Practical Guidelines On Fluid Therapy 2nd Ed

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Contents
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1. BASIC PHYSIOLOGY .................................................................................... 1 .
2. PRINCIPLES OF FLUID THERAPY AND

PHARMACOLOGY OF 1.V. FLUIDS ........................................................... 11
3. FLUID AND ELECTROLYTE DISORDERS ............................................... 56
4. FLUID THERAPY IN MEDICAL DISORDERS ......................................... 128
5. FLUID THERAPY IN DIABETES MELLITUS ........................................... 172
6. FLUID THERAPY IN RENAL DISEASES ................................................ 186
7. APPROACH AND MANAGEMENT OF ACID BASE DISORDERS ........... 195
8. FLUID THERAPY IN CHILDREN ............................................................. 231
9. FLUID THERAPY IN SURGICAL PATIENTS ............................................ 262
10. FLUID THERAPY IN SPECIAL SURGICAL DISORDERS ...................... 286
11. EVALUATION AND PRESCRIBING FLUID THERAPY ............................ 308
12. PARENTERAL NUTRITION THERAPY ................................................... 317
SUG.G ESTED READINGS ........................................................................ 376
INDEX ......................................................................................................... 379
ABBREVIATIONS ....................................................................................... 390
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CHAPTER ~
ONE
BASIC PHYSIOLOGY
BODY WATER 1 UNITS OF MEASUREMENT 4

Distribution 1 Moles and millimoles 4
Normal value 2 Equivalent and milli equivalent 5
ELECTROLYTES 3 . Osmotic pressure 9
Distribution 3 Osmolality and osmolarity 1O
Normal value 3
First of all let us see the distribution of fluids in the body, which will help us
in understanding the subject.
Total body water:

Total body water content.is about 60°/o of body weight in an young adult male
and about 50°/o in an young adult female. Since fat contains less water, an
obese person will have proportionately less body water as compared to a
lean person. In new born infants the proportion of body water in relation to
weight is as high as 80°/o, which declines with ·age.
Distribution of body fluid : ·':.

:-·.
Out of total body water two third (40o/o. of body weight) is intracellular fluid
(ICF) and one third (20% of body weight) is extracellular fluid (ECF)
(Fig-1.1).
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For b~tter Ul'.'\derstanding, distribution of fl_uid volume in :a 70 kg .man is
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summarized below :. .
Table No. 1.1 ~ Di.stribution of fluid volume

Fluid Type Total ICF ECF Inte rstiti al Plasma
..
% of Body Weight 60% 40% 20% . i 5°i~ · · ·53 ·
Volume for 70 kg weight 42.0''L 28.0 L 14.0 L 10.5L ·- 3.5 L

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Normal water balance
Fig. : 1.3 shows how body maintains its water _balance. The Kidney have a
major role in this· balance.
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CH. 1 : Basic Physiology 3
Oral (or l.V.) fluid intake and urine output are important measurable parameters
.of body fluid balance. To determine daily fluid requirement of body we need to
know insensible fluid input and loss as summarized below :
Insensible fluid input= 300 ml water due to oxidation.
Insensible fluid loss= 500 ml through skin
= 400 ml through lung
= 100 ml through stool
Fluid loss - Fluid input - 1000 - 300 ml - 700 ml.
NORMAL DAILY INSENSIBLE FLUID LOSS= 700 ML
Fluid loss = 500 ml. through moderate sweating
(Abnormal) = 1.0 - 1.5 liter through severe sweating/high fever
= 0.5 - 3.0 'liter through exposed wound surface
(burns) and body cavity (laparotomy)
So h.i~her amount of water ~s lost during exercise, abnormal perspiration,

pyrexia, burns and surgery. This basic information is needed to calculate
daily fluid requirements in patients on 1.V. fluids.
. . - . .
In a no"rmal pe.rson daily fluid requirement is the sum of urine output and
insensible losses. In normal person daily insensible loss is 700 ml. So daily
.fluid requirement = urine output+ 700 ml.
After water distribution, we will see distribution of electrolytes (summarized
i~ Table No. 1.2). Majo.r cation is sodium in _ECF and potassium and
magnesium in ~ ICF, while .major anion .is chloride in ECF an.d phosphate,
sulphate and proteins in ICF (Table No. 1.3). ·· ·
Table No·. {.2 : The electrolyte cone. of body fluids. (mEq/L) .
Electrolytes (mEq/L) ECF ICF
Sodium 142.00 10.00

: Potassium . . 4 .30 .
.. 104.00 _,. 2.00
Chloride
Bicarbonate 24.00 6.00
Calcium 5.00 .. . 0.01 -/
Magnesium . 3.00 40.00 ./
Phosphate and .Sulphate 8.00 150.00/
4 CH. 1 Basic Physiology
Table No. 1.3: Major ions in ECF and ICF .
ECF ICF
Major Cation Sodium Potassium and Magnesium
Major Anion Chloride and Bicarbonate Phosphate, Sulphate and Protein
Units of measurements
It is important to understand basic terminology ·used to measure
concentration and composition of body fluids and their inter relationship.
Ions · An ion is an atom or group of atoms with an electric charge.
Anion : When ion has a negative electric charge it is called anion (i.e.
er HC0 3-). ·
Cation : When ion has a positive electric charge it is called cation (i.e.
Na+, K+, Mg+2 ).
If cation and anion is confusing, here is the simple method to remember.
Anion - 11 n 11 - negative charge
Cation- "t"- + positive charge
Different ways by which solute concentrations can be measu.red are
milligram p_er decilitre (mg/di), milliequivalent per litre (mEq/L) or
niilliosmoles per litre or per kg (mOsmol/L or mO_smol/kg).
Moles and millimoles :
A mole refers to a specific quantity. One mole of any nondissociable
. .... .·.- substance contains the same number of particles (approximately 6.023 x ·
-.. <· :.- 10~.3 ). So 1 r:nmol of Na+ contains the same number of atoms as 1 mmol of
··. ·'.cr_:-·ev.en though their atomic weight differs (1 mmol contains 23 mg Na+
·:·· .. , · against . 35.~ mg Cr) e.g. If one dozen mango and one dozen banana are
·. cO"nipared .theirrnumbers are same but weights differ ..
. ·>.M~le : .On_e mole .(mol) .of any substance is defined as the atomic or
· .- · · ·. molecular weight of that substance in grams.
·· . :. ·. _ ~imilarly, ·one millim~le ~(mmol) is equal to one-thousandth of a mole or
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CH. 1 : Basic Physiology 5
So to determine amount of any substance in one mole, we need to know

atomic (molecular) weight of that substance (Table No. 1.4).
Table No 1.4 : Atomic and molecular weights of important substances
Substances Symbol or formula Atomic or molecular weight
Calcium Ca 2 + 40.1
Carbon c 12.0
Chloride ion er 35.5
Hydrogen ion H+ 1.0
Magnesium ion Mg2+ 24.3
Oxygen 0 16.0
Phosphorus p 31.0
Potassium ion K+ 39.1
Sodium ion Na+ 23.0
Ammonium NH .. 18.0
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Bicarbonate ion HCO. 61.0
3
Phosphate ion PO 3 • 95.0
4
Water H20 18.0
The atomic weight of Na+ is 23. So 23 mg is 1 mmol and 23 mg of Na+ in 1

litre of water presents a Na+- concentration which is 1 mmol/L.
Equivalent and milliequivalent :

Equivalent is a relative term, it refers to mole of ionic charges.
Equivalent : An equivalent is the atomic weight in grams, multiplied by
the valence.
For ions which carry a single charged mole equals an equivalent (i.e. Na+,
K+, c1·, H•). But if the ion carries charge that is greater than one, numbers
are no tonger equal. For example a mole of calcium ion (Ca+ 2 ) equals two
equivalents.
So equivalents = moles x valence
Comparision of normal value of serum electrolytes concentration in mEq/L
and mmol/L is shown in Table No. 1.5.
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6 CH. -1 : Basic Physiology
Table No·. 1.5: Normal plasma electrolyte concentrations
Electrolyte m'Eq/L mmol/L
Cation·s
Na+ 142.00 142.00·
K+ 4.30 4.30
Ca2+* 2.50 1.25
Mg2+* 1.10 0.55
Anions
c1- 104.00 104.00
Hco - 3
24.00 24.00
* The values ~f Ca 2+ and Mg 2+ include only the ionized (unbounded) form of these
ions.
Molecules must be quantified in moles (e.g. 'a mole of glucose') because

they carry no charge. However in practice they are usually measured in .mg
or gram because of simplicity and convenience. To conve~ from mg/di to
mmol/L the following formula can be used
mmol/L = mg/di x ·1O
Atomic weight
Ions can be quanUfied as either"moles or e·quivalents.
a. Why terms mmol or mEq are us.ed rout'inely instead of. moles ·or
equivalents ? ·
A. As concentration ·of most of the molecules ·and ions are very low in
serum, their measurement is convenient in mmol or mEq rather than
moles or equivalents. In day to day· work we use millimeter which .is
·. '1/1,000 of meter. :In same. way .mmol ·or mEq is 1/1,000 of. mole or
equivalent. If we look at value. of serum potassium . it,is 0.004 mole or
. . . equivalent/L. But after conversion it is 4 mmol/L or mEq/L, which is a
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CH. 1 Basic Physiology 7
The relationship between mEq ·and mg ~
1. To convert from milligrams per deciliter (mg/di) to milliequivalerits

per · I it re ( m·E qIL) , · the to 11 owing f'o rm u Ia can be · u·s e d
m Eq/L = mg/di x 10 x valence
mol. weight
Example:
If 1 gram salt (NaCl) is added to 1 litre of water, what will ·be ·its
concentration in mEq/L?
NaCl 1 gm/L = 1,000 .mg/L = 100 mg/di .
Valence of NaCl = 1
Molecular weight = 58.5 (Na mol. wt. 23 and Cl mol. wt. 35.5)
mEq/L=100x10x1 =17.1
58.5
1 gm NaCl/L = 17.1 mEq/L
So 1 gm of NaCl contains 17.1 mEq sodium and 17.1 mEq chloride ·
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or Na concentration of NaCl = 17 .1 mEq/gm .
2. To convert mEq/L to mg/di following formula can be used
mg/di = mEq/L x rriol. weight
10 x valence
Example:
If 1 litre of NaCl solution contains 154 mEq of NaCl, how much (mg/
di) is the amount of NaCl ? . .
' '
NaCl mEq/L = 154

Molecular weight = 58.5 (Na mo~ wt 23 and Cl mol wt 35 ..5)
Valence= 1
So mg/di = 154 x 58.5 = 900.9
10 x 1
So for NaCl 154 mEq/L-= 9009 mg/L (900.9.mg/di)
1 mEq/L = 58.5 mg/L
.·. ~o t mEq contains 58.5 mg salt
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8 CH. 1 : Basic Physiology
. the end of both equations (Na

If we look at these values derived at Eq contain 58.5 mg NaCl)
· · 17 1 Eq/gm of NaCl and 1 m
concentration .1s ·. m · . h eability of routinely used
it will be ·useful in the calculation and interc ang ·
substances.
Conversion factors useful in day to day practice are summarized in Table No.
1.6.
Table No. 1.6 : Conversion between mEq and mg
Salt mEq Cation or Anion/gm of salt mg of salt(mEq

. 58
NaCl 17
KCI 13 75
NaHC0 3 12 84
Calcium gluconate 4 224
Calcium chloride 14 73
Mg SO~ 8 1-23
Examples of conversion :
1. Find out k+ concentration .in mEq in 10 ml ampoule of 15o/o KCI
1O ml of 15°/o KCI = 1 .5 gram KCl/ampoule :
1 gram of KCI contains 13 mEq of K+ (as per table no. 1.5)
So 1.5 gram KCI = ·1.5 x 13=·19.5 mEq of K+
Answer: 1O ml amp. of 15°/0 KCI contains 19.5 mEq of potassium.
2. Find .out Na concentration in mEq in 25 ml amp. of 7.5% NaHC0
3
.... ·25 ml of 7.5°/o NaHC0 3 =1.86 gram NaHC0 /ampoule
3
1 gram of NaHC0 3 contains 15 mEq of Na (as per table no. 1.5)
·:s o 1.86 gram NaHC0 3 = 1.86 x 12 = 22.3 ·mEq of Na '. ·
): 1 nswer : 25 ml amp .. of. 7.5% NaHC03 contains 22.3 mEq .of Na.
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CH . 1 Basic: Physiology 9
Os·m otic pressure -and osmolality

Osmotic pressure
Osmotic pr.essure determines the ·distribution of water among the different
fluid compartments, particularly between -the ECF and ICF.
The osmotic pressure generated by a solution is proportional to the number
of particles per unit volume of solvent, not to the type, valence or weight
of the .Particles. To generate .osmotic pressure, the solute must be unable
to cross the eel.I membrane.
Osmole (Osm)
It is the unit of measurement of osmotic pressure. One osmole is defined
as one gram mo,ecular. weight (1 mol) of any nondissociable substance
(such as glucose) and contains 6.023 x 1023· particles.
Milliosmoles (mOsm)
mOsm is 1/1,000 of an osmole. So in relatively diluted fluids in body; the
osmotic pressure ·is measured in milliosniole per kg of water (mOsm/kg).
An osmole (or mOsm) of substance such as glucose which does not
dissociate into ions, is the same as mole (or mmol). However; a .mole of
salt such as sodium chloride, which dissociates almost completely into
sodium and chloride ions, equals 2 osmoles.
Osmolality and osmolarity
These laboratory values reflect the .relationship between solute and . solvent.
Osmolality
Osmolality of a .solution is determined by the amount of solute dissolved
in a solvent (i.e. water) measured in weight (kg).
If a solute is dissolved in 1 kg ·of water (solvent), the concentration of
solution is called· osmolality and is expressed as mOsm/kg of the water
solvent.
When osmolality is high, solution is more concentrated. and when osmolality
is low solu-tion is diluted.
Osmolarity
Osmolarity of a solution is determined by amount of .solute dissolved in a
solvent (i.e. water) measured in volume (litre).
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·cH. 1 ·: · Basic Physiology
If a solute is di~solved rn 1- litre of .water (solvent), the ·concentration

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solution is called osmolarity and is expressed as mOsm/L. · .· : ". . f
Remember : ·when solvent is measured in ·litre - "r" - Osmolarity
11 11
and when solvent is measured in Kilogram - 1 - Osmolality
As' temperature can affect volume of solvent as well as volume of solute
in-the solution, it can affect the value of osmolarity of the solution.
. .
So osmolality ·(mOsm/Kg), which is determined ~y . weigh~, of solvent is more

accurate than osmolarity. However, the difference between these two values
is negligable and osmolarity is easier to measure, so it is used more
commonly.
Osmolality of any solution is measured by measurement of its freezing point.
Plasma osmolality :
Plasma osmo_lality is determined largely by sodium salts, with less~r
contribution from ions, glucose and urea. Normal plasma osmolality is 285 ~
(275-29!;>) mOsm/kg
·. Plasma = 2 x Na + Glucose (mg/di) + BUN (mg/di)
Osmolality 18 2.8
Effective osmolality :
The .effective plasma (~CF) osmolality is determined by those 'so!utes in
the plasma which do not freely permeate cell wall and act to hold wate·r
within the ECF.
S6·lipid ·so1uble solutes such as urea, which can cross the cell membrane,
does not contribute to osmotic pr.essure gradient between ECF and ICF. So L'
·urea, . although .contributes to determination of plasma osmolality, it does '
not contribute to effective osmolality. Therefore there is a difference between
· .; ·.::~:·.. - .·total osmolaltiy and effective osmolality.
. j · ,;, .' · Effective Osmolality · = 2 x Na (mEq/L) + Glucose (mg/di)
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.· Under ·n ormal. circumstances, glucose accounts for only 5 mosm~kg in

·.effe.c tive .osmolality. ·So ·normally plasma sodium· concentration 15 the
.. . -·: ·determinant and reflector .of:. ~he plasma osmolality .. : · ·
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CHAPTER
TWO .
BASIC PRINCIPLES OF FLUID THERAPY AND

PHARMACOLOGY OF l.V. FLUIDS
INTRODUCTION 11 SPECIAL FLUIDS 32

BASIC PRINCIPLES OF Sodium bicarbonate 32
FLUID THERAPY 12 Potassium chloride 35
COMPOSITION OF l.V. FLUIDS 14 25% dextrose 36
BIRD'S EYE V{EW ON · COLLQID SOLUTIONS · 37
CHARACTERISTICS l.V. FLUID 15 Albumin 38
CLASSIFICATION OF l.V. Dextran 40
FLUIDS . 18 Gelatin polymers 42
PHARMACOLOGY & CLINICAL Hetastarch 43
BASIS OF l.V. FLUIDS 18 Pentastarch 45
5% dextrose 19 GUIDELINES FOR FLUID
Inverted sugar solution 21 THERAPY
Isotonic ~aline (0.9% NaCl) 22 . Fluid therapy in hypovolemia 45
5% dextrose, 0.45% NaCl 23 Monitoring fluid therapy 47
Dextrose saline 24 CVP monitoring 48
Ringer's lactate 25 Pulmonary artery wedge
lsolyte-G 27 pressure measurement 50
lsolyte-M 28 Methods to calculate rate of
. lsolyte-P 30 fluid infusion " '
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al1 ;sp ecialitie·s ·th~re arises a need ·to give .l.V. fluid. ·
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1
:. · ' f .o r .proper ·fluid therapy it is necessary to know :

.· ·:<(J} · E~io,logy . qf. fluid defici_t and typ~ _of ~lectr~lyte imbala~ce pr~sen-~.
~;:..-\:<:(2)~ ·:_, Assbciated·· illn~ss · (i.e. OM, HT, IHD, r~nal or hep~tic disorders _etc.)
_<;:.:J3) : cli~ical status (hydr~ition, vital -d.ata, urine oµtput etc.) ..
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·.. \{'};f'6traHonai"ahd>adeqtiater·t1uid therapy "it is neces·s ary to answer following

~:'.~{titttffi-esti.on~ · : · · ·.- .· . · · · · ·" ~ · · ,, . ·
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to·giveJ .v ~ flt.Jid . ~nd. when to ~yoid ?
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::.' ~~)~~~y3~:·;\":\'Hov/' h1uch · fluid to"give and ·how to calculate it ?
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4. At which rate l.V. fluid is to be infused?

How to calculate the drop rate ?
5. What are the contraindications of different. types of 1.V. fluids and why?
6. How to correct electrolyte im.b alances ?
7. When and how to use specific fluids ?
After such detailed evaluation necessary fluid therapy is planned and ordered.
BASIC PRINCIPLES OF FLUID THERAPY

As a principle, oral route is always preferred over I. V. route. But I. V. fluid
therapy has great importance in. various clinical problems.
Basic principles of l.V. fluid therapy are summarized.
Advantage:
.Y Accurate, controlled and predictable way of administration.
L Immediate response due to direct infusion in intravascular
compartment.
/ . Prompt correction of serious fluid and electrolyte disturbances.
Indications :
Fluid therapy is widely used for restoration of fluids and electrolytes, as a
drug carrier and for nutrition . Most common and important indications are :
1. Conditions when oral intake is not possible e.g. coma, anesthesia,
surgery.
2. Severe vomiting and diarrhoea.
_3. Moderate to severe dehydration and shock, where urgent and rapid .
:·_: . ,- c-~~~:::--· ·_·,' .: .. . r:~'-tfuid replacem'ent is' needed.
-"
4. Hypoglycemia where 25°/o dextrose is life saving.

· _?· .- ~s _
a vehicle for various l.V. medic~tion e.g. antibiotics, chemotherapeutic
agents, insulin, vasopressor agents.
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-- 6. Total parenteral nutritio~. ~

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.Treatment of critical problems : Shock, anaphylaxis, severe asthma
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cardiac arrest and forced diuresis in drug overdose, poisoning, urinary

stone.
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CH. 2 Basic Prl ncipl.,s of Flui d Thomp y nod Pt'H.tmrnco logy of LV . Flu ids 1a
Disadvantag s :
1. Mor :. exp nsivel needs strict asepsis.

2. Pos sibl e only in hospitalized pa tient un der skill ed upervi sio.n .
3. Improper selection of type of fluid used can lead to seri ous probfems .
..i. Improper volume and rate of infusion of fluid can be life threatening.
5. Improper technique of administration can lead to compfications.
Contraindications :
1. l.V. fluid should be avoided if patient is able to take oral ·fluid.

2. Preferable to avoid l.V. fluid in patient with congestive heart 'failure or
volume overload.
Complications :
1. Local:
Haematoma, infiltration and infusion phlebitis.
2. Systemic :
Circulation overload with rapid or large volume infusion espe.cially in
patients with cardiac problem.
Rigors, air embolism and septicaemia.
3. Others :
F;~uid C'·onta~i~ation,
fungus in I. V. fluids, mixing of incompatibl.e,drugs.
·improper technique of infusion, ·1.v. set or l.V. catheter related problems
and human error related problems.
u-~
.. . .
· Table No .. 2.1.: Compos~tion of common 1.V. solutions (mEq/L) ....I.
·-.
Dext.*.: . ·.. Na K Cl Acet. Lact. NH 4 CI Ca Mg HP04 Citr. mOsm/ ()

' :c
I\)
5% Dextrose 50 - - - - - - - - - L
CD
Q)
U>
,. 0.9% Saline - ·154 - 154 - - - - - -- - 278 (')
·1 •••
iJ
:::!.
::::J
" D-5%, 0.45% Saline 50 77 - 77 - - - - - - - 308 (')
"'O
CD
U>
Dextrose Saline 50 154 - 154 - - - - - - - 432

-,,
0
c:
c.
Ringer's Lactate - 130 4 109 - 28 - 3. - - - 586 -t
::::J"'
..,
CD
lsolyte-G 50 63 17 150 - - 70 - - - - · 274

Q)
"'O .
'<
Q)
::::J
c.
lsolyte-M 50 40 35 40 20 - - -. . - 15 - .580
iJ
::::J"'
Q)
..,
lsolyte-P 50 25 20 22 23 - - - - 3 3 410 3
Q)
(')
0
.. 0
lsolyte-E 50 ·140 1_0 103 47 - - 5. ·3 - 8 .. 368 cc
'<
Dext. : Dextrose Cl : Chloride NH4 CI: Ammonium Chloride _HP04 : Phosphates

-
0
<
Na : Sodium · Acet. : Acetate
,,
Ca : Calcium Citr. : Citrate c:
a.
K : Potassium Lact. :·Lactate Mg : M~gnesium en
* Dextrose concentration is in gms/L

CH. 2 Basic Principles ·of Fluid Therapy and Pharmacology of l.V. Fluids 15
COMPOSITION OF LV. FLUIDS
For proper selection of 1.V. fluid we : nee~ to r~memb.er its comp9sition

(Table No. 2.1 ). . · · ·
1
BIRD S EYE VIEW ON CHARACTERISTICS OF l.V.-FLUIDS
Before . going to fluid therapy let us assess ·and dear the b~sic. concept
about I. V. fluids.
Q. Which is the most physiologicalLV. fluid ? W~y?
A. Ringer's lactate is the most physiological ·fluid becau·se its constitution

:is similar to extracellular fluid (Na-130, K-4, . Cl-109, Lactate
(bic·arbonate) 28, and Ca-3 mEq/litre)
·a. What is the daily requirement of sodium "in a normal person ?

How much sodium does one litre of isotonic saline contain ?
How much I~ V. Isotonic saline should be given to supply the same ? ·
A. The daily requiremet of sodium is about 100 mEq (5.9 gram salt - NaCl)
. . 1·
One gram .of NaCl contains 17.1 mEq Na. , .

One litre of isotonic saline contains 154 mEq Na or 9 grams of NaCl.
. So -650 ml of l.V. isotonic saline is enough to.provide normal requirement
of sodium (provided there is no abnormal lo~s).
a. Among.st routinely.used 1.v~ fluids, which fluid has maximum sodium and
chloride ? How much ? · '
A. (1) Amongst routinely used l.V. fluids, isotonic saline and DNS (154
· mEq/Lor 9 grams ·of NaCl/L) have maximum sodium. · '. ·
~ - . (2) Amongst routinely ' us,ed l.V~. fluids, . isoto~'ic sal°ine, DNS and
·.· · · : lsolyte-G (154 mEq/L) ·have maximum chloride. :· ·· ·
16 CH . 2 : Basic Principles of Fluid Therapy and Pharmacology of f.V. Fluids
a. What is the sodium content of various I. V. fluids?

A. Sodium concentration (mEq/L) of various I. V. fluids is as follows :
Table No. 2.2 : Sodium concentration of I. V. fluids
Sodium N. S. lsolyte-E Ringer's lsolyte-G lsolyte·M lsolyte-P 3%-Naci

ONS Lactate
rnEqil 154.0 140.0 130.0 630 40.0 25.0 513.0
Q. Which I. V. fluid contains maximum potassium ? How much ?
A Potassium content of various J.V. fluids is summarized below.
Table No. 2.3: Potassium concentration of J.V. fluids
l.V. fluids tsolyte-M lsolyte-P lsolyte-G tsolyte-E Ringer's
Lactate
K· (rnEq/L) 35.0 20.0 17.0 10.0 4.0
So it is very important to remember that lsolyte·M has maximum

35 mEq/L potassium while Ringer's lactate has Just 4 mEQ/L potassium.
Q Which l.V. flu ids directly correct acidosis and how?
A. I. V. fluids which directly correct acidosis are lsolyte-E, lsolyte-P,
lsolyte-M and Ringer's lactate.
lsoly1e-E, lsolyte-P and lsolyte-M contain acetate (lsolyte·E =47, P=23
and M=20 mEq/L). This acetate gets converted into bicarbonate in
the liver and thereby corrects acidosis.
Ringer's lactate has 28-mEq/L lactate. This lactate gets converted
into bicarbonate in liver and lhereby corrects acidosis.
a. Which I. V. fluid directly corrects metabolic alkalosis ?
A lsolyte-G is the only I. V. fluid which directly corrects metabolic
alkalosis. Ammonium chloride (NH,CI = 70 mEq/L) present in lsolyte-
G gets converted into H· and urea in the liver. Addition of this H· corrects
alkalosis.
a. Which fluids are avoided In renal failure ? Why ?
A. Fluids usually avoided in patients with renal failure are lsolyte-M.
lsolyte -P, lsolyte-G, lsolyte-E and Ringer's lactate.
CH . 2 : Basic Prlnclplos ol Fluid Therapy and Pharmacology ol 1.v . Fluids 17
Because of fear of develop Ing hyperkalemia, I. V. fluids with high

potassium like lsolyte-M, lsolyte-P and lsolyte-G are used cautiously.
Ammonium chloride in lsolyte-G gels converl ed into H· Ion and urea
and therefore may aggravate uremic acidosis.
In severe uremic acidosis, conversion from lactale lo bicarbonale by
liver may be impaired. So lactate in Ringer's lactate may aggravale
metabolic acidosis.
a. Which l.V. fluids are avoided in liver failure? Why?
A. Usually Ringer's lactate and lsolyte-G are avoided in patients with
liver failure. Lactate in Ringer's lactate gets converted into bicarbonate
by liver. In liver disease laclate metabolism is impaired and may lead
to laclic acidosis so Ringer's lactate is avoided.
Ammonium chloride in lsolyte-G gets converted into H· ion and urea
by liver. In liver disease this process is impaired, so lsolyte-G leads
to accumulation of ammonium chloride. Collection of ammonia may
precipitate hepatic precoma or coma. So lsolyte-G is avoided in severe
liver diseases.
0 . Which flu id does not contain glucose ?
A. Isotonic saline and Ringer's lactate do not contain glucose and,
therefore, are the preferred fluids for diabelic patients.
a. Which fluid does not contain sodium and chloride ?
A. 5°;0 , 1Q0/o and 20°/o·dextrose are the only flu ids which do not contain
Na and Cl. lsolyte-M and lsolyte-P have low Na and Cl.
Q. Which fluid does not contain potassium ?
A. Isotonic saline, DNS and 5°/o, 1Oo/o and 20o/o -dextrose do not
contain potassium (so no fear of hyperkalemia in presence of renal
fai lure).
a. Which fluids do nol treat metabolic acidosis and alkalosis directly ?
A. Dextrose solutions, isotonic saline and DNS do not treat metabolic
acidosis and alkalosis directly. (Because they do not contain acetate,
lactate or bicarbonate which correct acidosis or ammonium chloride
which corrects metabolic alkalosis).
18 CH. 2 Basic Principles of .Fluid Therapy and Pharmacology of I. V. Fluids
CLASSIFICATION OF l.·V.· FLUIDS
I. V. fluids can be divided into three groups.
1. Maintenance fluid 2. Replacement fluid 3. Special fluid
Maintenance Fluids :
Maintenance fluid replaces fluid lost from lungs, skin, -urine arid faeces.
These losses are poor in salt so this. maintenance fluid should be
hypotonic to plasma sodium. Routinely used maintenance fluid is 5%
dextrose, dextrose with 0.45°/o NaCl solution (dextrose with half isotonic
saline). · ·
Replacement Fluids
Formulate~ to correct body fluid deficit caused by losses · suc·h as
gastric drainage, vomiting, diarrhoea, fistula drains, intestinal oedema,
oozing from trauma, infection, burns etc. Commonly used replacement
fluids are Isotonic saline, DNS, Ringer's lactate, lsolyte-M, P and G.
Special Fluids
.Special fluids_ are . used . for the special indications such as
. .
hypoglycem_ ia, hypok~lemia and me.tabolic .acidosis.

Commonly used speci~I, fluids are 2~ /o-dextrose, inj. sodium _bicarbonate 0
and i~j. p~tassium c~loride:
PHARMACOLOGICAL AND -C LINICAL BASIS OF l.V. FLUIDS

\
. For p/oper· ~electio_n, . of I. V. fluids we need t<? know composition,

pharma'.colog.ical basis, iriiporta~t indi.cations · ~nd contraindications of
,c ommonly used I. V. fluids. Following flwds are discussed here.
· c1°> .5%-bextrose, (2) i n~~r~ed sugar solutions, (~) 1soto~ic s_~rine, (4)
·,, _ %-Dextrose, Sodium ~hlo~rde 0.45%, (5) Dextrose saline (6_) Ringers lactate,
5
'._ · :<·'ir)~·:::J~oJyte-G_ , _ ;(~) rsolyte-M, (9) lsol~te-P, (10) ~so_lyte-E~ ·
' .· .·. :~>.: >:? .: ~:~~· ::·:~~ . . >. .: · . :·~-- · ··. :. .
. ' :·· · ·; ·' . . _ .. .

·
. :-· · .... . . .,
' .. .
.~ ' ,·~: :
.. . · ..·· . :' . ' .

-·. ·:
.- ...·. '
.
; .
·-'- ; .
.
.,
..
CH. 2 Basic Principles of Fluid .Therapy and Pharmacology of l.V. Fluids 19
5o/o·Dextrose
1. Composition :
One litre of fluid contains :
Glucose 50 grams'
2. Pharmacological Basis :
5°/o-dextrose (D-5°/o) corrects dehydration and Supplies energy. After
consumption of glucose, remaining water is distributed in all
compartments of body proportionately. Therefore D-5°/o is the.best agent
to correct intracellular dehydratign. D-5o/o is selected when there is
need of water but not electrolytes.
5°/o-dextrose solution (50 gm dextrose per litre) provides 170 Kcal/L.
1 gm of hydrous dextrose supplies 3.4 Kcal.
3.. Indications :
1. Widely used fluid for prevention and treatment of dehydration due to
inadequate water intake or excessive water loss.
·2. Cheapest fluid fo ·provide adequate calories to bodt ·
3. For pre and post-ope.rative fluid replacement.
4. For l.V. administration of various drugs.
5. For treatment or prevention of ketosis in starvation, diar.rhoea,
vomiting and high grade fever. ·· ·
6. Adequate glucose infusion proteets the liver against toxic substances.
~rrection of hypernatremia due to pure water los~ (e.g. diabetes
- i'nsipidus)_. Hypernatremiadue to salt poisoning or excessive use
_of electrolyte solution needs infusion of 5%-dextrose with frusemide.
_!Q. promote Na excretion and correction .of hypernatremia..,· ·
4. C«~Jl.'raindications : · . ·· · ·
~ · . Ce~ebral oedema· : Because :of its hypoton~c ~atur~ 5%-~.extrose
- aggravates cerebral_ oedema,
-~Neurosurg· i~al pro~edures: As 5°/.o-dextrose increases intracranial_
... . presspre, it can cause .damage during neurosurgery and so .must
be avoided.
·-
. , ,:
·' ; . · , ·· ·
20 CH. 2 : Basic Principles of Fluid Therapy and Pharmacology of 1.V. Fluids
3. Acute ischaemic stroke : Glucose containing fluid should not be

used after acute ischaemic stroke as hyperglycemia aggravate~
cerebral ischaemic brain damage.
4. Hypovolemic shock : 5°/o-dextrose is not the right fluid to select
because it does not substantially increase intravascular volume.
Moreover, fast replacement by large volume of D-5o/o can lead to .
hyperglycemia and osmotic diuresis leading to increased urine
.. output. s.o correction of dehydration w·ill be delayed.
5. Hyponatremia and water intoxication : By providing . electrolyte
free water 5°/o-dextrose worsens both conditions.
6. Hypernatremia : Fast infusion of 5°/o-dextrose· rapidly corrects
severe hypernatremia, but this correction occurs slowly in brain
cells, so swelling of hypertonic brain cells occur. This may lead to
serious or permanent neurological damage. Moreover, rapid
infusion of dextrose induces osmotic diuresis, which can aggravate
hypernatremia. So correction of hypernatremia should be done
gradually with D-5°/o or with low sodium containing fluids.
7. Blood transfusion :' Dextrose
.
solution
.
and whole blood should not
be administered thr~ug~ the same l.V. line as haemolysis and
clumping can occur.
8. Uncontrolled diabetes and severe hyperglycemia.
5. · Precautions :
' '
1. l.V. administration of dextros~ s9lution (especially hypertonic)

may cause local pain, vein irritat~on
. .
and thrombophlebitis.
2. . Pr~lori"ged l.V. administration of 5°/~~d~xtro~e can cause hypokalemia,
hypomagne,saemia and ~ypophosp~atemia.
#9
. 6. Ra~e of administration :
Dextrose in water can be given intravenously safely at a rate of
0.5 gm/kg body wt./hour without causing glycosuria. This is ~quiva!ent
to '6 66 nil/hour 5°/o-dextrose or fructose solution, or 333 ml/hour
1Q0/o-dextrose. 1 litre of 20°/o-de,Ctrose should be infused slowly within
. 6 hours. It is useful to test the urine for sugar at regular .i.ntervals
·· ; .. / during .dextrose infusion to . rule out glycosuria and the assodated
:_:.- .~-<::.": : f1hictross due to osrp.o tic di_uresis. ,
. ·.
,. ;. :· .·· ~--·,-..;· '. .~·~:/'~<·:_.>· . . '"'. ·. ._ . ' .· '-: _,_:··:< ...
... ......
> -· .
, r l • • ' • ,
' ' . ~. ! .... . ~ .- .:-·~ -~:· . .. .
.· ·•
: . . .• •::· . -.
'·-· .. ·-.. . . ... :'.' '
·, . : ~
.·· ·.• . .
'• • • I - • ' • .
~ : I ·.: ~·;' ..._ '~- '
~ ' .~ .. . .
CH. 2 Basic Principles of Fluid Therapy and Pharmacology ·of 1.V. Fluids 21
Inverted sugar· solution

1. Composition :
One litre of fluid supplies :
Inverted sugar 100 gm
' . .
Inverted sugar ·is a·n equimolar mixture, which contains half dextrose
and half fructose. Fructose is considered . to be metabolized ·ih the
absence of insulin. Therefore, it can be utilized mo,r,e rapidly than
dextrose, especia.lly in a diabetic patient. However, glucose is a
metabolic product of fructose and requires the presence ·of insulin for
its metabolism.
3. Indications :
1. Treatment of nausea, vomiting including vomiting of pregnancy.
2. In patient with liver disease it provides glucose, prevents glyc'ogen
depletion and exerts protein sparing effects.
4. Adverse effects :
Large dose of fructose can cause lactic acidosis, hyperuricemi~ and
_. _... hypophosphatemia.
Contraindications :
· ·:- ~.l. · ·, Hereditary fructose intolerance.
2. -Cautious use ·in ·patients with impaired -kidney ·function 'or severe
.. ;· · .-.: ..:, liv_e.Ldamag~.
"
· · 3; · Less effective in treatment of hypoglycemia.·

·.' . ..
~~ 4. Gener~lly mor_e than 25 gm of fructose per day _is not
~{\·;.~. 14.~~. . .
~\~~:.~~:~;~ir-~9~:;r,» j·.. ,... (ecommended. .
1:;.~t't~r~;:5'.~1;~;~€1,.; {~iY~~-·~iJi':":,:;."". . - - .
~1~1.fr:.,:t~~~~~~{· :~~~~;:~tl.O V.~ft~~d ·:-sµga_r solution is ·m·ore ·expensive fluid.
~~t:~ ~ t~~~l~'f?:_y:t ,::< ,;~ <.\ 0' : ;>.: , . ..
, . I f F-,,,id Therapy nnd Pl·u nrnacology of l.V. Fluids
22 H' ~ , - ns1c Pnnc 1p os o - ~' - __
'~ '
Isotonic Saline (0 . 9~b NaCl - Normal Saline)
1. Con1position :
Sodiun1 154.0 n1Eq
Chloride 154.0 n1Eq
Each 1oo n1l contains : SodiLm1 Chloride 0.90 gm
2.. Pharmacological Basis :
Sodiun1 chloride is present chiefly in extracellular fluid maintaining
osn1olal-ity of ECF. So isotonic saline is used to provide major
extracellular electrolytes.
During von1iting and diarrhoea along with water loss, there is a
substantial loss of sodium chloride. 0.9~'<> isotonic saline is very useful
to correct both fluid and electrolyte deficit.
As isotonic saline is distributed chiefly in extracellular fluid, it will
increase the intr~vascular volume substantially. There.tore, isotonic
saline is a very useful l.V. fluid to raise blood pressure in the patient
with hypovolemic shock. -
3. Indications :
1. Water and salt depletion as in diarrhoea, vomiting, excessive
diuresis or excessive perspiration.
2. Treatment of hypovolemic shock.
3. Treatment of alkalosis (e.g. vomiting) with dehydration.
4. In severe salt depletion or hyponatremia when rapid correction of
sodium is necessary.
-,· .. 5. Miscellaneous ·:
• Initial fluid therapy in diabetic ketoacidosis.
• Treatment of hypercalcen1ia.
• Fluid challenge in prerenal ARF.
• Irrigation for washing of body fluids .
.__ As a vehicle for certain drugs and can be given safely with blood. -
•r -:. ,"; ·.. " :, ~: • .- '. ; ;:)(· .:'.~ ·_:-;:); , _ ,~_· ;:; :· -.' · ' . . •' ; ,
·.,,
·i ~
. ·1:·
:' . '
-: · , _;
," ,·.,
~ ; :..
_.,· -, , · ~ ·. '::~ r·'"·_ ..~·: .
, • I •
-·.
' .: '·
~ .......
CH. 2 Basic Principles of Fluid Therapy and Pharmacology of l.V . Fluids 23
6. Hypertonic saline 3°/o NaCl is used in treatment of hyponatremia

due to SIADH or water intoxication (along with frusemide), as it
provides greater sodium in lesser fluid volume (Na concentration
513 mEq/L in 3°/o NaCl versus 154 mEq/L in 0.9°/o Na.Cl). 3°/o. NaCl
is available as 250 ml bottle commercially.
4. Contraindications : ·
1. Cautious use or avoid in . hypertensive or preeclamptic patients
and in patients with oedema due to congestive heart.failure ,. renal
disease and cirrhosis.
2. Careful administration to very young or elderly patients.
3. Dehydration with severe hypokalemia : With severe hypokalemia
there is deficit of even ICF potassium so infusion of isotonic saline,
without additional potassium supplementation, will aggravate
electrolyte imbalance of ICF.
Dextrose with half strength saline
(5°/o-O,extrose with 0.45 °/o NaCl Solution)
1. Composition :
Sodium 77 mEq Glucose 50 gm
Chloride 77 mEq
Each 100 ml contains : Glucose 5.0 gm and Sodium chlo'ride 0.45 gm
2. · Pharmacological Basis :
As this fluid contains 50°/o salt as compared to NS or DNS, it .is used
.. I
when there is need for calories, more water and lesser salt
·.~ :' "· . ' replacement. ' . .,. . ..·
-. . ;f . ~- ... • ' . . . ' . : • ' .' •, ' . .
.· -. ... ~· · ·:._ : A~qufrem.ent of w~ter is. greater in paediatric group as compared to

.. ., ) '' . t ~ • • ' • ' • ~ • • . .
(:~:-~·:: ...<::_-:·'. .a(fult~. · Jitoweve{, sal't requirement is same in both groups. In paediatric
:. "-.: :. ,:,:- '_.. . '~iroup. ratio of requirement of water : NaCl is about double as compared
t6 _ a~ult . group ~ ·so·: this· is a suitable replacement fluid in paediatric
~-,_ ;. . ··p atient.' "' ·: :..
· .· .· .· _in a no,rmal person loss of NaCl by skin, urine ·and stool is very less .
. .:· ·<··.:;.:;~imilarly :in ·the . eaEIY post -operative period there is retention _of salt
·:_: ·.·. .· _.·so,_only minor loss occurs~ Thus by·supplying .calories, moderate NaCl
. . . . •' . . . .
~
. · ' t
·;i ' : '
.
• ' I .·, ', • . • ' . ..
' . . . ~ .
·.,'t '°
24 . Therapy an d Pharmacology of I. V. Fluids
CH. 2 : Basic Principles of Fluid
· and required water, this. fluid

. becomes su1·table for maintenance
. and
early post operative fluid therapy.
3. Indications :
1. Fluid therapy in paediatric patients.
2. Treatment of severe hypernatremia: As it corrects hy~ernatremia
gently, it avoids cerebral oedema, and is therefore sa e .
.3. As maintenance fluid therapy.
4. Early post operative period.
4. Contraindications :
1. Hyponatremia.
· 2. Severe dehydration due to diarrhoea and vomiting where there is
need for larger salt replacement.
Dextrose Saline (DNS)

(5o/o Dextrose with 0.9°/o NaCl Solution)
1. Composition :
Glucose 50 gm Chloride 154 mEq
. Sodium 154 mEq
Each 100 ml contains : Glucose 5.0 gm and Sodium chloride 0.90 gm
This fluid has advantage of both 5°/o-dextrose (to provide energy} and
. '· isotonic saline (to provide salt). So DNS is_useful to supply major
extracellular electrolytes.(sodium and chloride) and energy a'iong with
fluid to correct dehydration.
'.
Like 0.9% isotonic salin_e it rapidly corrects NaCl deficit ·of ECF. As ··
DNS is distributed chiefly in ECF compartment, unlike D-5o/o it does
not correct intracellular dehydration. ,
:As .bNS increases only ECF volume, it can be considered in treatment
· · :··.. "' .oLdehydration
.. with hypovolemic shock. . But like D-5%, faster
.
. .~ . .. ' . ·. .·~ .
_.: __!\ .
.:= ·_ !' - ..... •• ,, -
. .· ··;
. .· . ' .
CH . 2 ~ Basic Principles of Fluid Therapy and Pharmacology of 1.v. Fluids 25
infusion of large volume of DNS will lead to large glucose load (> 25
gm/hr)J leading to hyperglycemia induced osmotic diuresis. So in
presence of incompletely or partially corrected shock patient will have
increased urine. output.
Unlike D-5o/o DNS is not hypotonic (due to NaCl) and hence it is
compatible with blood transfusion.
3. Indications :
1. Correction of salt depletion and hypovolemia with supply of energy.
2. Correction of vomiting or nasogastric aspiration induced alkalosis
and hypochloremia along with supply of calories.
3. Fluid compatible with blood transfusion.
4.. · Contraindications :
1. Anasarca : Cautious use in anasarca of cardiac, hepatic and renal
disease.
2. Hypovolemic shock: Not preferred in severe hypovolemic shock,
when rapid replacement with larger volume of fluid is required.
Rapid infusion of DNS can cause hyperglycemia and osmotic
diuresis even in presence of fluid deficit. So the simple logic tp use
DNS for supplying salt solution to correct shock and providing
energy simultaneously is not correct.
Ringer's lactate (RL)
Calcium 3mEq
Bicarbonate 28 mEq
. . _: .- '
Each 100 ·ml contains :

.· . .. Sodium lactate 320 mg, Sodium chloride 600 mg, Potassium chloride
. -;·: ~ · Ao mg .and ~a. 16ium ch10.ride.. 21 mg
.... ·.' _.,: .. ,. . .~ ' . ' . :"": ..~ .. .
' ' '
• • • J •.•• •• :_ .' •
.·•':<f {~;~n· P
26 CH .' 2 · · Basic Pri nci pies of Flu id Therapy and Pharmacology of I. V · Fluids [:i. ·~lt1
-. . · ..... , •.
!' -.·
('. ~: > .-~ ·:. •c I'
- . -~ ! -. . . . .1;1
.... j I -
;,:>.·.:-'_.j
2. · ·Physiological Basis : 1 • _ ·· it
!.
" Because of high sodium concentration p'30 mEq/L), Ringer·~ lactate 1·- -
-·
'. .
.
'
· "
"" :~1
..
(
f . .,
.
-6·
,
.A
;-
rapidly expands intravascular volume and so it is very effective in a:
treatment of severe hypovolemia. Ringer's lactate is the most
-._-(~;~
.. .
.
physiological fluid as its electrolyte content (i.e. Na, Kand Ca) 'is nearly r • 8.i
f
~-·· :<~... similar to the free concentration in plasma. So even larger amount of
.·.
. .. .
·· '
•
~~
1
RL can be infused rapidly without risk of electrolyte im~alance. .. <! ••

·o
• • • ' .r
.. ~)
. . . . ''1
. ·:~ Sodium lactate in Ringer's lactate is metabolized in liver to bicarbonate . . . 1. r

. . .·')
~ As RL provides bicarbonate, it is useful ·in correction of metabolic tt
.: :..,
. . ·~-.'~ acidosis. As Ringer's lactate not only supplies all electrolytes but also b
. ·. : ...~
. · . ·.~. < provides bicarbonate, it is very useful in many surgical conditions .
-:>-_)J
·. · ·.:; 3. Indications :
1. Correction of severe hypovolemia rapidly with large fluid volume. 1·. com1
2. For replacing fluid in postoperative patients, burns, fractures, One I
peritoneal irrigation etc. I
I Glucc
·3. Diarrhoea induced hypovolemia with hypokalemic metabolic acidosis I Sodil
-·is effectively treated. with RL. RL is the fluid of choice for initial Pota~
.~ . '
treatment of diarrhoea induced dehydration even in paediatric practice.

I ., ~oo r
4. · In diabetic ketoacidosis, RL provides glucose free water, so corrects
· ·.- Nac1
metabolic acidos.is with added advantage of supplying potassium.
I. · · Sodil
I - .
5. For maintaining normal ECF fluid and electrolyte balance during
and after surgery .. . !_ · } .· Phy-~
. I" ~~ :·· :.~ _:· Durn
·
:..
_.. _.• .
4. Contraindications : 1
· 1 ~-: ·i, . ·· : _ 9ast
1. ~n liver dise_ase,. sever~ hyp~xia a~d ~hoc~, lactate m~tabolis~ ·:: J ,- : . .:\: Po .·
.1s severely 1mpa1red. Ringers lactate infusion can lead to lactic .. ·; --·:::·)< ·, ta
acidosis in such patients. . ·. . · .; !J~? ~orn
. 2. In severe CHF lactic acidosis takes place, which is more in he~rt ~ ): '.~_ {!?~· ; '. . ' ~~c
tissues. Lactate given cannot be utilized, so it worsens the problem_ ~ ,L:~ - ~~:<!\~-~:>l:~?l~
·-. ,:. - -<:.. ~-,~ - ·1 . A~~l
<1. ~} -~~< i~t- 1
3. A ddison's
. disease. . . · . -·,. ,
· · · 4. . seVere ~etabolic a?idosis where conversion fro;,, lactate to bi~~rbonate':fr :~7[t~~~~~

is impaired. So Ringer's lactate may worsen metabolic acidosis<;.:.: ~~ ,.~~~~~
. ~! ·~ '
,·,. ' r-;>
~ - :: . : .- .
...
· CH. 2 : Basic Principles of Fluid Therapy and Pharmacology of I. v. Fluids 27
5. ·1n vomiting or continuous nasogastric aspiration : Her~ hypovolemia·.

is associated with metabolic alkalosis. As AL.provides bicarbonate,
it wrn worsen metabolic alkalosis and, therefore, is riot preferred .
. 6. Along with blood transfusion : Calcium in HL binds.wi.th the citrate
anticoagulant in blood transfusion. This can inactivate the
anticoagulant and promote the formation of clots in donor blood .
.For this reason simultaneous infusion of RL and blood product in
one l.V. line Is contraindicated.
7. The calcium in RL binds with . cert~in drugs (i.e. amphotericin,
thiopental, ampicillin., doxycycline etc.), and reduces their
. bioavailability and efficiency.
•'
lsolyte-G
1. Composition : .
Glucose 50 gms Chloride .150 mEq
Sodium 65 mEq Ammonium 69 mEq
Potassium 17 mEq
100 ml of fluid contains :
: NaCl 0.375 gm, KCI 0.130 gm, NH 4CI 0;370 gm, Glucose 5.000 gm,
Sodium metabisulphite 0.015 gm
2. Physiological Basis :
During vomiting or continuou~» nasog.astric aspiration there is loss of
gastric juice. Gastric juice contains 60 mEq/L so·dium, 1 o mEq/L
potassium and 130 mEq/L chloride along with acidic content. So
vomiting or continuous nasogastric aspiration will lead to
hypochloraemic, hypokalaemic metabolic alkalosis .
.lsolyte-·G is gastric replacement solution. It provides all electrolytes
lost by gastric juice, corrects alkalosis and provides calories.
Ammonium .ions in lsolyte-G are converted into urea and hydrogen
:. · ion· by liver .... H+ ion produced will replace the deficit of H+ ion. cau~ed .
· .~ :_. ·, by .IOS$ of gastric juice. lsolyte-G is the only available 1.V. fluid .which .
· · directly corrects metabolic alkalosis of any nature. ·
{~,~..... '_ '.
7·' . _ £.
··. .'_
. • ! . • -. ·~
. ·.
:." i
... . ·. ·
~\
'· ·' ....
..··
_. ' _. ..· . " . ~ '
.. , _ . . ·"::''- .-.-·: ·':'.
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• • ' · .- • •• • ' • •\ ·- ' ; '• •
., . .._, ~ )- ~ ~~: ./': . - . . . ._,-.
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. .
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. . .... ... .. ~ ~
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- .·. ·.: ~ . .
' '\ ,: ... ·i .. . . .- . . .. .' -~· -.· • . .: ....
. . . . :. _.,
.. . : , ·. . , • - · :·
. . ·2ti .• . - 6-~t . 2{ :-
.. •' .. : .: ..~. . .. · .. ·. , ;..
·. ··.
..•. . . 3.- ' · lrldicatiOns,: Z~~if{~~~~;}' 'i .' . ··· . . . . ... • ~ , · · . .. ..•. • . · · .:C;: /< ·'\ .. ,
·_ ,;"~. '.:'.:·~::-JI;,.·:~-·~tlf:: v~mmA~f~~riti·~·~-ontinuo"u·s gastric _aspiration 'to- replace loss ot/?_~
. . ·... :·, _ ~-. ::<·?t\:~~: \.· >:gastric ju'ice ~ ·. >-': · · · · ··· · · · · · ·. . Y
·,•>::i.<_::··'·~~.~/:;:,~ 2. In treatnierH of metabolic alkalosis due to excessive administration -·,
/·."< :- .,_ " · of sodium bicarbonate or aggressive diuretic therapy. ·
1. Hepatic failure : In severe liver disease ammonium ions in lsolyte-G
will not be converted into H+ ion. Accumulation of such unchanged
am_monium ions may precipitate hepatic precoma ·in severe liver
disease. Moreover this process of conversion ·of ammonium ions
into H+ ions will be an additional load to the already sick liver cells.
2. Renal failure : lsolyte-G may aggravate uremic acidosis (due to
addition to H+ ions) and may lead to hyperkalemia in renal failure
(due to 17 mEq/L potassium). So in patients with renal failure
lsolyte-G should be used judiciously or avoided.
3. Metabolic acidosis : By providing H+ ions, lsolyte-G will aggravate
metabolic acidosis.
4. Severe vomiting with shock : lsolyte-G is contraindicated for
the initial therapy of shock due to vomiting because it carries risk
·. of hyperkalamia due to its high K+ concentration and poor ability
to raise blood pressure due to comparatively low Na+
concentration.
_lsolyte-M . ..
(Maintenarice solution with 5 °/o-Dextrose)
1. Composi~ion :
.. ' ... ·-
g~u:~!; of fluid su:g~:s: · Chloride 38 mEq :·§~

~~1~~~um
Each 1oo ml. Contains : . ·
~~· ~~~ ::~:!:ate .,J~~~~ >t<~ · · ·. · ·.:~ ,~:. .-·:: ::.··:~:?);j
.... Glucose 5.0 gm, NaCl 0.091 gm, Na ·acetate ·0.280 gm, ~KGI O~ ~:.5··0' · :)~.··.• fu..1.:·«·).~~
.
· Dibasic potassium phosphate 0: 130 gm, Sodium · met~~i.sul8hit~(Q:; 9?·1r~;~()J1~

.... 9 1~
gm · ·x .• ?)'
2
\,,if~l§f~fi~::~:.
·CH. 2· Basic Principles of Fluid Therapy and Pharmacology of I. V. Fluids 29
2. · Pharmacological Basis :
lsolyte-M is the richest source of potassium (35 mEq/L), so.very useful
to treat hypokalemia. However, always ensure good urine output or normal
renal status before its infusion.
Proportion of electrolytes in lsolyte-M is almost similar to the
maintenance requirements of the body. Additionally, it corrects acidosis
and supplies energy. So this fluid fulfills the -needs of body electrolytes,
pH maintenance, caloric supply and water replacement and, so it is
the ideal fluid for maintenance fluid therapy and, therefore, named lsolyte-
. M. ,.
. .
As concentration of sodium is low (40 mEq/L) in lsolyte-M, it should be

avoided in hyponatremia. It is not the preferred I. V. fluid in patients
with significant salt and water depletion.
3. Indications :
1. For parenteral fluid therapy, it is the ideal maintenance fluid.
2. To .correct hypokalemia secondary to diarrhoea, .bilious vomiting,
. prolong~d infusion of potassium free l.V. fluids, ulcerative colitis etc.
4. ContraindiC.a tions :
1. Renal failure : Cautiously used or totally avoided in presence of
significant renal failure (ARF or CRF) due to potential risk of
hyperkalemia.
-· 2. ·Hyporiatreniia and water intoxication : As ·Na+ concentration of
lsolyte-M is much low (40 mEq/L), it should be avoided.
··· :- 3~· AdrenoC"ortical insufficiency : These patients have abnormally high
potassium. concentration and, therefore, should not receive fluids
with high potassium.
: .:. _~ :·: ~- Burns,: In patient~ with severe burns potassium concentration may
. ,::·_ .' ·: :
. be ~bnormally
. ..
high
. .
due. .to tissue destruction and acidosis.
.
Moreover'
· such patients require fluid with high sodium concentration such as
· Ringer's _la<?t~te rather than hypotonic fluid such as lsolyte-M.
' ·.. \ ~. . . . . ·. ·, ·f;· . . ·~ ~ '. "; : .
' .. ·. . .' ' .. : ··.
: . ,:_;_ ..
I ' t ~ ,, :' I 1' • •
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• " l,',
. . ~
'·
<
. . .. .. .. ·· ~
. . . f "FI 'd Therapy and Pharmacology ·of 1.V. Fluids

30 - GH. :2 :·. Basic Principles o u1 - _
lsolyte-P
I:
t ··· .composition :· ·
· . One litre of fluid supplies :
Acetate · 23 mEq
Glucose 50 gms
HPO . 3 mEq
Sodium 25 mEq 4
Potassium 20 mEq Magnesium 3 mEq
. Chloride -- 22 mEq
Each 100 mi contains :.
Glucose 5.0 gm, Sodium lactate 0.260 gm, KCI 0.130 gm, MgCI 0.031
gm, Di_b asic potassium phosphate 0.026 ~m, Sodium
metabfsulphafe 0.021 gm.
2. Pharmacological Basis : -
lsolyte-P is designed to suit maintenance fluid requiremen_t.of children.
It provides electrolytes, maintains pH, supplies calories and replaces
water deficit. As c'ompared to adults, children need more water and
· s·ame electrolytes. So lsolyte-P provides almost double water but same
-electrolytes as lsolyte-M. Roughly lsolyte-P has half concentration of
electrolytes compared to lsolyte-M. lsolyte-P can be used in adults
when there is chiefly water loss and only small loss · of eiectrolytes
(e.g. ·hypernatremia)
3. Indications :
1. Chiefly used as. maintenance fluid in infants and children to provide
daily water and electrolytes. -
2. ~x~e~sive water loss or inabilit_y to concentrate urine (i.e. diabetes
ms1_p1dus). _ _. . · _
1. Hyponafrerriia: Am~ng all sod.ium containing l.V. fluids, lsolyte-P
has- least concentration
·h ·. - _ ·t w1·11 aggrava t e
of sodium (20. mEq· /L) , s o- 1
_yponatrem1a. -
2. Renal fail~re : Cautiously used in renal failure due to high
concentration of potassium (20 mEq/L).
' - ·. , • ,.
...
Basic Principles of Fl u1'd Th erapy and Pharmacology of 1.V. Fluids 31

'' ....·._.
·
:. .<.:. ":· 3_- . Hypovolemic shock : lsolyte-P is not the suitable l.V. fluid to
. . . correct ~ypovolemic shock (as with diarrhoea or vomiting) . due·
. . to following reasons :
(a) Becau~e of low Na concentration, ability of lsolyte-P to
correct mtravascular volume and hypotension is poor.
(b) In oliguric child, high K+ conce~tration (20 mEq/L) is not ·safe.
(c) Rapid infusion of large volume of lsolyte-·P can · c·ause
hyperglycemia and osmotic ·diuresis even in child with fluid
..... ,-- : deficit, which is not desirable.
lsolyte-E
(Extracellular replacement solution)
1~ ·: Composition :
Glucose 50 gms Acet.ate 47 mEq
.Sodium 140 mEq. Calcium 5 mEq
Potassium 1 O mEq Magnesium 3 mEq
Citrate . 8 mEq
Chloride 103 mEq
Each 100 ml contains : ·
Glucose 5.0 gm, NaCl 0.5 gm, Sodium acetate 0.64.0 gm, KCI 0'. 075 gm,
Sodium Citrate 0.075 gm, MgCI 0.031 gm, Sodium metabisulphate
·0.020 gm.
Pharmacological Basis :
lsolyte-E is extracellular replacement solution .. lsolyte-E has
electrolytes similar to ECF except that it has double the concentration
of potassium and acetate (which will get converted into bicarbonate).
Patients on long term fluid therapy may develop magnesium deficiency.
lsolyte-E is the only 1.V. fluid available which will correct magnesium
deficiency. So lsolyte-E provides all ECF electrolytes, additional . -~
potassium and acetate for maximum Capacity to correct metabolic .

·acidosis, supplies .energy and replaces water deficit. . _ ·
32 . CH. 2
. ·. '..
' • 3. ~ .~~i~~~~~~~'; ;' :,.;·/~'. 4 • ' • • ·' • • • : •• ~; • : p. ··.:- };/ '', ' ·. ' . . ·.. ' .. ; . . .
..
.,.
-:~
··.1
· .·.-·· _1. · Diarrhoea. . __ .· · ·i::··. . ,. : · ·> 1 :~. · · •
' 1
J
I
>: ·.2. ·. . Me.t.aboli~ acidosi~. ·. .': ~ ·_,: ·. :~: -~~ . ;J
. I
·1
' ' .. 3. '' In maintenao~~
J .. ·~ • ' - • ' >" f
of .~CFvolUme preoperatiVely.
.~~~ ~ ?~
... ~-··. . : .- • .~ .. .
· 1
. 4. :..~ontraindication~
-
:- . '
r • •
-
·>. ·.. . '
~ . - II
· ·'1:··_· · Vomiting·or continuous nasogastric aspiration will lead to metabolic

alkalosis due to loss of H+ ions in gastric juice. As lsolyte-E
. provides maximum bicarbonate (acetate 47 mEq/L) among all
commercially available l.V. fluids it will significantly aggravate
metabolic alkalosis.
2. Metabolic alkalosis due to diuretics or sodium bicarbonate.
SPECIAL FLUIDS
Commonly used special fluids are sodium bicarbonate (NaHC0 3 ), potassium
chloride (KCI) and 25°/o-dextrose.
Sodium Bicarbonate (NaHC0 3 )
1. Composition :
1. Commonly available and routinely used preparation is Injection
sodium bicarbonate 7.5°/o, 25 ml ampoule.
2. Each ampoule contains 22.5 mEq sodium and 22.5 mEq
·bicarbonate.
2. Indications :
1. Treatment of metabolic acidosis. ' '·
... ,..,: - ·.'
..._ ·~· ,•, \ -·.·.

· · 2. For cardiopulmonary resuscitation and shock.
3.
4.
• · .-· · t •
. . CH. 2 : Basic Principles of Fluid Therapy and Pharmacology of 1.V. Fluids 33
3. Guidelines for using sodium bicarbonate in metabolic acidosis
(A) When to use ?

MiJd .to mod~rate metabolic acidosis can be treated with Ringer's
lacta1e or lsolyte-E in addition to treatment of underlying disorders.
But in severe metabolic acidosis or in critically sick patients,
conver$ion of acetate or lactate to bicarbonate may be impaired.
So effective way to treat is with sodium bicarbonate.
(B) Why ·tO' treat metabolic acidosis ?

(i) Metabolic acidosis suppresses cardiac contractility. So if it
is severe and not treated well, it can lead to hypotension.
(ii) Persistent metabolic acidosis will consume bone buffers and
cause osteoporosis and rickets. Release of bone calcium will
lead to hypercalciuria and may lead to nephrocalcinosis and
nephrolithiasis.
(iii) Acidosis induced reduction in urinary citrate concentration
· (which is inhibitor of stone formation) also aggravates the stone
formation . .
(C) How much to give ?
Amo.unt of sodium bicarbonate required depends upon severity
of acidosis.
Amount'of,· NaHCO~ Required ( in mEq/L ) =
0.5 x Weight in Kg x (Desired HC03 - Actual HC0 3 )
Do not correct metabolic acidosis rapidly or completely.
Desired, value of HC0 3 is usually 10-1'5 mEq/L, and riot normal
· value of 24 mEq/L
; ' . ' .
· .· . (D). How to .infuse ? ·
,. '" fn absence of. contraindications, approximately 50°/o of the

.· . ··~ ..... ·. . "· . ·calculated deficit is corrected in 4 hrs and rest gradually over 24 hrs.
· · ·To avoid ·irritation of vein and sudden sodium loading, sodium
· bicarbonate is added to D-5°/o and infused at desired rate for correction.
•,' ..
' : .
·~:~ •' ,•·,
~ ~· ;~ .. ; '. .
~ . .. .
34 ·. c~:,·2 '.·Basic11;~{d~~;}~1i~~~~!!~:~:r:py:·a0d PhMmaCOl~gy:of.

.:\ ;I,:V./Flulds···.•.
.. .., , ..:i . '" ·.· .·
.. :·,
:•t; ~:'P'· Y:
-·.:~:_ 1~'.~~~l ":: ~pec~al·; pr~cautions .. .: 1 \<'·:::· '
· ,, · ..·.· ··. · ·. ·.. ·.· .· ·. .
- ~ ~:
..
:: ,_,.;· :_· ·, ·. '
,.· .':.' .. •.•....·.· • .
.·~ <··:··:>•. ···::·--~ ' ·:· ,_, ·· ·-
:· :\\~
.. >7~
: · . ::··_.>':.:··"'--).<·~··:, Ji) :·: Sodi.um bicarbonate should not be. gi:v~r--: a~. _bql,us ex~~pt i~ · .:;~~
· -': .· ·· emergency cases. . ·. ' ·- ··'" · . :"c
. · - ~'.,:~·"°:" ·:,·;.; (iif ·: As-sodfum bicarbon·ate·is-very: frritarit, " est~blis~ prop·e r large ·. :· ~
.::_'. ~ -~ ..-, <'- ·,. Lv·.-·. nne ·fof-infusioh .-:" Extravasatioh . of the same can lead to·
':·.;,: -~-- . . '·,· <: : .extensivejis~iit3· necrosis. ". . ."
. · ·. · .''(mf A~~id:·oJ~~Ci6~'~ 'and alkalosis by giving repeated small doses
'. I, ;. ' , " ~ .'·::; • ''! '• • ,,·--:, ' . , I • '
·· ··anctf1l_o·nitoring pH. ···

:(iv) .Never treat acidosis .without treating the .etiology. Common
r ~. ·etiologies are hypotension, diabetic ketoacidosis, diarrhoea,
:. · . • ;
. y-. . ,-~- sepsis, hypoxia, postoperative catabolic patients, uraemia etc.

(v) In presence of renal failure, treatment with sodium bicarbonate
may cause tetany or pulmonary oedema. So the safer treatment
will be dialysis, if acidosis and renal failure are severe.
(vi) Never correct acidosis without correcting associated
hypokalemia. By correcting acidosis, NaHC0 3 will shift
· potassium from . the extracellular compartment into the
intracellular compartment. It will aggravate hypokalemia which
can be life threatening. This is very important in treatment of
diabetic ketoacidosis.
(vii) Do not mix lnj. calcium with lnj. NaHC03 in the same syringe or
line: Combination can precipitate calcium carbonate as white
crystals.
(viii) Avoid mixing of lnj. NaHC0 3 with inotropes.
4. Complications :
l
1. Over· shoot, post treatment metabolic alkalosis.
l
I-
2. Hypokalemia ·:· Due to shift of potassium from ECF to ICF.
3. Volume overload : 25 ml of 7.5°/o sodium -bicarbonate contains
22.5 mEq sodium. (Normal requirement is 60-100 mEq/day). So · "~
aggressive treatment with large volume of sodium bicarbonate ... .·.~~·
will lead to sodium overload. If renal · status is normal it will be ..-. ·>
excreted. But if renal function is poor or if large volume is infus~d ~ ._:'._; :j:
rapidly, it can lead to volume overload, pulrnonafY _ oedema and : ):~ ,~~
hypernatremia. ·. . ·. -· ~--/~~'>j} ff,
,.., ,~\0t~1~~~f~' r
~<.: ~' . t ..
:. ... .
~·;, ·:-i. ~ ~
. ' :.. ·.
.,
·"· .
•• 1
r_. .,' ·
...
/ .· .
.
:, ·•
· ·.· CH: ~ : · Snsic Principles of Fluid Therapy and Pharmacology of I. V. Fluids 35
: ~ ·, Hypocalcemia - Tetany : Decrease in pH will lead to ·decreased

· ,:· . , · ionic calcium. I~ patient with chronic renal failure where pre-existing
hypocalcaemia is likely, rapid alkalization can lead to tetany. 1.V.
calcium gluconate will improve hypocalcemia-induced tetany, with
additional advantage of counteracting acidosis induced suppression
\,I "' of cardiac contractility.
5. · Contraindications :
- -~ · ·· 1.' Respiratory alkalosis, metabolic alkalosis and hypokalemia.
2. Correct dehydration, hypokalemia, and hypocalcemia prior to or
alorig with sodium bicarbonate treatment.
3. Cautious use in congestive heart failure, chronic renal failure,
cirrhosis of liver or hypertension. ·
Injection Potassium Ghloride

1. Composition :
lnj. Potassium Chloride 15% 10 ml ampoule contains :
1 ml = 150 mg potassium chloride = 2 mEq potassium
·1 Amp. = 1O ml = 1.5 gm potassium chloride = 20 .mEq potassium
Potassium is chiefly intracellular cation, but its presence in ECF is
; ·;.:: _very _important .for neuromuscular regulation. .
.· _··:·i;" ._
.Ability
of kidney to retain potassium is incomplete (unlike sodium) so
. ·. ··. about 20 mEq potassium is lost daily even in presence of hypokalemia .
.." . .. $0 to avoid hypokalemia, K+ supplementation is required in patient
· on maintenance fluid therapy.
·.·: .. Moreover in many conditions where sodium and potassium both are
.. :. .lost (Le. diarrhoea, vomiting, diuretic therapy etc.), kidney retains
.. sodium at the cost of potassium with resultant hypokalemia: Potassium
. ~~, · "" chloride is added .to various potassium free 1.V. fluids ~s potassium . . .· ,.
· . ~ ":-.·. ~. upplement.
.' ·.· :
··
. . ', "" •• t ·: • •
.. ·.:'1 ..·
· i ,·
. '
. . '•
. ,. '·
~.::~,· -'.~.:.>; , ' • ', , l "
. . .. . .. •. . . . . . -
i
t· •• ·, '. • • " , ; ,t ' ,' ,
l~<~i ' .' ·-~· ,'. ~.• ~ . '~ · t.i.t:°"•
I
-,..· • I'• ', 4 '• ' ' •; • ••• '.•: • -. ! • • •• ·. I ' . .,, ,
;' ;.·•··. ·.·.· ·...·. .·./ .·. • --> ·• .·. ,· · ·-.· .,•..•_. ;:~:- • ,;, ~· :.<~ 'c: -~ / ~ ' · ·..·..•.- -~uid~- -~ ; ~;.f v
· · ·· ·... .as . - CH>2 :\ Basic·: Principles «:>rF1ulc$i: J;.ft.e raP:yJifrrd ~~h~rm~c<;>logv:~rr. _ : ·<~- · -.-·_...,:_,·:. ,··/,"h~3~
. ' .. ,' ... ....· .. '. . . . :. '' :·, ;'.\},i·;': .•i~i 2'ef
.a .·. lnd1cat1ons . . . :.:,1·1_..,,.,
' • : ' ' '. ' I ' ' • • ·,_ .,, • • / • • '
< c., " •. ', .·h' ..:
' .- • ( . :• ... •
··--i·.~
j•. ·, ' • •_ ';. '
f
1 rr-'.· <' ' .·. .. •.· . ~ ' .:.-_: :,' : -~:~ ' --J; ~};:~i
'' t' ' • ' : •
' • • • • • ,•' ' ' r
.
~ •
' •• ~
'
:'·, ''.; '.· '
' ' • ~:.•
.. _ . - . : 1 ~ -·:.··Pot~-ssi~u· rll "ch.lo'rid~·:.i~-;~dded to various p«)tassiurfr.tree· }.V~':· ffuids ,-, :

. . ·. ':.·, .\:· ~.;~~.fb'r- f:>'ret~ntion hypokalemia in the patient on maintenance fluid · . of
·. · . .
.~ <.:~>: ·>·tnerapy or for treatment of hypokalemia. Normal' requirement of ..
· <·<;.:~~· '.: ;·;. · ·" potassium in an adult is .about 60 mEq/day. Improper use of injection
potassium chloride can cause hyperkalemia, which can be
dangerous and can cause sudden death due to cardiac arrest.
2. Added to potassium free peritoneal dialysis fluid to maintain proper I
potassium level.
3. During cardiac bypass surgery for achieving cardiac stand-still
after preparation of heart-lung bypass.
Basic Rules in Use of Injection Potassium Chloride

a Never give d~rect l.V. potassium chloride injection.
b. Always use injection potassium chloride diluted in infusion.
c. Never add more than 40 mEq potassium/litre
d. Never infuse more than 1O mEq potassium/hour.
e. Never add potassium chloride in lsolyte-M.
· f: Monitor serum K+ level closely and, if possible, also by ECG
monitor during infusion of high dose potassium.
1. Cautious use in renal failure as hyperkalemia is a potential risk.
2. · Never use injection potassium chloride without kndwing potassium
status. · · , .
Injection 25o/o-dextrose
. ·,
1. Composition :
' '
-· .·
Available as 25 ml ampoule and 100 ml infusion ·bottle. : . . .. ". '
100 ml· of 25°/o.;.dextrose contains 25 gm glucose. :. .; " , ; ...
··1.->.
\" '.
~·\~'.: _. · : CH. 2 : Basic Principles of Fluid Therapy and Pharmacology of l.V. Fluids 37
., · ---------------------------
·2. · Pharmacological Basis :
I:
Dextrose supplies energy and prevents catabolism. 25°/o-dextrose is a
·concentrated form, so it is useful when faster replacement of glucose is
:needed (like in hypoglycemic coma).
When patient is on fluid restriction (i.e. CHF, volume overload, cirrhosis,
oliguric renal failure) 25°/o-dextrose provides larger glucose in smaller
volume to provide nutrition.
3. Indications :
1. Rapid correction of hypoglycemia or hypoglycemic coma.
2. To provide nutrition to patient on maintanence fluid therapy.
3. For the treatment of hyperkalemia, with 1O units of regular insulin,
25°/o-dextrose 100 ml is infused to prevent hypoglycemia.
1. 25°/o-dextrose is contraindicated in dehydrated patient with anuria,
intracranial or intraspinal haemorrhage and in delerium tremens.
2. To be avoided in diabetic patient unless there is severe hypoglycemia.
5. Caution :
Rapid infusion of 25°/o-dextrose can cause glycosuria secondary to
hyperglycemia. So in absence of hypoglycemia, 100 ml of 25°/o-dextrose
.~ho.uld be infused slowly over a period of 45-60 minutes.
·.'
. ,.
.J • '
COLLOID SOLUTIONS
- ·Colloids are large molecules so when infused into the vascular space
· they are retain-ed within the vascular system unlike crystalloids. So colloids
_:are more effective than crystalloids as plasma volume expander. Colloids
·,~- . are about three times more potent than crystalloid fluids for increasing
:··Vascular volume and supporting the cardiac output. So in patient with
·- <h'aemorrhagic shock, when plasma or blood is not available immediately,
_·.<infusion of ·colloids to correct circulatory fluid volume is vital and often
,-.·,.life : s·~vih,g. However, to maintain adequate capacity to carry oxygen, blood
;:·~ransfusion is :required subsequently. The potency of colloid fluids as
: ...'. .~.. ' :
·-.·,..
.. ·.:. ,::
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. . .. ··_ ·'. ,;_:
. /;, '.· ...
... ~,...:;/;1l~~~;,;~',;, j~'. >:<i· <·.···... .•.•. :.·...·.· ' : ..' . :. : ..··. ;·/~!]
·;.: '. ~;~'.-~·, ;~~~,;!£.(9~~~. :~ _\!\~t'.Basi·q ;·Pri. nciptes 'Of - Fl~ld Therapy and Pharm-acotogy .(>f·. 1. V. · Fl,utds ~· :':,.- .·. ':.::. ~~
::~}_i~~k~i::;f: ; .:'. .. . . . . . . ' '
. . : .. . . ... . . • ;- ·, ~ ~:· •'· .
: ~-; ;.
I .' •. . i:. ;"
.. _< .·· ·~ ~itasm~ volu~e-expander differs with differ~ntcomm~rcia_lly.availabffco1loid<; ?ll

. fl~_i _~~--q_s . showr:Un.Table No. :2..4:.-- ;. .:: _-'i ··,I:. = :- ~ :-~ -: · - .•_·_,. - ·~ .' ,· · : ·' - ;· ·. - \ · -_:: :_ · - --~.~,? ~
.. . ~. : ·· . ~- ··.- . ~ -.. · . ·· .· .- . _.. .' ' ,: ·- -· · ·~., ~:~ ... · . : · t~· ~ . ~· .. ~. .! ..~ ~_;f':. · ~ j ·:: ~ · .:~ ' ~ • • : ' • • · - : . •• ·-~ • • _· : _ ',~· . · : '· . • ..
. - ·· c:::-r:·~ :~
:. .'. Table-No. _2.4 ·:· C..haracteristfC:s~>of:t.-v.

. .· . .: ' . . ...
. .
-coiloid :fluid_s per .1oo ml:i~fu~ion ._· ..·Vi~
. .. -; ..
:··_ . ~
. •...: . type offluid > _:._'.; : .$.ttecHv~'._ p.lasma 'volume expansion Duratioh" of\~xpan·si'o~ '{:1 ;;
· ·'. -5°/o - Atbull,li &\:~·E:~> :_r: fr-;\. :.'-:. ·.<;. · 70-130 ml · 16. hrs· · · ..
: ~2.5%: --. Albtfm{nt_.:/:.~ .:::}(_= . ·~ · · 400-500 ml 16 hrs ·..
. : ~
...
~% _ . ·ti~fa·s1a:rot(-.
. . .- -. . ·- · '\
"· _.:· ·1_. •. 100-130 ml 24 hrs
... 1 O~/c> , ; P~entastarch 150 ml 8 hrs
·: t.0. 01~;~....b~xi~~n~4o 100-150 ml 6 hrs
>. :.·;_~o/~ ..·Dextran-70 . 80 ml 12 hrs
Albumin
Albumin is a physiological plasma protein. Chief function of albumin is to
maintain plasma oncotic pressure (responsible for 75°/o of the oncotic
pressure of plasma). Other function of albumin is binding and transport of
low molecular substances like bilirubin, hormones, certain drugs etc.
Heat-treated preparation of human serum albumin is commercially available
in a 5°/o solution (50 gm/L) and a 25°/o solution (250 gm/L). As sodium load
is small, 25°/o albumin is also called salt poor albumin.
1. Pharmacological basis :
a. A 5°/o albumin solution (50 gm/Lor 5 gm/di) has a colloid osmotic
pressure of 20 mm of Hg (which is similar to that of plasma), and
expands the plasma volume to roughly the same as volume infused.
Approximately half of the infused volume of 5°/o albumin stays in
the vascular space. The oncotic effects of albumin last 12 to 18 hrs.
The 25°/o albumin solution has a colloid osmotic pressure of 70 ··
mm of Hg and expands the plasma volume by 4 to 5 times the . :
volume infused. Thus infusion of 100 ml of 25°/o albumin can · -·
increase the plasma volume 400-500 ml. This plasma_, volume. . . ·:t
expansion occurs at the expense of the interstitial fluid volurli~'-. ::):
(fluid shifts from extravascular to intravascular cornpartm~n.9,~~<~_ Ji:
so 25°/o albumin should not be used for volume resµsqitatiqn.,'.: .i.f!Ji.f~ f
patient wit~ fluid. deficit (~~povolemia). F~_r the ..- sam~{ r.e~~~9:?t4~j~i;
hypovolemic patient receiving hyperoncot1c _c.~.~cr:D~r~l~~-;~;N?;.~~::~"'·-. ~~
· ··),{~f~~ii~r :.
.? ,~ /·{I. ~:~.~~
....:~ -~~-<;~, ~~ .
~........
~ .. . . · CH. 2 ; Basic _Principles of Fluid Therapy and Pharmacology of 1. v. Fluids 39
-~'l· ·--~-----~------------------
·.
[: 25°/o) albumin should be adequately hydrated with I. v. fluids such

~~ . . .as isotonic saline or 5%-dextrose. Albumin is preferred in patients
t/ . with hypoproteinemia along with anasarca and oliguria where intention
~ - · ,. of albumin infusion is shifting fluid from the interstitial space to the
vascular space.
2. Indications :
a Plasma volume expansion : When rapid volume expansion is
required, as in acute hypovof emic shock, burns and severe acute
albumin loss, albumin is an ideal solution for replacement.
\ b. Correction of hypoproteinemia : Jn liver disease, diuretic resistant
nephrotic syndrome or malnutrition, infusion of 25% albumin is
f' very effective for short term management.
-~ c. As an exchange fluid : In therapeutic pfasmapheresis, albumin is
..
'• J
used as an exchange fluid to replace removed plasma .
3. Adverse effects :
~
Adverse effects are rare and include nausea, vomiting, febrile reaction
and allergic reaction including anaphylactic shock.
4. Precautions and contraindications :
a Fast infusion wiff rapidly increase circulatory volume with resultant
vascular overload and puf mo nary oedema.
b. Infusion of albumin solution is contraindicated in patient with
severe anaemia or cardiac failure.
c. . ·It should be given with caution to patients with low cardiac reserve
or cardiac insufficiency.
d. Dehydrated patients may require additional fluids along with
albumin infusion.
e. Albumin solution should not be used for parenteral nutrition.
· 5. How much to give ?
· The amount of albumin solution administered will depend upon the
clinical condition of the patient and his response to treatment.
..... . For adults .an initial infusion of 25 gm of albumin is suggested. (e.g. 5~0
.·, . ml of a 5% solution or 100 ml of a 25% solution). A suggested rate. IS
· -·! ·• 1 to .2 ·m'- per·minute {5% albumin) or 1 ml per minute (25% afbumrn)
a~though high rates may be needed in the treatment of shock. . ·
. .
• • •· 'I
.. - ,. ; ·:·.: · ..-· .. •• • • J
..... . .. . . . .· ·:. . .. . :·'·>·..'·; #

40 CH.2
•
Basic •. .
Pnnctples of· Fl uId Th e· ra p:y and Pharmacology of I..V._Fluids
Dextran
The dextrans are . gIucos · · e· polymers produced by
. bacteria
. (Leucohostoc)
._ ..
incubated in a sucrose medium. Dextran is avat!able in two forms, .with a.
·· · 1·1t· of 70 , ooo (dextran 70) and with a molecular weight of
mo 1ecu lar. we1g
40,000 (low molecular weight dextran, dextran 40).
1, Pharmacological basis :
1. Plasma volume expansion :
Both forms effectively expand intravascular volume but dextran
is not a substitute for whole blood because it has no oxygen
carrying property. It is not a substitute for plasma proteins
because it has many limitations including lack of clotting factors.
Dextran-40 as 10°/o solution produces greater expansion of plasma
volume than dextran 70 as 6°/o solution. But comparative duration of
expansion with dextran 40 is shorter due to its rapid renal
excretion.
2. Improvement of microcirculation & prevention of thromboembolism :
Low molecular dextran improves microcirculation independently
of simple volume expansion. It minimizes the sludging of blood
that may accompany shock and prevents intravascular
aggregation of RBC and improves microcirculation in conditions
or procedures associated with impaired circulation.
2. Indications :
1. Correction of hypovolemia : For short term rapid expansion of
plasma volume in conditions such as shock or impending shock
from burns, surgery, haemorrhage or trauma.
2. Prophylaxis of deep vein thrombosis and postoperative and
post traumatic thromboembolism.
3. To improve blood flow and microcirculation in threatened vascular
gangrene.
3. Side effects :
1. Acute renal failure : Rapid renal excretion of dextran 40 · t· t
. , . · - . m pa 1en s
with reduced unn e flow can res ult in high urinary conce t ... ·t·
· h· . .· . n ra 1on ,
. w.h 1c increases urinary vi scosity ancf may ca use oliguria or renal
failure.
' .. · .; '
•. . ··"· .; . • '. ·. ·- .. . :· .. . .
CH .. 2 : Basic Principles of Fluid Therapy and Pharmacology of I. v. Fluids 41
•.-.- ----------------------------
·~ ·Hypersensitivity reaction : As dextran is a potent antigen,
sensi.t ivity . reactions are known to occur, but with better
manufacturing techniques incidences have decreased (less than
.·10°/o)~ Untoward reactions consist of itching, urticaria, joint pain
· and on rare occasion anaphylactic reactions (incidence as low
as 0.032°/o) .
. -
3..-. .Dextr~n may interfere with blood grouping and cross matching.
1. Severe oligo-anuria and renal failure.
2. Known hypersensitivity to dextran.
3. Sever~ CHF or circulatory overload.
4. Bleeding disorders such as thrombocytopenia, hypofibrinogenemia
etc.
5. ·. Severe dehydration.
5. Precautions :
1. Dextran should be administered with caution in patient with
a. lmpair~d renal function or oliguria
b. Active haemorrhage.
c. Chronic liver disease
d. Patient at risk .of developing pulmonary oedema or CHF .
. 2. The haematocrit should not be allowed to fall below 30.
·: 3. . Correct ·dehydration before or at least during dextran infusion to
maintain adeq·uate urine flow arid prevent ARF.
:.· · 4~ The anticoagulant effect of heparin is enhanced by dextran.
-.·" ··,. 5. · As d~xtran m~y interfere with blood grouping and cross matching,
co.llect a~~ · p_re~erve _ blood sample prior to infusion of dextran.
·. : . r· . ·
· .: ..> 6.. .-.;Along with de>e~ran infusion, patient may requirf3 blood, coagulation
' •, \ ' - • ' ' •' ' I ~ I
'":... _.- ·-, .. . .: factors or ~1~.c.!rqlytes .

;. ; ,.
,:; ' ' .

; -~ .
.. ... . . ~ .
- . . .
.',IJ
- . ,. ·~ . . . .~·.: ~ :;,i
: ;~· . - ·: . .· .. .!
: ..' ~: . ;
; ' ' ,·
. - . .
". ~'
.. · .. .
42 CH. 2 Basic Principles of Fluid Therapy and Pharmacology of I. V · Fluids
6. Administration :
A. Dextran-40
It is given by l.V. infusion as 10°/o solution in 0.9o/o NaCl or so;0
glucose. The dosage depends on the pa~ient's ~eed: Adult person
with shock usually requires 500 ml of rapid I. V. infusion. In the first
24 hours total dose should not exceed 20 ml/kg. Dextran-40 can
be given subsequently in dose of 10 ml/kg/day upto 5 days.
Regimen for thromboembolism

Day-1 : 500-1,000 ml over 4 to 6 hours.
Day-2 : 500 ml over 4 to 6 hours.
Up to 1o days : 500 ml over 4 to 6 hours on alternate day.
Regimen for surgical prophylaxis :
500 ml of dextran given preoperatively and daily postoperatively
for 3 days.
8. Dextran-70
Dextan-70 is given l.V. as 6°/o solution. The total dose should not
exceed 20 ml/kg in the first 24 hrs and 1O ml/kg on subsequent
days.
Gelatin Polymers (Haemaccel}

Haemaccel (500 ml plastic bottle pack 3.5o/o solution).
It is a sterile, . pyrogen free, colloidal plasma volume substitute, which
contains a polymer of the degraded gelatin with electrolytes.
1. Composition :
Each litre contains : Polymer from degraded gelatin 35 gm

(Molecular weight 30,000-35,000)
.. ·· ·. · Sodium 145 mEq
Calcium 12.5 mEq
· - Chloride . 145 mEq
Potassium 5.1 mEq
,. -·
· .: • •.•• t,
.. ' .
,•. - .
.. : i,
.. ·
CH . 2 Basic Principles of Fluid Therapy and Ph armacology of l.V. Fluids 43
2. ·• Indications :
· ·· i. · ·For
. .· rapid
. . expansion
. of intravascuar volume and correc· t'ion of
hypote~sion in shock, burns, trauma and intra or postoperative
blood loss.
ii. Prophylactic use in major surgery to reduce total volume of
·fluid replacement.
iii. For priming of the heart lung machine.
3. · Advantage :
i. It doe~ not interfere with coagulation, blood grouping and cross
matching.
ii. It remains in blood for 4-5 hours and expands plasma volume by
about 50°/o of infused volume.
4. Precautions :
L ·,It contains no preservative, so ensure clear solution before infusion.
ii. Gelatin is plasma expander like dextran so needs almost similar
precaution.
iii. It contains calcium, so it should not be mixed with citrated blood
as calcium may cause clotting. ·
5. Side effects :
i. Hypersensitivity reaction (flushing, urticaria, rigor etc.)
ii. Bronchospasm and fall in blood pressure.
Hetastarch (Hydroxyethyl Starch)
Hetastarch is a synthetic colloid available as 6°/o solution in isotonic saline.

Hetastarch is .a: starch that is composed of more than 90% esterified
. · amylopectine·. Esterification retards degradation, which leads to longer
plasma expansion·. 6°/o hetastarch, which is normally used, has molecular
:_:.·:_weight of 4,~0,000.
~ - . -: ;
Pharmacological basis :
J After LV. hetastarch infusion, molecules with lower molecular weight
. .. -
· -~ '" ' , (about40°/o . of dose) are readily excreted in urine in 24 hours. Larger ·.
molecular weight fractions are metabolized and eliminated slowly. · · c . ·,
,·· ' '
- - ;(:·~ :. ' '

. '• .: .:. - -- .
~\~t - ' - ' .. l .• ~. ~ . .
' .. - ~ . ·' .. .. ... ~ . ·. . . . . : ..

'
. :. • .. · . . . •.: · . .-
·· : ·' · : -·
: . . . . . ._ :
_ . __> --. _; • _- · • •._. -_ • >;Ai_Ji~:~f_ff~::-_> ·-_._.- .•. -.-.. :•·- :. -·•._.-·. ·
-44 CH. 2 : : :·a~s.IC··. Prlnclpl~~,~of ~· Fl_uld 'f ti. ~t~PY ~nd ·Pharm~cotogy of.I. v.·Ftu1 0$._
· _, .- :.i
.. .. :,. .. . •, .....· <·· :~ .. ·; ::·;=-. -~: :. ...-.~. .' . : . .; ' ... _ · 1~· ~f~
. .. .·. Heta~~a~ch ~xpand~ ~;r~ulatory

plasma volume Ilk& serum
· _. , :···,· .d~xtran. It ha.s a calculated osmoJarity.of approximately 31 OmOsrnJL ··:
~l~um1n a~~
· · · ·._· . ·Hetastarch i_ s slightly ·more potent than 5°/o album.~n : ~s coHoid. Jt has·~·- ·
higher colloidal osmotic pressure .than 5% albumm (30 versus 20 ·mm.
. Hg, respectiveiy) a~(:t9_a9.se~ . g·reater plasma.volume expansion (upto,
. ·30°/o greater than~~n.eJnfused volume.) The expanded plasma voJurrie. J
. may last for ~4 h~U~s: ·. _ ~j
2. ~dva_!'~ag~ -::·: · ...
i
·.· : _
.-.·.· -~: :._:.. L ·. ·> Nonantigenic, fewer antigenic properties as compared to dextran.
~ . ,. ,
l '
.'. :, ·'; ,' .'. . ii. Hetastarch does not interfere with blood grouping or crossmatching.
:". ' ~ --.
! .. .·. ·. .~
.! l ~ ..
iii. Hetastarch is less expensive than albumin .
i·
iv. Plasma volume expansion greater than 5°/o albumin.
v. Expands plasma volume for a longer period, effect lasts fo r
about 24 hours.
3. Disadvantage :
i. Increase in serum amylase concentration during and 3-5 days
after discontinuation of hetastarch. So serum amylase
concentration can not be used to diagnose acute pancreatiti1s
during this period.
ii. Like other colloids, it has no oxygen carrying capacity, so one
should not allow haemotocrit to fall below 30°/o after an infusion.
4.. Adverse effects :

Hetastarch is not antigenic. However allergic or sensitive reactions .
can occur i.e . vomiting, feverishness, urticaria wheezing etc~ · I . .
Anaphylactic reactions are extremely rare (incidence $S l·o. ..

0.0004°/o) · · · ·· ._,,
.
. ' -'~
· . r,• !
. .: !. -. __ .~
Indications : .- _;._'. <.· .- ·· .··: :..:.:>~'.~

5.
It is a safer and effective plasma expander, whtch ~IQtai~s' ~~f
volume tor a longer period. Indications are to· co.rr c~1-~~~*~.}Jl~,,;;~
and shock· same as descrlbod under dextran . .- ·:.:;;·.:\>t~2~·i~~~'. f.~ · "'
.' • !ci;:1~t~~' .
··<:;~·~.'.".· '.~·'". ~- .·
·~- ' - ,/
'
I •
· ·CH.
. .
2.:
. .'
Basic Principles of Fluid Therapy and Pharmacology of 1.V. Fluids 45
Contraindications are similar to dextran, chiefly bleeding disorders,
congestive heart failure or impaired renal function.
7. Administration :
The dose of hetastarch depends on the patient's needs. The usual
adult dose of hetastarch 6% solution is 500 ml to 1 litre. The total daily
dose should not exceed 20 ml/kg
Pentastarch
Pentastarch is a low molecular weight derivative of hetastarch that is
available as 3°/~, 6°/o and 10°/o solution in isotonic saline. Pentastarch
differs from hetastarch in having a lower degree of e·sterification. As
pentastarch contains smaller but more numerous starch molecules, it has a
higher colloidal osmotic pressure. So it is more effective as a volume expander
than hetastarch. 10°/o pentastarch can increase plasma volume 1.5 times of
the infused volume.
Indications, contraindications and side effects are similar to hetastarch.
GUIDELINES
'
FOR FLUID THERAPY IN HYPOVOLEMIA
.
Q. What are the common causes of hypovolemia ? .
A. Common c~uses of hypovolemia (loss of salt and water) are diarrhoea,
vomiting, excessive diuresis due to diuretics or renal diseases, burns
and high grade fever.
Q. How to evaluate severity of hypovolemia?

A. Clinical ·evaluation of volume depletion :
Mild (<2 litres in adult) ·
Thirst
Concentrated urine
Moderate (2-3 litres in adult)
As above, plus :
··Dizziness, weakness.
· ·Oliguria (< 400 ml/day)
Postural hypotension > 20 mni Hg systolic. ·
Low .JVP
' . : . : .·. - .
.. . ~- . ·.. .
. " . . ...
,. ·
..
'
- . ' .· :·' ' ' - ·. . ·,:
( . ..
- ~~ ..:· .~ '. ,:, . .. . ." - '" ,'.
.·...· .·.•·. · .· .~Y;R< \ :' . ;";:.:'~'i~;\:;''. ·· .< .. . · . · . . . . .

e;,'.2·.:;~asic
·..·· .• •·••• ·. . .46 · ·• Princ1p18s ~; Fluid T~e~apy; ~nd •Phar~a~~~i;f:?t~•:f fluids
. .- .· /. ;''. : •' :. . ~ .
- ' .•
. " '. .
.. Severe (>3 l_itresin adult).~. - ~~ ·,:~·:.~·:· -:.:<:;_:,__:--· . ·. ·_::. . . · ~. '' ~ . ·, -· ·.. :::. _>\f
<... · . , As .a.bove, plus . _; .:;.-.::~-~(~-}~~<<_. :·":,:·.· . :: :. · ·. > ·.-· ,'_.· ·
Confusion, stupor.~:. ; ·':--~:·,~ ·,·.- . . · · -. · · - ·
' Systolic BP -~- '1.-00" mm Hg . .
, . Tachycardia (not in elderly), low pulse volume
, -.... .... -Cold -extremities, poor capillary return.
::,.· ,·.. ,_.:;... '. ·Reduced skin turgor (doughy feel) I·
·. Q . . ~ow much fluid should be given to correct hypovolemia ? f

·A:
?.
It is usually difficult to estimate volume deficit in a hypovolemic patient. t
1
If patient's normal weight prior to fluid deficit is exactly known, loss

of weight will reflect the extent of fluid deficit. Above mentioned clinical
criteria can provide only rough idea about severity of fluid deficit.
If the haematocrit (Hct) value prior to fluid deficit is known and there is
no blood loss or haemolysis, following formula can be used to calculate
extracellular fluid deficit.
ECF deficit (L) = 0.2 x lean body weight x ( Current Hct - 1 )
Normal Hct
As extent of fluid deficit in a hypovolemic patient cannot be calculated
precisely, patient should be closely monitored clinically and by
laboratory data to assess adequacy of fluid repletion.
Q. Which fluid should be selected for initial replacement to correct
hypovolemia associated with hypotension ?
A. Fluid selected for initial volume replacement in patient with hypotension
due to hypovolemia is isotonic saline. Saline corrects hypovolemia
effectively by replacing lost sodium and water. As simple water or 5%-
dextrose infusions are salt free, they are less effective in correction of
hypovolemia and can lead to hyponatremia, and are therefore avoided
in initial therapy (also see Chapter No. 4). Colloids are preferred when.
hypovolemia coexists with hypoalbuminemia (burns, nephrotic .,
syndrome, cirrhosis of liver, etc.) . · j
For subsequent fluid therapy, selection of fluid for replac-e ment -varies .- .j
from patient to patient. The type of fluid lost, serum electrolyte status, '.: <-
acid base balance and renal status or coexisting disorders~ all.mustbe ". ·,;:
taken into account for appropriate selection. · · ·~. _. . ,~.>.
'· . .
. :.. -
CH. 2 :· Bas.ic ,Principles of Fluid Therapy and Pharmacology of l.V. Fluids 47
0. What should be ·the optimal rate of fluid replacement in hypovolemia?

A. Immediate aim of fluid therapy in hypovolemia is to get the patient out
of danger and to induce positive fluid balance.
Hypovolemic ·patient with hypotension or shock requires .rapid fluid
replacement. In patient with shock approximately 1 to 2 litre of fluid
should b_e given in first hour to restore adequate tissue perfusion as
_quickly as possible, under close medical supervision.
In hypovolemic patient who is haemodynamically stable, gradual
repletion is _preferrable, since it will restore normovolemia while
minimizing the risk of volume overload and pulmonary oedema.
The aim of fluid therapy is not just to administer fluids but to induce
positive fluid balance. If a patient with diarrhoea losses average 300
ml/hour fluid and I. V. fluid is infused at the same rate, there will not
be correction of fluid deficit. On the contrary, as urine output and
insensible losses are not considered, inspite of infusion of fluid, fluid
deficit will worsen. So fluid therapy can successfully correct hypovolemia
only if it provides 50 to 100 ml extra fluid in addition to losses, as
summarized below.
Effective rate of fluid replacement per hour
= 50 to 100 ml
+ Urine output per hour
+ Ongoing loss (such as diarrhoea or tube drain) per hour.
Monitoring fluid therapy
a. How to monitor fluid therapy ?
· · · flu'id therapy needs careful monitoring with frequent
A Patient receiving .
• • • • t' n and with proper laboratory tests to determine
clmica 1 examma 10
adequacy. . ·
, ., h' h uggest correction of hypovolem1a and adequate
Parameters w 1c s
fluid replacement are : . .
. . the weight loss due to fluid loss. .
1 Weight : Regammg d
. . . . . . Cold clammy extremities, dry tongue an
. 2. -: Skin and ton~ue · .d. . change to warm extremities, moist .
·. decreased skm turg1 1ty w1 11 . .
tongue and normal elasticity of skin. . . ' ... ·- .,
) ._· '.·
.....
\
. . . .. ' ~ . ' . '·. ·.

' :. ;
. ~ .
..
. · ·.·. .
·
..
· '
..
.~ ~·: .~ ·. ~- ' • '. . .
"'.;:· ,• . .·. . . -
. "
·-·:: . . · ' ·- .
:,, .· ...
. 48 CH . .2 : .Basic. Principles ·of Fluid Therapy and Pharmacology of I. V. Fluids
3. · Sensorium : Improvement of anxiety and restlessness_.

.. 4. · Urine output : Urine output > 30-50 ml/hour in adu!ts or > 0.5 ~o
1.0 ml/kg/hour in · children in absence of glyc~suna o~. osmo~1c
diuresis. Increased urine output with decreasing unne spec1f1c gravity
and osmolality are other dependable parameters.
5. Pulse rate : ·Correction of tachycardia to pulse rate less than
11 O/min in young adults as well as change from low volume
collapsing pulse to bounding pulse.
6. Blood pressure : Patient with shock, hypotension or orthostatic
hypoten.sion becomes normotensive.
7. . Haematocrit : Decreasing haematocrit in absence of blood loss
or ha~molysis.
8. Blood urea an.d Serum creatinine : Both will become normal. High
ratio (> 20: 1) of blood urea:serum creatinine will become normal
(10:1).
9. Urinary Na : Increase in urinary Na excretion (> 25 mEq/L). If the
urinary Na remains under 25 mEq/L the kidney is sensing persistent
volume depletion and patient requires additional fluid replacement.
10. Metabolic acidosis : Improvement of acidosis with improved
peripheral perfusion.
11. CVP or PAWP: Low central venous pressure (CVP) or pulmonary
· · arterial wedge pressure (PAWP) will become normal with adequate
fluid replacement.
Central Venous Pressure (CVP) Morlitoring

Q. What is CVP ?
A. Central venous. pressure is the pressure of blood measured · th

Vena.cava at 1'ts ·1unct1on
· · wrth
· the right atrium. in e
Q. Why to use CVP monitoring during fluid therapy?

A. . Close CVP monitoring permits rapid correction of fl ·d d · · .
.
1
, .. · ~ arge vo Iume of I.V. fl u1d
• •
· while
· protecting
. against th LI 1
· k e f IC It W 1th
. overload. e ns of volume
CH. 2 : Basic Principles of Fluid Th erapy and Pharmacology of I. V. Fluids 49
a. When to use CVP monitoring ?

A. CVP measurement is very useful for proper and safe fluid infusion in
the patient with shock, cardiac or critically ill patients in ICUs and during
major surgery (e .g. cardiothoracic surgery, transplant surgery).
Q. How to measure CVP ?
A. CVP is measured by placing a specialized catheter near the right
atrium in superior vena cava through the peripheral veins (antecubital,
femoral, jugular or subclavian) and connecting it with a water filled
manometer. Level of water in the transparent tube attached to a
measuring scale (calibrated in cm) reflects CVP. For correct
measurement it is important to keep zero of the scale at the level of
right atrium (mid axillary point at the level of ~th costal cartilage). It
is important to ensure free movement of the water column in the tube
along with respiration, which rules out partial obstruction, or blockage
of the catheter and hence false high CVP value.
Q. Which factors determine CVP ?
\,
A. Factors which determine CVP are vascular volume, right ventricular
function, intra thoracic pressure and vascular tone.
Q. How to interpret value of CVP ?
A. Value of CVP should always be interpreted with clinical status.
1. Normal value :
The normal value of CVP ranges from 2 to 14 (usually 6-10) cm
of water, which suggests normal blood volume and cardiac
function.
2. Low CVP:
a. True hypovolemia as in blood loss and dehydration.
b. Relative hypovolemia caused by peripheral vasodilatation as
in spinal anaesthesia, septicemia and anaphylactic shock.
3. High CVP (> 14 cm H 2 0)

a. Volume overload.
b. cardiac causes like congestive heart failure, cardiac tamponade,
constrictive pericarditis and tricuspid regurgitation.
': '
50 . CH. 2 Basic Principles of Fluid Therapy and Pharmacology of I. V. Fluids·
c. Pulmonary causes like embolism, t~nsion P~~umothorax,

COPD and cor pulmonale and intermittent pos1t1ve pressure
ventilation (IPPV).
Pulmonary arterial wedge pressure (PAWP) measurement
For the measurement of PAWP, Swan-Ganz flow direct catheter is introduced

through a peripheral vein and is placed with the tip in a pulmonary artery.
Pulmonary artery is in direct continuity with the left atrium and, therefore,
with the left ventricle during diastole. So pressure measured by this catheter
reflects left ventricular end diastolic pressure (LVEDP). Hypovolemia produces
low PAWP. High PAWP suggests volume overload in absence of left ventricular
failure, mitral stenosis or regurgitation, cardiac tamponade or constrictive
pericarditis.
Q. When and why measurement of pulmonary arterial wedge pressure

is the better guide for fluid replacement compared to CVP ?
A. In young patients with normal cardiac function CVP correlates well
with LV filling pressure ·and is a good guide for rapid but safe fluid
rep.lacemen~. But even hypovolernic patients can have high CVP due
to nght ventricular failure (right ventricular infarct, tricuspid or pulmonary
valve defect etc-}, pulmonary hypertension (COPD-cor pulmonale,
pulmonary embolism etc.) or patients requiring mechanical ventilatory
. support. In all these conditions PAWP is low in ·hypovolemic patient.
As P~W~ ~ccurately reflects left atrial pressure and left ventricular
function, it is a better guide for fluid replacement.
A marked elevation in PAWP f
alteration in th .req~e~tly occurs prior to overt CHF. Timely
erapy can avoid clinical CHF.
0. What are the indications of pulmon
fluid therapy? ary artery pressure monitoring during
A. 1. In critically ill, haemodynamically b .
. unsta le patients.
2. . In elderly patients or in patients with histo . . .
requiring massive fluid repla 1
ry of schem1c heart disease
· cement e g .
· shock; burns etc. · · severe dehydration and
------------ -~· . --- -
CH. 2 Basic Principles of Fluld Therapy and Pharmacology of LV. Fluids 51
· 3. In ARDS, for controlled optimum fluid delivery.

4. ·. To differentiate cardiogenic versus noncardiogenic pulmonary
oedema.
5. - Pre and intraoperative monitoring of fluid replacement in seriously
. ill patients or high-risk cardiac and noncardiac surgery.
Methods of delivering l.V. fluids

Most frequently used method to infuse l.V. fluid is by conventional (routine)
1.V. sets or micro drip sets. However for more precise and controlled
delivery, infusion pumps and I. V. sets with calibrated chambers are
available, although they are more expensive.
Methods to calculate rate of fluid infusion

Calculation of the rate of fluid infusion for conventional (routine) l.V. sets,
is not mentioned in most of the medical text books. Due to lack of such
guidelines, we often feel that the calculation of fluid volume to be infused is
a tedious and a complicated exercise. The methods that we are using and
have found to be simple, practical and user friendly are mentioned below.
1 Calculation for routine l.V. set

When fluid is infused with routine 1.V. set these methods calculate rate
of infusion quickly with reasonable accuracy.
The methods consist of :
1. RULE OF TEN 'I
2. RULE OF FOUR
Q. How many drops will make one ml of fluid ?

A. . Simple fact to be remembered is,
For routine I. V. set 15 drops = 1 ml. ',.
-_Q. How to calculate rate of fluid infusion in ?4 ho~rs (for routine i.v. set) ?
· A. Simplest and best method is to follow · _'!~~-_LJLE OF TEN". -. --- -
.... '1
- .~ '• t . .
' j .. .- ·:·'
... ·
. .. · . .. ; · ,
52 CH . :2 : Basic Principles :of Fluid Therapy and Pharmacology· of /. V. Fluids
Q. From fluid volume to be infused in 24 hours how to calculate dro

rate of infusion ? p
A. As per 11 RULE OF TEN", by multiplying fluid volume in litres to be
infused i~ 24 hours with ten, it will give us drop rate per minute.
I. V. fluid in litre/ 24 hrs. x 1O =
Drop rate/minute
'
)
.
I
2.0 litre in 24 hours = 2.0 x 10 = 20 drops/minute
3.5 litre in 24 hours = 3.5 x .1 0 = 35 drops/minute
Q. From drop. rate of infusion, how tq calculate fluid volume in 24 hrs.?
A. As per "RULE OF TEN", roughly the is drop rate divided by 10 will
give us volume in ·litre in 24 hrs .
. I
Drop rate per minute ·+ 10 - I. V. fluid in litre/ 24 hrs.
15 drops/min = 15/1 O = 1.5 litre I 24 hrs
.' ' .·. 20 drops/min = 20/1 O - 2 ·litre I 24 hrs
I
I I As this rough calculation is 96 °/o perfect, at end of 24 hrs. 4% less fluid

. '
:I will be infused. -
Q. How to calculate rate of fluid Infusion in One·hour (for routine i.v. set)?
A: Simplest and best method is to follow "RULE OF FOUR"
Q. . From fluid volume to be infused in One hour, how to calculate drop
rate per minute of infusion ?
A. . As per "RULE OF FOUR"; by dividing ·fluid volume (in ml) to be infused
in one hour by four will give us drop ·rate per minute.
Volume in ml I hour + 4 - . Drop rate I minute
60 ml I hour = 60 + 4 = 15 drops I minute
· 200 ml I hour = 200 + 4 - 50 drops I minute
Q. From drop rate of infusion, how to exactly calculate fluid volume
in one hour?
A. As per "RULE OF FOUR", drop rate per minute multiplied by four
will give fluid volume in one hour.
Drop rate I min x 4 - Volume in ml I hour
1o drops I min = 1o x · 4 _ 40 ml I hr
80 drops I r:nin = 80 x 4 - 320 ml I hr .-
I
"
·. ;;
,: -·.t
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\ CH.2 Basic Principles of Fluid Therapy and Pharmacology of l.V. Fluids
53
Oth,e r useful calculations for fluid therapy
Perfect method to calculate fluid volume from drop rate in 24·hrs.

Drop rate x 96 =volume in ml per 24 hour.
10 drops I min = 10 x 96 = 960 ml I 24 hrs
20 drops I min = 20 x 96 = 1,920 ml I 24 hrs
11 Drop rate calculation for any parameters .

Volume to be infused {in ml} = Drop rate I minute
Duration of infusion in hours x 4
Example : If 660 ml. fluid is to be infused in 3 hours.

660 = 660 = 55 drops I minute
3x4 12
Caution : If due to manufacturing defect, routine I. V. set fails to provide 15
-drops per each ml of fluid, these methods (rule of ten and four) will not be
accurate in fluid delivery. So always counter check calculated rate of fluid
admininstration with actual fluid delivery.
2 Calculation for micro drip l.V. set
Q. How many drops will make one ml of fluid ?

A. Simple fact to be remembered is,
For micro drip set 1 ml = 60 drops.
· Q. How to calculate volume .from drops in micro drip. set ?
A. Number of micro drops per minute = volume in ml/ hour
Micro drop rate I minute = Volume in ml I hour
35 micro drops I minute = 35 ml I one hour
50 micro drops I minute - 50 ml I one hour
Similarly :
Volume in ml I hour . - Drop rate per minute
30 ml I one hour . =
30 - micro drops I minute ·
45 ml I one hour.'-.:'= .. ·45 micro dropsiininute . ~ ..' :
'
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.
. . . .. .
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1. 5o/o-Clextrose :· Provides fluid and calories without ele t . \

. f . c rolyt .
The best agent for correct1on · ~ o ·intracellular dehydrati . es. !
maintainance fluid therapy. . on and ;
2. Isotonic saline : The ·best' ·agent to treat shock and salt de I .

Pet1on..
3. 5°/o-Dextrose, 0.45°/o-Sodl·um Chioride : Suitable for paedi .
·
patient, genta I; correc t'ion o f h yperna trem1a~
· · postoperative atnc
. . . a~
maintainance fluid therapy.. ., ·
4. DNS : Suitable to treat salt depletion with calorie supply.
5. Ringer's lactate : Most· physiological, glucose free fluid. Useful in

diarrhoea, diabetic, surgical (intra operative and post operative
period) and burns patient.
6. lsolyte-M : Best agent to provide potassium. Ideal ~s maintainance

·· fluid for parenteral fluid therapy. -.
7. lsolyte-G : Only fluid to correct metaboli.c alkalos_is. Used}o replace_

fluid loss due to vomiting or continuo'us ncisogastric a·spiration.
8. lsolyte-P : Provides less electrolytes (half of ·lsolyte-M) and more ·

water. Useful chiefly in paediatric patients.
9. lsolyte-E : Corrects all ECF el~~trolytes, acidosis ~n·d supplies g~ucose.

So useful in treatment of diarrhoea and hospitalized patient on
long term fluid therapy. ·
i
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Table No. 2.5: Characteristics of l.V. fluids . .
. ';
~
Characteristic Type of Fluid

Most physiological Ringer's lactate (AL)
Rich in sodium Isotonic saline, DNS
Rich in chloride Isotonic saline, DNS, lsolyte-G
Rich in potassium lsolyte-M, P and G
· Corrects acidosis · Ringer's lactate, lsolyte-E, P & M
Corrects alkalosis lsolyte-G
Cautious use in renal failure Ringer's lactate, lsolyte-M, G, P & E
Avoided in liver failure Ringer's lactate, lsolyte-G
Glucose free Isotonic saline, Ringer's lactate
Sodium free 5%, 10%, 20% and 25%-Dextrose
Potassium free Isotonic saline, DNS, Dextrose fluids
Calculation of fluid infusion ·
1. FOR ROUTINE l.V. SET

A. 15.drops =.1 ml
B. .·"RULE OF TEN" for fluid calculation for 24 hours.
l.V. fluid in litre I 24 hrs x 10 = Drop rate I minute . .
Drop rate per minute + 10 = 1.v_. fluid in litre I 24 hrs.
C. "RULE OF FOUR" for fluid calculation for one hour.
Volume in ml I hour 4 = Drop rate I minute
Drop rate I min x 4 = Vo_lume in ml I hour
D. Drop rate calculation for any parameter
Volume to be infused (in ml) = .Drop rate I minute

Duration of infusion in hours x 4
2. . FO.R MICRO DRIP l.V. SET

A. For micro drip set 1 ml .= 60 drops.
B. Number of micro drops per minute = Volume in ml I hour
..' r-· .r •
'f~
CHAPTER
THREE
FLUID .AND .ELECTROLYTE DISORDERS

DISTURBANCES IN ECF --.........
PHYSIOLOGY OF WATER AND
SODIUM REGULATION 56 COMPOSITION
ECF CONCENTRATION DISORDERS OF POTASSIUM 95
DISTURBANCES 59 Basic physiology 95
Hyponatremia 59 Hypokalemia 96
SIADH 73 Hyperkalemia 104
Hypernatremia 78 DISORDERS OF CALCIUM 112
ECF VOLUME DISORDERS 82 Basic physiology 112
ECF VOLUME EXCESS 82 Hypercalcemia 113
Water and Salt excess 82 Hypocalcemia 117
Predominant water excess 83 DISORDERS OF
ECF VOLUME DEFICIT 85 PHOSPHATE AND
Hypovolemia 86 MAGNESIUM 120
Pure water deficit 86 Hypophosphatemia 120
Polyuria 87 Hyperphosphatemia 122
Central diabetes insipidus 90 Hypermagnesemia 123
Nephrogenic diabetes insipidus 93 Hypomagnesemia 124
Introduction
For better understanding of fluid and electrolytes abnormality in clinical
practice let us review basic physiology of fluid and electrolyte balanc~.
A : Water Regulation
In a normal person water in the body is balanced by adjustment in
input and urine output.
1. Response to water deficit
a. Water intake is regulated by thirst, stimuli for which are :
i) Dehydration
ii) Fall in BP and
iii) Increased solute concentration (osmolality).

b. Water excretion is tightly regulated chiefly by antidiuretic
hormone (ADH). .
Regulation .
Fluid deficit increases osmolality (du.e to increased serum sodiurTl)
r
I
!
+
I .
CH .- 3 · :· FILiid·:and ·Electrolyte Dis6rders ~ 57
or decrease circulating blood volume~ which stimulates the .hypothalamus

for ADH release. ADH acts on the kidney at distal tubules and collecting
duct and increases water permeability. The result will be that as much
as 18 litres of water is reabsorbed under the influence of ADH. ADH
mediates increased water reabsorption and decreases urine output, which
preserves body water. · ·
.· 2. Response to water excess
i. Decrease ADH
.When amount of wate.r in the body increases secretion of ADH
will decrease, so water reabsorption by collecting duct will
decrease and there will be increase in urine volume.
ii. Increase ANP
Volume expansion will also lead to increased secretion of atrio-
natriuretic peptide-ANP (due to atrial stretching) which promotes
. diuresis and natriuresis.
So decreased ADH and increased ANP will decrease water
reabsorption and increase urine output and thereby maintain
required water status in the body.
B : Sodium Regulation
1. Physiological basis
i. Sodium is the major ECF cation (sodium value 140 mEq/L ECF
vs 25 mEq/L intracellular).
ii. Total body sodium is about 5,000 mEq in a normal adult person.
iii. 85-90°/o sodium is extracellular.
iv. Sodium is res·p onsible for more thah 90o/~ of total osmolality
I
of extracellular fluid. I
!
v. Major function of sodium is to mJintain ECF volume and
I therefore maintain blood pressure. 1. · .
i~ ;
vi. ECF volume is reflectio~ of total body sodiu.m content (amount).
vii. Daily requirement of. s.odium is about 100 mEq or 6 gm of
sodium chloride.
1):
!
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· sa [-·:
CH. 3 · - Fluid and Electrolyte Disorders r,..
l
~ ..
I.
. viji. ·Excess salt is excreted chiefly by kidney. Loss .of ·sodiufl1 · t\,
. sweat is poor (30-65 m Eq/L). · .· · . · ·. - . n, 1
~I 2. Response to sodium deficit · · - · · : . \

: ' . . . I
i. Deficiency of sodium in bo9y will lead to hypovolemi~ and ~
I activates Angiotensin-11 and Aldosterone. ·
I
!
li ii. By acting on the kidney, angiotensin-11 helps to increa '.
sodium absorption at the proximal tubules and . aldosterone:~ l
I
I,
the collecting duct. :
iiL In a state of so di Lim deficit, abso.r ption ·ot Na under :
aldosterone control is so perfect that almost no urinary Na '.
loss occurs. So by almost complete absorption of Na kidney :
helps to prevent sodium loss. 1
· Renal priority :
l
i. To reclaim sodium under aldosterone influ.ence, initially l
potassium and if needed later on H+ is lost in the urine. ·
ii. >·
D·ue to body's priority to reclaim Na > H K, during abnormal ;
loss of all electrolytes (like in diarrhoea) hypokalemia is the
•
II
commonest abnormality. 1
3. Response to sodium excess .. l

I
1. When there is excess amount (content) of sodium it will lead ~

. to increased ECF volume, which will lead .to decreased :
Angiotensin-11, Aldosterone and increase in ANP.
ii. Decreased angiotensin-11 and aldosterone level will lead to :
. decreased renal reabsorption of sodium.
iii. lnc~eased ANP will lead to natriuresis and diu.resis. .
5
Hence net result is increased urinary excretion of sodium. ThU \
extra sodium will be lost. · i·
rI
c : Potassium Regulation · J.
Discussed with disorders of potassium ·conCentratioii on page 95· j

j
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- . . ·~·;
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CH ~ 3 Fluid and .El.ectrolyter Disorders . 59
D : Fluid (volume) and electrolyte disorders. . : . .

Abnormality of fluid and el_ectrolytes is di_scussed as. foll.ow~ ...
1. ECF concentration disturbances ',I
·Sodium is the most important osmotically active ion in ECF. so

change in t~e ser~m sodium concentration produces ·change in
the osmolallty. Major abnormalities in fluid conc~ntration are :
a. Hyponatremia
b. Hypernatremia
2. ECF volume disturbances
Major fluid volume ·disturbances are
·. a. F;luid excess
b. Fluid deficit
i. Isotonic fluid deficit:: Hypovolemia
ii. Pure water deficit : Dehydration
3. Disturbances in ECF fluid composition
. Qisturbances in concentration of ions other than $Od,ium, are as
· follows : · · ·
. .
:
i ~ . Potassium Hypo~alemia and hyperkalemi~ . ..
ii. Calcium Hypocalcem_ia and hypercalcemia.
. . ' iii. .Phosphorus .
·• Hypophosphatemia and hyperphosphatemia .
iv. · Magnesium ..
.
Hypomagnesemia and hyper.magnesemia.
ECF CONCENTRATION DISTURBANCES

First we will discuss extracellular fluid concentration disturbances,
hyponatremia and hypernatremia.
• !
HYPONATREMIA
Hypon.a tremia i~ defined as plasma sodium. less than , 135 . mEq/L.
Hyponatremia is not uncommon in ahospitalized patient (incidence 1.5 to
2.5°/o), but is rarely s.e en in . an ambL1.lato.ry .patient (if present, r~flects a
chronic disease status).
:) ·· ' ¥~'
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60
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·CH. ·3 : · Fluid and Electrolyte Disorders
t
f
.:
I
Hyponatremia is clinically an important entity because : 1
.j '
" 1. Acute, severe hyponatremia has substantially high morb'd.
1
~.
and mortality. . ity \
2. Rapid correction of chronic hyponatremia can lead to neurologi
. ·t an d even death.
d e f 1c1 ca1
3. Etiology and treatment is not as simple ·a s that of other elec1rolYte ·
deficit.
A common understanding is that,
the deficit should be treated with supplementation
e.g. potassium deficit is corrected with K+ supplementation.
But in case of hyponatremia the treatment may be contrary to this common
understanding, thus
Hyponatremia = Sodium deficit
So salt replacement is required in all
is a wrong concept.
Serum sodium reflects the relative proportion of sodium and water.

Hyponatremia usually means water overload and not sodium deficit.
Hyponatremia can occur with normal, low or even high total body sodium.
So basically hyponatremia can be dilutional ( water excretion lesser than
water intake and so needs fluid restriction as the most important treatment)
or due to sodium loss (needs sodium and fluid supplementation)
Hyponatremia
Usually means
Water Retention 'f
Etiology
·a
Low serum Na leads to decreased serum osmolality, so true hyponatrern'. : 1
is characterized by hypoosmolality. ECF volume varies in hyponatr~~tc
patients, depending upon etiology. So etiology of hyponatremia is classified i .· ·
on basis of these two criteria, osmolality and ECF volume. t.
I:
~ '
~. .
!- :-.."''·
I
i
~
CH. 3 Fluid and Electrolyte Disorders ·s1
Pseudo hyponatremia ,
A. Normal osmolality Hyperlipidaemia, Hyperproteinaemia
B. High osmolality .. Hyperglycaemia, Mannitol
II Hypoosmolar hyponatremia (true hyponatremia)
A. Hyponatremia with ECF volume depletion

(Patient dehydrated, reduction in total body sodium exceeds
reduction in total body water)
1. Extrarenal loss (Urinary sodium < 15 mEq/L)
Vomiting, diarrhoea, peritonitis.
2. Renal loss (Urinary sodium > 20 mEq/L)
Excessive diuretics, S?tlt losing nephropathy, diabetic
ketoacidosis, cerebral salt wasting syndrome.
B. Hyponatremia with hypervolemia, increased ECF volume

(Patient ·oedematous - Increase in total body water exceeds
increase in total body sodium)
Urinary sodium< 20 mEq/L: CHF, cirrhosis and nephrotic syndrome.
Urinary sodium > 20 mEq/L : .Renal failure
C~ Hyponatremia with normal ECF volume

·(Patient normovolemic, increased total body water)
SIADH, post operative pain, hypothyroidi.s m, glucocorticoid
deficiency, psychogenic polydypsia, drug induced.
Clinical Features :
The severity of symptoms depends upon the severity of hyponatremia and
the rate at which the plasma sodium concentration is lowered. So acute
and severe hyponatremia is symptomatic but chronic and mild hyponatremia
.is well tolerated. The very young and elderly patients are more symptomatic.
Clinical features are summarized in Table No. 3.1.
_:s2~~C:H:·~3~~F~lu~id~a:n:d~E:l:ec:t:ro:ly:te:.:D:is:or~d~e-rs__.....-.------------------........~ /
~
,
'
Table No. 3.1 _:

erm1c
. al features of Hyponatremia ~
.Moderate ·.·
. Severe ~
I Mild
Drowsiness f
Anorexia . ..
Personality changes
Diminished reflexes I ~
Headache
Nausea
Muscle cramps
·. Muscular weakness ·.·
. . Convu!sions I ,1
Vomiting Confusion ..
Coma
'
I ,~I
Ataxia
D~ath j , ~I
Let~argy
Q. cal features of hyponatremia ?

What is the physiological basis of clini_ I ~
I ~
. . . ? . . .
Why symptoms are primarily neu_rogernc ·. . .
A. It is not the reduction of ECF Na.that .g lves rise to symptoms and signs I ' }lll
in hyponatremia. ·1ristea·d, it is the · increa_s e in volun:ie. of ICF and ~~
particularly increase in the volume of the brain cells which leads to I ~
signs and symptoms. · · m~rl
Hyponatrernia Jead_ s to hypoosmolality of ECF, so. water moves into , rn~r

. c~lls (ICF) and the cell swells. ln -.tissue such as skel~tal _ muscle this is I ~i m
of little consequence. When the cells of the brain swell, .this produces I ~,~
an in,creas~ in intracranial pressure because the brain is an enclosed I I ~l~I
space Witti ·a fixed volume. Increase in intracranial pressure causes ' i~ 1·
decrease in cerebral blood flow leading to hypoxic brain damage. In ~~c

severe cerebral oedema, swelling_of brain exceeds about 5-8°/o o.f. brain
~ra1
volume. As th. ~ skull is ·a·fixed closed space, s'uch _increa~ed brain cell
volume and ·resui'tant significant r(se in the intracranial pressure can r~,~ ~
· ·1ead to"·herniation. Herniation is characterized by unequal or fixed dilated l ~1~1
pupils, hypo\ientilation, cardiovascular instability, ·urinary .or faecal l~yl
incontinence or respiratory arrest. .
~~r
Diagnqsis . . · ~ ~ri1
q
• Histo~_Y ~n_d 'phys_ical e~amination is often helpful in identifying
M1
·hypov.olem1c ·hyponatrem1a {dia.rrhoea, vomiting, burn.s diuretics etc.)
. " I . , , ': , .. , . ! l1
• · The degree ~f hypo~~tremi_a often . co-relates with the s·everity ~
of the underlying cond1t1on and is an important prognostic factor. l Ur
• Three important diagnostic tests are (1) Plasma os r·t ( ) u ·nary
. d (3) U . mo 1a 1 y, 2 n
osmolaltty an nnary sodium concentration. (Table No. 3 .2)
CH. 3 :· · Fluid and .. Electrolyte Disorders 63
• Hyponatremia is usual'y associated with ,. low. plasma osmolality.. But if

osmolality is normal or high, .rule out pseudohyponatremia (Table No.
3.2). Normal plasma osmolality is 275-290 mOsm/kg.·
Plasm~ · ·" = ·2.· xNa . + .. ~l.u~bse :(mg/di) 7 BUN (mg/di)
Osmolality · · 18 : 2.'8 ·
-· ' . ,.
• If hyponatremia occurs in oedematous patient, rule out CHF, cirrhosis

of liver, nephrotic syndrome or other renal diseases.
• In hypovolemic patient rule out renal loss (Urinary · Na > .20 ,mEq/L
due to diuretics, diabetic ketoacidosis, salt loosing nephropathy) or extra
renal loss (Urinary Na < 15 mEq/L due to diarrhoea, vomiting, burns,
peritonitis). , , · · ·· -. ·· ~.
• Associated hyperkalemia suggests ·renal · 'insufficiency~·-or adrenal
insufficiency with hypo'aldosteronfam~.. · ··
I
Associated hypokalemia and metabolic alkalosis .suggest' vom.itlng or
I • diuretic therapy·. · .
I • Diuretics ·induced ·hyponatremia: is almos·t always. due to .thiazide
diuretics (Loop diuretics : Water diuresis > Natri~uresis, so
II
I
hyponatremia infrequent).' '. .- ' . ._: . . .· .. .· · . .
• SIADH (syndrome ·of ·inapp.ropriate antidiuretic hormone secretion)
is the most common" cause of normovolemic hyponatremia.
Characteristic of Sl~DH is high urinary sodium, osmolality and specific
gravity, inspite of low serum sodium and hypoosmolality.'.
Table Nb. 3.2 ':_Major steps in initi.al.. eval~atid'n of hyponatre~ia
1. Plasn:ia Osmbla'lity
: ··.
Low ·: True ·hyponatremia
Normal or elevated : Pseudohyponatremia or renal ,failure . .. , .
2. Urine Osm.olality ". . . . ·· . . . . ., ..
< 100 mOsm/kg or specific gravity < 1.003, diluted urine· s·uggest' . ..
primary polydypsia with normal water excretion. ... . · .
> 1oo mOsm/kg, other causes of hyponatremia in which .w_ ater.excretion
is impaired.
3. Urine Sodium Concentration : ._
< 15. mEqfL effective volume depletion e.g. diarrhoea,. vomi~i~g. ·
> 20 mEq/L SIADH (normo volemia) or renal salt wasting (d1uret1cs,
renal disease or hypoaldosteronism)
~ rv .
t'. ·
1> ..
1 .~
64 CH;· 3 : : Fluid and -Electrolyte Disorders
Diagnostic approach to hyponatremia is as per Figure No. 3.1.

Fig No. 3.1 : Approach to hyponatremia
Confirm .... Rule. out Pseudohyponatremia

diagnosis of
Hyponatremia
t-------11,..• Normal or high osmolality
l
Hypoosmolality
-- Impaired Renal
Assess
Renal function ....
. . - - - - -......,..~ Primary Renal Disease
Status
Normal
r---:-..;;:-•-~---r-------1. ~
. OEDEMA - CHF, Cirrhosis, ·
Assess ,.. Nephrotic Syndrome
Volume
Status VOLUME DEPLETION
~ Urinary Na excretion (mEq/L)
'1111 r
Normovolemic
Urinary Na < 15 Urinary Na > 20
Diarrhoea - Diuretics
Vomiting, Burns - Salt losing .
Pancreatitis nephropathy
Assess
Adrenal &
,.. Adrenal or thyroid insufficiency
Thyroid function
Normal
.... I r
Able to dilute Yes

urine in response
to water load
..------4111...• Diiute
,... Urine
----...1~~ Psychogenic
Polydypsia
No
.......
SIADH
. . .-~ ..
CH. 3 . . Fluid .and Electrolyte Disorders · 55·
· Treatment
Treatment of hyponatremia must be indivi'dualized considering etiology, rate

of development (acute vs. chronic), severity (severe vs. mild) and clinical
signs and symptoms.
Dictum : Hyponatremia, which develops quickly, should be treated fast,

whereas hyponatrernia, which develops slowly, should be corrected slowly .
. .
Goal of therapy
1. To raise the plasma sodium concentration at a safe rate.
2. To replace sodium deficit or potassium deficit or both.
3. To correct underlying etiology.
In general hyponatremia is corrected acutely by giving sodium to patients
who are volume depleted and by restricting water intake in patients who
are normovolemic or oedematous.
Treatment of hyponatremia is summarized in Fig. No. 3.2 .

. Fig. No. : 3.2
HYPONATREMIA
Clinical .L ± l
Features Hypovolemia Oedema Normovolemia
J. J. ·J.
Treatment Salt and water No salt . Water restriction
supplementation Water restriction
Loop diuretics
A. Specific treatment
• Removal of the drugs responsible for hyponatremia ·:
Diuretics, Chlorpropamide or l.V. Cyclophosphamide. ·
• Management of physical stress, postoperative pain.
• Specific treatment for adrenal insufficiency, hypothyro_idis~,
nephrotic syndrome, CHF, uncontrolled diabetes or ketoacrdosrs,
salt losing nephropathy etc.
66; CH; ·: 3 ": · Fluid and Electrolyte Disorders ·
B. How to correct Hyponatremia ?

. . 1. HyponatrE;!mia with hypovolemia .
. .. "· ~ . . . . .. . .. . .
Thes;e patients require fluid and salt supplementation which can be

done with l.V. isotonic (0.9°/o) NaCl (or even oral salt .containing
water) at rate appropriate for the ~stimated volume depletion. Intake
of ·simple 'water or I. V. fluid with ·1ow ,Na (0.45°/o NaCl, lsolyte-M :
5<%'-dextrose, 'etc.·) should be·restricted until the plasma sodium i~
within the normal range, because it will aggravate hyponatr~r:nia,
Diuretics induced hyponatremia is treated with saline with
potassium supplementation (30 to 40 mEq/L) ··
2. Hypona't remia with hypervolemia (O.edematous state)
Therapy is difficult in oedematous state since . sodium·
supplementation will worsen fluid overload. Such patients are
· treated with diuretics·, salt restriction, fluid restriction (intake< urine
output) and correction of potassium· deficit in addition · to ,the
etiological treatment.
3. Hyponatremia with euvolemia
Hyponatremia with, nprmal or ti_ igt:i ECF volume has impaired water
excretion with nornia·I or high tbt~I body sodium. In such patients
fluid restri.c tion is the 'rl1osf Important . freatment. Adequate
restriction of fluid intake will gradually: increase serum sodium
concentration.
c. Basic ·Principt·e s of Correction of Hyponatretnia = · · ..
Treatment of hyponatremia should balance.·ttl'e.·risk· of hypotonicity

due to hyponatremia and.the'·risk of. therapy.
Q. To tree1:t or not to treat ? . , .
A. How rapiolY. hyponatrert:lia should be . corrected is a .dilemma.
Patier)t~ with severe hyponat:erni_a (110-115 m,Eq/L) ~re at risk 0~
developing severe and potent1ally_1rreversible neurological da~~g
and sortietimes even death. On the other hand, too rapid corre~tion
· of severe hyponat rem1a . '
can produce central pontine myernos1s
1 .or
1
osmotic demyelinationsyndrome (ODS), which can cause substantia
morbidity and mortality. ..
CH. ·3 Fluid ·and Electrolyte Disorders 67'
So it is important to balance the risk of hyponatremia against the

·risk of correction. To avoid these problems controlled and limited
cofrection is advised after proper selection of patients who need
treatment for hyponatremia .
. Q. · How to diagnose central pontine myelihosis or ODS ?
A. · . This severe ne~rological disorder is characterized by dysarthria,
· · ·dysphasia,- flaccid paresis or coma. Diagn"osls is confirmed by C.T.
scanning or more acc"urately by MRI.
. . . .. .
Q. When to treat ?_ When not to treat ?

A. Pati.ent with seizures or other severe n.eurological .symptoms due
to .hyponatremia needs prompt treatment. , In thi~ ~.etting, risk of
untreated hyponatremia and cerebral o_ ed~ma is greater than the
potential harm of rapid correction. So rapid correction is ipdicated
in acute (< 48 hours) symptomatic or severe (serum:·Na < 120
mEq/L) hyponatremia
·on the other hand, chronic· (> 48 hrs) and mild hyponatremia,
· · with minimal neurological sympto:ms are at iittle risk due to
hyponatremia. However, these patients can develop demyelination
foll.owing rapid correction. So t~ere is no necessity to correct
these patients rapidly and they should be treated using slower
acting therapy such as fluid restriction ...Pay particular attention
to premenopausal women, elderly and YOl:Jng _chiidren" as they
·are more symptomatic and need early treatme~.t · · ·
Q. At which targeted rate is the correction of hyponatremia.sat~ ?
A. General guidelines for treatment are :
1. Chronic asymptomatic hyponatremia :
i. · The targeted rate of plf!sma sodium .should not be greater
than '. 0.5 to 1_
.9 mEq/L/hour. . . . ..
ii. Rais~ the plas111a .sodium by I. es~ tha.n .1 O_to .12 m~q/
L on th.e first da~y and less than 18 mEq/L over the first
two days. As per recent recommendations a 'targeted rate
of correction should not exceed 8 mEq/L on any day of
treatment.
. ;' I
' '
!' '
I: .
68 CH ;· 3 · : Fluid and Electrolyte Disorders
1·
I'
I: '
I~
t . iiL If the rate of correction .is faster or rise in serum sodium
is > 25 mEq/48 hours or correction is made until
t·
I·· normonatremia (serum sodium 140 mEq/L) is achieved
I;
I' there is high risk of central pontine myelinosis.
fl
I
i'I
2. Acute hyponatremia with severe neurological symptoms :
These patients require ·rapid correction of plasma Na with
hypertonic saline. Initial rate of rise of Na concentration should
be 1.5-2 mEq/L/hr for the first 3 to 4 hours or until the severe
neurological symptoms improve. Besides this initial rapid
correction rise in the plasma sodium concentration should
not exceed 10-12 mEq in first 24 hours. Patient with seizures
also require imme.diate anticonvulsant drug therapy and
adequate ventilation .
. Q. .How long to treat and when to stop acute correction of
hyponatremia ?
. A. Regardless of the initial rate of correction, chosen acute treatment
should be interrupted once any of the three end points is reached.
1. Patient's symptoms are abolished.
2. A safe plasma sodium (generally 120-125 mEq/L) ·is achieved
or
3. · A total magnitude of correction of 20 mEq/L is achieved. It is
necessary to correct hyponatremia accurately to a safer range,
rather than correcting completely to normonatremia.
Q. How to ·calculate need of sodium containing fluid for correction of
hyponatremia ?
A. Conventional method :
Conventional method of correction of hyponatremia is as follows
Na requirement = (Desired Na - Actual Na) x Total body water
This c'onventional method is complicated beca.use :
1. It only calculates the amount of Na required to raise Na.
2. After ·calculating the requirement of Na, it is confusing to
select Na containing fluid and determine its infusion rate.
CH. 3 Fluid and Electrolyte Disorders 69
8. · Newer method : . . ·
This method directly calculates ·
t · ·Change in serum sodium concentration ·for ·:given infusate
(select type and volume of Na containing fluid ·and calculate
expected change in Na).
2. For given target bf ch~ng. e in Na concentration, this formula can
directly
. .
calculate
.
the volume o'f selected Na containing fluid.
'
Change in serum sodium concentration :=

Infusate Na/L - Serum Na .· .
· Total body water (L) + 1 .or
·.1nfusate (Na.+ K)/L - Serum Na
·Total. body water (L) ·+ t
Total body water
= 0.60 x ·body weight (kg) in children and .non elderly. man
= 0~50 . x· body weight (kg) in non elderly· woman and elderly· man
= 0.45 x body weight (kg)
.
in elderly woman
' .
Q. ·. What is the sodium concentration of various l.V. fluids and solutions?

A. ·Sodium concentration of various l.V. fluids ·and ·solutions are as
per table No. 3.3.
Table No. 3.3: Sodium concentration of LV. fluids and solutions
Solution . Na (mEq/L) LV. fluid N~ {mEq/L)
.. 7'.5% NaHC0 3 900 0.45% . NaCl 70
5% NaCl 855 lsolyte-G 65
3% NaCl 513 · · ·1solyte-M ·40

' ..
0.9% NaCl ' 154 0.2% NaCl 34
. Ringer's lactate 130 5% Dextrose 0

70 CH: ·3 ·.: . Fluid· and Electrolyte Disorders·
..
I
Q. Which fluids should be used to correct hyponatremia and why ?
A. Aim of fluid infusion is to raise Na by correcting Na deficit. So
the . infu.sed f.luid should contain higher Na conce~tration than
.' .... desired or normal serum s9dium concentrati~:>n . .
0.9°/o saline (154 mEq/L Na) and 3°/o NaCl-hypertonic saline (513
.mEq(L Na) _are the only two routine!y us~d l.V. fluids which have
. higher.
. ~. . Na . concentration . and therefo're are qsed to correct
. ' .
hyponatremia. However, for the treatment of hyponatremia due to

SlADH, infusion of.·0.9°/o NaCl is ·inappropriate.
When hyponatremia is associated with hypovolemia or in absence
of ,fluid retention or oedema, 0.9°/o saline is the preferred fluid.
But when . patieqf'. needs salt supplementation along with fluid
restriction hypertonic saline is the preferred fluid (e.g. severe form
of SIADH).
Q. ·: How to monitor·Na during treatment of hyponatremia?

A~ . -. During·treatment pf hyponatremia,. many other independent factors
can modify the N;a conc.entrati~n (e.g. urinary. ~nd other losses of
Na, addition of oral fluid intake etc.). So frequent m~nitoring of the
serum sodium concentration (atleast ·at 4 to 6 hours interval
.iniUall,y),
. is n~cessary
. ..
tq ensure that the . rate of .correction
~ . ..
is as
desired and in order to make further adjustmen_ t in. the amount
and rate of fluid administration. Remember, in symptomatic/sick
paHents with: hyponatremia~ calculation of the: requirement of Na
-~ · ·· _ containing l.V. fluids for whole 24 hours and their infusion without.
. .... ·proper monitoring and.·modification can be dangerous. .. · .. . . t
Q. How much fluid should be given to correct hyponatremia and how

to calculate ?
A. For correction of hyponatremia, we need to determine
1. Goal of' correction
. : Determine how much Na is to .be
. '. raised
and in how much time.
2. · ~elect _the ~ppn)priate type_of _
Na c~ntaining 1.V. fluid for
correction of hyponatremia considering the clinical condition.
CH .. 3 Fluid and Electrolyte. Disorders 71-
Example· mentioned below will provide simple guideline for

calculation.
· .Example for .correction of hyponatremia :

45 year male (with 60 ~g weight), .a fter appendicectomy received
3 litres of ~. /o dex~rose/day along with liberal oral intake.
0
On the third day patient became confused and developed

convulsions. Clinically he was stuporo.us and euvolemic.
. . ' .
On investigation : serum Na 11 O mEq/L, serum K 4.1 mEq/L, serum

osmolality 230 mOsm/kg and urinary osmolality 480 mOsm/kg ·:
i . .
Q. What is· the diagnosis and how wili you treat ?

' I ' ~ ' ' ' • '· • ' "' '' :" •: ' l
A. DIAGNOSIS : Hypotonic hyponatremia due to pos.top~ratiye. yvater

retention (secondary to impaired water excretion due to pain induced
inc.r eased ADH) · .· · . ' . ·. · · ,
.. .
TREATMENT PLAN: Infusion of 3°(o NaCl, l.V. fruse.mide 20 mg and

:water . rete.n tion. For convulsions ph.enytoin .~nd: ,diazepam may be
given as per requirement
Calculation of expected change of ~a with pne litre of 3°/o Na91
Change in Na = lnfusate Nall - Serum Na./Total body water (L) + 1·.

= 513-11 O I 0. 6 x 60 + 1
= 403 I 36 . + 1 = 403 . I 37
= 10.9 mEq/L
INITIAL GOAL: To raise Na .by 4 mEq/L in the initial 4 hours .

To raise 10.9 mEq/L of Na, 1,000 ml of 3°/o NaCl is required.· So to
raise 4 mEq/L of Na, amount of 3°/o NaCl required is 366 ml ( 4/
10.9 x 1,000 = 366 ml)
So total 366 ml of 3°/o hypertonic·saline is required to raise serum
Na concentration by 4 mEq/L in the initial 4 hours.
Therefore, the required rate of infusion of 3% NaCl is 366/4 =92 ml/hr
72 CH. 3 : Fluid and Electrolyte Disorders
AFTER 4 HOURS : Serum Na was 115 mEq/L with no convulsion f.
and mild improvement in sensorium. f
Subsequent plan : Determine new goal _to ra!s~ serum Na and i

calculate volume and rate of infusion of 3% NaCl for given period I
as mentioned above (if goal is to raise 4 mEq Na in next 8 hours: I
rate of infusion of 3% NaCl will be about 47 ml/hour).
I
HYPONATREMIA
Summary
1. Hyponatremia is a frequently encountered entity with variable
clinical presentations as per duration of onset and severity of
hyponatremia.
2. Hyponatremia usually means water retention in euvolemic ,
patients. In hypovolemic patient, loss of Na is greater than loss of water. I
In oedematous patient , retention of water is greater than retention of [
Na. So hyponatremia occurs inspite of increased total body sodium. i
3. Treatment of etiology is most important in management of hyponatremia,
so arrival of etiological diagnosis is mandatory.
4. Severe, symptomatic, hyponatremia requires rapid correction with
hypertonic saline.
5. In asymptomatic, chronic hyponatremia rapid correction can be life
threatening and must be avoided. Water restriction is the most effective
therapy.
6. As per causes of hyponatremia preference of therapy are
Water restriction : SIADH, Oedema, Renal failure
Primary polydypsia
Salt supplement : True volume depletion, diuretics, and
adrenal insufficiency
CH. 3 Fluid and· Electrolyte Disorders 73
SIADH
SIADH. is a form .of dilutional hyponatremia produced by inappropriate or
excessive secretion of ADH.
A. Etiology
SIADH may be caused by enhanced hypothalamic ADH secretion,
ectopic hormone production (usually by cancer), potentiation of ADH
effect (as with chlorpropamide) or by administration of medication with
ADH like activity.
Commonest etiology of SIADH is neuropsychotic disorders, head injury,
malignancy (e.g. oatcell carcinoma of lungs), drugs like chlorpropamide
carbamazepine or l.V. high dose of cyclophosphamide and postoperative
pain.
8. Pathogenesis
1. In SIADH increased ADH secretion is independent of normal
osmotic or haemodynamic stimuli.
2. Because of increased ADH secretion free water cannot be
excreted normally . Retention of water causes dilutional
~yponatremia and progressive expansion of intra cellular and extra
cellular fluids.
3. Expanded ECF volume leads to increased secretion of ..ANP
(atrionatriuretic peptide) and decreased secretion of a~dosterone.
These changes stimulate natriuresis with an isotonic loss of ECF,
bringing ECF volume back to its baseline volume.
4. Natriuresis in presence of water retention leads to an inappropriately

concentrated urine. (Normally in patient with hyponatremia urinary
loss of · Na is negligible, in the · same way as · hypovolemia is
associated with oliguria).
5. Natriuresis prevents correction . of hyponatrem!a b.esides routine
salt supplementation .(in absence of fluid . restriction)~
· 1 of ·.hY
. pona·.tremia in SIADH is summarized in
· Pathop h ys10 ogy
Fig. No. : 3.3.
74 CH. ·3 .. Fluid and .Electrolyte Disorders
Fig. No. 3.3 : Pathophysiology of hypon~tremia in SIADH
.Excessive ADH activity

+
Free intake of water
.i. I
WATER RETENTION ~ J. Plasma osm~lality l
. .i. . . J. Plasma sodium !
Volume expansion ~ . . 1
Ren in ·~ · ,. · · ·' · t Renal 'pertu~ion I
,,·
-A-II · ~
· J. Aldosterone secr~etion· t ANP secretion 1
' J. ~ .
.. . Natriuresis
.
- . . . Diuresis.
. .
J.
c.
. . .
4. . Inappropriately high urinary sodium (> 20 mEq/L) insplte of low

- . . ~ -plasma sodium because u·rine does not contai'n enough water.
s·: .Rule ~~t hypothyro_i.dism, hypoaldosteronism, renal faiiu:re or diuretic
th_erapy .befor~ diagnosing SIADH. In SIADH potassium and acid·
.. : . . . base balance are normal.
. ·. p. __ Low ~erum .µric acid ~nd BUN are commonly associated findings.
D. Clinical features · ·
' SignS cin~ symptoms are relcited to the rapidity of Water ~;:i exces:
severity of hyponatremia. These sympotms ·are chiefly neural 9. nt
as discussed. previously with hyponatremia. Additionally, the patte
I • .. . .. . .
will have features related to the primary etiology. · ..
. . ..
,.
~- .. -·~...:. ~ ~ --..:~ : .. .
-.-.,,,.~,:·:~~-:~:.;';~~=~~0fa~t;~£
..
CH. 3 · Fluid and Electrolyte· Disord.ers 75
E~ -Treatment · ·
. .. . : ~ '. r· l ·
·: · Aim of treatment is water restriction and·to pr.om : "ote' w ·t··. .· · · t.;

.. . .· a er excre ion.
1. .. S~a~dard first line therapy is wat~r rest.~icti.o~ ... · · · ·· · ·
2. If it. fai~s or patient remains symptomatic, then we need a r~gimen
~h1ch .in.Greases wat~r excretion i.e. diuretics, demeclocycline and
isotonic or hypertorn<? saline. · '
a. What is the 'role of fluid restriction in SIADH .? ·
A. _Water restr_iction is t~e mainstay of. therapy in acute ·SIADH with
· symptomatic hyponatremia( e.g. ·post head~ injury) as well as in ch ·r~nic
SIADH (e.g. small cell carCinoma of lung). Negative water balance due
to fluid rest_riction r~ises the plasma sodium .concentration towards normal.
Q. What
. . .
is the .role of loop diuretics
' . .
in SIADH
' .
?. -. .. .
' .
A. Loop diuretics like frusemide, which i111pair free water reabsorpti.on and
lower urinary bsmolality, will promote larger _e.xcretion of water.
Frusemide + Sodium··repl.ace~ent ·(I.\/.· or salt tablefa) can enhance
· · tree water excretion . ., ·
. I
Q. What is the role of Demeclocycline ?

A. Drug therapy with demeclocycline is used -in .chronic: SIADH. It causes
; nephrqgenic diabetes insipidus .and _ t hereby : decreas .~$ urJnary
·concentration of sodium. So it promotes la.rger r~nalexcretion of water as
compared to sodium and wilt grad.ually correct_hyp~nat~e.mia. ~h_e _eff~ctive
dose is 600-1200 mg/day and maintenance dose is 15 mg/kgi24 h.ours.
Si.de· effects of demeclocyclin·e indude ·aioteniia,' photose.nsitivity and
·· nause·a. It is contraindicated in patients ~ith . liver dis.ease· or renai ·failure.
' .... ' , . - ' " • • :' ' I ,• ; -
. Demeclocydine is av9ided in children as ~et~acycline ca.n interfere with

bone de~elopment. In such cases Lithium is used, ~I.though it .is less
effective and po·orly tolerated than demeclocycli~e .
. ...
·
. . '
.·a. · How NaCl infu$ion c_orrects hyponatr~mia in S.IADH ?

·A. . In SIADH there · is ADH mediated · abnormal fluid · retention but
·· · excretion of sodium is ·intact o·r normal. We know·that maximum urine
output is the direct function of solute excretion rate. Larger the amount
1q1 .
1 ! 76 CH> 3 Fluid · and Electrolyte Disorders
1lr
fd
'I
',j of urinary solute excretion, greater will be the loss of water. Serum sodium
ii'
. vvill -increase and hyponatremia will be corrected only if osn:iolality
1
1
(secondary to electrolyte's i.e. Na, K, Cl) of fluid infused is higher than

that of urine osmolality. 'so response to NaCl infusion can be determined
·by ·two factors.
1. · Urinary.osmolality·(reflect'ion of severity of Sift.DH) .
2. Osmolality of NaCl infusion (0.9o/o NaCl .= 308 mOsm/kg . and 3o/o
NaCl= 1026 mOsm/kg).
f the urinary osmolality .is· greater than the osmolality of · . N~CI inh1s_ion
l_
I • ' ', ' • ' • • •
It leads to WATER '1ETENTION and

aggravation of hyponatremia is the net end result
If the osmolality of NaCl infusion is greater than the urinary osmolality
. '
It leads to WATER EXCRETION and
correction of hyponatremia is the net end result.
So to correct hyponatremia osmolality of the fluid given must exceed
the osmolality of the urine .
.Q. . What is the response of sodium solution in SIADH ? ·

A. The response of 0.9% saline in SIADH depends upon severity (urinary
·· osmolality) of SIADH. lnfact, in severe form of SIADH · 0.9% saline
infusion may even worsen hyponatremia.
In .s~vere SIADH with hyponatremia, urinary osmolality is v'ery high
. and is fixed at 600 mOsm/kg. 1,000 ml of o·.9°/o NaCl contains 'roughly
· 300 'mosm solute (150 mOsm of each Na and Cl). As urinary osmolality
is· 600 mO~m/kg, excretion of this 300 mOsm solute will require only
· 500 ml of fluid.(3o~ · mosm in 500 '. m.1of water equals to soo· mosm)
. . . ' . . . . ..
So when .1,000 ml of isotonic saline is given, all NaCl is excreted with

just 500 ml of water. So end result is retention of one half (500 ·ml) of
infused water. Such retention will lead to further dilution and reduction
. in the plasma sodium concentration. with worsening of hyponatremia.
·. .' .
CH ;. 3 : . Fluid and Electrolyte .Disorders 77 .
a. Why and how, 3o/o :NaCl corrects hyponatremia-in severe SIADH ?

A. Osmolality ~f s:o
NaCl is 1,026 mOsm/kg (513 mOsm, ·e ach. ·Na~ elf'
and Cl") which 1s greater than urin~ry osmolality (~00 mOsm/kg). in'
severe SIADH. So when 1,000 ~I of. 3°/o N.aCI is given,· all the NaCl will
be excreted but in larger volume of 1,700 ml of urine. So net end result
is loss of 700 ml of the abnormally retained "Yater leading to correctio~
of dilutional hyponatremia. 3°/o NaCl.,is inf~sed slowly, preferably with
inj. Frusemide to avoid volume o:v erload:and ·LVF.
Q. How to calculate volume of water excess in .SIADH and requirement or

3°/o· Nacl?
Amount of water excess can be calculated as follows :
Excess water (litre) = TBW x (1 - Actual Serum Na) .
· · · · Desired Serum Na ·
Total body water (TBW) = 0.6 x Body weight
In severe SIADH each 1 litre ·o{3°/o ·Nac·1will excrete approximately 700

ml of excess water .
. ·However actual volume of hypertonic saline re·q uired to correct
. ·. . ·: '
hyponatremia is less in ·clinical practice becaus·~

1. Simultaneous administration of frusemide will ·reduce_ urinary
osmolality. So greater volume of water will be excreted w_
ith lesser
urinary sodium losses.
2. Simultaneous water restriction corrects hyponatremia. · ·· · ·
3 . . In less severe SIADH, 3o/o NaCl excretes greater volum·e of excess
water.
.·To assess efficiency ~f treatment, serial ~easurement of plas.~a sodiu;

. concentration is required and treatment 1s planned. and modrfred ~s P
·.the response.·
. ' . .
' '
, ·.. · ·.·..
~ ''
78 CH. 3· : Fluid and Electrolyte Disorders
· .. Summary : Treatment of SIADH
·• ·Treat ·underlying etiology

'
• ·Acute · . : Water restri.ction, avoid hypotonic fluids ·
, Hypertonic saline I oral sodium chloride
Fn.isemide ·
• Chronic Water restriction
High salt, high protein diet,
' .I
Frusemide, Demeclocycline, Lithium

· Aim fora gradual rise' of sodium to 125 mEq/L~ at a rate <1 mEq every 2 hours
HYPERNATREMIA
Hypernatremia is defin~-d as.. plasma sodiu.m concentration greater than
145 mEq/L. Hypern~tre.mia is a Jess frequent disorder and fndicates either
lack of water or primary sodium gain.
HYPERNATREMIA IS USUALLY DUE.TO
·WATER DEFICIT AND NOT SODIUM OVERLOAD.
The thirst mechanism is very effective in preventing hypernatremia. So '
hypernatremia usually does not occur . unless there is non-availability of
water', impaired thirst or comatose-confused patient unable to drink water.
Therefore, hypernatremia is seen chiefly in very young, very ·old and very
sick or debilitated patients. ·Pure water deficit leading to hyp·ernatremia is
called dehydration. :
Etiology
.. .... .Common
.: causes of hypernatremia are summarized
' . .
'tn Table
.
No. 3.4. -
·Clinical Features
: .· . i Clinical -features of hypernatremia are primarily neurological and they
depend . upon . the rapigity of onset, its duration and its magnitude.
This is the only state in which dry sticky mucous membrane is
characteristic and body temperature is generally elevated. Major
neurological symptoms include nausea, muscular weakness, altered
mental status, neuromuscular irritability, focal neurological deficit and
occasionally coma or seizures.
·- - .
'
CH.3 Fluid and Electrolyte Disorders 79
Table No. 3.4 : Etiology of hypernatremia

I Excess water loss.
A. Insensible loss :
Dermal : Heat exposure, severe burns,· severe exercise: ·
Respiratory : Patient on mechanical ventilator.
B. Renal loss :
Diabetes lnsipidus (central or nephrogenic)
Excessive diuretics, uncontrolled OM
C. Gastrointestinal losses :
Osmotic diarrhoea.
II Water deficit due to impaired thirst.
Primary hypodypsia, confused or comatose conditions.
Ill Sodium retention.
Excessive I. V. hypertonic NaCl or NaHCO
In severe acute hypernatremia brain shrinkage may be substantial,
, exerting traction on the venous sinuses. It can cause intracerebral
and subarachnoid haemorrhage which may produce irreversible
neurological deficit or even death. The patient may also complain of
polyuria or excessive thirst. Th -e signs and symptoms of volume
depletion are often present in patient with history o"f excessive
sweating, diarrhoea or osmotic diuresis. ,
Q. Even though there is equal volume of fluid losses, why the pat'ients
with hypertonic dehydration are haemodynamically more stable than
the patients with isotonic volume depletion ?
A. Pure water loss leads to dehydration with hypernatremia (hypertonic
dehydration), whereas proportionate combined loss of water and salt
in isotonic volume depletion leads to hypovolemia and has norr:nal serum
sodium.
In isotonic volume depletion, fluid loss leads' to reduction only in, ECF
volume (and therefore early reduction in intravascular volume) leadin·g
to hypotension and reduction in tissue perfusion. While in dehydratio·n
due to pure water depletion there is proportionate reduction in .total
body water (2/3 from ICF and 1/3 from ECF). As ECF volume depletion
(and therefore intravascular volume depletion, which is 1/4 of EC~) is
much less, clinical features are lesser in pure water depletion.
80 CH. 3 ·: Fluid and Electrolyte Disorders
Fig No. 3.4 and Table No. 3.5 simplify how diffe_rent type of fluid losses
are· distributed in various fluid compartments. ·
Fig. No. 3.4 : Distribution of fluid loss

· ~orm.r ·~· ·N.D·~~ t~t·
' - ~J · ' .. . . .. ' : •
Nonnu "™'t
' • • ,..I + " > • -. ...
Table No. 3.5 : Distribution of fluid loss
Reduction Loss of 1,000 ml of fluid by

in Isotonic loss Pure water depletion
ICF - 667 ml
ECF 1000 ml 333 ml
lntravascular 250 ml 83 ml
Diagnosis
Complete history and examination may provide the clue for etiology
of hypernatremia. Renal and glycaemic status, urinary volume,
osmolality and glycosuria and response to vasopressin in diabetes
insipidus are useful for etiological diagnosis of hypernatremia.
Treatment
The therapeutic goals are :
1. To stop ongoing fluid loss by tr~ating the underlying causes.
2. To correct water deficit.
Two important factors to decide treatment plan are :
i. ECF volume status and
ii. Rate of development of hypernatremia.
-i: ":
. .,.. .
-'('
CH . ·3. Fluid and Electrolyte· Disorders · Bf
The important tr.e atment aspects are-: .

. . .
t To di~gnose an~ . treat specific etiology (Le.· treatfng diabetes insipldus,

· '. OM~ hypokalem1a, hypercalcerhia etc. ·and stopping diarrhoea)
2. .Fluid deficit .: The amount of water .required. to .correct. the deficit can
be calculated from the f.01.1owing. equation. ·
Water deficit = Plasma Na-140 x 0.6 x body weight in kg ...
.140 .
• ' • 1 • •, •
In addition to water deficit, ongoing and insensible loss needs to be

replaced. Correct the· total ·fluid deficit over 48-72 .hours.
3. Rate of correction , ~ · In acute hypernatr'emia the water deficit can
be replaced relatively rapidly, without increasing the risk of cerebral
oedema. In acu~E3 ·hy.pernatremia targeted rate of correction of
hypernatremia is 1 mEq/Uhr. Rapid correction of chronic hypernatremia
. is dangerous'. It may leq.d to neurological problems due to d~velopment
of cerebral oedema. Safe rat~ of correction is reduction of .serum sodium
by 1 mEq/every 2 hours or 10 mEq/L over first 24 hours.
4. .. Goal of treatment : The goal is to reduce seru.m Na concentration to
145 mEq/L.
5. · Deterioration of neurological symptoms after initial improvement
suggests the development of cerebral oedema and requires temporary
discontinuation of water replacement.
6. Treatment of hyperna.tremia is water. The safest route of administration
of water is by mouth or via a nasogastric tube.
7. Acute hypernatremia is treated vigorously with 0-5°/o irtfusio'n ...
Large and rapid infusion of 0-5°/o will lead to hyperglycemia and:osmotic
diuresis, which may aggravate hypernatremia. If requi:red.,-
hyperglycemia can be combated with insulin therapy.
8. Hypernatremia with ECF volume contraction : If there is severe
· loss of ECF volume with. hypotehsion and azotemia, isotonic saline is
·given 'initially until the · ECF volume is restored: Subsequently water
deficit can be replaced with water by mo~th or l.V . .~ 0/o-d.extrose or
0.45°/o NaCL
'; , ·
' ,_
82 CH. 3 :· Fluid and Electrolyte Disorders
Sodium concentration of 0.9°/o NaCl (154 . mEq/L) is greater than the

_ nor~al serurri sodium (140 mEq/L), _but is g~n~~ally_lower th.a_n the serum
sodium concentraticm in hypernatremia. ~o m1t1al t~erapy with 0.9% Naci
~as . an ___ ~dyantag~ of rapid correction of hypotension and avoiding
unnecessary rapid fall :of seru.m sodium. _. . ·_ ·
1·
9. Method to calculate change in serum Na for given infusate : Change in
I'
serum Na concentratiori, for · the infusion . ()f ·one .litre 'of .appropriately
·I
selected l.V. fluid, can be calculated by formula mentioned below
:J:1
., . . . ., .
''•"
c ·h ang_e in serum sodium concentration = .
lnfusate Na/L - Serum Na
. Total body water (~) - + 1 or
. lnfusate (Na+ K)/L - Serum Na
· Total body water (L) + 1
(For details of Na co.ncentration of infusate and method .to calculate
tbtal"body water refer treatment of hyponatremia). .
10. Hypernatremia with increased ECF volume : In these patients
-_ hypernatr'emia is secondary to solute administration. The hypernatremia
is acute and can be rapidly corrected. These patients are usually-volume
overloaded. A loop diuretic is administered along with water to facilitate
. . sqdium excretion . .In patient with -·massive -overload _or renal failure
dialysis may be necessary. ·
'·
.. . . . -. f . · • ..
ECF Vohime Disorders

. . .· •. '·
. '
ECF volum.e pisorders c~n be divided. into

' . >';1 _. • !. I . ; '. ' . ' : ·
1. ECF. Volume ·excess. · ·'" .

.., ..
2~- · · ECF Volume depletion . .: · .,.;.
ECF Volume Excess - . .

. . , E.CF vol~m~ exces~. can ,be divided into (a) water. and salt excess ·and
... ~ (b) predC?minant water.excess (w~ter intoxication or over hydration)
·" (a) Water and salt excess :
j .. . .:· ..
Water and salt excess is a frequently encountered disorder in clinical
CH. 3· : Fluid and Electrolyte Disorders 83" ·
pr~ctice, c~aracteriz~d by oedema and occurs due to syst~rnic disease

. :or iatrogenic
.
excessive saline infusion. . . . ' . . .-.
Etiology ·· . .,
·(1) ·Systemic diseases : ·
Congest~ve heartf~ilure, cirrhosis of liver, nephrotic syndrdme, acute

or chronic renal failure -or hypoproteinemia. · .. . .·
(2) Iatrogenic : ..
In hospitalized paffehts excessive and prolonged administration of

saline can cause water and salt excess espedally in traumatic and
post operative patients.
Clinical features
Weight gain is the most sensitive and consistent sigr)·; The important
presenting feature oedema, is usually not apparent until 2-4 kg of fluid
is retained. Other features are raised JVP with hepatojugular reflux,
tachycardia with bounding pulse, increase ·in systolic blood pressure,
ascites, bilateral basal crepitations, raised CVP or.pulmonary capillary
·wedge pre·s sure and pulmonary oedema in untreated se\/ere form.
Treatment • I ~ , ';l r ' I o
1. Treatment of underlying etiology.

2. Water restriction, salt restriction and di~retics are mqst)mp~rtant
and effective measures.
3. Pulmonary oedema needs extensive treatment ·Le. - propped-up
position, O inhalation, l.V. aminophylline, nitroglycerine infusion
.. and, in non-~esponsive patients, phlebotomy, dialysis or ultrafiltration~
(b) Predominant Water Excess

Predominant water excess (water ·intoxic.ation, over' hydration or ·
dilutional syndrome) is ·1ess frequent and _is · ~-~ucilly · an -~i~trogenic
· disorder. Water excess occurs·when a patient receives more water th~n
the kidney can excrete. ·With normal functioning ofth~ kidneys, posterior
. pituitary gland and adrenal glands it is almost impossible.to t~ke e~ough
water by mouth to produce water excess (except in psychotic patients).
·, ·
.
·.··
.
· r i" ~
.
--· ·
;,. : ,
' ; :~~
: '
~
84 CH: 3 · : ' 'Fluid and Electrolyte ·Disorders ·
!.
)
l'
I:1; · . ·Etiology .
i:
1i! 1. Absorption of the irrigation fluid (Le. distilled water ··or glycin
!l 1 during transuretheral resection of prostrate (TURP). . e)
~.::
2. Excessive administration of dextrose in patient · with high ADH

secretion (i.e. severe pain, tr~uma and postoperative patients).
3. Correction of salt and water loss (i.e. diarrhoea, vomiting
excessive diuretics etc.) solely with 5o/o dextrose infusion:
.. 4. Syndrome of inappropriate .ADH secreti,on (SIADH) wh~ch occurs
with cerebral and pulmonary disorders, malignancy, drugs and
stress.
·,
..;:
. :;.1
5. Compulsive water drinkers (psychogenic polydyps_
ia)
'I
I!
:l::i Clinical Features ·
: ;j 1 The .clinical picture is predominantly neurological .d.ue to
11
,:,i '/. ·hypoostnolality, hyponatremia and increased intracranial press.ure.due
1
1: "to brain .cells swelling. ·
111 1
'J'
1· /11 . Common features are : Confusion, loss o_f attention, altered behaviour,
,1 11!
j: jl drowsiness, nausea and vomiting. In severe cases, it can cause
,:
1
·11 convulsions and even coma.
}~I 0 n investigations urine is diluted with low specific gravity and serum
.' 111' sodium arid osmolality are low.
I
I
I''
l· !./1 l
1
;, :1
1
Preventi.on , . . . . 1
I 111
,;. /Ii i • 1~ · Don't correct all fluid loss with 5% dextrose. Commonest form of
1
i lj ! , fluid loss (i.e. diarrhoea, vomiting) needs sodium containing fluid ;
111 i
·.,ill administration (i.e. 0.9% saline or R~nger's. lactate). . - _.~
; :/; 2. . .Avoid excessiv~ infusion of 5°/o dextrose in all hpspitq.lizeq patients
:(1'; requiring I. v.' fluid therapy' .main,taining strict input ' outp~t dcha~ I
·':: .. ; Calculate volume of fluid .and amount of electrolytes require a I

il:j i . ·. . a~co rdi ngly select Proper I. V. flu id for infus ion. . I
, :1;1i · •· a · If a patient undergoing TURP sliows signs and sympto~s of wa~~; I
r
i rj;:
It '1
!i\
:
intoxication~ the procedure should be terminated and patient shO
be treated promptly.
I
CH.3
Fluid and Electrolyte Disorders
85
Treatment
1. · Fluid restriction is the first · d . . . · .· · · . :
excess. It effectively correc~: most impo~ant treatment of fluid
. moderate fluid excess · "
2. Few symptomatic patients .(convulsions . . . . . . . . .
excess. require vigorous treat . or coma) ·with severe water
and frusemide. Corr.ection of ;e:~:;th h~pertonic saline (3% NaCl)
prevent central pontine de~pelin r~m1a should.be done sl;owJ~ to
syndrome) .as discussed un.d yh ation (~sm9tic d~myehnat1_on
· · · er yponatremia. · .
. 3. Seatch for the etiology of wat · · . · .. .- .
treatment. Treatment of SIADH . erd.excess and ~rov1de specific
is 1scussed previously.. .
ECF Volume Deficit · · ' ·
. Variety of .disorders lead to volume defi 't . ". d .· . " ..
· fl · . . . Cl in ay to day practice
Severe Uld def1c1t, if untreated can be leth I . P . " therapy
. . m ..
.. . . . , . a . roper flwd
sue h a patient 1s very much ·rewarding. .
,.. ECF volurlle deficit can be divided into :
1~ · Isotonic volume depletion :
· Combined loss of both water and salt.
2. Pure water depletion :
Predominant water deficiency with minimal electrolyte de:flciency.
l~portant differentiating points are :
1. Combined loss of water a·nd salt in isotonic volume dep.letion leads to
hypovolemia, while pure water loss leads to dehydration. ·
2. Most common causes of hypovolemia are diarrhoea, vomiting or excess
diuresis, while most common causes of pure water depletibn are poor
oral intake and diabetes insipidus.
3. Isotonic volume depletion has normal or low sodium while pure water
loss with dehydration ~s characterized by hypernatremia.
4. In isotonic volume depletion, fluid loss leads to reduction only in ECF
volume (and therefore early reduction in intravascular volume) leading
· to.hypotension an_d reduction in. tissue perfusion. While in dehydration
due to pure water depletipn there is proportionate reduction in total
body water (2/3 loss of water from ICF and 1/3 loss from ECF). So
86 CH. 3 : : Fluid and ·Electrolyte Disorders
ECF as well as intravascular volume (which is 114 of. EC~~ depletion is

. much 1.ess with less~r hypotension; .Table No. 3.6 simplifies how fluid
loss is distribute.d in v~rious fluid compartments.
Table No. 3.6 ~ Distribution of fluid loss .
Reduction Loss of 1,000 ml of fluid by
· In. · Isotonic loss Pure water depletiOil'
. ICF - '. 667 ml ----...
ECF 1.,000 ml 333 ml ---...
ln_travas~~lar 250 ml 83 .ml ---
--
5. Important teatuies of isotonic volume depletion ·are dry tongue,
tachycardia, postural hypotension, dizziness, oliguria and azotemia with
. disproportionate elevation of blood urea and dimif)ished urinary _sodium.
. l.n severe.form there are colc;f clammy extremities,·shrut:lken "eyes; and
· poor or absent peripheral pulses and hypotensiof1. While in pure water
depletion characteristic features are excessi_ v e thirst and CNS
manifestations secondary to · hypernatremia (altered sensorium,
confusion, convulsions and coma). As ECF and intravascula·r volume
are less affected, blood pressure and tissue perfusion are better
maintained.
6. In both types of fluid deficit, . etiological treatment is very. important.
In addition : I
A. Correction _of isotonic volume _

depletion (hypovolemia) is best done
with 0.9°/o NaCL
B. Pure water depletion (d,ehydration) is best treated ~ith. increased
ora~ wat_
er intake or dextrose-5°/o infusion.
1. Hypovolemia I ' '~
For furt,h er discussion of clinical features and treatment of

hy_povole~ia referChapter No. ~- and Chapter No. 4.
2. Pure water deficit

' I
Pure water·1.oss leads to deficit of water without significant elect~o1yte
l?sses leading to plasma concentration-hypernatremia. Pure water
CH . .3 Fluid and Electrolyte Disorders 87
loss oc~urs if loss is solute free. Hypernatremia is the hallmark.of

diagnqs1s of pure wat~r loss. Etiology, olinical features and tre~tment
. of pure water loss are. discuss~d :with hypernatremia . . ·. ' · ··
lmportant_.rena_Icause of pure water loss ·is diabetes .in. ~ipi~us (DI),'
characterized by polyuria. Approach and management of polyuric
patients and diabetes insipidus are discussed bei'ow.· :
! •
Polyuiia is a·frequen·t.ly encountered clinical problem: Polyuria is defined as

excretio'n of exc~ssive a·mount of urine. Average daily urine volume is 1.6
litres in a healthy adult ' and excretion of 'more than. 3-4 fitres/24 hours
suggests polyuria. · :· · · ·· · ·
It is important to differentiate polyuria from the more frequently encountered

din.ical problem urinary frequency, characterized b'y muitiple voids of
refatively small volume. In urinary frequency 24 hours urinary volume is
within the normal range.
Etiology
Etiology of polyuria is summarized in ·Table No. 3. 7. ·
Table No. 3. 7 : Causes of polyuda
I. Solute Diuresis
.. (Urinary osmolality ; 300 mOsm/kg)
tic ph.ase .of ATN,
A. ... Renal : Post obstructiv.e diuresis, diure_
salt losing nephropathy . .
B. ·uncontrolled diabetes mellitus, renal glycosuria .. .
C. Mannitol infusion, loop diuretics
. D. High protein tube feeding
· 11. Water Diuresis
· (Urinary osmolality < 250 mOsm/kg)
A · Increased water intake · · ·
Psychogenic polydypsia ·
;: B. . lncre~sed renal loss ·
1. Central diabetes insipid us ...
2. Nephrogenic diabetes insipidus
·. .. ~
·:
. ......
•!
.
-
1.- ..,.
I
88 CH. 3· : Fluid and El ectrolyt e Dlsordors
Diagnosis . .. . .
ortant step Is to measure urinary
In polyunc patient firs~ and the. most ~P
• • .. . . 1
diuresis (with high Uosm)
osmolality (Uosm), which can d1fferent1ate solute
from water diuresis (with low Uosm) (see Table No. 3.7}
I. Solute Diuresis
Concentrated urine with urinary osmolality gr.eater .than 300 mOsm/
kg is suggestive of solute diuresis in polyunc patients.
History : History of renal disease, recovery phase of ur in~ryh.
1
1.
obstruction or ATN-ARF, diabetes mellitus or treatmen wit
mannitol, loop diuretics or high protein feeding will be very
useful in arriving at the diagnosis.
2. To confirm diagnosis : Necessary laboratory and
r~diological investigations should be done (blood sugar to rule
out diabetes mellitus, renal function tests, electrolytes and
sonography to rule out renal disorders)
If. Water Diuresis
Diluted urine with urinary osmolality less than 250 mOsm/kg is

suggestive of water diuresis. The three important causes of polyuria
due to water diuresis are primary polydypsia, central diabetes
insipidus and nephrogenic diabetes insipidus. These disorders are
distinguished with the help of history, laboratory test (serum Na+,
2
K+, Ca+ , glucose, blood urea etc.), response to water restriction
and response to exogenous ADH (5 units of aqueous vasopressin
subcutaneously or 10 µg of dDAVP by nasal insufflation).
Fig. No. 3.5 summarizes simplified approach to polyuria due to
water diuresis which can be applied to most of the patients. At
times it i~ difficult to differentiate between partial DI and primary
polydyps1a. More definitive diagnostic approach in such patients is
to measure plasma .or urinary vasopressin and urinary osmolality
before and after suitable osmotic stimuli such as fluid restriction
or hypertonic saline infusion.
I
t
CH . 3 : Fluid and Electrolyte Disorders 89

l
I
I
Primary polydypsia (compulsive water drinking)

• Vagueness regarding onset of polyuria and variability regarding
severity of polyuria and nocturia. I I
• No complaint of thirst.
l
• Most often seen in anxious, middle aged women and patients with
psychiatric illness including those taking a phenothiazine which .
I
can lead to sensation of dry mouth.
• Normal or low serum sodium due to water overload. In response
to water deprivation urine output decreases and urinary osmolality
increases.
DID between prim ary polydyspia and diabetes insipidus

Prima ry polydyspia is a diso rde r of wa ter excess, so the serum sodium
co nce ntration is typica lly in the low normal range (135-140 mEq/L),
i.,•rhile diabetes insipi 1 1 ciiso rcle r of wa ter loss and the serum sodium
conc entration t r cf in Ui · ti igh normal range ( 140-145 mEq/L).
Urin ary osm ol ality v/s ur ina ry s pecific gravity

If there is no f ilt 1 m c..s 1r urinary osmolality how to approach a
polyuric p ati nt ?
In norm al urine. speci{ic c r vitv varies in a predictable way with urinary
osmol ality . So Nh n facili ties are not available for measurement of
uri nary osmol ality. urin ary specific gravity should be measured.
For every 35 mOsm/kg increa se in urinary osmolality, urinary specific

gravity will be raised by 0.001. Thus a urinary osmolality of 280 mOsm/
kg is associated with a sp ecific gravity of 1.008 approximately.
This correlation is lost if urine contains abnormal large solute e.g. glucose
(glycosuria in uncontrolled OM) , radio contrast media, mannitol or
carbenecillin.
. . . -,.-
.. .
. '
·,
90 OH. 3 :· Fiuld and Electrolyte · Disorders
' 'I i
Fig. No. 3.5 : Approach to polyuria .. ,
POLVURIA DUE TO WATER DIURESIS

(Uosm < 250 mOsm/kg)
J. .
· · 1
. .
Water Restriction
I
I· i
J:
Decreased Urine. Output No Response
· Uosm > 800 mOsm/kg J.
J. Diabetic lnsipidus
PRIMARY POLYDYPSIA ' J. '

Response to Vasopressin
.' J: I
Decreased Urine Output · No Response
lnci'eas·ed ·Urinary Osmolality
CENTRAL
J.. . J
NEPHROGENIC·
DIABETES INSIPIDUS DIABETES INSIPIDUS . : .
CENTRAL DIABETES INSIPID.u s (DI) '

Central . (Neurogenic, pituitary, hypothalamic or vasopressin responsive)
diabetes.· insipidus · is characterized by · the excretion of abnormally large
amount of diluted urine due to lack of suffident ADH secretion. ADH is
responsible for · renal re.a bsorption of water. Under influence of ADH,
.collecting tubule.s reabsorb upto 18 litres of water .per day and lead to
concentration of urine and water conservation. Central 0 ·1may result from
damage or loss of the pituitary centre of ADH synthesis or release.
Etiology
Causes of central diabetec insipidus (D.I.)
I. Idiopathic (more than 50o/o of all cases).
·r --·
f
CH. 3 Fluid and Electrolyte Disorders .91 .
11. Destruction of neurohypophysis

1. Trauma, brain surgery
2. Granulomatous disease (tuberculosis, sarcoidosis)
3. Brain tumour (benign, malignant), meningioma
4. Metastatic brain tumours (Carcinoma breast)
5. Vascular accidents (brain thrombosis, haemorrhage or aneurysm)
6. Infections (meningitis, encephalitis)
Clinical features
The hallmark of central D.I. is acute onset of se~ere polyuria and.severe
thirst in absence of osmotic diuresis. It begins so abruptly that patient
can date the exact onset. Characteristically, there is a ma·rked preference
for ingesting very cold or ice water and absence of any diurnal variation
so polyuria and thirst persist even at night.
Degree of polyuria in diabetes insipidus depends upon severity of diabetes
as well as the patient's volume status and solute intake. Urine volume
may vary from 3 to 15 litres per day.
In ambulatory patients with free access to water, plasma osmolal.ity.and
serum sodium tends to be on the higher side of.normal. If the patient is
unable to take free water due to bedridden condition, confusion or any
other reason, severe hypernatremia with neurological manifestations can
develop rapidly.
Diagnosis
Urine is markedly diluted (specific gravity < 1.005 and Uosm < 150
mOsm/kg). In severe central D. I. basal plasma osmolality and sodium
concentration is high and polyuria is abolished by vasopressin treatment
but not by water deprivation.
Treatment
The treatment of central 0.1. is summarized in Table No ..3.8.
92 . .. 3 : .Fluid and Electrolyte Disorders
CH
Table No. 3.8 : Tr~atment of central diabetes insipidus
ADH Preparations
Aqueous . t'
vasopres~m (short-ac mg,
used primarily
. for diagnosis) dDAVP
nasal spray
Drugs that increase ADH release
Clofibrate
Drugs that potentiate ADH effect
'chlorpropamide
Carbamazepine
Nonsteroidal anti-inflammatory drugs
Drugs and measures not requiring ADH
Diuretics (thiaz.ides and amiloride)
Salt restrietion ·
dDAVP nasal spray
dDAVP nasal spray is the most physiological therapy of central D.I.,

and requires one or two time administration. It has antidiuretic but. no
. . presser activity and is given by nasal insufflation. The usual starting
dose is 5 µg twice daily. Major hurdle in this therapy is the high cost.
Chlorpropamide
Chlorpropamide used in dose of 125-250 mg once or twice daily, often

lowers the urine output by 50% or more in responsive patients. It acts by
increasing responsiveness to ADH or by direct stimulation of NaCl
reabsorption in thick ascending limb of loop of Henle by raising medullary
interstitial osmolality. Major side effect of chlorpropamide is hypoglycemia.
The drug is more effective and less toxic when combined with thiazides
. in treatment of central D.I .. This combination can reduce polyuria to
asymptomatic levels in virtually all adult patients with this disorder.
Thiazides
Thiazide diuretics have paradoxical antidiuretic effect. They reduce

urinary output by about 50% and restricting sodium intake can further
enhance their efficiency. Unlike vasopressin, chlorpropamide, clofibrate
and carbamazepine, thiazides are equally effective in both central and
nephrogenic D. I.
_ . . ·. . . ..
rF .
Thiazide induced reduction of polyuria is primarily due to diuretic induced

hypovolemia. \jolume depletion is associated with enhanced prox.imal
tubular sodium and water reabsorpti6n. As a result, less water is delivered
to the collecting tubules (the site of ADH effect). So it enhances
vasopressin-independent wate·r reabsorption, and therefore less water
is excreted. Usually required dose of hydrochlorthiazides is 50 to 100
mg per day.
Addition of the potassium sparing diuretics can enhance the diuretic
response of thiazides, while also minimizing thiazide induced
hypokalemia.
Clofibrate
Clofibrate, which is used to treat hyperlipidemia, also reduces polyuria
in central D.I., but is less effective than chlorpropamide. Clofibrate
appears to enhance ADH secretion. Usual dose of clofibrate is 500 mg
four times daily.
Carbamazepine
Carbamazepine 400-600 mg/day may potentiate ADH release in state
of partial central D.I.
Like thiazide diuretics, carbamazepine and clofibrate can produce more
than 50°/o reduction in urine output in responsive patients.
NEPHROGENIC DIABETES INSIPIDUS .
Nephrogenic di,abetes insipidus is characterized by normal ADH secretion

but varying degree of resistance to its water retaining effect leads to p.olyuria.
It can occur due to
(a) Loss of medullary hypertonicity because of anatomical disorder of
kidney.
I
(b) Functional disturbances and inability of the collecting duct epit~elium
r
I
• · to respond to vasopressin.
~
I
I
I
I
.. l '
,;' .
"
•i'I
94· . CH : 3 · : . -.Fluid and Electrolyte Disorders

: I • ~ •
Etiology " :
Absent or decreased collecting duct resp~nse

. .
to va~opressin
. . - . :
' '
:i::
'· . j (1) Congenital · . · .. · ·
(2) .. Drugs : .Lithium, Demeclocycline, Amphotenc1n 8
(3) Hypokalemia
(4) Hypercalcemia
II . .Loss of medullary hypertonicity ~
(1) Chronic interstitial nephritis

(2) Medullary cystic disease
(3) Obstructive uropathy, amyloidosis
(4) Polycystic kidney disease
' ..
Ill · Both
(1 )_ Post obstructive diuresis
(2) Sickle cell disease
Clinical features and diagnosis f

I
Clinical picture is that of underlying etiology, dehydrati_on and 1
hypernatremia depending upon the severity of disease. Picture is similiar ·
. . . I
to centra_I diabetic insipidus but_onset is more gradual. Urine output is ·

moderately increased .(3 to 5 litre~/day) . 1
As discussed previously in diagnosis of polyuria these patients are .

non-responsive to both water restriction and vasopressin administration. i
Detailed history and laboratory tests may-identify the 3 major causes I
.of N~phrogE3ni9
.• ·. .
D. I. ; Lithiur:n toxicity, hypercalcemia
. . .
and hypokalemia. /
·T reatment -
Treatment of Nephrogenic D.I. is more limited because only modalities
.that act ~ independent of ADH are effectiv~. Treatment options are
mentioned in Table No. 3.9.
Like in central D. I., thiazid_es and salt restriction are effective in
nephrogenic D.I., but vasopressin and _ chlorpropcimide are totallY
ineffective in nephrogenic D.I.
- ·.
CH. 3 : . Fluid and Electrolyte Disord~rs · 95
Table No. 3.9 : Treatment of Nephrogenic Diabetes lnsipidus .. ·

Encourage adequate water intake
Eliminate drugs : Lithium, demeclocycline, Amphotericin B
Thiazide diuretics
Salt restriction, low protein diet
NSAID
Amiloride for lithium induced D.I.
High dose of dDAVP
Correction of etiology : hypokalemia and hypercalcemia
NSAID (lndomethacin) : By impairing renal prostaglandin synthesis,

NSAID potentiates ADH action and thereby increases urine osmolality
and decreases urine volume. ·
Amiloride : It is useful in treatment of lithium i_nduced nephrogenic
D.I. Amiloride functions by blocking entry of lithium into the collecting
duct cells and thereby reducing its cellular toxicity.
In lithium induced nephrogenic D.I., thiazides should be avoided.
Thiazides induced sodium depletion leads to increased. reabsorption
of lithium by proximal tubules and can lead to lithium toxicity.-
POTASSIUM
Potassium Regulation
1. Physiological basis
Potassium is a major intracellular catio·n. Total body potassium is about
3,500 mEq. Out of this 98°/o is intracellula~ and just 2o/o is extracellular.
The normal serum · potassium concentration is· 3 :5 to 5.0 mEq/L vs
intracellular concentration of 150 mEq/L. Normal requirement of K+ is
50-80 mEq/day. Potassium plays an important role in cell functions and
neuromuscular transmission so it is required for normal function of cells
and all muscles.
2. Regulation
i. Chief regulation of potassium is through renal excretion:.
Almost all filtered potassium is reabs~rbed. K+ i9n _excreted is the
. one secreted at distal tubules .and .collecting duct. . .. .
96 CH. 3 Fluid and Electrolyte ·oisorders
·;'
ii. K+ secretion (and therefore excretion) is controlled by aldost · >

distal fluid ·and sodium ·d elivery, serum H+ ion and ser~rone, '.·-
rn K' :·
concentration. i
iii. K+ secretion (and therefore excretion) is increased due to h'

aldosterone level, incre~sed distal fluid and sodium deliv~~h
alkalosis and hyperkalem1a. '
iv. Effect of acid base balance : Metabolic acidosis increases seru
potassium level while metabolic alkalosis reduces serum K+ leve~
v. Glucose insulin infusion pushes potassium inside the cell leadin
9
to lowering of serum potassium level.
3. How renal regu_lation of potassium and sodium differs ?
Unlike sodium, absorption of K+ is not complete. About 20 mEq K+ is
lost everyday even in absence of potassium intake. So hypokalemia
frequently occurs in the patient who is on potassium free maintenance
fluid therapy.
4. Correlation of serum and body potassium :
It is important to remember that whenever body potassium increases
serum potassium rises proportionately and may reach to a dangerous
level rapidly. But when there is deficit in total body potassium, reduction
in serum potassium is not proportionate because it is partly
compensated by shift from intracellular compartment. So hyperkalemia
suggests increased total body potassium but level of hypokalemia may
under estimate total body potassium deficit.
. DISORDERS OF POTASSIUM CONCENTRATION

Disorders of potassium are hypokalemia and hyperkalemia.
HVPOKALEMIA
Hypokalemia is defined as persistent reduction of serum potassium (K+)
below 3.5 mEq/L.
I. Etiology
Common causes of hypokalemia are summarized in Tab.le No. 3. 10 ·
,
(
~r . .
CH, 3 : Fluid and Electrolyte Disorders 97
!_able No. 3.1 O : Causes of hypokalemia

1. Poor Intake
Low dietary intake or potassium free l.V. fluids
2. Non Renal Loss
(Urinary potassium excretion < 20 mEq/d ) .
.. d' ay .
Vom1ting, iarrhoea, excessive sweating and Iarge nasogastnc
. aspiration
.
3. Renalloss
(~rin~ry potass~um excretion > 30 mEq/day) :·
D1.uret1cs, os.m~t1c diuresis, salt-wasting nephropathies
Mmeralocort1co1d
. , excess (primary or secondary aldosteroni sm )
Cus h mg s syndrome, steroid therapy
Magnesium deficiency, Amphotericin B, Bartter's syndrome
4. Redistribution (shift of K+ into cell)
Metabolic alkalosis
Insulin, 8 2 adrenergic agonist (i.e. salbutamol)
Hypokalemic periodic paralysis
II. Clinical Features

·• Clinical picture varies greatly and seldom occurs unless serum
potassium is less than 3 mEq/L. The manifestations of hypokalemia
are mainly neuromus~ular and cardiac.
• Fatigue, myalgia and muscular weakness of the lower extremity
are common complaints.
• Smooth muscle involvement may result in constipation , ileus or
urinary retention.
• More severe hypokalemia leads to progressive weakness .
hyporef.lexia,hypoventilation (due to respiratory muscle
involvement) and virtually complete paralysis.
• Hypokalemia leads to increased risk of arrhythmia especially in
patients on digitalis treatment.
.,_
• Hypokalemia can lead to polyuria due to nephrog~nic di~betes
insipidus. Hypokalemia can cause increased am~ornag~nes1s a~d
can precipitate hepatic encephalopathy in patients with hepatic .,i
' ~
failure.
·{
i
. ~
i
I
\
'
98 CH. 3 Fluid ·and Electrolyte ·Disorders
ECG changes
• Do not correlate well with the serum potassium .. r
• Early changes :
I
Flattening or inversi~n. of T waves
Prominent U waves
ST segment depression
Prolonged QT interval
• Severe potassium depletion :
Prolonged PR interval
Decreased voltage
Widening of QRS complex
Ventricular arrhythmia
Ill. oragnosis of etiology of hypokalemia

A. History : History of poor K+ intake, abnormal losses due to diarrhoea,
vomiting, diuretiG therapy, or transcellular shift of K+ due to insulin,
NaHC0 or salbutamol can identify cause of hypokalem.ia.. \
3 . . . I
8. Urinary K+ excretion: In patients with K+ deficit appropriate response i
is to excrete K+ less than 25 mEq/day. Measurement of urinary K+
excretion is very useful to establish etiological diagnosis ol
hypokalemia. . . . I
1. Hypokalem1a with low renal K+ excretion (< 25 mEq/day) i
It suggests poor intake of K+, diarrhoea, excessive sweat or
previous K+ loss due to vomiting or diuretics.
2. High urinary K+. excretion besides K+ deficit. 'd
The ECF volume status, blQod pressljre and associated .aci.
base disorders are useful for arrivi.ng at of etiological diagnosis
. Q.f K+ wasting with hypokalemia. .
. - . .n
.a . K~ wast_ing with m:tab~lic acidosis with no hy~erten~~A·,
.·. •'
. . .• D1a.b et1c ketoac1do.s1s, proximal and ,distal
amphotericin B.
j
I
l CH. 3 .. Fluid and Electrolyte Disorders .·99
I!
. . b. K+ wasting·with variable pH. . . .· .
Renal
. . salt wastin g ·· Recovenng
· · ATN postobstructive
·
d 1ures1s. '
c. K+ wasting "."ith metabolic alkalosis with no Jl~pertension :
i. L~w un~ary ch_lo~ide (~ 20 mEq/day) : Vomiting.
iL High urinary chloride : Diuretics, Bartter's ·syndrome.
d. K+ :wasting wjth metabolic alka.losis With hyperte~sion.
Pnmary and secondary . al.dosteronism,. .Gu~hing's
syndrome, .r~novasc~lar. hypert.en.sion, Liddle'_s syndrome.
IV. Treatment ·.'
A. Therapeutic goals : .:·
1. Prevention of hypokalemia ·
2. To p·revent life threatening complicatfons.
(arrhythmia and respiratory failure)
3. To correct the potassium.
' . ,. . . deficit
. .
4. To minimize on-going losses ·

5. To treat underlying etiology
B. ·Prevention of potassium depletion ·
Normal potassium intake of about 60 mEq/day ·is. sufficient to
prevent hypOkalemia. But patients receiving digit81is, !Ong term
· diuretics or la'rge doses of steroids should · receive potassium
Supplement. Conditions where prevention of hypokalemia is of
. special importance are digitalis therapy, hepatic failure, previous
myocardial infarction or IHD and diabetes mellitus.
Postoperative patients on parenteral fluid 'therapy shouid receive
40-50 mEq/day of potassium to preverit hypokaleri1ia.
c. How much total body potassium deficit occurs in

hypoka_le~i_a ? .
The degree of total body potassium depletion does not correlate
with serum potassium. ··
-· " --_
:.;!
.... : .•_:
100 . -CH. 3 Fluid. and Electrolyte Disorders
;,
Roughly 1 mEq/L fall in serum potassium = 200-400 mEq total · · •·

; 1
potassium deficit. . . · ; . . body
, I Table 3.11 : Potassium deficit, normal plasni·a pH ·
Serum K+
> 3.5 3 2 <2
-
(mEq/L)
Total K+ 450-600
-
0 300 > 600
deficit (mEa)
-
D. When to treat hypokalemia ?
Widely followed guidelines are as follows :
Serum Potassium : Treatment Guidelines
3.5 to 4 mEq/L : --
No potassium supplement
Increased oral intake of potassium rich food
Add potassium sparing diuretiqs or decrease dose of diuretics
l: 3 to 3.5 mEq/L :
" I
Treatment in selected high risk patients

:!
I
~
:
:I
( Risk of arrhythmia e.g. CHF, digitalis therapy, history
,,
;; j of acute myocradial infarction or IHD. ) ..

': !
:I :
:j j
< 3 mEq/L :
! '
i I
Needs definitive treatment
I '
! I
'
' '
' E. Precautions before initiating potassium supplements
'
;'
'
I
1. In oliguria-anuria, avoid or supplement K+ caut_

iously.
2. _Patient's receiving potassium sparing diuretics, ACE
inhibitors and patients with renal failure are at high risk of
developing hyperkalemia, so potassiu.m supplementation should
b~ done cautiously.-
3. Digitalis therapy .: In patients on digitalis, potassium enters the
cell at a slower rate so there is a risk of transient hyperkalemia with
faster I. v·. infus.ion. So rate of infusion should be < 20 mEq/
hour.
4. Continuous ECG monitoring and frequent ·serum potassium
20
level estimation is advisab.le. if the rate of infusion is >
mEq/hour in any patient.
l i
CH .. 3 : Fluid and Electrolyte Disorders 1Ot ·
F. How much pota~sium to give ? How long to treat ?

The amount of potassium required to correct potassium deficit cannot
be determined by any fixed formula.
When the average deficit of potassium is about 200-400 mEq, 50-
100 mEq/day of potassium slowly, but adequately corrects deficit.
With severe hypokalemia·or with high rate of ongoing loss, larger ·
dose may be required.
The deficit should be corrected ·slowly over a period of days. It may
take weeks to correct severe potassium loss. Failure to increase
serum potassium after sufficient dose and duration of potassium
supplement raises the possibility of associated magnesium deficiency.
G. Which potassium preparation is selected for supplementation ?
Potassium chloride (KCI) is usually the preparation of choice and
will promote correction of hypokalemia as well as of metabolic
alkalosis (vomiting and diuretics lead to both hypokalemia and
alkalosis).
Potassium bicarbonate and citrate tend to alkalinize the patient and
would be more appropriate for hypokalemia associated with chronic
diarrhoea or distal RT A.
Oral potassium administration is safer than 1.V. route because
I. V. route carries high risk of hyperkalemia. :·
H. Oral potassium supplementation

• Oral potassium is a safer mode of corr~ction of hypokalemia
as there is minimal risk of h~perkalem1a. .
• In mild to moderate hypokaler:nia (serum potassium 3 to 3.5
mEq/L) average dose of potassium chloride is 60 to 80 mEq/~ay
( mEq, _4 times) along wi.th treatment of underlying
3
20
disorder (such as vomiting or diarrhoea).
,.
. . t mati·c hypokalemia more rapid replacement \"
I .
• I.n severe or symp o

d d d b most easily done by oral replacement. In
1s nee e an can e ssium 2 mEq/L or less) .1t can be
severe cases (serum . P. Ota . .
. · d E 6 hourly under close ECG monitoring.
increase upto 40 .m q . .
102 CH.- 3 :· ·Fluid and · Electrolyte Disorders
• Potassium chloride solution, available in the market contains 20

.... . mEq potassium per 15 ml solution (~gm KCl=13 ..4 mEq of
potassium).
• KCI tablets available contain 8 mEq potassium per.tablet.
• Oral potassium preparation may frequently cause G.I. irritation
and therefore the patient is advised to take potassium chloride
solution with proper dilution in a glass of water, after food.
• Oesophageal or small bowel erosion and stricture are
uncommon side effects.
· I. l.V. Potassium Therapy
l.V. potassium supplementation carries higher risk of hyperkalemia.
So l.V. potassium supplementation should be reserved for severe
symptomatic hypokalemia (K+ < 3 mEq/L) or for patients who cannot
ingest oral potassium.
·No rule is absolute, but common guidelines for l.V. potassium
therapy are as follows :
• Always monitor l.V. potassium therapy closely with continuous
ECG monitoring and frequent serum potassium estimation.
• Avoid l.V. potassium, till urine output is established .
• Don't give> 10-20 mEq/hour .
• Don't give> 40 mEq/Litre .
• Don't give> 240 mEq/day .
• Never give inj. KCI directly intravenously, it can cause sudden
hyperkalemia and instant death from cardiac arrest.
• Never add KCI to lsolyte-M .
• Remember that hypokalemia is safer than hyperkalemia, so
avoid over enthusiastic treatment.
• Rapid I. V. correction can cause dangerous hyperkalemia even
in potassium depleted patients.
• Tre~t~ent of acidosi.s with l.V. NaHC0 may aggravate or
3
prec1p1tate hypokalem1a (due to intracellular shift of potassium).
•;' _
CH. 3 Fluid and Ele.c trolyte Disorders 103 ·
·• In severe hypokalemia, KCI should be mixed with isotonic .

saline. Don•t use D-5°/o ·as . diluent · because dextrose
stimulated insulin release will shift pota~sium intracellularly
and hence initially aggravates hypoka~emia. Here transient
reduction .of serum potassium can be 0.2 to .1.4 mEq/L if 20
mEq K+/L of D-5o/o is infused.
• Diabetic ketoacidosis and nonketOtic · hyperosmolar
hyperglycemia are amongst the commonest indications .of l.V .
.potassium therapy. ·
J.- How to give I. V. potassium and how long ?

Depending upon etiology readymade available l.V. fluid _ s can
be used to provide potassium supplement e.g. lsolyte-G in vomiting
or continuous nasogastric _aspiration, lsolyte-M for parenteral fluid
therapy etc.
To make tailor made potassium chloride infusion, 1oo·mEq of
·potassium. ( 5 ampoules of 1O ml, 15°/o KCI ampoules) is mixed
in 1 litre of isotonic saline. Infusion of this saline at rate of 100
ml/hour ( 25· macrodrops or 100 microdrops ) will deliver 1o.
mEq KCI per hour.
• Potassium concentration> 40 mEq/L can cause phlebitis and
should be infused only into large (femoral or subclavian) veins.
• Average rise in potassium level is 0.25 mEq/L, when 20 mEq
is given during one hour. Usually 80°/o of the administered
dose enters cells.
How long to give ?

As soon as cardiac rhythm retu.rns to normal or the respiratory
muscle strength is restored to normal, l.V. potassium drip is
gradually tapered and ·discontinued and oral KCI is initiated.·.:
K . Potassium supplements
• · .· .Potassium rich food : Fruit .juices, coconut water, ba~ana,
. · juicy fruits, dry fruits, chocolate, coffee, soup, salt substitutes ·
e.g. Lona salt.
.,
·, :j'\··
. ·. ' -"':,
104 CH. 3 Fluid and Electrolyte Disorders
• lnj. Potassium chloride : Most widely available and used is

inj. KCI 15°/o, 10 ml ampoule.
10 ml of 15°/o KCI = 1.5 gm KCI = 20 mEq of potassium
1 ml of 15°/o KCI = 2 mEq of potassium .
• Potassium concentration of commonly used l.V. fluids is
summarized in Table No. 3.12.
Table No. 3.12 : Potassium concentration of l.V. fluids
-
1.V. Fluid lsolyte-M lsolyte-P lsolyte-G lsolyte-E · Ringer's
Lactate
-
Potassium 35.0 20.0 17.0 10.0 4.0
(mEq/Litre)
HYPERKALEMIA
Introduction
Serum potassium level greater than 5.5 mEq/L is considered
hyperkalemia. Hyperkalemia is not as common as hypokalemia and
it's clinical manifestations are fewer but more severe than hypokalemia.
Mild hyperkalemia ( serum potassium 5.5 to 6.5 mEq/L ) is of slight
concern, but moderate to severe hyperkalemia can be life threatening.
Etiology
Common causes of hyperkalemia are summarized in Table No. 3.13.
Clinical Features
Hyperkalemia is often asymptomatic until plasma potassium
concentration is above 6.5 to 7.0 mEq/L and may lead to fatal cardiac
arrhythmia hence it is called a silent killer.
Vague muscular weakness is usually the first symptom of
hyperkalemia. Severe hyperkalemia can lead to hyporeflexia, gradual
paralysis affecting initially legs, then trunk and arms, and at last f~ce
and respiratory muscles. Paralysis usually spares the muscles supph_ed ·
· .by.cranial nerves and patient remains alert and apprehensive until cardiac
arrest and death occurs.
I • , -
CH 3 · Fl 'd · . .
. . u1 and Electrolyte Disorders 105 .
i:
.I
\.
,
Table No. 3.13 : Causes of hyperkalemia
f:
~
1. Increased intake )
'
i. I. V. fluid containing potassium

ii. High potassium containing foods I
2.
iii. Potassium containing drugs
Tissue Breakdown
!
i
i. Bleeding into soft issue, G.I. tract or body cavities I
ii. Haemolysis, Rhabdomyolysis
iii. Catabolic state \
3. Shift of potassium out of cell r
i. Tissue damage ( ischemia or shock), severe exercise
ii. Metabolic Acidosis
iii. Uncontrolled diabetes due to insulin deficiency
iv. Aldosterone deficiency
v. Hyperkalemic periodic paralysis, succinyl choline
4. Impaired Excretion
i. Acute renal failure or chronic renal failure
ii. Potassium sparing diuretics, ACE inhibitors, NSAID,
heparin, cyclosporine I
iii. Reduced tubular excretion : Addison's disease i

l !
!
hyporeninemic hypoaldosteronism and amyloidosis i
iv. Effective circulatory volume depletion
5. Pseudo hyperkalemia
i. Traumatic haemolysis during blood drawing
ii. Thrombocytosis, marked leucocytosis
The patient may complain of tingling around lips or in fingers but is

more likely to present with slow or irregular pulse rate or collapse due
to dangerous bradyarrhythmia.
Diagnosis
Diagn·osis of hyperkalemia depends on clinical susp1c1on, serum
potassium measurement and characteristic ECG changes.
Serum potassium greater than 5.5 mEq/L is diagnostic. If all patients
with ARF and CRF are excluded the incidence of hyperkalemia will be
rather insignificant. If the etiolog~ is not readily apparent and patient is
asymptomatic, pseudohyperkalemia should be excluded. One should
. ., .
. . ,. .
- -- -· . -~--~ ·~:~-~..::;.:;c~::;;:...;..•~~...-~ ·----'·--~~...~- -~::.:=~~-....._.___
___ ___.
106 CH .. 3 · Fluid and Electrolyte Disorders
remember that pseudohyperkalemia is caused by imptoper technique in ·

drawing the blood, extravascular haemoly.sis and leucocytosis. Tight or . •
prolonged application of tourniquet especially if combined with exercise
of the limb can increase the potassium concentration of the venous
blood sample.
In hyperkalemia ECG is a very important tool as correlation between
serum potassium and ECG abnormality is approximately at best
Progressive ECG changes of hyperkalemia must be treated as a
serious medical emergency. ECG findings are as per Table No. 3.14
Table No. 3.14: ECG findings of hyperkalemia
Serum potassium ECG findings

6-7 mEq/L Tall peaked T waves
7-8 mEq/L Loss of P waves
Widening of ORS complex
8-10 mEq/L ORS merges with
T waves forming sine waves
> 9 mEq/L Atrioventricular dissociation,
ventricular tachycardia or
fibrillation and cardiac standstill
Diagnosis of etiology of hyperkalemia

Clue to other etiological .factors should be sought in the history and
. la.boratory analysis. So -to establish etiological diagnosis of
hyperkalemia, ex'clude moderate to severe renal failure, c;trugs causing
hyperkalemia, pseudohyperkalemia, ECF volume depletion and severe
metabolic acidosis as underlying causes . .
The urinary potas_s ium excretion rate or transtubular potassium
gradient' (TTKG) . are most widely used ·to differentiate renal
(hyp~aldosteroni. sm) from extra re.nal causes of hyperkalemia.
·t Extra renal c~uses . (e.g. d_
i et) are associated with increased K+
excretion (urin·ary K+ excretion > 80 mEq/day and TTKG > ·_1O)
··.·
: . . -..
. ,:.;
CH. 3
Fluid and . Electrolyte Disorders 107
2. Renal. causes
. of hyperkalemia ·(e · g · hy·poaldost eronism
·· · · · ) •are
associated with decreased K+ excretion (urinaryK+ excretion< 20
mEq/day and TTKG < 3). · .
.Renal causes can be further differentiated by administration of
mineralocorticoid (0.005 mg fludrocorUsone) :
(a) Increased K+ excretion (urinary K+. excretion > 40 mEq/day
_and TTKG > 7) favours diagnosis of aldosterone deficiency
(Addison's diseases)..
(b) No increase in K+ excretion is suggestive of aldosterone
resistance (pseudo hyperaldosteronism, cyclosporine, K+
sparing diuretics).
Q. What is transtubular potassium gradient' (TTKG) and how to

calculate it and interprete its value ?
A. Transtubular potas~ium gradient (TTKG) is a rapid and simple test
designed to evaluate the driving force for net K+ secretion. TTKG
is useful to establish etiological diagnosis of K+ disorders, as it
differentiates renal (abnormal K+ secretion) from non renal causes
of hypo or hyperkalemia.
TTKG =(UK) + (Uosm I Posm) I PK
. UK and PK= Urinary and plasma potassium concentration.
Uosm and Posm = Urinary and plasma osmolality.
· Interpretation of TTKG :
Normal value : 8 to 9 on regular ·diet
Low value : <3 is suggestive of renal conservation of K+ (poor
· intake,· diarrhoea, etc.) or impaired secretion of K+
in patient with hyperkalemia (e.g. hypoaldosteronism).
High value : > 1 o is suggestive of i_ncreased urinary secretion

of potassium.
Treatment
. · d ·how aggressively,
The need to treat hyperkalemia, how urgent 1Y an . .
depends on·us·degree and clinical status. ·
~ : .
~~!: ~, . .
108 CH: 3 Fluid and Electrolyte Disorders
I. EMERGENCY TREATMENT
Potentially fatal hyperkalemia (serum potassium> 7.5 mEq/L, profound
weakness, absence of P wave, QRS widening or ventricular arrhythmia
on ECG ) needs urgent treatment. It is based on the following principle :
i Table No. 3.15 : Principle for the treatment of hyperkalemia
If. A Antagonism of membrane effects of hyperkalemia
Injection calcium gluconate
I
B. Potassium movements into the cells
Insulin and Glucose
Injection sodium bicarbonate
B2 agonist : salbutamol
C. Removal of potassium from the body
Loop or thiazides diuretics
Cation exchange resin ( Keyxalate )
Peritoneal dialysis or haemodialysis
1. Calcium Gluconate
• Calcium gluconate injection is available as 10°/o solution in 1O ml
ampoules.
• The usual dose is 10-20 ml infused over 5 to 10 minutes .
• It is the most rapid treatment available and the effect begins within
minutes but is short lived (30-60 minutes). The dose can be repeated
if no change in the ECG is seen after 5-10 minutes.
• Calcium administration decreases membrane excitability, and
protects the myocardium from toxicity due to potassium.
• It should be remembered that calcium does not lower serum
potassium level, so definitive treatment should be planned.
• Calcium can exacerbate or precipitate digitalis induced arrhythmia .
As a result calcium should be avoided if patient is on digitalis
therapy or, if necessary, should be used with great care.
2. Insulin and Glucose
• Fast way to lower serum potassium .
• · Insulin causes potassium to shift into cells. Glucose is administered
CH. 3 Fluid and Electrolyte Disorders · 109
with insulin to prevent hypoglycemia.

Caution : Hyperglycemic patients should not be given glucose along
with insulin.
• Administer 25 to 50 grams of glucose together with 10-20 units of
regular insulin. Dose of insulin is reduced to 50°/o in patients with
severe renal impairment.
• Initial bolus of glucose insulin should be followed by continuous
infusion of 5°/o-dextrose at 100 ml/hour to prevent late hypoglycemia.
• If effective, the plasma potassium concentration will fall by 0.5 to
1.5 mEq/L. This effect begins in 15 minutes, peaks at 60 minutes,
and may last for approximately 4 to 6 hours.
3. Sodium Bicarbonate infusion
• Alkali therapy with l.V. NaHC0 3 will shift potassium into the cei'ls .
• Sodium bicarbonate 7.5o/o, 50-100 ml ( 45-90 mEq ) is given as
bolus l.V. slowly over 10-20 minutes followed by l.V. NaHC0 3
drip. Onset of its effect is within 5-1 O minutes and effect lasts for
1-2 hours.
• The injudicious use of large amount of alkali can cause excessive
calcium binding to albumin and provokes tetany.
• Care should be taken to avoid contact between calcium gluconate
and sodium bicarbonate in the needle, syringe or infusion set, as
it will precipitate into chalky deposits.
• l.V. sodium bicarbonate is most likely to be useful in severe

hyperkalemia with metabolic acidosis.
• Patients with CRF-ESRD seldom respond to this therapy and may

not tolerate the sodium load and the resultant volume expansion.
4. Beta adrenergic agonists
B agonists such as salbutamol promote cellular uptake of
•
p~tassium and effecitvely lower serum potassium level.
Salbutamol is given in a nebulized form or parenterally. Dose
recommended is 20 mg in 4 ml of saline by nasal inhalation over
1O minutes, or 0.5 mg by 1.V. infusion. .
. : .~ . ..
CH. 3 : Fluid and Electrolyte Disorders
• ·It generally becomes .effective in 30 to 60 minutes and its effect ·

. persists for 2 to 4 hours. It lowers serum potassium level by 0.5 to ·
1.5 mEq/L.
• · Insulin and B agonists exert additive effect. 1.V. salbutamol is
preferred in E§Ro requiring a rapid lowering of serum potassium.
However nebulization is preferred in ESHD patients associated
with CAD, because heart rate is less elevated with nebulization
than with l.V. therapy.
Calcium, .glucose-insulin, sodium bicarbonate and 8 . agonists are
2
temporary measures. It does not remove excess potassium from the
body. Measures to remove potassium are diuretics, c~tion exchange
resins and dialysis .
. 5. . Loop and thiazides diuretics often in combination may.enhance

potassium excretion, if renal function is adequate.
6. Cation exchange r~sins

.. . .
• Cation exchange resins such as sodium polystyrene ·sulphonate
( Keyxalate ) promote the exchange of sodiuni for potassium in
G.I. tract. Each gram binds 1 hlEq of potassium and releases 2-3
mEq of sodium.
• ·. When given orally the usual ·dose is 25-30 grams mixed with 100
ml 20°10 sorbitol 3-4 times daily (sorbitol prevents constipation).
• It can also be given as retention enema consisting · of 50 grams
Of resins and 50 ml of 70°10 sorbitol mixed in 150 ml of water
every 4-6 hrly. It is retained for about 60 minutes after which
.rectum is washed with clear water. The rectal route is faster and
more reliable.
• Each enema can generally lower the plasma potassium concentration
by 0.5 to 1 mEq/L within 1-2 hours and effect will last for 4-6 hours.
•
Adve~se ~ffects of resins include anorexia, nausea, vofniting and
. const1pat1on. As sodium is released in exchange of potassium
. an~ absor?ed by G.I. tract, resins should be used cautiously in
patients with CHF or :volume overload. · · . , . . .··
·1
i
CK 3 : ·Fluid , and Electrolyte Disorders 111 :
I
7. . Dialysis. !I
• The most rapid and effective way of lowering the plasma potassium i
i:
concentration is haemodialysi·s ( removal· rate 35 mEq/hour ). I'
• Dialysis should be reserved for patients with. renal failure and those I
with severe life threatening hyperkalemia unresponsive to more
conservative measures.
• Peritoneal dialysis also removes potassium but is only ·15 to 20°/o
as effective as haemodialysis. . . · · . '. · . · · ,. .
8. Monitoring
Repeated ECG or serum potass.ium determination shoufd be - ~sed
to check the effectiveness of therapy.
II NON EMERGENCY TREATMENT
In mild to moderate hyperkalemia. and for prevention of recurrence of
severe hyperkalemia following measures are useful :· · ·
1. Dietary potassium restriction : Avoid fruitjuice, coconut water and food
rich in potassium.
2. Avoid medications like :
a. Potassium sparing diuretics, NSAID and ACE inhibitors (_all reduce
· renal potassium excretion). · ,, ,>I,
b. B-blockers ( decrease ECF to ICF shift of potassium ).. ·'

: '
3. Loop or thiazides diuretics to increase renal excretion of potassium.

4. Cation exchange resins : Dose required is 15-20 gram Keyxa~ate, 2-4 I~
i I
I
times/day. . . . '
5. Specific etiological treatment : · . .. · . · I,.

''
·. d' • ·d· eases · Glucocorticoid ( hydrocortisone) ·therapy.
a. Ad 1son s 1s · . . . · I
! I
b. Hypoaldosteroni~m : · Min~ralocorticoid s_ upplement ( 0.2 mg(day,

· fludrocortisone ·).
. · d. paralysis : Prophylactic 8 2 agonist inhalation.
c. Hyperkalem1c peno 1c . . · ·
Treatment of diabetic ketoacidosis. .. .
. d.
e. Correct volume depletion. ·
112 CH. 3 Fluid and Electrolyte· Disorders
f. Correct metabolic acidosis : Metabolic acidosis is generally

associated with hyperkalemia. So treat with sodium bicarbonate
( 600 mg tablets, 2-3 times/day) or sodium citrate ( Shohl's solution,
10-15 ml three times daily).
Calcium
Basic physiology
Calcium is essential for bone formation and neuromuscular function. If
calcium intake is truly inadequate, bone mineralization may be impaired in
children and bone loss will be accelerated in adults.
• Distribution : The body of a normal adult contains 1.2 to 1.4 kg of calcium,
so it is the most abundant cation in the body. Out of this about 99% is
present in the bone, 1°/o in the cells of soft tissue and 0.15% in ECF.
• Serum Calcium : Normal value is 10 ± 0.5 mg/di. About 40o/o of this
calcium is bound to albumin (protein) and 50-55% is in ionized form.
The remaining calcium is complexed with the anions of organic acids
such as phosphate, bicarbonate, citrate, lactate or sulphate.
• Ionized calcium : The ionized-free form is the physiologically active
form of calcium and measures 4.8 mg/di. The total serum calcium does
not always reflect the level of ionized calcium. Hypoproteinemia leads
to reduction in protein bound and total serum calcium but the ionized
calcium remains unchanged. In such cases hypocalcemia may be
wrongly diagnosed.
• Correction of total serum calcium in hypoalbuminemia : For corrections
add 1 mg/di to serum calcium for each 1 gm/di reduction in serum
albumin below 4 gm/di.
• Regulation : Parathyroid hormone (PTH) and vitamin D (1,25(0H) 2 D3)
are the main factors that maintain normal serum ionized calcium.
Fine control of serum calcium is achieved by their action on bone,
intestine and kidney.
. Role of PTH : PTH increases serum calcium by stimulating bone
reabsorption, increasing renal calcium reabsorption and promoting
conversion of vitamin D to its active form (1,25(0H) 2 0 3). Serum calcium
. ~ .'
CH. 3 : Fluid and Electrolyte Disorders 113
regulates PTH secretion by a negative feedback mechanism. _

Hypocalcemia stimulates and hypercalcemia suppresses PTH release.
• Role of vitamin D : Active form of vitamin D - Calcitriol (1,25(0H) 2 D)
increases serum calcium by promoting intestinal calcium absorption
and plays a major role in bone marrow formation and reabsorption.
Calcitriol is a potent suppressor of PTH. Synthesis of calcitriol is
stimulated by both PTH and hypophosphatemia, ·and is inhibited by
increased serum phosphate. -
Hypercalcemia
Hypercalcemia can have variable presentation. It can present with serious
illness such as malignancy or may be diagnosed accidentally by laboratory
testing in asymptomatic ·patient in primary hyperparathyroidism.
Etiology
Primary hyperparathyroidism and malignancy are the two most common
causes responsible for hypercalcemia in more than 90°/o of the patients.
Common causes of hypercalcemia as per their basic - pathophysiologi~al
mechanism are summarized in Table No. 3.16.
Clinical Features
Variable clinical features can be
1. Secondary to underlying disorders.
2. Secondary to hypercalcemia.
Clinical features of hypercalcemia are related to severity and rapidity of
onset. Mild hypercalcemia is generally asymptomatic. Features of severe
hypercalcemia are :
i. CNS Symptoms : Weakness, fati _
gue, depression, confusion,
stupor or coma.
ii. GI Symptoms : Constipation, anorexia, n~u.sea and vo~iting.
Abdominal pain may result from hypercalcem1a induced peptic ulcer
disease or pancreatitis.
iii. Renal Symptoms : Polyuria, nocturia and stone formation.
114 CH . 3 Fluid and Electrolyte Disorders
iv. . Cardiac abnormalities ·: .Patients with· hypercalcemia a.re more

prone· to digoxin _toxicity. ECG shows shortened QT interval.
Table No. 3.16 : Causes of Hypercalcemia_

I Increased. bone turnover
(1) Primary hyperparathyroidism
(2) Sec~ndary hyperparathyroidism
(3) Malignancy (lung, breast, ·kidney, . multiple myeloma)
(4) Thyrotoxicosis
(5) Lithium therapy
II Increased intestinal absorption
(1) Vitamin D intoxication
(2) Milk Alkali. syndrome .
(3) Granulomatous disease (i.e. sarcoidosis)
Ill Decreased renal excretion
(1) Familial hypocalciuric hypercalcemia
(2) · Thiazide diuretics
(3) Acute adrenal insufficiency
Diagnosis
It is important to diagnose the two most common disorders, primary

hyperparathyroidism and malignancy (which accounts for more than 90°/o
of total hypercalcemia), from other less common causes of hypercalce~i.a.
I History and physical examination .
(a) Patient with primary hyperparathyroidism is usually a~ymptomatic.
Hypertension is common in primary hyperparathyroidism .
.·· (b) . If hYpercalcem.ia is present fcir more than 6 months without obvious
cause, primary hyperparathyroidism is most certain.
(c)
In . m~lignancy,. symptoms of mal.ignancy bring the patient to the
physician and hypercalcemia is diagnosed by laboratory
investigations. ·
Hypercalcemia With renal stone favours long duration, so

malignancy is unlikely. · ·
(e)
Use of vitamin . D, calcium, antacid and lithium therapy may be
underlying cause of hypercalcemia.
CH. 3 : Fluid and Electrolyte Disorders 1.1s ·
(f) A chest X-ray should be obtained to rule out pulmonary malignancies

and granulomatous disorders.
11 Investigation .
Useful laboratory tests are electrolytes, BUN, serum creatinine,
phosphate, serum protein electrophoresis, intact PTH level etc.
(a) The presence of high serum chloride and low serum HCO in a
ratio > 33 to 1 is suggestive of primary hyperparathyroidis~.
(b) A low serum chloride, high serum HCO and elevated BUN and
creatinine are characteristic of milk alkaIT syndrome.
( c) In patients with high total protein with reversed AG ratio, suspect
multiple myeloma. Serum protein electrophoresis showing a
monoclonal spike is suggestive of multiple myeloma.
(d) If increased intact PTH, most common cause is primary
hyperparathyroidism. A low plasma phosphate is found in primary
hyperparathyroidism.
As a general rule, primary hyperparathyroidism is the etiology in
outpatients who are asymptomatic with a serum calcium concentration
lower than or at 11 .0 mg/di. On the other hand, malignancy is often
the cause in symptomatic patients with an abrupt onset of diseases
and serum calcium concentration higher than or at 14 mg/di.
Treatment
A Measures to increase urinary exc.r etion
( 1) Volume restoration, expansion and saline diuresis are the most
useful and effective measures to correct hypercalcemia.
o.9°/0 NaCl is infused to correct dehydration, for volum~ expansion
and natriuresis, which leads to. urinary excretion of calcium.
patient may need 4-6 litre of saline to achieve this goal. So use
cautiously in elderly and heart failure patients to avoid pulmonary
oedema.
Frusemide : After volume expansion forced diuresis can increase
(2)
urinary calCium excretion. Avoid de.hydration, hypokalemia and
hypomagnesemia during treatment with frusemide. Avoid thiazide
diuretics because it impairs urinary calcium excretion.
Haemodialysis : Reserved for treatment of patients with severe
(3)
hypercalcemia and little or no renal function.
. ··~
1.16 CH . 3 Fluid and Electrolyte Disorders
B Measures to inhibit bone resorption

(1) Bisphosphonates : Pamidronate is the potent and most widely
used bisphophonate in treatment of hypercalcemia due to bone
reabsorption. For severe hypercalcemia pamidronate 90 mg 1.V.
over 4 hours causes a fall in calcium, which is maximal at 2-3
days, and the effect lasts for a few weeks.
(2) Plicamycin (mithramycin) : It acts by inhibiting bone resorption.
· Currently it is used sparingly due to its high toxicity and because
of better effectiveness of bisphosphonates. Mithramycin should
be avoided in patients with severe hepatic, renal and marrow
disorders. Its effect begins in 12 hours and peaks at 48 hours. The
dose can be repeated at 3 to 7 days intervals.
(3) Calcitonin : It inhibits bone resorption and increases urinary
calcium excretion. Because of its rapid action it is useful for urgent
therapy of life threatening hypercalcemia along with rehydration
. .
and saline diuresis, but it is not useful for long term therapy.
(4) Gallium Nitrate : It inhibits bone resorption and corrects
hypercalcemia. It is not often used due to 5 days duration of infusion,
potential for nephrotoxicity and availability of safer and effective
agents.
C Measures to decrease intestinal absorption

(1) Glucocorticoids : It decreases intestinal absorption and increases
urinary excretion of calcium in pharmacological doses.
Alternatively ketoconazole and hydroxyl chloroquine can be used.
Glucocorticoids are effective in hypercalcemia due to vitamin D
intoxication, sarcoidosis and malignancies (multiple myeloma,
leukaemia, Hodgkin's disease etc.), but do not alter calcium level
in primary hyperparathyroidism or in a normal person.
(2) Oral phosphate : It inhibits calcium absorption and promotes
calcium deposition in bone and soft tissue. It should be used only
if the serum phosphorus level is less than 3 mg/di · and renal
function is normal. Summary of treatment options tor
hypercalcemia is shown in Table No. 3.17
CH. 3 ·:fluid and Electrolyte Disorders 117
Table No. 3.17 : Treatment of Hypercalemia

Drug Dosage
Isotonic saline 2-4 L/day initially
Frusemide 20-160 mg l.V. 8 hrly after volume expansion
Salmon Calcitonin 4 I U/kg s.c. 12 hrly
Pamidronate Disodium 60-90 mg l.V. over 24 hrs
Plicamycin 25 µg/kg l.V ~ over 4 hrs, 6 hrly for 3-4 days
Corticosteroids 200-300 mg hydrocortisone l.V. 6 hrly for 3-5 days
Galliu·m Nitrate · 100-200 mg/m 2 for 5 days
D Specific treatment
( 1) Discontinue drugs responsible.
(2) Surgical treatment of primary hyperparathyroidism.
(3) Specific treatment for malignancy, thyrotoxicosis etc.
Hypocalcemia
1: Etiology
Hypoalbuminemia is the common cause of hypocalcemia with normal
ionized calcium. True hypocalcemia is the result of decreased calcium
absorption from the gastrointestinal tract or decreased calcium.
reabsorption from bone, due to abnormalities of either PTH or vitamin
D (calcitriol). The most common causes of hypocalcemia are shown
in Table No. 3.18.
2. Clinical Features
Symptoms of hypocalcemia vary with degree and rate of onset and
are due to increased neuromuscular excitability. The patient may
complain of weakness, circumoral and distal extremity parasthesia, .
'
muscle spasm, carpopedal spasm, tetany and mental changes such i'
I
I
as irritability, depression and psychosis. On physical examination

patient may have increased deep tendon reflexes or signs of latent
tetany (Chvostek s sign, Trousseau•s sign).
1
• Chvostek s sign is a facial twitch $1icited by tapping on the facial

1
· nerve just anterior to earlobe, just below the zygomatic arch ·with
·the mouth slightly open.
:·. \
118 CH. 3 · : Fluid and Electrolyte Disorders
• Trousseau's sign is the development of wrist flexion

'
metacarpophalangeal joint flexion, and hyper extended fingers ·
and thumb flexion when a BP cuff is inflated above systolic
pressure for 3 minutes.
• The ECG may show prolonged QT interval. Digitalis effect may
be reduced.
• Severe hypocalcemia may cause lethargy, confusion, laryngeal
spasm, seizures or reversible heart failure.
• Chronic hypocalcemia due to hypoparathyroidism may cause
cataracts and calcification of basal ganglia.
Table No. 3.18 : Causes of hypocalcemia
1. Hypoalbuminemia
2. Hypoparathyrodisim
(a) Post surgical - Hungry bone syndrome
(b) Hypomagnesemia
(c) Idiopathic
3. Defect in vitamin D metabolism
(a) Nutritional, lack of exposure to sunlight
(b) Malabsorption and drugs (e.g. anticonvulsants)
(c) Liver disease, renal failure
(d) Vitamin D dependent rickets
4. Miscellaneous
(a) Metabolic or respiratory alkalosis
(b) Sepsis, toxic shock syndrome
( c) Acute pancreatitis, burns
(d) Massive transfusion of citrated blood
5. Severe acute hyperphosphatemia
Tumorlysis syndrome, ARF, rhabdomyolysis
Diagnosis
Detailed history and physical examination may give clue for underlying etiology ·
of hypocalcemia. Hypoalbuminemia is a common cause of decreased total
serum calcium. However the common causes of true hypocalcemia are
magnesium deficiency, re.nal failure, metabolic alkalosis and complications
of parathyroid surgery. Important investigations required for etiological
diagnosis of hypocalcemia are serum albumin, serum HC0 3 , serum
magnesium, serum phosphate and occasionally intact PTH. Differential

diagnosis of hypocalcemia is summarized in Table No. 3.19.
Table No. 3.19 : Differential Diagnosis of Hypocalcemia
Etiology Serum Calcium Serum Serum
I
Total Ionized phosphate PTH
Hypoalbuminemia Low N N N
Alkalosis N Low N N-high
Vit.-0 deficiency Low Low Low High
Chronic renal failure Low Low High High
Hypoparathyroidism Low Low High Low
Treatment
1 Acute Management
Symptomatic hypocalcemia should be treated as emergency with 10°/o
calcium gluconate (90 mg elemental calcium/1 O ml) 10-20 ml l.V .
slowly over 1O minutes. Severe symptomatic hypocalcemia may require
infusion of 60 ml of calcium gluconate in 500 ml of 5°/o dextrose.
Calcium concentration of the drip is 1 mg/ml and its requirement is
0.5 mg to 2 mg/kg/hour.
If 1.V. calcium does not relieve tetany, rule out (and correct)
hypomagnesemia. In treatment of metabolic acidosis with
hypocalcemia (e.g. CRF) , correct hypocalcemia before correction of
acidosis.
When citrated blood is transfused rapidly, hypocalcemia can occur.
So for every 4 units of blood, give 10 ml of 10°/o calcium gluconate.
2 Long term management
1. Treatment of underlying etiology.
2. Calcium supplementation : An asymptomatic hypocalcemic patient
needs oral elemental calcium 1 to 3 gram per day. Calcium is best
absorbed when taken between the meals.
3 Vitamin D supplementation
Calcitriol (1,25 (OH) D ) is the most potent of the vitamin D preparations
and has the fastest ~n~et and the shortest duration of action. So there is
no risk of vitamin D intoxication but disadvantage is the higher cost.
120 · CH .. 3 . . Fluid and Electrolyte Disorders
Vitamin D (ergocalciferol) requires several weeks to achieve full effect.

Although cost is low, because of long half-life and storage in fat, it carries
higher risk of vitamin D intoxication.
PHOSPHORUS
Ph6s.p horus is critical for bone formation and cellular energy metabolism.
Phosphorus is chiefly intracellular and only 1°/o is in the ECF. The normal
serum phosphate level is 3.0-4.5 mg/di. It is best measured in the fasting
state, since there is diurnal variation (lower value in the morning and higher
at night and post meals). Major regulatory factors includes PTH,
1,25(0H) 2 D 3 and insulin. PTH lowers serum phosphorus by increasing renal
excretion. 1,25(0H) 2 D3 increases serum phosphorus by enhancing intestinal
phosphate absorption. Insulin lowers serum levels by shifting phosphate
into cells.
Hypophosphatemia
Etiology ·
Important causes of hypOphosphatemia are summarized in Table No. 3.20
Clinical Features
Acute Hypophosphatemia can cause :
(a) Muscular abnormalities : Proximal muscle weakness,
.rhabdomyolysis, impaired diaphragmatic function, respiratory
. failure and congestive heart failure.
(b) Neurological abnormalities : Parasthesia, dysarthria, confusion,
seizures or coma.
( c) Haematological abnormalities :
i. · Enhanced oxygen dissociation causes tissue hypoxia, and
haemolysis.
ii. Impaired phagocytosis and opsonization leading to increased
susceptibility to bacterial and fungal infections.
· 11 Chronic hypophosphatemia causes mineralization defect leading
to rickets in children ahd osteomalacia in adults.
CH. 3 : Fluid and· Electrolyte Disorders · 121
Table No. 3.20 : Causes of hypophosphatemia

A Decre~se~ intestinal phosphate absorption
(1) V1tamm D deficiency
(2) Vitamin D dependant rickets type I and II
(3 ) Malabsorption, Phosphate binding antacids
B Increased renal phosphate excretion.
(1) Hyperparathyroidism
(2) Vitamin D - deficiency
(3 ) X linked hypophosphatemic rickets
C Shift of phosphate into intracellular fluid .
(1) Respiratory alkalosis
(2) Dextrose infusion
(3) Diabetic ketoacidosis
(4) Sepsis
(5) Hungry bone syndrome
Treatment
(1) Mild hypophosphatemia needs only treatment of underlying etiology.
(2) If serum phosphate level is > 1.0 mg/di and patient is asymptomatic,
oral phosphorus replacement is sufficient. Milk and milk product is
an excellent source of phosphorus. Milk contains 1 gram of inorganic
phosphorus per litre.
To correct hypophosphatemia, solutions containing sodium phosphate,
potassium phosphate and neutral sodium phosphate are used.
Depending upon severity, upto 3 grams can be given in four to six
divided doses in 24 hours.
(3) Severe (<0.5 to 1.0 mg/di) symptomatic hypophosphatemia may require
f.V. phosphate therapy. 1.V. infusion should be stopped when serum
phosphorus level is greater than 1.5 mg/di or when oral therapy is
possible. Extreme care must taken to avoid hyperphosphatemia, which
may cause hypocalcemia, ectopic soft tissue calcification, hypotension
and death. Hypophosphatemic patients .are frequently hypokalemic
and hypomagnesemic and need correction.
;,, ·-··.·: .. . .
· ··. ·- . -._., _ _.
-· -- ~
. .....- ./~
_
....
•.· ~
:122 CH. 3 . Fluid and Electrolyte Disorders
Hyperphosphatemia
·Hyperphosphatemia is defined as serum phosphorus level greater than 5
·mg/di in adults.
·Etiology .
The most common causes of hyperphosphatemia are acute , renal !ailure
and chronic renal failure. Important causes of hyperphosphatem1a are
mentioned in Table No. 3.21. ·
Table No. 3.21 : Causes of hyperphosphatemia

( 1) Decreased renal excretion
Acute renal failure
Chronic renal failure
(2) Acute tissue destruction
Tumor-lysis syndrome, severe haemolysis,
Rhabdomyolysis, crush injury
(3) Increased renal phosphate reabsorption
Hypoparathyroidism
Acromegaly
Thyrotoxicosis
(4) Miscellaneous
Excess phosphate administration
Vitamin-0 intoxication
Metabolic or respiratory acidosis
Clinical features
Chief clinical features of acute hyperphosphatemia are due to
hypocalcemia and ectopic calcification of soft tissues, including blood
vessels, cornea, skin, kidney etc.
Chronic hyperphosphatemia contributes to renal osteodystrophy.
Management
1 Treatment of underlying etiology.
2 ·Restriction of dietary phosphate to 600-900 mg/day.
Avoid phosphorus rich products like milk and dairy products and
carbonated beverages containing phosphoric acid.
CH. 3 . . Fluid and Electrolyte· Disorders 123
3 Oral phosphate binders : Calcium acetate and calcium carbonate are

preferred agents and are administered with meals. Aluminium hydroxide
may be used for the short term but its chronic use in patients with renal
failure should be avoided because it may cause aluminium toxicity
causing adynamic bone disease, proximal myopathy and anemia.
If hyperphosphatemia and hypocalcemia coexist (e.g. CRF), correct
hyperphosphatemia before correcting hypocalcemia. Monitor serum
calcium and phosphorus level frequently and adjust dose of phosphate
binders, so as to keep calcium phosphorus product below 60, so as to
minimize the risk of ectopic calcification.
4 Saline diuresis will reduce acute hyperphosphatemia in patients without
renal failure.
5 Dialysis may be required to treat hyperphosphatemia in severe renal
failure.
Magnesium
Magnesium is the fourth most common cation of the body (after Na, K and
Ca), second most common intracellular cation (after K) and is the
commonest intracellular divalent cation. About 60°/o of body magnesium
is in bones, only 1°/o in ECF and rest is within the cells. Since clinical
effects of magnesium disorders are determined primarily by tissue
magnesium content, serum magnesium levels have limited diagnostic
value. The normal serum magnesium level is 1.4 to 2.2 mEq/L (1.8 to 3.0
mg/di)
Magnesium plays an important role in neuromuscular function and
maintenance of cardiovascular tone.
Hypermagnesemia
Hypermagnesemia is defined as serum magnesium concentration above
2.5 mEq/L (3.0 mg/di). As a normal kidney c~n.effectivel~ e~crete magn~siu~
load, hypermagnesemia is rarely seen in clinical practice 1f renal function 1s
normal.
Etiology
1. Renal failure patients, receiving magnesium containing antacids,
laxative or 1.V. ·fluids is the most common cause.
i '. ·
,;,
· 124 CH.' 3 Fluid and Electrolyte Disorders
2. · Treatment of pre-eclampsia with 1.V. magnesium sulphate.

· 3. ARF with acute rhabdomyolysis.
4. · Diabetic ketoacidosis without treatment.
II Clinical features
Neuromuscular manifestations: It includes muscular weakness; lethargy,
loss of deep tendon jerks, muscular paresis leading to respiratory
depression and respiratory failure.
Cardiac manifestations : It includes hypotension due to peripheral
vasodilatation, bradyarrhythmia and, in severe cases, cardiac asystole.
ECG changes : Due to generalized depression of cardiac conduction.
ECG changes are prolonged PR intervals, increased QRS ·duration
and QT interval and lastly complete heart block.
Hypocalcemia may occur due to hypermagnesemia induced decreased
secretion of PTH and end organ resistance of PTH.
111 Treatment
1. Eliminate source : Stop magnesium containing antacids, laxative
and discontinue magnesium containing l.V. fluids.
2. 10°/o calcium gluconate, 10-20 ml l.V. slowly over 10 minutes will
effectively correct hypotension by lowering magnesium levels.
3. If renal function is normal Inj. Frusemide after rehydration with
isotonic saline will enhance renal excretion.
4. Haemodialysis can effectively correct hypermagnesemia and is
the treatment of choice in patients with renal failure.
5. Supportive treatment : Artificial respiration may be necessary if
respiratory failure occurs.
Hypomagnesemia
Hypomagnesemia is defined as serum magnesium concentration less t~~n
1.5 mEq/L (1.8 mg/di). However in symptomatic hypomagnesemia: 1.t 15
usually less than 1 mEq/L. Magnesium deficiency is a common clinical
problem, seen in about 10°/o of patients admitted in city hospitals and up
to 65% patients in ICU.
CH. 3 Fluid and Electrolyte 'Disorders 125
Etiology:
Common causes of hypomagnesemia are alcoholism loop diuretics diarrhoea

and poor nutrition. Causes of hypomagnesemia are ~ummarized in' Table No.
3.22.
Table No. 3.22 : Causes of hypomagnesemia

(a) Increased renal excretion
1· Loop diuretics, osmotic diuretics
2. Hypercalcemia
3. Acute Pancreatitis
(b) Increased gastro-intestinal losses
1. Chronic diarrhoea due to malabsorption
2. Vomiting or nasogastric aspiration
(c) Poor intake
Prolonged malnutrition or magnesium free l.V. fluids
(d) Chronic alcoholism and alcohol withdrawal
(e) Others
1. Primary aldosteronism
2. Hypoparathyroidism
3. Drugs : Aminoglycosides, Cisplatin, Amphotericin B,
Cyclosporine A etc .
Clinical features
Hypomagnesemia rarely occurs as a single deficiency. It often causes
hypocalcemia and hypokalemia, which contributes to the clinical picture.
Neuromuscular manifestations
They are similar to hypocalcemia and include lethargy, confusion,
tremor, fasciculations, ataxia, tetany and seizures.
Cardiovascular manifestations
ECG abnormalities include prolonged PR and QT intervals. Atrial and
ventricular arrhythmia may occur, especially in patients treated with
digoxin. Digitalis toxicity may be precipitated or aggravated by
hypomagnesemia.
126 CH . .3 -: Fluid and Electrolyte Disorders
Metabolic abnormalities
Hypocalcemia : Mg deficiency results in decrease in PTH secretion and
· end organ resistance to PTH leading to hypocalcemia. If patient With
hypocalcemia does not respond to calcium or vitamin-D replacement,
think of hypomagnesemia and correct it.
Hypokalemia : Mg deficiency enhances renal excretion of potassium.
Hypomagnesemia and hypokalemia often coexist. So when
hypokalemia does not respond to K+ replacement, rule out associated
Mg deficiency and correct it.
Treatment
( 1) Correct underlying etiology and-coexisting hypocalcemia and hypokalemia.
(2) Magnesium sulphate (MgSO 4 )
MgSO 4 is available as powder as well as 10% or 50% solution. 5 ml
of 10°/o or 1 ml of 50o/o MgSO 4 contains 4 mEq magnesium. The 50%
solution must be diluted before use.
Conversion equations for Mg therapy are
1 gram MgSO 4 = 8.1 mEq of magnesium
1 mEq of Mg is provided by 123 mg of MgSO 4
1 mmol = 2 mEq = 24 mg elemental magnesium
Onset of action : l.V. immediate, l.M.<1 hour
Peak effect: l.V. few minutes, l.M. 1-3 hours
Duration of action: l.V. 30 min, l.M. ·3-4 hours
(3) Treatment of mild hypomagnesemia
Mild deficiency (serum Mg concentration 1.5 mEq/L or 1.8 mg/di)
needs oral supplementation of 2 gram three times a day without
producing diarrhoea. For dietary supplementation, Mg rich diet includes
green vegetables, nuts and legumes, chocolate and fruits such as
bananas, grapes and oranges.
(4) Treatment of severe Mg deficiency
Patients with severe hypomagnesemia (serum Mg concentration less
than 1.0 mEq/L or 1.2 mg/di) need parenteral Mg supplementation.
..
•
: ~l
.~·· .
{
~I
. .
. c ·H: 3 : Fluid and Electrolyte Disorders 127 ·
2 ~ra~ (4ml of 50°/o, 16 mEq) MgS0 is given l.V. slowly over 10 minutes.
4
This 1s followed by 1 mEq/kg body weight/24 hours as slow continuous
infusion or 1.'M. inj~ction. For l.V. infusion 1o ml of 50% MgSO 4 is added to
500 ml of isotonic saline which will contain 40 mEq of magnesium.
Alternatively 2 gram MgSO 4 is given every 6 to 8 hours as l.M. injection,
which is quite painful. After first day, dose required is 0.5 mEq/kg/day
given for next 3 days to correct intracellular deficit.
(5) Caution and monitoring of MgSO 4 therapy
(a) Check deep tendon reflexes every 15 minutes. Disappearance of
the patellar reflex is a useful clinical sign to detect onset of Mg
intoxication. Knee jerk reflexs should be tested before repeating
dose. If they are absent, no additional Mg should be given until
they return.
(b} Periodic monitoring of serum Mg concentration is essential during
Mg therapy. Adjust infusion rate to keep serum Mg concentration
less than 2.5 mEq/L. If serum Mg level is more than 3.5 mEq/L
discontinue infusion, at least temporarily.
(c) Great care is required in supplementing Mg in patients with renal
insufficiency. In renal failure patients reduce the dose, infuse it
more slowly and monitor serum magnesium concentration more
frequently to avoid hypermagnesemia.
(d) Magnesium therapy is contraindicated in heart block or in patients
with extreme myocardial damage.
(e) . Maintain urine output at a minimum rate of 100 ml every 4 hours.
f) If over infusion causes life threatening hypermagnese~ia, tre~t it
( . gluconate 1o-20 ml followed by fluid loading
with 10°/o ca Ic1um ..
and diuretics.
CHAPTER
FOUR ,
FLUID THERAPY IN
MEDICAL DISORDERS
NORMAL MAINTENANCE FLUID THERAPY IN
FLUID REQUIREMENT 128 RESPIRATORY DISORDERS 161
FLUID THERAPY IN ARDS 161
HYPOVOLEMIC SHOCK 130 Asthmatic bronchitis 162
FLUID THERAPY IN Mechanical ventilator 163
G.I. DISORDERS 134 Aspiration diseases of lung 166
Vomiting 135 FLUID THERAPY IN NEURO-
Diarrhoea 139 LOGICAL DISORDERS 166
. Haemetemesis 144 FLUID THERAPY IN HEAT
Ascites in cirrhosis of liver 148 ILLNESSES 169
Hepatic encephalopathy 150 Heat cramps 169
Pancreatitis 153 Heat exhaustion 170
FLUID THERAPY IN CARDIO- Heat stroke 170
. VASCULAR DISORDERS 159
Congestive heart failure 159
Hypertension 160
FLUID THERAPY IN COMMON MEDICAL DISORDERS
In this chapter we will discuss about normal fluid requirements, fluid therapy
in . hypovolemic shock and fluid therapy in various important systemic
disorders. Basic pathophysiology of fluid, electrolytes and acid base
disturbances in these clinical conditions are also included here.
NORMAL FLUID AND ELECTROLYTE REQUIREMENTS
The normal maintenance fluid and electrolyte requirements of an adult on
parenteral fluid therapy are as follows :
1. Water
Adequate amount of water is necessary for proper body need,
hydration and excretion of nitrogen end products in urine. As a rule
of thumb fluid intake = urine output + 700 ml. But approximately 2
to 2.5 litres of fluid is necessary for an average normal person with
normal renal status. However in patients with abnormal losses like
diarrhoea, vomiting, fever, excessive perspiration, increased
catabolism etc., requirement is high. Need of fluid can be -roughly
calculated as mentioned below.
I ···
CH. 4 Fluid Therapy in Medical Disorders 129 ·
Water requirement
1. Measurable loss (Intestine+ Kidney)+ 700 ml.
2. 20-40 ml/kg/day ·
3. 1000-1500 ml/m2/day
4. First 10 kg : 100 ml/kg/day or 4 ml/kg/hour
Second 1 O kg : 50 ml/kg/day or 2 ml/kg/hour
· For rest weight : 20 ml/kg/day or 1 ml/kg/hour
Good urine output suggests proper hydration. With proper hydration urine
output should be more than 1 ml/kg/hour or more than 50 ml/hour.
2. Sodium
Average body requirement of sodium is 100 (60-150) mEq/day or 6
gm of NaCl/day. The kidneys are normally capable of compensating
for wide variations in Na intake. During sodium deficiency its urinary
excretion becomes almost zero. Sodium should be restrieted in the
patient with hypertension, cardiac disease, renal disease, cirrhosis
of liver, oedema or fluid overload.
3. Potassium
Normal requirement of potassium is 40-60 mEq/day (20 mEq K+ = 1.5
gm KCI). Ability of kidney to retain K+ is poor (unlike sodium). Even in
patients with K+ deficit, daily urinary loss of potassium is about 20 mEq.
So if potassium supplementation is not provided, hypokalemia easily
·occurs in the patient on maintenance 1.V. fluid therapy. Howe~er lar~er
and rapid potassium supplementation can ca~se hyp~r. kalem1a, .which
ngerous. To avoid hyperkalem1a, avoid or cautiously
can b e d a . · b ·
supplement K+ in pati:~nts with renal failure, excessive tissue cata o1ism
or burns.
4. Glucose
.. teral fluid therapy needs at least 100 gms of dextrose.
The patient on paren . .
It is necessary because :
I . .·
I ~ •
'1.. '
- ~
. . . ..
130 · CH. 4 ·.: Fluid Therapy in Medical Disorders
1.. It provides calories to the body.

2. It prevents breakdown and catabolism of endogenous protein.
3. It prevents depletion of liver glycogen and therefore prevents
excess fat mobilization and production of an excessive amount
of ketone acids.
4. Brain and red blood cells preferentially need glucose for their
calorie need.
1 gm of dextrose provides 3.4 Kcal. The patient who is unable to eat or
drink for a period of 4 to 8 days requires more calories (about 200 gm/
day) to prevent catabolism (2 litres of 20°/o-dextrose is infused I. V. slowly
into large vein to prevent local thrombophlebitis). Infusion of
concentrated dextrose should be followed by infusion of 5°/o or 10%
dextrose solution, to prevent reactive hypoglycemia. Hyperglycemia is
a potential risk with these solutions and requires careful monitoring of
blood sugar.
Maintenance l.V. fluid regimen
To provide adequate fluid, sodium, potassium and glucose to the patient
on parenteral fluid therapy we need to give :
1. 2 litre 5°/o-dextrose + 500 ml. isotonic saline with 5 ml injection
potassium chloride 15°/o, in each 500 ml. fluid (It will provide 2.5
litre water, 78 mEq sodium, 50 mEq potassium and 100 gms glucose)
2. 1.5 litre lsolyte-M + 1 litre 5°/o-dextrose (It will provide 2.5 litre
water, 60 mEq sodium, 52.5 mEq potassium and 125 gms. glucose)
Depending upon the need of patient, fluid therapy can be tailor made~
Calcium, magnesium, phosphorous, vitamins and protein replacement may
be necessary after one week of parenteral therapy. . ~··
FLUID THERAPY IN HYPOVOLEMIC SHOCK . ... .
Fluid loss leading to hypovolemia, hypotension and shock are common

clinical problems. Amount of fluid to be given is decided by clinical and
other guidelines. Most important question to be answered is which fluid
should be given ?
·. . /
'
J
~ j
CH. 4 : Fluid Therapy in Medical 'Disorders 131 .
i Table No. 4.1 provides very useful guidelines for selection of the 1.V. fluids
for the ·treatment of hypotension and shock.
q
Table No. 4.1 : Distribution of l.V. fluids in body fluid compartments
Fluid distribution (1,000 ml) ECF ICF

5%-dextrose 330 670
Isotonic Saline (0.9%) 1,000 Nil
Half Isotonic Saline (0.45%) 670 330
0. Why 5°/0-dextrose (D-5°!o) is not an ideal fluid to treat hypovolemic shock?

A. 5°/o-dextrose is not an ideal fluid to treat hypovolemic shock because:
1. Poor expansion of intravascular volume : 1,000 ml of D-5°/o will
increase 330 ml of ECF volume and only 83 ml (1 /4 of ECF) stays
in the intravascular space. As 1 litre of D-So/o will increase
intravascular volume only by 83 ml, rise in blood pressure would
not occur satisfactorily in the patient with shock.
2. Increased urine output due to osmotic diuresis: Larger and faster
infusion of D-5°/o will cause glucose load(> 25 gm/hour) and osmotic
diuresis will occur. So even in presence of hypovolemia, there will
be increased urine output, which delays correction of dehydration.
Increased urine output will also create false impression that now
there is no fluid deficit. In such a setting rate of fluid replacement
may be slowed down despite hypovolemia, therefore hypotension
may not improve. So 5°/o-dextrose should be avoided in the
treatment of shock.
Q. Why isotonic saline is selected as an initial fluid to treat hypovolemic

shock?
A. As isotonic saline is distributed only in ECF clompalrtme~, i3n0fuosioln of
litre of isotonic saline will expand intravascu ar vo ume y m , so
1
rise in the blood pressure will be much rapid as compared to 5°/o-dextrose.
132 CH. 4 Fluid Therapy in Medical Disorders
The other reason to prefer isotonic saline as initial therapy is its safety
in unknown glycemic status. Moreover isotonic saline is least
expensive, readily available, and reaction free (as compared to
colloids), so ·preferred for the initial treatment of shock.
Rate · of infusion is decided on the clinical status and vital data.
Depending upon the .nature of loss, NaHC0 3 and KCI is added to the
infusion.
Once the urine output is established preferred 1.V. fluid is Ringer's lactate.
Q. Why Ringer's lactate is the preferred fluid in sh·o ck after urine output
is established ?
A. Once urine output starts, correct remaining deficit by balanced salt
solution like Ringer's lactate because :
1. Ringer's lactate is the most physiological fluid. Its composition is
almost identical to ECF, so large volume can be infused without
fear of electrolyte imbalance.
2. It corrects acidosis (lactate is converted into HC0 3 ) produced
by lactic acid due to anaerobic metabolism during hypotension.
Q. Why Ringer's lactate is avoided in initial treatment of shock ?
A. Ringer's .lactate is not an ideal fluid for initial fluid therapy because.
1. Potassium in Ringer's lactate is unsafe till renal status is
uncertain.
2. In. shock state hepatic conversion of lactate to bicarbonate is
unpredictable.
So use of RL for initial .treatment of shock may cause hyperkalemia
or lactic acidosis and hence avoided. NaHC0 3 is preferred agent for
initial treatment of acidosis with shock.
Q. Which l.V .._agents are the best to raise blood pressure in shock? Why?
A. For prompt rise of blood pressure in shock, albumin, blood transfusion
or colloids (like penta or hetastarch, haemaccel or low molecular weight
dextran) ·are be·s t ·agents. As all these agents are primarily restricted
1
to the· intravascular compartment and selectively expand the plasma ,

v'o lume; they will raise blood pressure rapidly. :;
,....--··
~i :
CH. 4 ·Fluid Therapy in Medical Disorder~ . 133
a. When to use colloids in hypovolemic shock ? . .. .

A. Claimed advantage of colloid containing solutions (such as albumin,
polygelatin or hetastarch) are : . ·
1. More effective plasma volume expansion, since it remains in the
vascular space (in contrast to saline, where 2/3 of it enters the
interstitium).
2. Lesser risk of pulmonary oedema, since the increase in plasma
oncotic pressure favours fluid movements out of the interstitium
into the vascular space.
The primary indication of the use of albumin or other colloids is in
hypovolemia with hypotension in protein losing states such as burns.
Although these solutions are also used in treatment of shock or severe
hypovolemia, they appear to offer little or no advantage over the pure
electrolyte solutions. Isotonic saline is equally effective in producing
volume repletion, although volume required is 2.5 to 3 times greater
than that of- colloids, because of its extravascular. distribution.
Replacement of such large volume by colloids is not harmful. On the
contrary it replaces the interstitial fluid deficit that is induced both by
fluid loss and by fluid movement into the cells.
Q. When to use blood in hypovolemic shock ?
A. Hypovolemic patients who are bleeding or have marked anaemia
require administration of blood in addition to fluid. However with blood
transfusion haematocrit should not be raised over 35°/o. A hi_g her
haematocrit level is not necessary for oxygen transport and may produce
an increase in blood viscocity that can lead to stasis in the already
impaired capillary circulation.
Table No. 4.2 is a summary of increase in intravascular volume (which is
required to correct hypotension) with various types of 1.V. agents.
Table No. 4.2: Rise in intravascular compartment with l.V. agents
Type of Fluid (1,000 ml) 5% Dextrose Isotonic Saline Colloids/B. T.
Increase in Roughly
75-100 ml 300 ml · ·
1000 ml
lntravascular volume
:·.· · -~
134 CH. 4 : Fluid Therapy in Medical Disorders
To clear the basic concept, rough guidelines about distribution of various l.V.
infusions in different fluid compartments are shown in Fig No. 4.1. ·
Fig. No. 4.1 : Distribution of I. V. infusions in different fluid compartm_ents
. . ., ', . .. ~·-. ~
1 ·lit,~ iwx .·100 · ~ 3QQi. · JnfifSJYQoouf~Gllr~pprD:dmet:ty··: 1 00%

FLUID THERAPY IN GASTROINTESTINAL DISORDERS .
Pathophysiology of fluid, electrolytes and acid base disturbances and fluid
therapy of the following important G.I. disorders are included here~
1. Enteric disorders :
Vomiting or nasogastric aspiration, diarrhoea and haemetemesis
2. Hepatic disorders :
Ascites in cirrhosis of liver and hepatic encephalopathy
3. Pancreatic disorders :
Acute pancreatitis
.. •.
CH : 4 : -Fluid Therapy in Medical Disorders . 135
·· · ·Fluid Therapy in Vomiting

Upper··gastrointe·stinal losses (vomiting o'r nasogastric aspiration) is a
commonly encountered. problem. For proper. selection of fluid, i,t is
necessary to understand the basic physiology.
Q. Which type of fluid and electrolyte abnormality occurs due to vomiting
and why ? . . . .· ·
A. Important features are su.mmarized below.
1. Hypovolemia : Due to loss of fluid there is dehydration-:
decreased ECF volume.
2. tlypokalemia : Decreased ECF volume and loss of sodium in
gastric juice will lead to increased secretion of aldosterone. Under
aldosterone influence, there will be increase in reabsorption of
sodium and increase in secretion of potassium leading to greater
loss of potassium in urine (Table No·. 4.3). So hypokalemia occurs
partly due to loss of potassium in vomiting but chiefly due to its
loss in urine (renal loss) .
3. Metabolic alkalosis : Metabolic alkalosis in upper gastxointestinal
loss is multifactorial :
a. Gastric juice is acidic. During upper gastrointestinal loss H+
ion will be · lost leading to alkalosis. (Normally this H+ ion
secreted in stomach is reabsorbed distally in the intestine· so
~· no acid base disturbance occurs).
b. Hypovolemia (due to fluid deficit) v:'ill lead to g~eater reabsor~tion
of HC0 in proximal tubules of kidney, leading to alkalos1s.
3
During severe upper G.I. loss there may be a stat~ of sev~re
c. · depletion So in. collecting duct of kidney high
potassium · · h' h
will secrete H+ ion (instead of potassium), w 1c
aldosterone , · · · · lk I · u ·
. .d . and aggravation of metabolic a a os1s. nnary
leads to ac1 una 11
. 'd . ..
. + . . etabolic alkalosis is paradox1ca 1 ac1 una .
loss of H ion in m .
. . L of hydrochloric acid will lead to loss of
4. . Hyp~chloremia · . ~~: hypochloremia. Loss of chloride will lead
1
chloride so t~ere WI HCO reabsorption, which will aggravate
to increase in renal s ·.
' ..
136 CH. "4 Fluid Therapy in Medical Disorders
So during vomiting or continuous nasogastric aspiration there will be

Hypovolemic, Hypokalemic, Hypochloremic metabolic alkalosis
Abnormalities of urinary electrolytes in patients · with vomiting 18
Table No. 4.3 : . Variation in urinary electrolytes with vomiting
Time Potassium Chloride HC0 pH
" 3
Day 1-3 Increased Decreased Increased > 6.5 alkaline
Late Decreased Decreased Decreased < 5.5 aciduria
Abnormalities of fluid and electrolytes in patients with vomiting is
summarized in Fig. No. 4.2.
Fig. No. 4.2 : Fluid and electrolyte abnormalities in vomiting
Vomiting or nasogastric aspiration
Na loss Dehydration Loss of Cl· Loss of H+

J, J/ .j, .j,
1'HCQ3· ~ Hypochloremia
1' Aldosterone
J, absorption in
~
1' Na absorption proximal tubules Metabolic
1' K secretion Alkalosis
. : & urinary loss
J,
Hypokalemia
. J,
When severe hypokalemia 1' H+ Secretion Paradoxical

~
for increased Na absorption in distal tubules aciduria
End result:
Hypokalemic, Hypochloremic, Metabolic Alkalosis
Treatmen.t .
In upper G:I. loss-electrolyte losses are as follows: Na 50 mEq/L, Chloride
mEq/L, K 10-20 mEq/L and variable H+ ions. Volume by volume
100
replacement of fluid loss should be made.
CH. 4 Fluid Therapy in Medical ·Disorders 137
Fluid used to correctdeficit due to upper G.I. losses are isotonic saline and
lsolyte-G. .
1. Isotonic saline : 0.9°/o NaCl is used with addition of 30-40 mEq/L
potassium to restore previous and ongoing losses. In patients with
shock and oliguria, potassium supplementation should be done
cautiously or avoided.
2. lsolyte-G : This is the specific fluid used for the replacement
of upper G.I. loss. By its ammonia (70 mEq/L), high chloride
(154 mEq/L), potassium (17 mEq/L) and sodium (63 mEq/L) content,
it corrects H+, c1-, K+ and Na+ losses respectively. This is the only
available fluid which corrects metabolic alkalosis directly by
providing H+ ion.
Q. How isotonic saline is an effective l.V. fluid in treatment of vomiting/
nasogastric aspiration ?
A. Isotonic saline effectively corrects abnormalities due to upper G.I.
loss in the following ways :
1. It corrects deficit of fluid and so increases ECF volume and
decreases HC0 3 reabsorption by proximal tubules. So by reducing
renal HC0 3 reabsorption and thereby increasing renal excretion, it
corrects metabolic alkalosis.
2. Correction of volume and sodium deficit will decrease aldosterone
secretion. Easy availability of sodium at distal tubu.l es and
decreased aldosterone level will lead to decreased potassium and
H+ ion secretion at distal tubules. So it will prevent further
hypokalemia and alkalosis.
However additional potassium supplementation is nece~sary to
correct already existing hypokalemia.
3. Maximum concentration of chloride (154 mEq/L) in isotonic saline
corrects hypochloremia. Increased chloride in collecting duct will
permit increased rate of cr/HC0 3 -. exchang_e. It favours HC0 3 -
secretion which will correct metabolic alkalos1s.
so isotonic saline corrects all biochemical abnormalities caused by
vomiting or continuous nasogastric aspiration (except K+ deficit).
Fig. No. 4.3 : Summarizes role of isotonic saline in treatment of upper G.I.
loss
Infusion of isotonic saline
Volume Sodium · Chloride

Correction ~ Supplementation Supplementation
J. ~ J. . J.
J.Renal . J. Aldosterone . Corrects
HC03- .i Hypochloremia
Absorption J. Urinary. J.
H+ lossand Favou.rs HC03 -
Corrects
l J K+ loss
J.
Prevents
Secretion
Metabolic Alkalosis Hypokalemia

1'
Prevents Hypokalemia and
Corrects Hypochloremia, Alkalosis and Dehydration
Q. How to assess efficacy of fluid therapy in upper G.I. loss ?
A. Besides the clinical criteria and urine output monitoring, urinary pH
i~ very important to assess efficacy of fluid therapy. Acidic urine
suggests need for more vigorous treatment and alkaline urine suggests
response to therapy.
. .
Q. Which fluid is ideal for gastric irrigation ? Why ?

A. Isotonic normal saline is ideal for gastric irrigation .(especially in
electrolyte disturbances, hypovolemia and haemodynamically unstable
patients). Remember never to use plain water for irrigation. Plain water
draws more gastric secretions iri to the stoma.ch in attempt to make
the fluid isotonic for absorption. Removal of this electrolytes containing
fluid can deplete fluid and electrolytes. ·
For the same reason, in patients with contiriious hasogastric
aspiration, it is important to restrict the amount of ice chips given by
mouth. Nasogastric suctioning of ice chips : can cause fluid and
electrolytes loss from the stomach.
CH. 4 Fluid Therapy In Medical Disorders 139
Fluid therapy in diarrhoea

In diarrhoea stool contains large amout of sodium chloride, potassium and
bicarbonate along with water (Table No. 4.4).
Table No. 4.4 : Electrolyte content of diarrhoea

Average electrolyte content, mEq/L
Na· K+ er HC03-
Cholera
Adults 140 13 104 44
Children (below 5 years) 101 27 92 32
Non-cholera diarrhoea
Children below 5 years 56 25 55 14
Fluid and electrolyte abnormality in diarrhoea is summarized below :

1. Hypovolemia : Loss of fluid in diarrhoea occurs due to
a. Abnorma.lly increased secretion of fluid into the small bowel
(secretory diarrhoea due to G. I. infections e.g. E. coli, Vibrio
cholerae or rota virus).
b. Decreased absorption of fluid by intestine (osmotic diarrhoea
due to purgatives like magnesium sulphate or malabsorption of
glucose or lactate in children).
c. Additional loss of water can also occur due to associated
vomiting or fever.
2. Sodium deficit : Diarrhoea causes loss of Na, resulting in Na
deficit in all patients, but proportion of Na loss as compared to
water loss will decide serum Na concentration and type of dehydration.
a. In most frequent cases of diarrhoea loss of water and sodium
are in the same proportion leading to isotonic dehydration-
hypovolemia.
b. In some infants with diarrl1oea net loss of water is in excess of
Na (deficit of water is greater than deficit of Na), which ·1eads
to hypertonic (hypernatremic) det1ydration.
c. If net loss of Na is greater than loss of water (deficit of Na is

' v
140 · CH. 4 Fluid Therapy in Medical Disorders
greater than deficit of water), diarrhoea will cause hypotonic i:
(hyponatremic) dehydration. ;:
:
usually adult patients with diarrhoea· who drink large amount of ,
water, hypotonic fluids or receive 1.V. infusion of 5°/0-dextrose may
develop hyponatremia.
3. Hypokalemia : Hypokalemia occurs because. fluid. lost in diarrhoea !s
rich in potassium. (Normally 8-15 mEq potassium ions are excre~ed rn
faeces daily. Much greater loss occurs with diarrhoea). Moreover in the
process to retain sodium under the influence of aldosterone, potassium
is lost in urine and secretion of potassium in intestine also increases,
which aggravates hypokalemia.
In patiehts with hypokalemia due to diarrhoea, the actual serum
potassium concentration may be misleading due to acidosis, water
and sodium loss. Therefore, serum potassium concentration may be
normal (or high) inspite of loss of total exchangeable body potassium
and a low potassium concentration in the cell.
4. Hyperchloremia : The ileal and colonic mucosa possesses
a luminal ci-/HC0 3 - exchanger that is capable of reabsorbing chloride
1
in exchange of bicarbonate. So during diarrhoea when more HCO - is
' ' 3
secreted, more chloride is absorbed from intestine causing
hyperchloremia. In attempt to increase sodium absorption (to maintain
ECF volume) from intestine and kidney, simultaneous chloride
absorption by NaCl transporter will also aggravate hyperchloremia. So
during ·diarrhoea hyperchloremia occurs.
5. Metabolic acidosis : Fluid secreted distal to pylorus is rich in
bicarbonate. Diarrhoea leads to large amount of HCo - secretion (30-
3
45 mEq/L) in the gut which is excreted, and leads to metabolic acidosis.
If diarrhoea causes severe hypovolemia or renal failure, renal
compensation to loss of bicarbonate is lost and severe metabolic
acidosis may develop rapidly. Acidosis may also result from excessive
· production of lactic acid when patient has hypovolemic shock. i •.
i;
l '
So hyperc~loremic, · hypokalemi.c, metabolic acidosis occurs in ·Ih.

'patients with diar'rhoea. \' '
I~ .
I
I
CH. 4 : Fluid Therapy in Medical Disorders 141
Abnormalities of fluid and 1 . . . . ·

in Fig. No. . . e ectrolyte in patients with diarrhoea are summarized
44
Fig. No. 4.4 : Fluid and eIect ro Iyte abnormalities in diarrhoea
DIARRHOEA
Ri c h ·m K+ and HC0 -, Contains water and Na+
3
l
Kloss Water loss Na loss HCOi loss ·
~ ~
Dehydration~ 1' Aldosterone Intestinal luminal
• / -1- exchange of
1' K Secretion 1' Na Absorption Hco - with Cl-
3
& Urinary loss ~ ~
Associated 1' Renal 1' G.I. Cl-
Absorpt~on of Cl- / absorption
/
HYPOKALEMIA HYPERCHLOREMIA ACIDOSIS
END RESULT
HYPOKALEMIC, HYPERCHLOREMIC, METABOLIC ACIDOSIS
Treatment
A. Specific treatment for control of diarrhoea
B. Fluid therapy
Aim of fluid therapy is :
1. Correction of dehydration.
2. Correction of sodium deficit (which ·indirectly prevents potassium
loss and chloride retention).
3. Correction of hypokalemia and metabolic acidosis. Treatment of
both need to be done simultaneously and meticulously. If only
metabolic acidosis is treated, due to its correction potassium
will be shifted intracellularly. If patient is hypokalemic only
correction of the acidosis can precipitate dangerous hypokalemia.
on the contrary, ·w ithout correction of acidosis · potc:issium
supplementation can cause dangerous hyperkalemia. This' is due
142 · CH. 4 : ·Fluid Therapy in Medical Disorders
to .failure of K+ shift into .the intracellular compartment {due to

acidosis) even in state of potassium deficit of the body. .·
Q. Which fluids are used to treat fluid and electrolyte abnormalities due
to diarrhoea ?
A. Fluid and electrolytes losses can . be replaced either orally or
intravenously. Intravenous route· is usually needed only for initial
rehydration of patients with severe diarrhoea ..
1. Oral rehydration therapy (ORT) : As oral rehydration therapy is
easily available, simple to use and safe, it is a preferred method of
fluid replacement. Losses due to diarrhoea can be effectively
corrected by oral rehydration solutions (ORS). Readily available
ORS provides Na+, K+, Cl- and bicarbonate along with glucose, .
which effectively corrects fluid and electrolyte abnormalities, and
also provide calories.
Oral rehydration therapy is based on the principle that the intestine
actively absorbs glucose and Na is carried with it. Glucose
enhances Na and secondary water transport across the mucosa
of the upper intestine, even in presence of infective d,iarrhoea.
Avoid correction of losses due to diarrhoea, totally with electrolyte
free solutions (i.e. water, glucose water, tea, soft drinks or
commercially available fruit drinks). As it provides only fluid, but
lacks electrolytes, it can cause hyponatremia and is ·not effective
in correction of hypovolemia. For detailed discussion on ORT, please
refer to Chapter No. 8 ("Fluid therapy in children").
2. · . Intravenous fluid therapy : l.V. ·fluid therapy is indicated when
rapid correction of blood volume is required for severe dehydration
and shock,. inability.of patient to take ORS due to pe,rsistent vomiting
or ORT fails to correct volume depletion due to greater losses.
The preferred · LV. fluids to correct losses due to diarrhoea are
Ringer's lactate and isotonic·saline~ But no l.V. fluid is ideal, because
· they all are deficient in atleast some of the electrolytes required to
correct the deficiency found in · patients dehydrated :by acute
diarrhoea. .. ,
j
j
.]
I
J CH. 4 .Fluid Therapy in Medical Disorders 143
To ensure adequate electrolyte replacement, · patient needs ·

supplementation of potassium and I or .bicarbonate to l.V ..fluiqs, or
ORS should be given as soon as the patient on I. V. fluid is able to ·
· drink.
·a. ·Ringer's lactate solution : It is the best commercially
available solution. It is the preferred solution because it not
only provides an adequate concentration of.sodium but also
provides bicarbonate (by hepatic conversion of lactate) for
the correction of metabolic acidosis. How~ver its potassium
concentration is low (4 mEq/L) and solution provides no
glucose to prevent hypoglycemia. So the patient with diarrhoea
may require additional potassium, glucose and at times
bicarbonate supplementation (1.V. or oral). ·
b. Isotonic saline : It effectively corrects hypovolemia and
provides Na along with water. Isotonic saline does not contain
potassium to replace potassium deficit or base to correct
metabolic acidosis. So patient may require . additio~C:ll
supplementation of potassium (10-20 mEq/L) and NaHC0 3
(20-30 mEq/L) to correct existing hypokalemia and metabolic
acidosis. .
Although isotonic saline lacks ·K+, adequate supply of sodium
and water will prevent urinary loss of K+ by . suppressing
aldosterone. . .
Similarly isotonic saline does not correct metabolic acidosis
directly, but adequate correction of hypovolemia will improve
renal perfusion, which will permit renal correction of f!letabolic
acidosis. ·
c. 5o/o dextrose : It is not an acceptable I. V. fluid because it
does not correct acidosis, hypokalemia; and sodium 9eficit.
50;0 de.xtrose :is not effective in correction of hyopovolemia.
Rapid infusion of large volume of 5°/o dextrose also carries
the risk of hyponatremia and hyperglycemia leading to osmotic
diuresis. However D-5°/o with 45 mEq NaHC0 3 (2 ·amp - :50
ml of 7.5°/o NaHC0 ) and 20-30 mEq of potassium ·chloride ·
3
·is effective.
144 CH. 4 · : fluid Therapy in Medica·1 Disorders ·
Combined Loss - Vomiting and Diarrhoea

Basic pathophysiology and principles of treatm~nt_ are same ~s desc.ribed i.n
vomiting and ·diarrhoea. When vomiting and diarrhoea ~oex1st, pa~1ent w111
have predominantly loss of fluids, sodium and potassium. If patient has
predominant vomiting, it will lead to associated metabolic alkalosis. If patient
has predominant diarrhoea, it will lead to associated metabolic acidosis.
Treatment: Preferred l.V. fluid to treat this combined loss is isotonic saline
with necessary potassium supplementation (oral or l.V.).
Upper G.I. Bleeding (Haemetemesis)

Upper gastrointestinal bleeding is a frequently encountered problem with
haemetemesis and melena as the common presentation. Melena develops
after as little as 50-100 ml of blood loss, whereas massive upper G.I.
bleeding (> 1,000 ml) may present with haematochezia. Most important
causes of upper GI bleeding are peptic ulcer (50o/o), erosive gastritis
(about 20o/o) and oesophageal varices due to portal hypertension.
Management
Treatment of acute · GI bleeding must beg.in with initial assessment,
resuscitation and stabilization of patient. Subsequently, further evaluation
is done and specific therapy planned accordingly.
Initial Evaluation and Resuscitation

A. Initial assessment
• Ha~mod.ynamic . assessment . lntravascular volume and
haemodyna~ic status should be assessed immediately. In the
~ae_modynamicall~ compromised patients, resuscitation should be
instituted concomitantly with initial assessment. Vital signs (heart
rate, B.P. and postural changes) are cru · · th. · d
. .. . c1a 1 1n e eva 1uat1on an
management of s1gnif1cant bleeding Vit I · b d d
·re 1·1a bl y an d f requen ti y. - · a signs must e recor e
. A sudden increase in pulse rate or a cha .n · ·. BP · ft n

. . . ge in postura 1 1s o e
th~ only ~arly ind1cat1on of recurrent bleeding. In absence of other
evident etiology, postural hypotension (supine to upright fall inSBP of> 10
-1 "-
il'
1J
1
I
L CH. 4 : Fluid Therapy in Medical Disorders 145

I
I
mm Hg or increase in heart rate of> 20 beats/min) indicates moderate
blood loss (10-20°10 of circulatory volume). Supine hypotension suggests
severe blood loss (usually> 20°10 of circulatory volume). Further blood
l~ss resul~s in shock with hypotension, tachycardia, vasoconstriction,
d1aphores1s and ischemic organ damage and requires ICU admission
and rapid restoration of circulatory volume. ··
• Signs of distress : It includes confusion, obtundation, diaphoresis,
cold clammy skin and hypotension. Such a patient needs urgent
intervention.
• Determining initial treatment strategy : The urgency with which
gastrointestinal (G.I.) bleeding is managed is dictated by the rate of
bleeding.
The patient with trace haem-positive stools and without severe anaemia
can be managed as an outpatient.
·visible blood loss requires hospitalization and inpatient evaluation.
Persistent bleeding or rebleeding with haemodynamic · instability
necessitates ICU admission.
Massive bleeding is defined as loss of > 30°10 of estimated blood
volume or bleeding requiring blood transfusion of 6 Units or more in
24 hours.
• Estimating blood loss : This can be estimated by measuring the return
from nasogastric (NG) tube. An approximate estimate of blood loss
can be made by the haemodynamic response -to 2 litres of isotonic
saline (crystalloid fluid challenge). - .
If blood pressure (BP) returns to normal and stabilizes, blood loss of
15o/o to 30o/o has occurred. If BP rises but falls again, blood volume
loss of 30-40% has occurred. If BP continues to fall, blood volume
loss of more than 40°/o has occurred. _ _ . ·. .
• -Assess co-morbid disease : The presence of co-morbid disease (1.e.
OM, HT, IHD) must be determined. . · . _
• History and examination : Attempt to localize the most likely source
of bleeding. .
The presence of_melena indicates upper G.I. bleeding.
Haemetemesis indicates upper G.I. bleeding . .When small amount of
. ht d blood is passed per rectum, the lower G.I. tract can be
brig re . .
assumed to be .the source.
146 · CH. 4 : . Fluid Therapy in Medical Disorders
. In patients with large volume maroon stools, NG t.ube aspiration should

be performed to exclude upper G.I. haemorrhage. lt_should be noted
·· , that in about 15°/o of patients with upper .G. L ·bleed mg, NG . aspirate
.would fail ·to obtain blood or coffee-ground material.
• · Insert nasogastric tube : A NG tube should be inserted i_n all p~tients
with upper G.I. bleeding to decompress the stomach. N~ data suggests
that NG tube placement may initiate or aggravate bleeding in patients
with oesophageal varices. NG tube placement is :essential to monitor
ongoing bleeding. Nasogast.ric aspiration of blood also prevents hepatic
encephalopathy in cirrhotic ·patients.
8 Initial resuscitation
• Establish two large-bore intravenous lines or large-bore central line .
• Bloo_
d is sent immediately for a complete blood count, platelet count,
.pro~hrombin time, serum creatinine, liver enzymes and cross matching.
• Insert the NG tube and aspirate (gently by hand, to avoid gastric injury) .
• Initial volume expansion can be done with isotonic saline, Ringer's
lactate or colloids in haemodynamically unstable patients, urlti.I blood
product is available.
• .. Blood .replacement
(a) . When to transfuse ? ·
There is no hard and fast rule about indications of blood
·t~ansfusion. Patients: with large blood loss who ·continue to bleed
' d~spite ...therapy, w~o .are in shock, who have low haematocrit
(e.·g ~ less than 20:.25} or who have symptoms related to poor
tissue. o_x~~ -~natio~ __ (~.g. angina) require volume expanders and
blood should be transfused as soon as possible. ·
. (b) Why to transfu$e and what should _be the goal of transfusion ?
Aim of blood _ transfusion is to achieve haemodynamic stability,

and to maintain haematocrit at about 30. Transfusion therapy must
, ,. continue ta: keep ;pace with ongoing losses. When ·the blood
pressure and · pulse rate have been restored to normal limits, the ,..
rate of transfusion can be slowed. It. is very important to note that .
. ·1 '
CH. 4 : : . Fluid Therapy in Medical Disorders 147
reduction in haematocrit may take 24-72 hours.after bleeding. So

blo~d transfusion ~hould not be withheld from actively bleeding
~at.1 ent based on their haematocrit (BP and pulse are better
mdt~ators). Do not correct anaemia completely. It may aggravate
vanceal bleeding in cirrhotic patients ·due to expansion of
intravascular volume.
( c) Which · blood product to transfuse ?

(i) PCV: Packed red blood cells transfusion is ·recommended to
correct blood loss in haemetemesis. In absence of.continuing
bleeding, the haematocrit should rise by 3°/o for each unit of
PCV. Patient who requires massive ·transfusion(> 3,000 ml)
. should receive warmed blood to prevent hypothermia.
(ii) FFP : In patients with active bleeding, .fresh ·frozen plasma
. (FFP) should be given if the prothrombin time is atleast 1.5
times the control value. Initially 4 unit~ of FFP can ·b.e given.
Further therapy is based on clinical assessment. In patients
with massive bleeding, 1 unit of fresh frozen plas.ma should be
given after each 6 units of packed red blood cells transfused.
(iii) Platelet transfusion : It is indicated if the platelet count is
under 50,000 per cubic mm, along with therapy directed at
the cause of thrombocytopenia (i.e. hypersplenism, drugs).
Platelet transfusion should also be considered if there is
impaired platelet function due to aspirin use (regard.less ~f
the platelet count) a.nd after 10 units of PCV transfusion.
. . . . ~ .
• Monitor BP, pulse and urine output.

• Other measures include
1. Airway protection : . . .
. •.
Espec1a • ·
11 y in ma
ss·ive bleeding 6r a"!tered
. . rnental
. . status·
: . ,
2. 0. ctreotide or so~atostaHn infusion :

If there is severe G.I. bleeding due to varices.
:~ .-
-V
I
;
i
-t_
148 CH. 4 : _Fluid Therapy in Medical Disorders
- _ · C· Risk assessment
Factors which suggest high risk and poor prognosis are :
(i) - S~vere blood loss (>5 units of blood).
(ii) Shock, low haematocrit and coagulopathy on admission.
(iii) Bright red haemetemesis or nasogastric aspirate.
(iv) Persistent haemodynamic instability despite fluid resuscitation.
(v) Recurrent haemetemesis (within 72 hrs)
(vi) Advanced age (> 60 years)
(vii) Serious comorbid illness or advanced liver disease.
These patients require ICU admission and vigorous treatment.
D Subsequent evaluation and treatment
With proper evaluation, establish diagnosis of underlying etiology and
accordingly decide further treatment plan.
Fluid therapy in Hepatic and Pancreatic disorders

Basi_c principles of fluid and electrolyte management in patients with
ascites due to cirrhosis of liver, hepatic encephalopathy and pancreatitis are
discussed.
Ascites in cirrhosis of liver
Pathophysiology
In cirrhosis of liver, ascites is thought to result from
(1) Portal hypertension (increased hydrostatic pressure).
(2) Hypoalbuminaemia (decreased oncotic pressure).
(3) Peripheral va~o~ilatation, perhaps mediated by endotoxin induc~d
release of nitric oxide, with resulting increase in renin and angiotensin
levels and sodium retentio"n by kidney.
(4) Impaired liver' in.activation of aldosterone.
(5) Increased aldosterone secretion secondary to increased renin production. -
CH. 4. Fluid Therapy in Medical Disorders 149
Basic treatment guidelines:

(1) Salt restriction
The most important measure is to restrict. salt to 1-2 gram/day. Salt

· · restriction induces a negative sodium balance and permits diuresis.
(2) Fluid restriction
Restriction of fluid intake (800-1,000 ml/day) does little to enhance
diuresis but may be necessary to correct hyponatremia. So if serum
so9ium is less than 130 mEq/L fluid restriction is required.
(3) Diuretics ·
Spironolactone is the diuretic of choice. Starting dose is 25 mg twice
a day, this may be increased to maximum 150 mg six hourly. Loop
diuretics are more potent so they may be added when spironolactone
fails to initiate a diuresis. The goal of weight loss in the ascitic patient
is 1 kg/day in oedematous patient and 0.5 kg/day in patient without
peripheral oedema. Avoid overaggressive diuresis, which may cause
azotem.ia or precipitate hepatic encephalopathy.
(4) Bed rest
It is occasionally helpful in mobilizing ascites in the patient with
refractory ascites.
(5) Paracentesis
(a) Indications : Paracentesis is indicated ·for diagnostic purpose,
massive tense ascites causing respiratory compromise, ascites
refractory to diuretics, or intolerable diuretic side effects.
(b) Safety : Up to 5 litres of ascitic fluid can be safely removed provided
that the patient has oedema and the fluid is removed slowly (over
30-90 minutes).
( c') Risk : Ascites tapping leads to hypovolemia. So large volume
paracentesis can lead to hypotension and even shock (more
frequently in non-oedematous patients). In advanced cirrhosis it
can precipitate even hepatic coma.
(d) Plasma volume expansion during paracentesis : Plasma volume
expansion with albumin, colloids, plasma protein or blood transfusion
prevents hypotension and permits large volume paracentesis even
··. ·...· -. -~
· 1'50 CH . .4 · Fluid .Therapy in Medical Disorders
in non-oedematous patients. Albumin is more effective than other

plasma expanders (dextran, polygelatin) at prevent.ing cirGu.latory
. dysfunction. So when more than 5 litre ascitic _fluid is removed,
. . albumin is the 'treatment. of choice. The total ascitic fluid can be
removed in' one sitting without complications, if 6-8 gm of albumin
is replaced per litre of ascitic fluid removed. If the ascitic fluid
removed is less · than 5 litre, albumin .can be replaced . by less
expensive colloids. · ,
Plasma niay be transfused for patients with coagulatfon ·disorders
and is less expensive than albumin. If patient is anaemic· even
· · whole blood can be transfused for· replacement · ·
·(e) Current
. .
status : In last decade
.
paracentesis has become the .
treatment of choice in management of severe/large ascites in

cirrhosis of Hver. Paracentesis with p·lasma volu'me expansion is
more rapid .and effective and is associated with ·lower n'umber of
·com'plications than conventional diuretic therapy. However the
patient should be given diuretics after paracentesis to avoid
reaccumulation of ascites.
(6) Other measures
(a) Peritoneovenous shunts
(b) Tr~nsjugular intrahepatic portosystemic shunts (Tl PS)
(c) Other.agents : Beta-.blockers, etc . .
(7) Liver transplantation .
Standard therapy· for patients With end stage cirrhosis
1·
HEPATIC ENCEPHALOPATHY
/;
Hep~tic encephalopathy represents a reversible ·decrease in neurological
function caused by liver diseases . . • I ' '
Ii Principles of treatment :are

Iiij
/i 1. Identification and ~reatr:'ent of the pr:e~ipitating causes.
1,,1. 2. lnitiate ,.a~monia lo~ering therapy. .
~ . , '.
ji
3. -· Agents to modify neurotransmitter balance . . .
I!
F
} . .
~ .
CH. 4 Fluid Therapy in Medical Disorders 151
~
~
I 4. Minimize potential medical complications of cirrhosis.
Treatment of hepatic encephalopathy is summarized in Table NO'. 4.5.
Table No. 4.5 : Treatment of hepatic encephalopathy
1. Identify a.nd correct the precipitating cause(s)
.a . Monitoryolume status and vital signs
h Assess for gastrointestinal bleeding ·
c. Eliminate ~edati.ves, tranquillizers, or similiar drugs
· d. Perform screening test for hypoxia, hypoglycemia, anaemia,
hypokalemia and other metabolic factors and correct it ·
e. .Maintain calorie, fluid and electrolyte balance
2. Initiate animonia lowering therapy
a Empty bowels containing nitrogen material. Perform nasogastric
lavage. Stop G.I. haemorrhage. Avoid constipation
· . Lactulose or phosphate enema if required
h ·· Protein restricted diet, raise dietary protein slowly with. recovery
, c. ·. Lactulose or lactilol to produce 2-4 soft stool per day .
" d. Antibiotics to reduce intestinal bacterial counts
· 3. To modify neurotransmitter balance directly (bromocriptine;
flumazemrl) or indirectly (branched chain aminoacids)
4. Minimize potential complications of cirrhosis/depressed consciousness
Supportive care for airway, haemodynamic and metabolic status .
·5.. Approaches with anecdotal benefits : Dietary zinc, levodopa, eradication of
H. Pylori, charcoal haemoperfusion
1. Diet
Dietary protein should be withheld during the acute episodes. Caloric
intake is maintained at 2,000 cal/day or above, orally or intravenously.
When the patient resumes oral intake; protein intake is started at 20
· ·gram/day and increased by 1O gram every 3-5 days to 60-80 gram/day
as tolerated (vegetable protein is better tolerated then meat protein).
In cirrhotic patients without encephalopathy, it is important to avoid
protein restriction because these patients have a higher than normal
protein requirem·ent (1.2 gram/kg/day) to remain in positive · balance.
· Zinc deficiency should be
corrected, if present, with oral zinc sulphate,
600 mg/day in divided doses.
152 . CH. 4 . Fluid Therapy ·in Medical Disorders
2. Medical Therapy· .
It includes chiefly lactulose, neomycin and metronidazole. 0th ·
alternative antibiotics are ampicillin, vancomycin and rifaximine. er
3. Fluid and electrolyte management
(a) Avoid hypoglycemia
Patients with hepatic encephalopathy with renal failure are more
prone to hypoglycemia due to decreased glycogenolysis. and ,
gluconeogenesis. So oral glucose supplementation (200 gm/day
approximately) or 10°/o or 20°/o dextrose should be given l.V. slowly
continuously.
Frequent blood sugar should be monitored to rule out hypoglycemia
and to avoid hyperglycemia.
(b) Avoid metabolic alkalosis
Overzealous use of diuretics, vigorous paracentesis or vomiting
can lead to metabolic alkalosis, which can precipitate or aggravate
hepatic encephalopathy. Systemic alkalosis causes increase in
the amount of NH 3 (non-ionic ammonia) relative to NH 4
(ammonium ions). Only nonionic ammonia (NH 3 ) re_ adily crosses
the blood brain barrier and accumulates in the CNS. All precautions
should be taken to prevent alkalosis.
( c) Hypokalemia
Vomiting and diuretic therapy causes hypokalemia. Hypokalemia
directly stimulates renal ammonia production, which can
precipitate or aggravate hepatic encephalopathy. Hypokalemia
should be corrected by adding KCI in l.V. fluids or by oral K+
supplement.
(d) Avoid hyponatremia . . ·
Ad~inistration of only glucose containing electrolyte free fluid
can lead to hyponatremia, which can aggravate cerebral .oedem~
So l.V. fluid therapy should be carefully planned so as to avoid
hyponatr~mia.
(e) Selection of l.V. fluids .
0) Glucose containing fluid is preferred, but avoid So/a-dextrose, 1
as it is hypotonic. Hypotonic fluid can aggravate cerebra
oedema.
CH. 4 Fluid Therapy in Medical Disorders 153
(ii) Avoid lsolyte-G, as it contains ammonium chloride, which

gets converted into H+ and urea by liver. In liver failure this
conversion is defective so there is accumulation of ammonium
chloride. Subsequent collection of ammonia may precipitate
hepatic precoma.
(iii) Avoid Ringer's lactate as it contains lactate, which gets
converted into bicarbonate by liver, and can cause alkalosis,
which is not desirable. Moreover in liver disease lactate
metabolism is impaired, so it can cause lactic acidosis and
therefore, should be avoided.
(iv) Which fluid to give and how much ?
1.V. fluid usually preferred is 10°/o dextrose, 20°/o dextrose and
dextrose saline. Potassium chloride (1 Amp of 15°/o inj. KCI
contains 20 mEq of potassium) may be added to l.V. fluid as
per requirement. Instead of l.V., oral potassium supplement
is preferred.
Volume of fluid infused depends on hydration status and urine
output. In oedematous cirrhotic patients fluid supplement may
be restricted along with salt restriction. In cirrhotic patients salt
should be restricted to 1-3 gram/day. Normal salt (sodium)
requirement is about 6 gm (100 mEq) per day.
Acute Pancreatitis
Acute pancreatitis is commonly associated with excessive alcohol

consumption or gallstones. Less common causes include hypercalcemia,
hypertriglyceridaemia and variety of drugs.
Q. How to classify acute pancreatitis ?

A. The most useful classification of acute pancreatitis distinguishes
between mild and severe disease.
Mild pancreatitis : Up to 90°/o of patients with acute pancreatitis have
mild and self-limiting course. Such mild pancreatitis with minimal or
no organ dysfunction has uneventful recovery.
-154 CH. 4 Fluid Therapy in Medical -Disorders
· ·severe Pancreatitis : In 10-15°/o patients .it ·i·s· severe requiring

hospitalization, extensive treatment and has s1gmf1cant morbidity and
mortality. Pancreatitis should be considered severe if there is evidence
,0 f organ failure (shock,· pulmonary insufficiency, renal failure or G.I.
bleeding) or local complications such as necrosis, abscess or
.p s_eudocyst.
Management
Treatment Guidelines
• Control ·of pain with analgesics.
• Fluid resuscitation vigorously.
• Correction of metabolic and electrolyte disorders.
• No oral ._alimentation initially.
• · Nasog_ astric suction : Only in patients with protracted nausea, vomiting
. or ·paralytic ileus.
• -Monitor arterial blood gases and I or pulse- oxymetry.
• Antibiotics : No benefit of antibiotics in mild to moderate pancreatitis.
However, it is indicated if there is established infection. Prophylactic
antibiotics in severe pancreatitis have .improved outcome i.e. reduced
. risk of infection and /.or mortality. Broad-spectrum antibiotics with
: penetration in the pancreatic tissue and ·anaerobic cover reduce the
risk of pancreatic abscess. lmipenem· or piperacillin I tazobactum
are recommended.
• Peritoneal lavage : As per recent studies therapeutic lavage is of no
value.
• . .· Eliminate precipitating factors : A!cohol, medications etc. Prophylaxis
for alcohol withdrawal.
• Drugs ineffective : Glucagon, protease inhibitors such as aprotinine_ ,
glucocorticoids, calcitonin , NSAID etc. ·
• H2 r·ecepto·r antagonist ·: Although they have no proved beneficial
I
I
effects in the therapy of acute paricreatitis, they may be necessary in
severely ill patients.·with significant risk factors for· stress ulcer
·bleeding. _
• Octreotide : It reduces··mortality, not complications.
I
CH. '4 : Fluid Therapy in . Medical Disorders 155
• Gabexate : It reduces pancreatic damage but no effect on mortality>'

• En'doscopic therapy : Detection ·a·nd extraction of common bile duct
. stones by ERCP is indicated in acute severe pancreatitis complicated
by progressive jaundice or ·c holangitis. ·ERCP has no role · in the
treatment of patients with acute gallstone- pancreatitis in the absence
of cholangitis.
• Surgical therapy : It may be required for severe haemorrhage or
necrotising pancreatitis, pancreatic abscess .and persistent p~eudocyst.
I. V. fluid therapy in pancreatitis

Correction of intravascular volume loss with proper l.V. fl~id therapy is an
essential component of treatment of severe acute pancreatitis. ·
Fluid resuscitation
Q. What is the importance of fluid therapy in pancreatitis ·7
A. 1. Fluid therapy prevents hypotension and renal'failure.
2. Fluid therapy may help in the protection of the microcirculation o.f
the pancreas. Compromised microcircula.tion of the pancr~a~ may
lead to intensification of local inflammation . and may ~ause
necrotizing pancreatitis.
Q. What are the causes of hypovolemia in pancreatitis ? . .
A. Important causes of hypovolemia are : .
1. . Accumulation of fluid within the bowel lumen secondary to paralytic
ileus.
2. Marked oedema in peripancreatic region.
3. Vomiting and excessive perspiration ..
Q. How much fluid is required fo~ fluid resusc.itation in acut~ pancreqtitis ?
· . · · · d ding upon severity of fluid loss.
A. , It varies .from patient to P.at1ent . .epen . . . .. h d f r the
Requirement of the fluid may be in excess. a~ - litre ~a~. =~e~uate
5 5
first few days and at times in excess of 1o litre to main am . ..
· · · · p . t 'th hypotension and vascular mstab1hty
intravasc.ular v~lume_. at.1en ~1 . a .need CVP monitoring. . .:
. requiring mass1ve ·flu1d resusc1tat1on m Y
'
156 CH. 4 : ,: Fluid Therapy in Medical Disorders
a. What should be.used for resuscitation in pancreatitis ?

A. . .Crystalloid solutions (i.e. isotonic saline) are .generally used for initial
. fluid resuscitation. Because large amount of proteins are lost from the
. . circulation as part of the retroperitoneal inflammatory process, it is
advisable to use colloid especially if albumin falls to a level less than
2 gm/L.
Severe haemorrhagic pancreatitis with low haematocrit needs PCV
.or blood transfusion. It should be transfused to maintain haematocrit
of approx. 30°/o. For correction of abnormal coagulation status, patient
may need transfusion of clotting factors. If, despite appropriate fluid
resuscitation, hypotension persists l.V. dopamine drip may be helpful
in maintaining adequate systolic blood pressure.
Metabolic and electrolyte abnormalities in acute pancreatitis

Hyperglycemia
About 1 Oo/o of patients with severe pancreatitis may develop transient
hyperglycemia during the first several days. Blood sugar usually normalizes
as ·the inflammatory process subsides. Permanent residual diabetes
meilitus ··is muc~ less frequent, occurring in less than 2% of patients.
Because of the instability of blood sugar, insulin should be administered
cautiously and at widely spaced intervals of not less than 6 hours.
Hypocalcemia
Hypocalcemia occurs in 3°/o to 30°/o patients with acute pancreatitis. The
magnitude of the hypocalcemia correlates with the degree of illness. It
may occur as a result of decrease in nonionized calcium, which is usually
caused by loss of albumin from the circulation as a result of tissue
inflammation and third space losses. These types of hypocalcemic patients
are asymptomatic and require no specific therapy. . .
. .
In comparision, a reduction in serum ionized calcium ·may cause

neuromuscular irritability. Reduction in ionized calcium is due to its
deposition within the area of fat necrosis, metabolic abnormalities involving
inhibition ·of PTH secretion, refractoriness of bone to stimulation by PTH,
and associated hypomagnesemia. Symptomatic patients should be treat~d
with inj. calcium gluconate in absence of hypomagnesemia. As hypercalcem1a
. I
I~ .
j .
I
CH. 4 · : Fluid Therapy in Medical Disorders · 157
is one of the u~d~rlying causes of acute pancreatitis, inj. calcium gluconate

should be administered only if indicated.
Hypomagnesemia
Cause~.of magnesi~m deficiency include vomiting,Joss of Mg in the urine or

~epos1t1on of M~ in the ~rea of fat necrosis. Mg should be replaced
intravenously, which helps tn restoring the serum calcium level to normal.
Hypochloremic· contraction alkalosis

It may follow persistent vomiting and is treated with vigorous volume
replacement with isotonic saline supplemented with exogenous KCI.
Nutritional support in acute pancreatitis
Q. When to start oral intake ?

A. In patients with acute pancreatitis oral intake is initially _prohibited.
There are no uniform guidelines about the proper ·timing of initiating
oral feeding. Patients with mild to moderate pancreatitis usually require
treatment with l.V. fluids, fasting and possibly nasogastric suction for 2
to 4 days. A clear liquid can usually be started after 3 to 6 days and
regular diet by 5 to 7 days. In severe pancreatitis oral intake can
generally be resumed when abdominal pain and tenderness have
improved, paralytic ileus resolves and patient experiences bowel function
and becomes hungry and serum amylase has approached normal levels.
Q. . Why to avoid premature oral _
intake ?
A. Premature return to oral intake has been associated with the formation
of pancreatic abscess and reactivation of pancreatic inflammation. So,
in patients with persistent pain, paralytic ileus or the occurrence of
complications such as pseudocyst or abscess, return to eating should
be delayed.
Q. · How to initiate oral intake in pancreatitis ?
A. Theoretically it is advantageous to initiate ·oral i~take w_ith
carbohydrates along with water, which stimulates pancreatic secretion
lesser than fat or protein.
·~
'. ·.
~
158 CH. 4.· FluidTherapy.in ·. Medical 'Disotders
Total·parenteral nutrition (TPN)
Q. When and why to provide TPN ?

. .
A. Most of the patients (80°/o) ha~e mi.Id dise~se and recover over the
first 5 days without' requiring nutritional support In severe pancreatitis
the patient .who may not be able to recs.iv~ oral nouris_hment for 3. to 6
weeks should recei.ve 'TPN. TPN can decrease pancreatic secretion
provide nutritional support and can reverse t~e metaboli~ eff~c~ of severe
'
pancreatitis and may improve mortality. ·
Standard parenteral nutrition include$ carbohydraJe arid aminoacid
based solutio'ns. l.V. lipids can also be used as a calorie source in most
patients (except in patie_nt~ with ·hyperlipidemia). It is important to
remember that the choice of route is less important than the need to
provide adequate calorie and to establish positive nitrogen balance ..
.. . .
Q. What is total enteric nutrition .(TEN) and its status in acute p_a~creatitis?
A. , Feeding via 11asoenteric tube placed distal to the ligament of Treitz (distal
to third part of duodenum) is called enteric feeding. ,.
·· Conventionally gut rest with parenteral nutrition or I. V. ·fluid therapy
remains the treatment of choice in acute pancreatitis.
Howevernumber of rece.nt trials have demonstrated safe and effective
· us~ of ·oral feeding in mild pancre.atitis and total .ehteral riut_rition (via
nasojejunal tube) in patients with severe pancreatitis.
Enteral feeding is well tolerated and reduces· pancreatic and systemic
· inflammation and reduces the· incidence of . intra-abdominal sepsis·,
multi organ failure, need for operative ·inten.ientions and mortality,
when compared with the parenterally ·fed patients. Advantage.of enteric
feeding is that it.-is less expensive, ·safe and atleast ·as· effective as
parenteral nutrition. So it will be reasonable to attempt enteric feeding
in most patients. At the sam.e time clinical judgement shoL1ld be used
to detect patient~ who are unable to tolerate enteric feeding.
CH. 4 : Fluid Therapy In Medical Disorders 159
FLUID THERAPY IN CARDIOVASCULAR DISORDERS

Congestive heart failure (CHF)
Q. Which fluid and electro! t b ..
congestive heart failure (~~F~ ?normalities are seen in patients with
A. Oedema in CHF is d
water and sod·
more than th
dilutional
tm . ue to water and salt retention . So tofal body
is more in these patients. But retention o'f water is
a . of s.alt, so hyponatremia is frequently seen which is
'CHF · As diu_re~ics are the first line of treatment for oedema in
' hypokalemia is a frequently encountered side effect. 1
Q. How to ·provide fluid to patients with CHF?
A. Oral route is always preferred because it can provide better nu1rmon
and. salt restriction along with fluid ·restriction. Moreover oral fluid also
avoids the possible risk of pulmonary" oedema due to accidental
overrunning of I. V. fluids . .
Basic guidelines of fluid management
DON'T
( 1) Don't correct hyponatremia with salt supplementation : Remember that
hyponatremia is usually dilutional and needs fluid restriction and loop
diuretics for correction. Loop diuretics induce greater water loss than
sodium loss, so it will not aggravate hyponatremia.
(2) Don't chase urine output : In CHF with anasarca, when diuretics are
instituted urine output will increase. Don't follow routine guidelines
(i.e. total fluid required per day = urine output + 700 ml) of fluid
replacement. Our aim is to remove accumulated extra fluid from the
body so restrict fluid intake despite good urine output.
(3) Don't treat hypotension with sodium rich fluids, without establishing
cause for the same : Patient with CHF with poor cardiac performance
(very low ejection fraction) may develop hypotension. Such. pa't i:nts
require treatment like dobutamine infusion and not saline infus10~.
But at the same time patients with CHF may develop hypovofem1a
and hypotension due to abnormal losses i.e. diarrhoe~1 vomiting etc. .i
Such patients require gentle and careful, but adequate fluid replacement.
. ,f,:
F
J••
160 CH ~ 4 Fluid .Therapy in Medical Disorders
oo·s
(1) Give less fluid : Depending upon severity of anasarca amount of fl . . ·
. 'th Uld
replacement is reduced. Pat1ents wt severe anasarca require restriction
of fluid i~take (oral+ l.V.) as low as 500-600 ml/day.
(2) Restrict Sodium : If patient requires 1.V. fluid select proper fluids so as
to provide water with less sodium. Preferably avoid sodium rich fluid
like Isotonic saline or Ringer's Lactate as 500 ml of same contain 4.S
gram (77 mEq) and 3.8 gram (65 ~Eq) of salt ~sodium) respectively
(Compare it with 1-3 gram salt permitted per day in patients with CHF).
(3) Correct potassium deficit : Hypokalemic patients are more prone
to digitalis induced cardiac arrhythmias. So all patients on diuretic
therapy need to be evaluated for potassium status. While prescribing
fluid therapy, adequate potassium supplementation should be made.
Oral route is safer and hence preferred over intravenous fluid
replacement.
Essential Hypertension
fJn:1vl1cal guidelines
(1) Restrict total sodium intake to roughly 50 mEq (or 3 gram of salt -
NaCl/day).
(2) Avoid rapid replacement of total sodium requirement within shorter
duration with the sodium rich I. V. fluids (0.9°!o NaCl or Ringer's lactate).
Such rapid sodium replacement can aggravate hypertension.
(3) To deliver required sodium uniformly, all throughout the day, select
I. V. fluid with low sodium concentration (i.e. lsolyte-M or lsolyte-
P). Infuse these l.V. fluids slowly, preferably over 18 hours. -
(4) In uncomplicated hypertensive patients there is no need to restrict fluid
intake. Potassium supplementation should be done adequately.
CH. 4 : Fluid Therapy in Medical :Disorders 161
FLUID THERAPY IN RESPIRATORY DISORDERS.

Pathophysiolo~y of fluid, electrolytes and acid base disturbances in clinically
important respiratory disorders and fluid therapy in same are summarized
below. .
F~uid therapy in acute respiratory distress syndrome (ARDS)

Q. Why fluid balance should be maintained optimally in patients with
ARDS? .. · .
A. Although pulmonary oedema in ARDS patients is a consequence of

increased permeability of the alveolar capillary membrane, elevation in
the intravascular hydrostatic pressure may also contribute to the
• accumulation of alveolar fluid and result in worsening of oxygenation.
Therefore, the optimal fluid management for patients with ARDS
requires a balance between fluid restriction, which may cause
hypotension and decreased pedusion of vital organs and fluid
administration, which may increase oxygen requirements.
Q. How to achieve fluid balance in ARDS and with what precautions?

A. Small decrements in the intravascular volume with diuretic use and
fluid restriction produce significant decrease in extravascular lung water.
· Caution must be exercised in reduci.ng intravascular volum~, since
vigorous diuresis, especially in the setting of PEEP (positive end
expiratory pressure) may reduce cardiac output and pertusion of critical
· organs. Ideally the lowest intravascular hydrostatic pressure (or
pulmonary capillary wedge pressure) that also achieves an adequate
cardiac output and renal perfusion should be maintained.
. . . '
Crystalloid solutions should be used when intravascular volume

expansion is necessary. lnotropic agents may be required to maintain
an adequate cardiac output and perfusion pressure (mean ar~erial
pressure > 75 to 80 mm Hg). Measurement of pulmonary capillary
wedge pressure may be useful to optimize haemodynamics in ARDS
I
patients, but its role is presently unclear. Packed red blood c~lls I
transfusion is given to keep the haemoglobin above 1Ogm/di, a practice "I
that maintains a reasonable arterial oxygen content. I
i
i
, ..
162 CH.. 4. : ·Fluid Therapy in Medical Disorders
Q. How to provide· fluid fhe·rapy-. in .patients ·who develops ARDS after

._trauma or major s.urger.y _? .
A. , These patients. may need massive amount of ·fluids to ·. maintain an
adequate cardiac output. In these settings, circulatory considerations
outweigh the goal of minimizing lung oedema. Until loss of intravascular
fluid slows, crystalloids or colloids shou.ld be i'nfused aggressively to
· keep the pulmonary arterial wedge pressure above 1O mm Hg. Several
days later, excess fluid can be removed by diuresis, dialysis or CAVH
(or CVVH) with the goal of . reducing lung water .and improving
oxygenation. · ·
In conclusion, patients with ARDS should be kept as dry as possible
without compromising the cardiac output, to minimize accumulation of
· excess fluid in the lungs. .. -
Fluid therapy in chronic bronchitis or asthmatic bronchitis

I , . , .· . .
In addition to specific therapy, patients with chronic bronchitis or asthmatic

bronchitis should be well hydrated. Proper hydration avoids thickening of
secretions. Intravenous fluid may be required for acute exacerbatidris.
· Fluid therapy in status asthmaticus
Keep th.ese pq.tients optimally_hydrated ~ As there is no .convincing evidence
that fluid administration hastens mobilization of thickened secretions in
the airways, fluid the.rapy should be conservative unle'ss there is significant
dehydration. Av,oid excessive fluiq administration bec~use it may increase
pulmonary capillary .hydrostati~ pressure and decrease plasma oncotic
pressure. Cor:Dbin_ed with.the .marked negative pleural pressure transmitted
to the bronchovascular interstitium, these changes in vascular pressure
gradients promote : pu_lmon~ry oede.ma formation, which might further
complicate management. . .
t:lectrolyte ~nd Acid basedisturban~es i.n asthma !_COPD
EIE3:ctrol.yt·e abnormalitie~ . : Hypokalemia_is the . most frequently. seen
abnormality. . ,·
P a:t·1en ts . w1
. ·t·h· ·---b r· onchial asthma or COPD- receiving B2 I agonist·
(i.e.
'd therapy··are prorie -to develop hypoka em1a.
-salbutamol) or stero1
CH. · 4 . Fluid Therapy in Medical :Disorders · 163
coPD patients receiving diuretic therapy also contribute to hypokalemia. It

is important to diagnose and treat hypokalemia because associated hypoxia
and administration of theophylline can increase risk of cardiac arrhythmias
in such hypokalemic patients.
Acid base disorders in bronchial asthma :
1. Hypoxemia : In patients . with bronchial. asthma there is regional
inhomogenecity in _the dist_ribution of inspired ~ir, : which leads to
ventilation-perfusion (V/Q) ,mismatch and impaired gas exch.ange. Area
of low V/Q contributes to ._ the d.evelopment of hypoxemia . .
• • - -.. . • .J •
2. Mild :to moderate attack : Hypoxemia .with respiratory .alkalosis : In

mild to moderate asthma with dyspnoea, C0 2 elimination is adequate
or excessive . . So patient may develop hypoxemia with respiratory
alkalosis in early stage.
3,. Severe attack : Hypqxemia with respiratory acidosis (hypercapnia) :
·_ In severe asthma the c?mbine.d effect of augmented ~0 2 · production,
. _impaired. co2 elimi~atio~, ~nd. respir~tory _
muscle fatigue leads to the
qevelopment of hypercapnia and respiratory acidosis ..
COPD patients with respiratory failure will develop respiratory acidosis.
While those patients receiving aggressive ventilatory support may
·develop · respiratory· alkalosis. ,
Mechanical ventilation
.
In volume depleted patients, what care should _be taken before initiating
.
Q.
positive pressure ventilation, and why ? · · ·· ·
A. Basic pathophysiology : Venous blood flows passively from the low
pressure venous system into the right _atrium, right ventricle an.d finally
.to lungs. • ' • ·, I '
Effect of nor.m al inspiration on venOU$ return : During normal

spontaneous inspiration, intrathoracidpressure (IT_P) decreases, which
accel~·rate_s return of the venous blood flow to the heart and lungs.
Effect of positive pressure ventilation on venous return : In the patient
on positive pressure mechanical ventilation, ITP will increase during
inspiration (effect opposite to normal inspiration on ITP). Increased
. :". ".':"i
164 · CH. 4 . : Fluid Therapy in Medical Disorders
intrathoracic·pressure will reduce the systemic venous return. As·cardia .

output is primarily dependent on venous return, positive pressure
· ventilation will have detrimental effect on cardiac output. e
Clinical aspects : In euvolemic patients with normal cardiac function

positive pressure ventilation increases ITP, resulting in decreased
venous return and left ventricular stroke volume.
However this reduction in venous return is more pronounced in the
setting of hypovolaeniia, and decreased venous tone (sepsis,
hypoglycemia, etc.). So in the setting of hypovolaemia, acute
haemorrhage or spinal shock, if positive pressure ventilation is instituted,
patient may develop hypotensive crisis.
Prevention : Correct hypovolemia before initiating positive pressure
ventilation.
Management : It consists of intravascular volume replacement, use
of vasopressures (in low vasomotor tone states), and smaller tidal
volume ventilation. Avoid" large tidal volume or excessively high levels
of PEEP, because it will further reduce venous return as well as cardiac
output and blood pressure. .
Q. What will be the effect of mechanical ventilator on CVP and its clinical
significance ?
A. Normally CVP fluctuates with respiration. CVP decreases with a
spontaneous inspiration and increases with a positive pressure
ventilation. However CVP measurement taken at the end of exhalation
minimizes this effect.
· CVP measured · in a patient receiving PEEP (positive end expiratory
pressure) is higher, but this effect is rarely significant if PEEP is less
than 7 .5 cm of water. So common practice to disconnect the ventilator
· for a brief period during CVP measurement, is not favoured. Removal of
PEEP even for a short period maicarry risk of hypoxia.
CH. 4 Flu id Therapy In Medical Disorders 165
a. Which acid base disorders can be expected in patients on mechanical

ventilator ?
A. Patients on mechanical ventilator can develop following acid base
disorders.
1. Respiratory alkalosis : To correct hypoxemia, patient on
mechanical ventilator may receive hyperventilation which can
washout PaC0 2 causing respiratory alkalosis.
If required, the respiratory alkalosis can be reversed by increasing
the dead space or by reducing either the tidal volume or the
respiratory rate.
2. Respiratory acidosis : Inadequate setting of respiratory rate and
tidal volume can lead to respiratory acidosis in the patients on
mechanical ventilator. In these patients hypercapnia is usually
associated with hypoxemia.
3. Post hypercapnic alkalosis : The renal compensation of chronic
respiratory acidosis (as in COPD) is an elevated plasma HC0 3
(due to increased urinary H+ secretions). So these patients will
have increased PaC0 2 , increased HC0 3 and near normal, acidic
pH.
Mechanical ventilation in patients with chronic respiratory acidosis
can reduce PaC0 2 to near normal. However, as there is no
immediate effect on plasma HC0 3 , elevated HC0 3 can lead to
Q. Which fluid and electrolyte abnormalities can cause failure to wean
from mechanical ventilator ?
I A. Following electrolyte and fluid abnormalities can cause failure to wean
or inspiratory muscle fatigue.
1. Hypophosphatemia : It occurs in patients on ventilator because of
intracellular shift of phosphorous due to respiratory alkalosis
(because of over ventilation), sepsis and B2 agonist therapy.
Muscular weakness due to severe hypophosphatemia may
contribute to failure to wean from mechanical ventilator.
2. Hypokalemia : Hypokalemia can occur due to therapy with
steroids, diuretics and B agonist. Hypokalemia. can cause
2
weakness of respiratory muscles. Severe hypokalem1a can cause
166 CH. 4 Fluid Therapy in Medical Di sorders
,. even respiratory paralysis, which .can cause failure to wean from

ventilator.
3. Hypomagnesemia: It can occur due to therapy with diuretics and
antibiotics (e.g. aminoglycosides). Hypokalemia and hypocalcemia
are difficult to correct, unless Mg deficiency is corrected.
4. Hypocalcemia : It can occur due to Mg deficiency, respiratory
a\kalosis and drugs (aminoglycosides, heparin and theophylline) .
s. Pulmonary oedema : It can be due to fluid overload and I or
increased alveolar permeability.
Aspiration disease of lung
This is a frequently encountered problem in semicomatose or critical
patients. Aspiration pneumonia occurs commonly due to aspiration of
gastric acid or solid material (e.g. food).
Fluid management : Hypotension in the course of aspiration is usually the
result of loss of intravascular volume resulting from increased permeability
of the pulmonary capillaries and flooding of the pulmonary parenchyma
(noncardiogenic pulmonary oedema). lntravascular volume must be
replaced to maintain a reasonable blood pressure. However, pulmonary
capillary wedge pressure should be kept as low as possible during the
infusion of fluid to minimize the hydrostatic component of intrapulmonary
capillary leakage. Crystalloids should be used for fluid replacement
because colloids are likely to leak into the extravascular space and may
retard fluid reabsorption as the lungs begin to heal.
FLUID THERAPY IN NEUROLOGICAL DISORDERS
Basic principles of fluid therapy in patients with stroke, increased

intracranial pressure and meningitis are as follows.
1. Maintain euvolemia. Avoid hypovolemia and hypotension
Previously fluid restriction to achieve moderate to severe dehydration
l
i· was advocated with an aim to avoid increasing brain water and cerebral
1. .oedema. But as cerebral blood flow is determined by cerebral perfusion
\:
pressure (CPP) in ischemic brain tissue, hypovolemia can rapidly lead
·1+1·
I ·.
['
; :
' '.
/.
.I
~.. r
•' .
CH . 4 : Fluid Therapy in Medical Disorders 167
to decreased CPP and global hypoxic-ischemic injury. There is no

. evidence that fluid restriction improves cerebral oedema. So avoid fluid
restriction,. which can exacerbate volume depletion leading to an
increased risk of cerebral ischemia. Hypotension and hypovolemia needs
to be treated aggressively even in patients with CV stroke. First step in
treatment is volume repletion, followed by administratio~ of vasopressors
if needed.
2. Avoid hypotonic fluid and hypoosmolality
Hypoosmolality can induce or aggravate cerebral oedema so avoid
infusion of hypotonic fluid (e.g. 5°/o dextrose, 0.45°/o saline and eriteral
free water). Normal plasma osmolality is about 285 mQsm/kg while
osmolarity of 5o/o dextrose and Ringer's lactate is 278 and 27 4 mOsm/L
respec~ively. · ·
So avoid 5°/o dextrose because of its hypoosmolality, as well as its
ability to cause hyperglycemia.
Ringer's lactate (RL): It is an appropriate fluid if volume of infusion is
small. But avoid RL if large amount of fluid administration is required
because RL is mildly hypotonic (approximately 114 ml of free water
is contained in each litre of solution). Moreover as RL contains 3
mEq/L of calcium, it may promote reperfusion injury and so it should
be avoided.
3. Isotonic Saline (0.9°/o NaCl), the ideal l.V. fluid
Maintaining fluid therapy at isoosmolality will not worsen neurological
outcome. So .isotonic saline is the best solution, especially when large
volumes of fluid are to . be. infused, because it is slightly hypertonic
(osmolality 308 mOsm/L) with respect to plasma (osmolality 285
mOsm/L) and it does not contain calcium. There is no evidence that
colloids are better at maintaining CPP.
4. · Avoid hyperglycemia
Hyperglycemia in the immediate period after. stroke. is · ass~ciated
with increased morbidity and mortality in patients with nonlacunar
stroke. Hyperglycemia enhances brain injur~ · ~nd breakdown of. th.e
blood brain barrier. In patients with stroke, clinically hyperglycemia ~s
associated with increased cerebral oedema and haemorrhag~c
transformation of infarct. So in immediate period after stroke, avoid
168 CH. 4 .. Fluid Therapy in Medical Disorders
dextrose containing fluid to av~id .hyp~rglycemia and existing

hyperglycemia should be treated with insulin. It seems reasonable to
avoid glucose solutions during the first 24 hours after a patient presents
with an anterior circulation cerebral infarct and ·tor 72 hour after pnsterior
circulation events. These are the periods during which evolution of stroke
may occur. It should be noted that it is the glucose concentration at the
time of infarct that is critical in determining stroke severity, so the
purpose of avoiding glucose is to prevent hyperglycemia at the time of
any extension of the infarct.
5. Caution while feeding
Nutritional requirements are increased in patients with stroke and brain
injury so feeding should be started as soon, as possible after stroke,
using nasogastric tube. The majority of commercially available tube feeds
provide 1 calorie per ml and contain significant amount of free water,
which can aggravate cerebral oedema. So in individuals with significant
cerebral oedema, concentrated tube feeds (2 cal/ml) should be used at
full strength and the remainder of fluid requirements should be supplied
with isotonic or hypertonic intravenous fluids. Avoid nasogastric feeding
.of free water and other hypotonic fluids, which can aggravate cerebral
oedema.
6. Avoid hypovolemia during mannitol therapy
Mannitol is used in the management of elevated intra cranial pressure.
One should remember that mannitol acts as a diuretic and continued
use will inevitably lead to hypovolemia, and potentially hypotension
and cerebral ·hypoperfusion. So during mannitol therapy care should
be taken to avoid hypovolemia, which can aggravate ischemic brain
· injury. ·
7. Achieve hypervolemia in vasospasm .
Amongst survival of nontraumatic subarachnoid haemorrhage (SAH),
· symptomatic vasospasm is a leading cause -of morbidity and mortality,
which usually occurs 4 to -14 days after aneurysmal rupture. In
· vasospasm, vascular lumen narrows leading to impaired cerebral
autoregulation and ultimately to ischemia ~ Low systolic blood pressure,
dehydration, and increased serum viscosity may exacerbate the
. ischemic injury .. Vasospasm may be detected in upto 70°/o of patients
~
. . ' I • - •
CH. 4 : Fluid Therapy in Medical Disorders 169
after SAH, but causes symptoms in less than 30o/o. Adequate hydration
is essential in prevention and treatment of vasospasm and cerebral
protection from ischemic complications. Medical treatment of vasospasm
consists of triple-H therapy: Hypervolemic, hypertensive, and
haemodilution therapy, which are aimed at optimizing cerebral blood flow
in ischemic territories with impaired autoregulation.
a. Restrict fluid in SIADH
Small numbers of patients with evidence of syndrome of inappropriate
antidiuretic hormone - SIADH (characterized by euvolemia, hyponatremia
and increased urinary osmolality) will require fluid restriction .
FLUID THERAPY IN HEAT ILLNESS
Basic principles of fluid therapy in heat illness (heat cramps, heat

exhaustion and heatstroke) are summarized below.
Heat Cramps
Prolonged or unaccustomed exposure to hot environment causes heat
cramps. They are caused by salt depletion with hypotonic fluid replacement.
It chiefly affects calf and thigh muscles. They are self-limiting and cause
no permanent damage.
·T reatment
1. Rest in cool environment with icepacks to affected muscles.
2. Adequate oral saline solution (1 teaspoon of salt in 500 ml of water)
to replace both salt and water.
3. l.V. fluid is rarely required but cramps responds rapidly to 1.V. isotonic
saline.
4. 1-3 days rest, dietary salt supplementation ~n~ ~eat avoidance is ..
\
advised before resuming work or strenuous act1v1ty in the heat.

,-··;· .... ;. · • . .
Heat Exhaustion (Heat Syncope)

. Heat exhaustion results from prolonged heavy a.ctivity with inadequate salt
·i.ntake ·in. a hot e'n vironment and is characterized by hypovolemia and
'hypotension. The patient complains of .he~dache, .nausea, vomiting,
dizziness, weakness, cramps or persp1rat1on. Patients present With
syncope, orthostatic hypotension, tachycardia, tachypnoea and normal to
40°C temperature.
Treatment
1. Rest in cool environment and fan evaporation for heat loss.
2. Adequate hydration (1-2 litre over 2-4 hours) with salt supplement,
orally if possible.
3. If vomiting occurs or haemodynamic status is unstable, electrolytes
should be checked and 1-2 litres of l.V. isotonic saline is given.
Heat Stroke.
Heat stroke is a life threatening medical emergency resulting from failure
of the thermo-regulatory mechanism. Heat stroke is imminent when the
. rectal temperature approaches 41°C. It presents in two forms : (1) Classic
heat stroke occurs in patients with compromised homeostatic mechanism
and (2) . Exertional heat stoke occurs in previously healthy persons
.undergoing strenuous exertion in a thermally .stressful environment.
Morbidity or even death can result from cerebral, cardiovascular, hepatic
or renal damage due to rhabdomyolysis.
The hallmarks of heat stroke are cerebral dysfunction (from confusion to
delirium and coma), high fever (usually 105°F or 40.5°C or above) and
absence of sweating. It is important to differentiate heat stroke from
malignant hyperthermia, neuroleptic malignant syndrome, severe
. hyperthyroidism, sepsis and meningitis. : ·
Treatment
A : Immediate Cooling : Various measures used are cold water sponging,
continuous cooling by large high speed electric fans with maximum
body surface exposure and application of ice packs at groin, axilla
and chest. Ice water immersion may interfere with other treatment
measures and therefore should not be used. Rarely used measures are
cold water gastric lavage, bladder irrigation or peritoneal dialysis and
,.... .
t· . .
~ .. CH. 4 : Fluld Therapy in Medical Disorda.rs :·111
cardiopulmo~a1y bypass. Antipyretics (aspirin, acetaminophen) have no I
effect on environmentally induced hyperthermia and are contraindicated. :f

'(
The r;ctal ten;,peratu~e should be monitored closely and when it reaches
I
38.8 C (102 F) active cooling should be stopped because once

temperature falls below 39.4°C (103°F) it may fall precipitously and
shock may develop. Chlorpromazine can be given to control shivering.
B: Baseline laboratory studies : These include CBC, platelet count,
prothrombin time, PTT, electrolytes, BUN, creatinine, glucose, calcium,
CPK, LFT, ABGs, urine analysis and ECG.
C : Fluid Therapy : If shock occurs, initially isotonic saline or Ringer's
lactate is infused, subsequently 5°/o dextrose with 0.45°/o NaCl is used.
The patient may need 1,200 to 1,400 ml or more l.V. fluid during the
first 4 hours. In patient with heatstroke, initially there is marked
peripheral vasodilatation and vasoconstriction occurs as temperature
falls. So during initial period fluid replacement should be done only
optimally with isotonic saline, and vigorous fluid replacement should
be avoided because the circulating blood volume may become
excessive when vasoconstriction occurs and it may lead to pulmonary
oedema. As these patients are prone to CHF, cardiogenic shock and
cerebral oedema, invasive monitoring may be helpful. l.V. isoprenaline
or dobutamine may be helpful if shock occurs. An alfa-adrenergic
vasoconstrictor (i.e. dopamine or noradrenaline) should not be infused
when temperature is still high because it decreases the dissipation of
heat. Volume expansion with dextran is contraindicated due to its
anticoagulant effect.
D : Prevention of renal failure : Rhabdomyolysis or urine output less than
30 ml/hour should be treated with adequate volume replacement.
Mannitol (12.5 - 25.0 gram) and bicarbonate (44 mEq/L in 0.45°/o
isotonic saline) are used to promote osmotic diures.is an~ ur~n~ry
alkalization. Intermittent doses of frusemide helps .m mamtammg
·
con t .muous urine ou t p ut . Established severe renal failure may need
dialysis support. . . .
E : Other complications : Treat other complications like hypoxia, ARDS
seizures, DIC, hepatic injury etc. !
. :
"
·. i
.,
.,
CHAPTER
FIVE
·FLUID -THERAPY IN
DIABETES MELLITUS
DIABETIC KETOACIDOSIS
Pathophysiology 172 Avoidance of complications
Treatment 175 of therapy . _ . 181
Insulin therapy. 176 To monitor .treatment. 181
Replacement of fluid HYPEROSMOLAR
and electrolytes. 177 · NONKETOTIC COMA
Treatment of Diagnosis . 183
precipitating factors. 181 Treatment 183
FLUID THERAPY IN DIABETIC KETOACIDOSIS

Diabetic ketoacidosis (OKA) is a medical emergency condition that can
be life threatening if not treated promptly. OKA is one of the common
complications of type-I diabetes mellitus (IDDM) associated with significant
fluid and electrolyte imbalance. ·
Definition
Diabetic ketoacidosis is characterized by the triad of hyperglycemia (blood
glucose> 250 mg/di), acidosis (HC03 < 15 mEq/L, pH< 7.3) and ketonemia.
Pathophysiology
Q. ·why diabetic ketoacidosis (OKA) occurs ?

A. OKA o_ c curs due to reduction in effective concentration of the
circulating insulin (decreased insulin secretion or utilization) and
concomitant effect of counter-regulatory hormones (catecholamines,
glucagon, growth hormone and cortisol).
This hormonal alteration brings about three major metabolic events :
1. Hyperglycemia resulting from accelerated gluconeogenesis
(increased hepatic glucose production) and decreased peripheral
glucose utilization.
2. Increased proteolysis and decreased protein synthesis.
3. Increased lipolysis and ketone production.
CH.· 5 ·: Fluid Therapy in Diabetes Mellltus . 173
Insulin deficiency leads to increased lipolysis, leading to increased plasma

and subsequently hepatic free fatty acids (FFA), which leads to increased
production of ketone bodies. Glucagon is the primary hormone responsible
for inducing hepatic ketogenesis. Common precipitating factors for OKA
are inadequate or discontinuation of insulin, irregular diet, infectio.n, trauma,
surgery, emotional stress, myocardial ischemia etc.
a. Why and which fluid electrolyte imbalance occurs in OKA ?
A. Pathophysiology of fluid and electrolyte imbalance in OKA is
summarized below and also in Fig. No. 5.1.
1. Fluid and Electrolyte loss
The renal threshold for glucose is approximately 170 mg/di.
Hyperglycemia in OKA leads to glycosuria. This glycosuria leads
to osmotic diuresis. So large amount of water and electrolytes
are lost. Hyperglycemia indu.ced hyperosmolality causes the
movement of water out of the cell with subsequent intracellular
dehydration, extracellular fluid expansion and diuresis. Urinary
loss then leads to progressive dehydration and volume depletion
which causes diminished urine flow and greater retention of
glucose in plasma. Vomiting due to OKA also leads to loss of
water and electrolytes aggravating hypovolemia.
2. Metabolic Acidosis
In OKA fat is mobilized at an excessive rate to supply energy. As
a result, large amount of ketone bodies (B- hydroxy butyric -acid
and acetoacetic acid) are formed. These ketoacids are neutralized
by bicarbonate buffer, thus serum bicarbonate level decreases
leading to metabolic acidosis. Due to large amount of ketones,
the anion gap is high.
Severe dehydration induced hypoperfusion leads to impaired renal
function, which also contributes to the metabolic acidosis.
3. Potassium Imbalance
Hyperkalemia may occur because of metabolic acidosis and lack
of insulin (so potassium will shift from intracellular to extracellular
compartment leading to hyperkalemia).
In OKA, hyperglycemia induced osmotic diuresis leads to
l
· 174 CH. 5 Fluid Therapy in Diabetes Mellitus
Fig. No. 5~ 1 : Pathophysiology of fluid-electrolyte disturbances in DKA

· Dacraasad ift&ullni, : ·
lncreaaed g1ueagone, hormone & ~holamlne 11rowt.,,t
i 'i l
lnclB88ed Upmysls ~.~ ·
and
TG Breakdown
P1oteolyela.
,, i'
Increased FFA. '"'' .
Increased Plasma
in Plasnu• . Afni~ A.~ (BUN)
i ,.. l
HYPERGLYCEMIA lner~Amrno
fl,Ciels IC ~iver
l
·.· ... -..............
I ncr9S6~
l
KelN"'i&A-ia lncreasea
· ···-· -·~·~~ -·..
· sru~en~s
,,.
K&TONUAIA
.,
Lo.Qt ot aecu:o~ U .···· · t!i.~t•
nY;p.fJfg!!l.J1¥¥!!'! 1fll!!ll!
Decreased Alcali
i
. .. .. ., - ... ,, ,_ ..... .. ,,,, ........ ,,.,..,,,.. ~ - - -·
Ft~ Volum1i Dep.ltrilon
l
-AC1DOS18.,•4llt-..---1mp•fNH:.1 R..,.. ......1 - - - - C>smot
.·•IC
F1a1.d:1- .
-..L11U,n Dilntsls
CH. 5 : Fluid Therapy In Diabetes Mellllus 175
continuous loss of K• in urine. Potassium is also lost due to vomiting.

This Ki- loss leads to deficit of total body potassium. So in OKA,
serum K+ may be high, normal or even low but there will be deficit
of total body potassium.
~ Other losses
In addition to loss of water, sodium and potassium there is loss of
magnesium and phosphorous.
So in OKA, the patient has salt and water loss, hyperkalemia
(besides deficit of total body potassium) and metabolic acidosis
(with high anion gap). Pathophysiology of loss of fluid and
electrolytes is summarized in Fig. No. 5.1.
Q. Roughly how much loss of fluid and electrolytes is expected in OKA ?

A. In diabetic ketoacidosis, usual loss is :
Water 5-8 litre or 100 ml/kg body weight
Sodium 400-700 mEq or 7-10 mEq/kg body weight
Potassium 250-700 mEq or 3-5 mEq/kg body weight
This loss represents loss of water in excess of loss of sodium and
therefore, fluid lost in OKA more closely resembles hypotonic saline
solution rather than isotonic solution.
TREATMENT
Q. How to treat diabetic ketoacidosis ?
A. Treatment of OKA can be discussed as follows :
1. Insulin therapy
2. Replacement of fluid and electrolytes
3. Treatment of precipitating factors
4. Avoidance of complications of therapy
5. To monitor treatment
.l
·176 CH. ·5 Fluid Therapy in Diabetes Mellitus
· ·.:1.. lnsulin·therapy
·. · Selection of insulin : Insulin preferred in treatment of OKA is purified,
·regular or short acting insulin. As hal~-life of l.V. insulin is not more
than 5 minutes, insulin therapy with large loading dose followed by
bolus at large intervals is discarded.
Insulin therapy preferred is loading dose followed by frequent small
bolus or preferably insulin infusion drip . .With continuous low dose
. infusion method lowering of blood sugar is smoother, hypokalemia
is less severe and th.ere ar~ lesser chances of hypoglycemia and
cerebral oedema.
Loading dose: 0.4 unit/kg body weight (half l.V. and half l.M.)
Subsequent therapy : Loading dose is followed by 5-10 units (or
0~1 unit/kg) of insulin hourly. Insulin infusion is preferred if patient
is in ICCU, otherwise insulin is given IM. This bolus is continued till
blood glucose reaches 250 mg/di.
.Q. How to prepare and infuse the insulin drip ?

A. In one litre fluid 100 units of insulin is added. After connecting
l.V. set, initial 50 .ml fluid is rapidly run through and discarded
as insulin particle.s stick to the wall of the tubings. If 1 ml/min
(15 macrodrops or 60 microdrops/min) is the rate of this
infusion, it will deliver 6 units insulin/hour.
Q. When to increase dose of insulin bolus ?

A. If blood glucose level does not decrease by at least 10% or
50-70 mg/di from the initial value, loading dose is repeated, or
the drip rate doubled until blood glucose starts declining
satisfactorily. Conversely, if the blood glucose has fallen by
greater than 150 mg/di per- hour, the infusion rate should be
halved. With insulin therapy control of hyperglycemia is faster
than that of ketoacidosis. So once blood glucose falls below
250 mg/di, D-5°/o infusion is started. D-5oi0 infusion prevents
hypoglycemia and helps in early ·resolution of ketoacidosis.
I
II
I
CH. 5 : Fluid Therapy .in Diabetes Mellitus 177
2. Replacement of fluid and electrolytes . ..
A. Fluld therapy
As large amount of fluid is lost in OKA, initial treatment priority is
restoration of fluid deficit with proper fluid.
Q. Which fluid to be infused ?
A. Isotonic sali'ne, Ringer's lactate and 5°/o-dextrose are the
available and commonly used fluids. For initial treatment, only
glucose free fluids ·(isotonic saline and Ringer's lactate) are
given. In shock or hypotensive patient isotonic saline is
preferred. Ringer's lactate is given in absence of shock,
hypotension and in patient with good urine output. After initial
· fluid replacement, depending upon the serum sodium, the fluid
should be changed to 0.45°/o saline. This allows more free water
to be delivered. In OKA there is a greater deficit of free water
in comparision to sodium. Ata later stage (once blood glucose
falls below 250 mg/di), D-5°/o is i~fused. . ·
Q. How much to infuse ? ·
A. Most of the patients require about 5-8 litres of fluid to correct
volume depletion. Fluid resuscitation should be started early
and continued until the resolution of the ketoacidosis.
Q. How rapidly to infuse ?

A. The optimum rate of infusion of isotonic saline. depends on
the clinical status of the patient.
Severe hypovolemia and shock: In such patients fluid should
i
be infused as quick as possible. Patients with normal cardiac /1
I
function should receive the first litre of fluid within the first !
hour. Fluid replacement should be conti~ued ·at the rate of Il

one .litre per hour (or more) till the correction of intravascular I
deficit and haemodynamic stability. Such rapid fluid infusion _I
:I
needs proper, close monitoring. :I
:/
Maintanence requirement : After rapid fluid replac~ment ~~d i
l
in those patients who do not have significant fluid def1c1t, ·i
[
Ir
t
.t
l
·t· i
. iI
·I I
.178 CH. 5 Fluid Therapy in Diabetes Mellitus
l.V. fluid should be administered slowly. Initially fluid is

infused at the rate of 500 ml for the first 4 hours followed
by 250 ml/h~ur.
Q. When and why dextrose solution is given ? ·

A. In OKA D-5o/o is started once blood glucose falls below 250
m.g/dl. N.eed of 5°/o-dextrose at .this stage is :.
1. For b.etter intracellular distribution of free water
. (corrects intracellular dehydration) .
2. To p·revent hypoglycemia and to help in resolution of the
· ketone bodies.
3.· As a prophylactic measureto prevent the late cerebral
oedema syndrome.
· Q. How to asses·s fluid status during therapy ?

A. Norm.ally good urine output reflects proper fluid therapy and
reasonable hydration. But in DKA, only urine output will not be
a dependable criterion for it. In DKA due to hyperglycemia
·,, induced osmoti~ diuresis, urine output will be high even in
· ·presence of yolu _
me deficit. ,So other parameters need to be
. . consid~red to assess hydration.
8. Potassium supplementation
. Q. Why hypokalemia occurs during treatment of OKA ? .

A. Mar_ked urinary and G.I. loss of potassium (about 250-700 ·
mEq or 3 to 10 m'Eq/kg) occurs in OKA. However, initially serum
potassium is usually normal or high due to insulin deficiency
and metabolic acidosis. Regardless of .the serum potassium
. levef, total body .reserves are depleted. With insulin and fluid
. therapy. hyperglycemia:and ac.idosis are corrected and so K+
will shift into the .int,racellular co~.
.. .
p~rtm~nt
. . ' which
'
can cause
life threa:tening hypokalemia. .· · · ·
' .. ,.
CH. 5 : : ·. Fluid Therapy in Diabetes Mellitus . 179 · ·
Q. When to start potassium ·replacement ?

A Potassium replacement is always n·ecessary but the time of
· administration varies ..It is dangerous to give potassium in shock
or oliguric patient. After initiation of therapy when blood
pressure becomes normal, urine output is established, blood
sugar starts declining, level of serum potassium is < 4 mEq/L
and when .there is no clue of hyper~alemia on EQG, than only
potassium supplementation is started. Usually ·potassium is
replaced after few hours of treatment with insulin and reversal
of acidosis. However in patients with low or normal initial level
of potassium, replacement may be done earlier.
Q. How to tre~t hypokalemia ? .;
A. An initial rate of potassium supplementation is 1O mEq/hour,
when there is no hyperkalemia in · ECG ,and urine output is
adequate.
Once the potassium concentration falls below 4.5 mEq/L
20-40 mEq of potassium is added to one litre of infusion.
If hypokalemia is severe and causes serious cardiac
arrhythmias, potassium should be supplemented in doses upto
20-40 mEq/hour under close ECG monitoring. Many patients
require oral potassium supplementation for several days after
treatmenrof OKA to correct potassium deficit.'
C. Treatment of metabolic acidosis
. .. '
Q. Why bicarbonate therapy is required only in. few patients

with OKA? . .
. .· A.~ , , Proper .fluid ; and . insulin therapy ccin e~fectively correct
metabolic acidosis in most of the patients with DKA. Only few
patients with metabolic ac::idosis are tree:tted with .bicarbonate
therapy because : .
. -: :. J,' '
1. Bicarbonate therapy can paradoxically increas·e ketone

· p·roductio.n. The basic cause ·of ·the acidosis·is the lack of
insulin and the accumulation ·ofketoacids. Therefore insulin
180 · CH. 5 · Fluid Therapy in Diabetes Mellitus
therapy · and metabolism of ketone bodies will correct

acidosis .
.2. NaHC0 3 may.paradoxically increase spinal fluid acidosis
and may precipitate coma due to cerebral oedema.
3. Bicarbonate therapy may worsen tissue oxygen delivery
by depleting RBC phosphate (2-3 OPG) .
.'
Indications of bicarbonate .therapy in OKA are :
1. Severe metabolic acidosis (HC03 < 9 mEq/L, pH< 7.0-7.1) . .
2. OKA associated with shock.
3. Severe hyperkalemia.
Q. How long to give bicarbonate therapy ?
A. Provide NaHC0 3 supplementation cautiously. Bicarbonate
therapy is stopped when pH reaches 7 .2 to minimize possible
detrimental side effects and to prevent metabolic alkalosis as
circulating ketones are metabolized to bicarbonate with reversal
' '
of ketoacidosis.
Q. . How to provide NaHC0 3 supplementation ?
A. Bolus infusion of bicarbonate should be avoided except as
an emergency resuscitation measure. A solution of NaHC0 3
. ' :
44-88 mEq (2-4 Amp of 25 ml 7.5°/o NaHC0 3 ) per litre of
0.45°/o saline can be infused as a substitute for isotonic saline,
as per the requirement.
D. Correc~ion of hypophosphatemia
Decreased oral intake and increased urinary loss of phosphate
is known to cause phosphate depletion. Hypophosphatemia
frequently occurs during treatment of OKA (in similar way as
hypokalemia);
However rout.i ns use of phosphate supplements in DKA has not
shown improvement in morbidity. In addition to lack of efficiency,
phospha_ t e. adrni .n istration . is not without ·risk, since
_hyperphosphatemia and hypocalcemia may occur. So reserve
, phos.phate administration for the occasional patient who develops
....
CH , 5 : FJuld Th '>r'1 py in Ol'nbores Melfttus 181
a seve re, symptom ati c reduction In th e pfaa ma pho sphate

concentration. Early Initiation of oral intake co ntaining milk can
effectively and rapidly correct hypophosphatemfa in most o1 the
p tients .
3. Treatment of precipitating factors

80°/o of OKA occurs due to lack of insulin or due to presence of
infection. By careful history and evaluation , precipitating factor for
OKA is diagnosed and treated meticulously.
4. Avoidance of therapy related complications

Care should be taken to avoid treatment-related complications.
a. Hypoglycemia
b. Hypokalemia
c. Cerebral oedema
d. Hyperchloremic acidosis
Possibility of cerebral oedema during treatment of OKA is due 'to

too rapid administration of fluid and correction of hyperglycemia
leading to imbalance between the brain and ECF. Cerebral oedema
can also occur due to excess use of bicarbonate, development o f
hyponatremia or allowing blood glucose to fall rapidly below 200
mg/di.
5. How to monitor treatment ?

For proper monitoring , in all patients with OKA a th erapeutic fl v
sheet should be maintained, where time and amount of in ufin .
fluid and electrolytes administered , vital da ta . urin ut ..ut.
laboratory parameters are record ed. Chi ef pa r m t r · u · d f r
monitoring of treatm ent are :
a.. Blood glucose level
b. Plas ma keton e I keton urla
c. pH - a nion gap
182 CH .- s- Fluid Therapy in Diabetes Mellitus
a Blood Glucose
·· · · · Effective therapy reduces the blood glucose level. But as
hyperglycemia responds faster than ketoacidosis, once blood
glucose falls below 250 mg/di, insulin is continued along with
glucose infusion till ketosis disappears.
b. , Plasma ketone I ketonuria

. .
Presence of ketosis is important .t or diagnosis and to decide

how long to · treat s·uch patients aggressively. But in DKA,
therapeutic .response and extent .o f recovery in ketosis is not
parallel, so this test is not very useful in monitoring the treatment.
Nitroprusside reacts chiefly with acetoacetate, to a lesser extent
with acetone and not at all with B-hydroxybutyrate. Usually ratio
of B-hydroxybutyrate to acetoacetate is 3: 1 and may reach up
to 7: 1 in severe hypoxia or shock.
With proper treatment in OKA patients with shock-hypoxia,
. circulation is reestablished and tissue oxygenation is restarted.
This leads to conversion of large amount of the accumulated
B-hydroxybutyrate to acetoacetate with clinical recovery of the
patient. But as the test picks up only acetoacetate and not at all
with B-hydroxybutyrate, although total ketone concentration is
. falling, paradoxicall"y ketosis may seem to WOr?en.
c. pH and anion gap

Therapeutic progress can be more accurately. monitored with
se~um pH and a~ion gap measurement Rise in the pH and
normalization ·of increased anion gap suggests response to
. therapy. If the anion remains elevated ahd pH is persistently
low, this indicates insulin resistance and requires an aggressive
increase in the amount of insulin needed. ·
6. Supportive treatment
Supportive treatment is discussed later, along with treatment of
hyperglycemic, hyperosmolar nonketotic coma.
CH. 5 Fluid Therapy in Diabetes Mellitus 183
Hyperosmolar Nonketotic Coma (HO~K) ; .. .

Hyperglycemic, hyperosmolar rionketotic coma (nonketotic hyperdsmolar
syndrome) is usually a complication of NIDDM·in the elderly, in whom severe
dehydration and severe hyperglycemia occurs without the development of
ketoaCidosis. · · ·
I
This syndrome occurs over a longer interval than. OKA, usually in the patient
unable to .drink sufficient amount of water to keep up with the t.frinary fluid
loss. A full blown picture does not occur until volume depletion has b~c ome
1
severe en9ugh to decrease urine output. The severe .glycemia is p·artly

caused by decreased renal glucose excretion due to either intri'nsic
underlying renal disease or due to decreased glomerular filtration. and
prerenal azotemia secondary to marked dehydration.
When ketoacidosis occurs nausea, vomiting and air hunger brings the patient
to the physician before extreme dehydration occurs. As· ketoacidosis is
absent, clinical symptoms are mild at the early stage and so dicl'griosis is
delayed. Usual precipitating factors are drugs (steroids,·mannitol, diuretics,
and phenytoin) infections or cerebrovascular accident. ·.- :
Diagnosis
1. Variable CNS symptoms (disorientation to coma).
2. Severe dehydration - hypovolemia.
3. Hyperglycemia, blood sugar > 600 mg/di
4. Absence of ketonemia and acidosis.
5. Plasma osmolality > 320 mOsm/kg
6. · Severe azotemia.
Treatment
Therapy of hyperosmolar nonketotic coma should include correction of
fluid and . electrolyte deficit, correction of hyperglycemia and
hyperosmolarity. Even with the best possible treatment mortality is very
high (75°/0 ).
184 CH. 5 Fluid Therapy in Diabetes Mellitus
a Fluid therapy
. The most important measure is rapid administrati~n of large amount of
intravenous fluid to reestablish the circulation and unne flow. The.aver.age
· fluid deficit is 10-11 litres. Initially 0.9°/o isotonic salin.e without additive
' is pr.eferred to correct fluid deficit and 2-3 litres is given in the first ?
hours. Subsequently, half strength (0.45°/o) saline can be used to correct
relative free water deficit. As hyperglycemia i.s controlled and blood
glucose reaches to 300 mg/di, 5°/o-dextrose is s~arted, especially to
·correct intracellular dehydration (to supply tree water). Dehydration in
hyperosmolar nonketotic coma is usually more severe than in OKA and
'approximately 12°/o of total body weight fluid 'replacement is required in
firs·t 12-24 hours.
b. Insulin treatment
' '
To control severe hyperglycemia, insulin therapy preferably by infusion

is given in similar way to OKA. Larger dose of insulin may be necessary
.especially in obese patient.
c. Electrolyte management
Potassium salts are usually required earlier in the treatment .of
hyperosmolar nonketotic coma than in OKA because the intracellular
shift of plasma potassium during therapy is accelerated in the absence
of acidosis. If lactic acidosis is present, sodium bicarbonate should be
given until tissue perfusion is reestablished. Method and need of
administering electrolytes and bicarbonates is similar to OKA.
d. Monitoring of therapy
Blood sugar sh~uld be monitored half or one hourly and electrolytes

frequently. Detarls of therapy, vital data, urine output and laboratory
parameters are recorded in continuous flow sheet.
e. ·Supportive treatment
Oth~r additional supportive measur~s to be kept in mind are :

1. Nasogastric tube in unconscious patient.
2. CVP line in patient with cardiovascular disease.
r .:. . . .
I
:
' . . .. ;
\. · CH. s : · "_Fluid Th~rapy jn oia.betes· M~llitus .. · ;'1a·s ·

!• •.• .
..
•
.
:• .' • t
•' '.; . ' .:. .
3. Plasma or plasma expander in persistent hypotension.

4. Low dose heparin in comatose obese patient to prevent deep
vein thrombosis.
5. Recognition and treatment of precipitating factors i.e. drugs (steroids,
mannitol, diuretics'. and phenytoin), infections or cerebrovascular
accident.
6. Antibiotics, if infection i~ detected or suspected~
7. ECG : Cardiac monito"ring as a guide to potassium therapy.
a. Bladder catheterization if sensorium is altered.
9. Frequent monitoring of pulse, BP, respiralion and level of
consciousness.
' .
CHAPTER
SIX
fLUID THERAPY IN
RENAL DISEASES
.GENERAL PRINCIPLES OF
FLUID AND ELECTROLYTE Oliguric acute renal failure 190
MANAGEMENT 186 Diuretic phase of AR.F
. .
191
SPECIFIC GUIDELINES 187 Chronic rerial'failu.re 192
Nephrotic syndrome 187 Due to glomerular d!sease 192
Acute renal failure 188 Due to tubulointerstitial- .
Prerenal azotemia. 188 disease' · f 93
Non oliguric ARF 190
Kidney plays a major role in the regulation of fluid, electrolytes and blood
pressure in addition to excretion of nitrogenous end products. Despite
ingestion of various types of food and fluid, the volume and composition of
body fluid is maintained. Due to renal diseases this regulation is altered. So
modification in intake of dietary food and fluid is necessary to minimize
these abnormalities in fluid and electrolytes.
A. General Principles of Fluid and Electrolyte Management in Renal

Disorders
1. Fluid restriction : Oedematous and oliguric patients need fluid

restriction to avoid volume overload, pulmonary congestion,
aggravation of hypertension or hyponatremia. Amount of fluid
permitted varies, depending upon severity of anasarca and daily
urine output. In anuric patients, intake should be restricted only
upto 500 ml (which is equal to the insensible loss). If patient has
pulmonary oedema more rigid fluid restriction is necessary.
· In oliguric patient_, fluid intake= urine output+ 500 ml/day
Monitoring :
Strict urine output chart and daily weight should be maintained for
assessing volume status. Loss of weight suggests reduction in
accumulated fluid and therefore reduction in oedema. Any· weight i
gain suggests more fluid intake and possibility of fluid overload.
I
i
f
. i
. l
r-
1'
I
I
!
CH. 6 : Fluid Therapy in Renal Diseases 187
.2. · Do not chase urine output In oedematous patients :.In oedematous

patients urine output will increase in response to diuretic therapy.
Aim of diuretic therapy in such patients is removal of the
accumulated body fluid so continue fluid restriction besides increase
in urine output. Do not increase fluid intake by following routine
guidelines i.e. fluid intake per day = urine output+ 500 ml.
3. Salt restriction : Salt restriction is required to reduce oedema,
to avoid pulmonary congestion and for the control of hypertension.
Amount of salt permitted varies from patient to patient, according
to severity of anasarca and hypertension. Usually 2 to 3 grams
of salt (NaCl) per day is permitted to the patients with mild to
moderate oedema and is restrict.ad to 1 gram per. day in severe
oedema.
4. ·A void hyperkalemia : In patients with oliguria or renal failure,
potassium supplementation carries risk of hyperkalemia, which can
be life threatening. So avoid food rich in potassium (fruits, coconut
water, dry fruits etc.) or potassium containing l.V. flulds. l.V. fluids
with high K+ concentration are lsolyte-M (35 mEq/L), lsolyte-P (20
mEq/L) and lsolyte-G (17 mEq/L). Ringer's lactate contains only 4
mEq/L of potassium.
B. Specific Guidelines of Fluid and Electrolyte· Management in Renal
Disorders
In . addition to general principles, following conditions need special
considerations.
1. Nephrotic syndrome.
2. Acute renal failure.
3. Chronic renal failure.
1. Nephrotic Syndrome
Nephrotic syndrome occurs more commonly in children and is
characterized by anasarca, significant proteinuria, hypoalbuminemia
and hyperlipidemia.
a. Fluid and salt intake : Fluid and salt which are restricted
during oed~matous state, need . liberalization as oedema
188 CH . 6 : Fluid Therapy in Renal Diseases
. . '.:· . . _. decreases, and normal salt and fluid intake is permitted during
.remission in -asyptomatic, normotensive patients.
b.· Prevention of hypokalemia ·: Nephrotic patients ·receiving
diuretics as well as steroids are prone to develop hypokalemia.
To prevent hypokalemia in patients on diuretic.therapy, potassium
sparing diuretics or·potassium supplementation is given.
c. Specific treatment : Prednisolone is the drug of choice and
is the only required agent in most of the patients·. Small group
of patients who do not respond to _steroid therapy, or are
steroid dependant need therapy with alternative agents (i.e.
cytotoxic drugs, cyclosporine, etc.).
2. 'ACUTE RENAL FAILURE
Acute renal failure is characterized by relatively rapid decline in
renal function, leading to· accumulation of water, . crystalloid
solL:Jtes and nitrogenous end products in the body. Severe acute
· renal failure .can be a potentially life threatening but completely
re'versible condition. ·
We
.
need to remember
. .
that presentation of acute renal failure
varies. It is a wrong concept that all patients with acute renal
failure ~re oliguric and have oedema and need flu!d restriction. In
non-oliguric acute renal failure and during diuretic phase of acute
renal failure urine output is normal or high.
So fluid management of ARF varies as per the presentation
mentioned below :
1. Prerenal azotemia.
2. Non oliguric acute renal failure.
3. Oliguric acute renal failure.
4. . Diuretic phase of acute renal failure.
1. · Prerenal azotemia.
In the patients with oliguric acute renal failure, it is essential
to differentiate prerenal azotemia from established ATN by
careful history and meticulous clinical evaluation.
CH. 6 Fluid Therapy in Renal Diseases 189
Patients with prerenal azotemia improve with early and adequate ·

fluid therapy.
a. Fluid challenge
In the oliguric patients who are not volume overloaded and in
whom prerenal azotemia is likely, fluid challenge is
appropriate. The quantity of fluid to be given must be
determined on an indiyidual basis. Usually 500-1 ,000 ml of
isotonic saline is infused over 30-60 minutes under close
observation. Such a volume challenge may result in increased
urine flow in prerenal azotemia. If there is no response,
volume infusion can be followed by 100-400 .mg of l.V. frusemide
to promote urine flow.
b. Monitoring of fluid administration
·The best monitoring of adequacy of fluid therapy in the patients
with ARF is the bedside estimation of the ECF volume status,
urine flow chart and daily weight. The simple method to
evaluate fluid status is close monitoring of pulse, BP (including
orthostatic changes), and JVP. The presence .of basal rales
and third heart sound is suggestive of cardiopulmonary
congestion. Maintenance of strict urine output chart and daily
weight chart are essential to avoid fluid overload.
Fluid replacement in critical patients need measurement of /
CVP or pulmonary artery wedge pressure by Swan-Ganz
catheter.
c. Diagnosis of prerenal azotemia
Ratio of blood urea : serum creatinine > 1O : 1, urinary sodium
< 20 mEq/L, fractional excretion of ·sodium < 1 and urinary
osmolality > 500 mOsm/kg, are usually suggestive of prerenal
azotemia.
d. . Selection of l.V. fluid.
I. V. fluid selected in hypotensive state is isotonic saline. Till
·urine · output is not established, potassium supplementation
should. be done very cautiously or avoided.
190 · CH.· 6 · : · Fluid Therapy in ·Renal Diseases
, , . ... 2. Non oliguric acute renal failure . · ·. '· . ·

As many as 20-30°/o of ARF (espe~ially ~~e ·to sep~i?emia,
aminoglycoside toxicity and a~u~e in.terst1~1~I nephnt1s) are
non oliguric in nature. Diagn~s1s_ 1s often d1ff1~~lt, ~s there is
no reduction in urine output. High index of susp1c1on 1s needed.
Diagnosis 'is often made on evaluating unexplained anorexia,
nausea, vomiting or hiccup. . ·
Fluid and electrolyte management : These patients do not
need fluid or salt restriction. These patients carry higher risk
for hyperkalemia and metabolic acidosis and· need periodic
evaluatlon. Potass:ium intake should be restricted.
Hyperkalemia and acidosis, if altered significantly, need
treatment.
. 3. Oliguric acute renal failure
In oliguric ARF urine output is less than 400 ml/day in adults
_or less than 0.5 ml/kg/hour in children. This oliguric phase
due to acute tubular necrosis usually lasts for 1-3 weeks.
During oliguric phase of ARF, excretion of water, electrolytes
and nitrog.enous end products are diminished, resulting in
fluid overload, hyperkalemia, acidosis and azotemia.
a. Fluid and salt intake : In oliguric phase intake of fluid,
salt and potassium are restricted, as mentioned
· previously in general principles .. Maintain strict urine
output chart and daily weight in order to determine daily
fluid intake of the patients and to avoid fluid overload. A
daily weight loss of 0.2 to 0.3 kg is ideal in oliguric phase.
Hyponatren.iia in patients with ARF is usually secondary
to volume expansion with hypotonic flui _ d, whereas
hyper~~tre~i~ ·is most often caused by over aggresive
d1uret1cs With Inadequate intake of free water.
b. Establish urine flow : Oliguric ARF should be treated with
diuretics (l.V. frusemide). Diuretic administration may
. convert oliguric ARF to non-oliguric ARF, which simplifies
... . .- manage~e~t and may improve prognosis'. During initial
pryase (within the first. 6 hours), 20o/o. mannitol can be
CH.· 6 Fluid Therapy in Renal Diseases 191
given at the rate of 10-20 ml/hr. If no effect is seen by 12

hours, then the infusion should be discontinued.
Low_ dos~ dopamine (less than 3 µgm/kg/min) may initiate
natnures1s and diuresis (by selective dilatation of renal
~rteries) in certain patients of oliguric ARF. A response
1s usually seen within the first 6-12 hours of therapy. If
the patient remains oliguric, therapy with low dose
dopamine should be discontinued.
c. Hyperkalemia : In oliguric renal failure there is risk of
hyperkalemia, which can be life threatening if not treated.
Mild hyperkalemia (serum K+ < 6 mEq/L), can be treated
with dietary restriction and potassium binding resins.
Acidosis , hypoxia, shock or hypercatabolic state may
aggravate or precipitate hyperkalemia. Administration of
proper carbohydrate, correction of acidosis and shock, I
and treatment of infection will help in pr~vention of .,!
hyperkalemi a.
Severe t1yperk alemia requires immediate medical therapy
(e.g. insulin and glucose, lnj . calcium gluconate, lnj.
NaHC0 3 ) (Chapter No. 3). Hyperkalemia refractory to
medical therapy is an indication for dialysis.
d. Metabolic acidosis : Mild acidosis (serum HC0 3 > 12
mEq/L) does not require therapy. More marked acidosis
should be corrected with sodium bicarbonate. NaHC03
should be used cautiously, because the additional sodium
may exacerbate volume overload. If acidosis is
unresponsive to medical therapy, dialysis is indicated.
e. Selection of l.V. fluids : If patient needs LV. fluid the
preferred fluid is 5°/o-dextrose or 1 Oo/o-dextrose.
4. Diuretic phase of acute renal failure · .·
Pathophysiology : This is the period during which the pa~ient's
renal function recovers through repair and regeneration of
renal tissue. The diuretic phase is due to (1) defective tubular
function during the . phase of recovery, (2) excretion ~f
accumulated sodium, water and high urea (acting as osmotic
· · ~
192 · CH. 6 : Fluid Therapy In Renal Olseasos
diuretics), (3) high level of atrio .. natriuretic peptides and (4)

treatment with diuretic agents. This phenomenon is more
common after relief of bilateral urinary tract obstruction.
Fluid and electrolyte management :
The most important principle of fluid therapy at this stage is
not to chase urine output by large fluid replacement. But at the
same time volume depletion and dehydration should be
avoided, because decreased ECF volume can decrease renal
perfusion and may delay the renal recovery. In addition to proper
fluid replacement, deficit of NaCl, HC0 3 , Kand Mg should also
be replaced. Usually l.V. fluid preferred is half strength (0.45%)
saline with addition of potassium as per requirement.
3. CHRONIC RENAL FAILURE
To simplify the guidelines, patients with chronic renal failure are
divided into two major groups.
1. CRF due to glomerular disease.
2. CRF due to tubulointerstitial disease.
CRF Due to Chronic Glomerular Disease

CRF due to glomerular disease has defective glomerular filtration
leading to oliguria, anasarca and hypertension. Urinary abnormality
(i.e. proteinuria and haematuria) are common in this group. Common
clinical disorders in this group are diabetic nephropathy and chronic
glomerufonephritis.
Hypocalcemia and hyperphosphatemia are frequently seen in
patients with CRF. In CRF, excretion of phosphate declines with
falling GFR, leading to hyperphosphatemia. Hyperphosphatemi ~
leads to secondary hyperparathyroidism. In patients with CRF
hypocalcemia occurs due to lack of 1, 125(0H).)D (calcitriol the
active form of vitamln-D), by causing decreased g·ut absorption of
calcium. Additional hyperparathyroldism by direct suppr • si n
calcitriol production also contributes to hypocalcemi a.
CH. 6 Fluid Therapy in Renal Diseases 193
Hyperphosphatemia, hypocalcemia and secondary hyperparathyroidism

contributes to renal bone disorders. . ·
Treatment
1. Restrict fluid and salt intake : As com~on pres.entation is volume
overload and hypertension, fluid and salt restriction are
important, which avoid volume overload and helps in control
of hypertension.
2. Diuretics : Oedematous patients need. frusemide to increase '1
urine output and reduce anasarca.
3. Avoid hyperkalemia : As hyperkalemia can be a silent killer I
in the patients with CRF, follow general ptinciples to avoid it. Ir
4. Fluid administration : Whenever l.V. fluid supplementation
is necessary D-5°/o or D-10°/o is preferred. During a surgical I
procedure in CRF, l.V. fluid given should be minimum and is l
decided on the basis of urine output of previous 24 hours and ~
l
the current fluid status.
5. Treatment of other disorders :
I
I
I
a. Metabolic acidosis (discussed in tubulointerstitiaf disorders)

b. Hypocalcemia and hyperphosphatemia : These patients
I
t
need restriction of phosphate rich diet, calcium containing 1:
phosphate binders (calcium C8;rbonate and acetate, and I

:1
supplementation of active form of vitamin~D 3 (i.e. calcitriol). i.
I.
c. Hypermagnesemia : Prevent hypermagnesemia by avoiding 1:
magnesium containing antacids or laxatives.

CRF due to chronic tubulointerstitial disease
CRF due to chronic tLibulointerstitial disease has defective urinary
acidification and concentration, natriures·is and diuresis. So
clinical features in these patients .are absence of oedema or
volume ·depletion due to polyuria, normal blood ··pressure and '! '
I
' :
anaemia, along with metabolic acidosis and hyperkalemia. Urine i
I
is diluted with low and fixed specific gravity, mild proteinuria, no /,
haematuria with presence of variable pus. cells. .I

11
. ~
'!i J1
ii
ii
. •I
. , ·1
' :
.194 CH.- 6- .·: Fluid Therapy in Renal Diseases
Treatment ··
1. Fluid and salt intake : Practically all patients are advised to
take enough or plenty of fluids to prevent dehydration. There
is no need to restrict salt in these patients.
2. ·. Correction ~f metabolic acidosis .: Most of the . patients with
·significant metabolic acidosis need oral sodium bicarbonate
tabi'et, which corrects deficit of both bicarbonate and sodium.
650 mg NaHCO tablet contains 8 mEq of Na and 8 ~Eq of
bicarbonate:. Us~ally 16-32 mEq dose is optimum but varies
as per the clinical .status.
3. .Avoid and tre.at hyperkalemia: Potassium restriction is needed
. to avoid -hyperkalemia ; Treatment of same is discussed
. previously.
Q. Why to treat metabolic acidosis in the patient with CRF ?
A. Metabolic acidosis is a .common complication of advanced renal
disease and results from inability of the diseased kidney to excrete
the daily dietary acid load.
1. Metabolic acidosis is detrimental for renal function.
In patients with CRF number of functioning nephrons reduces, so
each remaining nephron excrete more acid, as ammonia. This
· adaptive increase in NH 3 production per nephron can lead to local
complement activation, which leads to secondary tubulointerstitial
disease -and worsening of renal function.
· Correction of acidosis (HC0 3 > 20 mEq/L) will prevent renal injury.
- ·2. ·· Prevention of osteopenia : Bone buffering in ·chronic acidosis due
to CRF leads to loss of bone calcium and osteopenia.
Correction ·of acidosis. reduces loss of bone calcium and prevents
osteopeni~. It also prevents secondary hyperpa~athyroidism and
related bone disorders.
3., . Prevention .of muscular weakness.
Metabolic acidosis can , lead to increased skeletal muscle
. '.. - breakdown and decreased ·albumin synthesis which . leads to
muscle weakness and -loss of lean body mass. These effects can
be prevented by the correction of the acidosis.
CHAPTER
SEVEN
OIAGNOSIS ·AND TREATMENT OF

ACID BASE DISORDERS .
INTRODUCTION 195 -BASIC INVESTIGATIONS 204

BASIC TERMINOLOGY 196 STEP BY STEP DIAGNOSIS 208
BASIC PHYSIOLOGY 197 EXAMPLES 209
CLINICAL DISORDERS DIAGNOSIS AND TREATMENT
CAUSING ACl.D BASE OF SIMPLE DISORDERS . 213
DISTURBANCES 199 Metabolic Acidosis 213
PRIMARY DISORDERS AND Metabolic Alkalosis 223
COMPENSATION 199 Respiratory Acidosis 225
MIXED DISORDERS 202 Respiratory Alkalosis 229
pH Regulation
Why pH is important in medicine?

Precise .regulation of the pH in a narrow range of 7 .35 to 7 .45 is essential.
pH is vital for ~ormal cellular enzymatic reaction, and . for nor.mal ionic
concentration. Change in pH can cause cardiac arrhythmias. Extreme ranges
o.f pH . (less than 7 .2 or more than 7 .55) are potentially life threatening
because of disrupti_on of many vital cellular enzymatic reactions and
physiological processes.
Acid base disorders commonly occur in very ill patients or it may be the first
presentation and mark~r of an unde.rlying disease (i.e. Kussmaul s breathing
1
as presentation of diabetic ketoacidosis or renal ·failure).

Proper evaluation
.
and treatment of acid base disorders need understanding
.
of following :
1. Basic terminology
2. Basic physiology
3. Knowledge of clinical disea$e·s causing acid-base disturbances
4. Basics of acid-base disorders and compensation
5. Interpretation of arterial blood gases (ABG) and laboratory tests
i
I
6. Step by step analysis of acid base disorders ·i
l
7. Confirmation of diagnosis of acid-base disorders I
I.L
.. ~ ..
' ·. .
. '. · ~ . .; . . • ; • . r
.: 1·;~6 .· . CH. : 7 : Di~gno~.i~· a_nd Treatment ·of Acid .Base Disor~ers : ..
8. Diagnosis of underlying etiology and planning of the treatment;.

Basic Terminology ·
Basic terminology and their values in simple acid base disorders are summarized
below (Table No. 7.1 ). ·
Table No. 7.1. : Acid-Base terminology
Clinical terminology Criteria
Normal pH 7.4 (7.35 - 7.45)
Acidaemia pH< 7.35
Alkalaemia pH> 7.45
. Normal PaC0 - 40 (35 - 45) mm of Hg
2
Respiratory acidosis (failure) PaC0 2 > 45 mm of Hg and low pH
Respiratory alkalosis PaC0 2 < 35 mm of Hg and high pH
(hyperventilation)
Normal HC0 3 24 (22 - 26) mEq/L
Metabolic acidosis HC0 3 < 22 mEq/L and low pH
Metabolic alkalosis HC0 3 > 26 mEq/L and high pH
pH - pH signifies free hydrogen ion concentration. pH is inversely

related to H+ ion concentration.
Increase in pH means H+ ion is decreasing.
·Decrease in pH means H+ ion is increasing
Acid A substance.that can "donate" H+ ion or when added to solution
raises H+ ion (i.e. lowers pH).
Base 11
A substance that can accept 11 H+ ion or when added to solution
lowers H+ ion (i.e. raises pH)
Anion : An ion with negative charge is anion (i.e. Cl, HC0 )
3
Cation: An ion with positive charge is cation (i.e. Na, K, Mg)
If cation and anion i~ confusing, here is the simple method to
remember.
Anion - "n";. negative charge
Cation- "t"- positive (+) charge
11
Acidaemia and Alkalaemia : The -aemia 11 in acidaemia and alkalaemia
CH. 7 Diagnosis and Treatment of Acid · Base Disorders : 1.97 -
is the same suffix (word ending) found in anaemia and ischemia~ . It .m·eans
"blood". . - - _ . - . -_
Acidaemia means· "acid blood" refers to a blood pH · below normal

(pH < 7.35) and increased H+ ion concentration. - · :
Alkalaemia means "alkaline blood" refers to a blood pH abo-ve normal
(pH > 7.45) and decreased H+ ion concentration. - -
Acidosis : Abnormal process or disease, which reduces pH due to -increase
in acid or decrease in alkali is called acidosis.
Alkalosis : Abnormal process or disease, which increases pH due to
decrease in acid or increase in alkali is called alkalosis.
Basic physiology of acid base regulation
The body maintains pH within a normal range in spite of variation in dietary
intake of acid and alkali, and endogenous acid production.
Endogenous acid production ·

Normally when food is metabolized, two types of acids are added to ECF.
1 Volatile acid in the form of carbonic .acid (H 2 C0 3 ), -which
_ determines level of C0 2 in blood (PaC0 2 ) and is excreted by
lung. About 22 ,000 mEq volatile acid is produced daily. -
2 Nonvolatile (fixed) acids (lik_e sulfuric and phosphoric acids) are
produced by dietary and endogenous protein cata~olism '. roughly
at the rate of 1 mEq/kg ~ They are excreted by the kidney.
Regulation of acid bas_e .

The regulation of the pH in a narrow range is the funct1.on of buff~rs, lungs
·
and kidneys. - Th e H en derson-Hasselbalch .Eq11at1on . descJ1bes
. - _. the
correlation of metabolic and respiratory regulations, which maintains pH.
_p H -- 6 . 1 + '.log
'"" HCO
- 3
/0.3 x PaCO 2 =pK +Kidney/Lung _
·ical systems · which -either release or
1 Buffers : Buffers are c h e m . ' . 'd
. . . e change in pH induced by an ac1 or
accept H+. So buff~rs ~rnnim~~ t defence Buffers act fastest but has
base load an_d provide im~e ~a ·~portant. buffers are bicarbonate,
1
least buffering -power. os • one bicarbonate.
phosphate, proteins, haemoglobin, and b
198 CH ..7 : Diagnosis and Treatment of Acid Base Disorders
2 Respiratory regulation : By excreting volatile acids, lung regulates

PaCO . Normally CO 2 production and excretion are balanced, which
2
o r ·
maintains C0 2 at 40 mm of Hg. When rate of C 2 pro d uc ion increases
it will stimulate PaCO sensitive chemoreceptors at central medulla with
resultant rise in rate ~nd depth of breathing. This hyperventilation will
maintain PaC0 2 at normal range. Respiratory regulation acts ·rapidly
(in seconds to minutes) and has double buffering power as compared
to the chemical buffers.
Q. w .hen the respira~ory regulation fails ? What will be its consequences?

A. a. If the underlying disorder (respiratory or CNS) causes
hypoventilation, C0 2 excretion is reduced. Retained PaC0
2
(hypercapnia) causes fall in pH leading to respiratory acidosis.
b. If the underlying disorder causes inappropriately high
hyperventilation, C0 2 is washed out. Low PaC0 2 (hypocapnia)
causes rise in pH leading to respiratory alkalosis.
3 Renal regulation : The role of kidney is to maintain plasma HC0
3
concentration and thereby pH regulation. It has the most powerful
buffering system, which starts within hours, and take·s 5-6 days for peak
effect. The kidney regulates HC0 3 by excreting nonvolatile-fixed acids
by following three main mechanisms :
1. Excretion of H+ ions by tubular·secretion.
2. Reabsorption of filtered bicarbonate ions.
3. Production of new HC0 ions.
3
Q. How kidney responds to metabolic acid base disorders and

regulates HC0 3 ?
A. a. In response to acid load, normal kidneys are able to increase
net acid excretion greatly (more than 1o times). Increased
excretion of H+ ions along with regeneration of bicarbonate
will correct plasma HC0 3 to normal range.
b. When there is primary increase in plasma HC0 or when
3
PaC0 2 increases there will be increased renal HCO excretion
. h e urine.
int . 3
CH . 7 · · · Diagnosis a·nd Treatment of Acid Base Disorders · 199
... .. • .. ~I , . , , ... ., / • .J , '" '~ 'I " 1 J;JrJ1.. 4 ' ,~ •• · ~ ~,- ,..~., , -
a. When does the metabolic regulation fail ? •I " •
A. a. M~tabolic acid?sis occurs when excess .HC03 _:is ' lost'.

(d1arrh.oea), acids are added (OKA /' ·laoti'c :acidosis) or
bicarbonate is not generated (renal fa!lure). · ·.. · " ·· ..... . . . . .
b. Metabolic alkalosis occurs when excess H+ is lost (vomiting), :
increased HC0 3 is generated (salicylate poisoning) or ·re.nal ;
bicarbonate excretion fails (hypovolemia.,· hypokalemia 'and :
hypochloremia).
Knowledge of clinical diseases causing acid-base -disturb.a nce ·;
Q. In which clinical settings can one suspect acid base disorders? .. .

A As underlying disorders provide clue for possible ·acid-base '.
disorders, it is important to have ·basic knowledge of clinical diseases ~
causing it (Table No. 7 .2). On this basis, existing underlying .'clini.cal ;
problem should alert the clinician to the likelihood of an acid~base :
disorder (i.e. diarrhoea may cause metabolic acidosis and vomiting=rTiay "
cause metabolic alkalosis). .· . "
Basics of acid-base disorders and compe·n sation ..
Q. . Which are the primary acid base disorders?

A. Four primary acid base disorders are defined depending upon initial
•disturbances. ·
If the initial disturbance affects HC0 3 · ~JiL
)I
/1
'
1.
2.
Metabolic acidosis (Fall in bicarbonate) ·
Metabolic alkalosis (Rise in bicarbonate)
. If the initial disturbance affects PaC0 2
·..t~E
3. 'Respiratory acidosis (Rise in PaC.0 2)
. 4. !. Respiratory alkalosis ·(Fall in PaC0 2 )
~ j
···cWhen you see Metabolic Think of HC0 3

11 11
11
and when you see Respiratory Think of PaC0 2 )
11
I
;}
i
200 CH. 7 : Diagnosis and Treatment of Acid Base\~isorders
Table No 7.2 : Clinical diseases that may cause acid base disorders
J
CLUES TO POSSIBLE TYPES OF ACID BASE
ACID BASE DISORDER DISORDERS OFTEN SEEN
Central nervous system
Coma Respiratory acidosis or alkalosis
Seizures Metabolic acidosis
Cardiovascular system
Congestive heart failure Respiratory alkalosis
Shock Metabolic acidosis I Respiratory alkalosis
Respiratory system
Tachypnea, hyperpnea Respiratory alkalosis
Bradypnea, hypopnea Respiratory acidosis
Gastrointestinal system
Vomiting Metabolic alkalosis
Diarrhoea Metabolic acidosis
Abdominal pain Respiratory alkalosis
Renal excretory system
Oliguria-anuria Metabolic acidosis
Polyuria
Metabolic acidosis I alkalosis
Endocrine system
Myxoedema
Respiratory acidosis
Hypertension
Metabolic alkalosis
9haracteristics of primary acid-base disorders are summarized in

Table No. 7.3.
' f,,1·
I I
Table .No. 7.3 : Characteristics of primary acid-base disorders
Basic Disorder pH H+ Primary Secondary
Change Change
Metabolic acidosis Low High HC0 low PaC0 decreased
Metabolic alkalosis 3 2
High Low HC0 3 High PaC0 increased
Respiratory acidosis Low 2
High PaC0 High HC0 increased
Respiratory alkalosis 2 3
High Low PaC0 low
2 HC0 decreased
3
CH . 7 : Dlngn Is nncl Trontm nt or !\cl Bn o Ol sorc.J or 201
COMPENSATION IN ACID BASE DISORDERS
\Nli at is th e mp n ·1ll n rind h w It cur ?

1.
The body' r p ns lo neutrali se the off ec t of the Initi al in sult on pH
110111 o t is is called compensation.
To und rstand compensation first of all it Is important to remember that
pH is maintained by ratio of HC0 3 /PaC0 2 (Henderson-Hasselbalch
equation)
To maintain normal pH, primary metabolic disorders (primary change
in HC0 3 ) lead to compensatory respiratory responses (secondary
change in PaC0 2 ).
Example : Metabolic acidosis (Fall in HC0 3 ) leads to low pH. Low pH
stimulates the respiratory centre causing hyperventilation.
Hyperventilation leads to C0 2 washout and decreased PaC0 2 . So in
short, low HC0 3 leads to compensatory low PaC0 2 ,. which returns ratio
of PaCO/HC0 3 towards normal. This compensation keeps pH within a
normal range as far as possible.
Similarly, to maintain normal pH, primary respiratory disorders (primary
change in PaC0 2 ) lead to compensatory metabolic (renal) responses
(secondary cha_ng.e in HC0 3 ).. ; .
11 11
2. What is the Same Dir_e ction .Rule· ?
From the above discussion (as well as Table No. 7.3), we can conclude
that in each case the compensatory changes-are in the same direction
as the primary changes. Decreased HC0 3 leads to decreased PaC0 2
and increased HC0 leads to. i~~rease.q P~C0 2 (i.e. up yields .up, down
3
yields down). _ . . .
This is known as 11
Same Direction Rule" of compensation.
3. What is the expected comp·e~satjon? . ..

..
Expected compensation for simple aCid base ~isorders is summarized
in Table No. 7.4. · · · ~. .
202 CH. 7 : Diagnosis and Treatment of Acid Base Disorders
. ?
4. Why to calculate and cfleck compensation ·
Importance of calculation and checking compensation in acid base
disorders :
1. Useful in differentiating simple from mixed disorder.
2. If e. pected change = actual change, disorder is simple.
3. If actual change is more or less than. predicted, disorder is mixed
4. compensation follows "same direction rule". If changes are i~
opposite direction, think of mixed disorder.
Table No. 7.4: Prediction of compensation for simple acid base disorders
Disorder Expected compensation -
Metabolic acidosis PaC02 = (1.5 x HC03) + 8
(Fall in HC03) · PaC02 ~ HC03 + 15
Metabolic alkalosis Rise in PaC0 2 = 0.75 x Rise in HC0 3
(Rise in HC03)
Respiratory acidosis (Rise in PaC0 2)
Acute: ·Rise in ~CC? 3 . = 0.1 x ~ise in PaC0 2
.( 6-24 hrs) Fall in pH ~ 0.0·1 x Rise in PaC0 2
Chronic : Rise in HC03 in
" = oA ~ ·~ise Paco 2 ·
(> 24 hrs) Fall in pH =0.003 x Rise in PaC0 2
Respiratory alkalosis (Falt'in .Paco 2 ) · . · ·.
Acute : Fall in HC03 =0.2 . x Fall in, Paco2
Rise in pH . =0.01 x Fall in PaC02
Chronic : Fall in Hco 3
·= 9,.4 x Fall in Paco 2 .
Rise in pH
- 0.002 x Fall in PaC02
MIXED ACID BASE DISORDER

. ·• .
Definition: Mixed a~id base disorder is defined as independent coexistence

of more than one pnmary acid base disord·
er.
~ixed dis~rders ~ccur iii very 111, critlCai patients . .fhe most common mixed
drs~rder 1s ~ mrx~d metabolic and respiratory acidosis. The ·most
detnm~ntal mixed d~sor~ers are mixed metabolic with respiratory acidosis,
and mixed metabolic with respiratory alkalosfs.
CH . 7 : Di agno sis
nd Treatm ent of Acid Base Disorders 203
Different mixed acid base disorders and t .

in Table No. 7.5. heir common causes are summarized
Table No. 7.5: Common mixed acid b ase disorders

.
Disorders
Common causes
1. Metabolic acidosis and a Cardiac arrest (hypoventilation +
Respiratory acidosis
lactic acidosis)
(low pH, J.Hco 3 , 1'Paco ) b.
2 Shock with respiratory failure.
c. Diabetic ketoacidosis with
respiratory diseases
2. Metabolic acidosis and a Salicylate intoxication
Respiratory alkalosis b. Gram-negative sepsis
( N.pH, J..HC0 3 , J.PaC0 ) c. Liver failure
2
3. Metabolic alkalosis and a. COPD with diuretics
Respiratory acidosis b. Metabolic alkalosis with severe
( N.pH, 1'HC0 3 , 1'PaC0 2 ) hypokalemia and respiratory-\
weakness leads to hypo~entilation
4. Metabolic alkalosis and a Liver failure with vomiting
Respiratory alkalosis b. Patient on ventilator with continuous
(tpH,tHC0 3 ,iPaC0 2 ) nasogastric aspiration.
5. Metabolic acidosis and a Diabetic ketoacidosis with vomiting
Metabolic alkalosls b. Vomiting with severe volume
( near N. pH and HC0 3 ) . I depletion causing lactic acidosis
6. Respiratory acidosis Do not co-exist
Respiratory alkalosls
Triple mixed disorders

1. Metabolic acidosis, metabolic alkalosis, with respiratory alkalosis.
Example : Alcoholic patient ~ith vomitirt9 (metabolic acidosis +
alkalosis), who develops superimposeq respiratory alkalo~is from sepsis
or liver diseases. --
2. Metabolic acidosis, metabolic alkalosis, with respiratory acidosis.
Example : COPD hypercapnic (respiratory acidosis) patient, who
develops metabolic alkalosis from diuretics or vomiting, develops
sup~rimposed metabolic acidosis from sepsis, hypotension or hypoxemia .
.I
204 CH. 7 Diagnosis and Treatment of Acid Base Di sord ers
Evaluation and investigations of acid base disorder

Stepwise evaluation of patient with suspected acid base disorder is as follows:
1. History and Examination : Careful history and examination can
provide clue for underlying clinical disorders. Diarrhoea or ketoacidosis
may cause metabolic acidosis. Presence of Kussmaul's breathing
suggests underlying metabolic acidosis.
2. Primary Investigations : Basic investigations are essential as they
may provide clue for underlying disorders as well as acid base disorders.
Most useful investigations are serum sodium, potassium, chloride, HCO
and anion gap. Other relevant investigations are CBC, urin~
examination, urinary electrolytes, blood sugar, renal function test
etc.
3. Arterial .blood gases (ABG): It is mandatory for diagnosis of acid base
disorders.
Arterial Bloo~ Gases (ABG) : When and Why?

There- is no single right method for deciding when ~o get ABG. It needs to
be determined after proper evaluation of indiyidual patient.
Why to go for ABG selectively .?

As blood gases require arterial puncture (which is painful and carries
small risk of arterial occlusion) and is relatively expensive, it should not
be performed as a routine investigation.
When ABG is n·ot needed?

Ex~ept for emergency, or_der prir,nar:y, less invasive tests first
(Electrolytes, HC0 3 etc). On basis of theh· results decide about need
for ABG. If clinical findings and labo-ratory data suggest mild, primary
or no acid base disturbances, usually ABG is. not required.
When ABG is needed?

Indicatio·ns:
1. In emergency, ·c-ritical and un~table pati~nts, )Vh.ere significant
acid base disorder is suspected, ABG is .needed immediately.
CH . 7 Diag nos1s
· and Treatment of A .d B .
c1 ase Disorders 205
.
2. If history, examination and serum el t 1
progressive acid base disord ec ro ytes suggest severe or
ers.
3. Sick patient with significant respirat d.
· ory 1stress secondary to
acu t e respiratory diseases or exacerbat' f h . .
diseases. ion °
c ronic respiratory
How to collect blood for Arterial Blood Gases (ABG) ?

Technique for Radial Artery Puncture : -
1. Perform modified Allen's test.
2. Clean the site (local anaesthesia is optional).
3. Use 21 gauge needle with syringe.
4. Flush syringe and needle with heparin.
5. Palpate artery with one hand and enter skin at 45-degree angle.
6. Obtain 2-4 ml of blood preferably without aspiration.
7. After withdrawal of syringe , apply firm pressure at punctured site.
Special Precautions
1. Collect blood in a low friction syringe under arterial pressure. Avoid
pulling (suction) of syringe as it may reduce value of both PaC0 2 and
Pa02 .
2. Heparinized syringe is used to avoid blood clotting. But avoid excess
heparin, which can dilute the sample.
3. If sample contains air bubble, it ·should be "tapped" to the surface and
pushed out of the syringe. Air bubbles can lead to increase in Pa0 2 and
decrease in PaC0 ~
2
4. If laboratory analysis will be delayed for more than a few minutes, the
sample should be refrigerated. (Place the capped syringe in a glass of
ice water). At normal temperature RBC_!11etabolism can produce lactic
acid and may-acidify the sample.
Interpretation of Basic fJ1vestigations
It is important to remember that ABG. and serum electrolyt~s should
b~ Performed . simultanously for correct interpretation of acid base
disorders. . .
206 CH. 7 Diagnosis and Treatment of Acid Base Disorders
1. pH
Normal value: 7.4 (7.35 to 7.45)
-
Normal pH : It suggests either absence of disorders or pres~nce of mixed
disorders (i.e. metabolic acidosis with respiratory alkalos1s).
Low pH (<7.35): suggests acidosis I acidaemia_
High pH (> 7.45): suggests alkalosis I alkalaemia
pH is determined by and inversely related to H+ concentration. Relation
of pH and H+ (nEq/L) is as follows
pH 6.9 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7
H+ 125 100 80 64 51 40 32 25 20
(Note that the H+ falls by 20°/o for each 0.1 pH unit increment.)
Equation which defines relationship between H+, HC0 and PaC0 is
3
H+ = 24 X (PaCOiHC0 ) 2
3
2. HC0 3 (mEq/L)
Normal value : 24 (22 - 26) m Eq/L
Low (< 22 mEq/L) : Metabolic acidosis (primary change) or
Respiratory alkalosis (secondary change)
High (> 26 mEq/L) : Metabolic alkalosis (primary change) or
Respiratory acidosis (secondary change)
Normal HC0 : Does not exclude acid base disorders.
3
Acute respiratory disturbances or mixed
disorders (metabolic acidosis with alkalosis)
can give normal HC0 •
3
3. PaC0 2 (mm of Hg)
Normal Value : 40 (35-45) mm· of Hg
High (> 45)
: Respiratory acidosis (primary change) or
Metabolic alkalosis· (secondary change)
Low (< 35)
: Respiratory alkalosis (primary change) or
Metabolic acidosis (secondary change)
\
CH.7
Diagnosis and Treatment of Acid B .
7
_...------~~~~~~~~~~~~~~~:.:::.:a:s:e~D:1s:o~rd:er:s~~2~0:.
Anion Gap (AG)
4.
Anion Gap (AG) = Na - (Cl + HC0 3 ) = 12 ± 2 mE /L n
charge difference between unmeasured an·i q ( ~rmal value). The
· on and cation is t
Anion Gap (AG). (Important unmeasured anions a . ~rmed the
re anionic prot .
phosphate , sulphate and organic acids. Important u _em,
· · · nmeasured cations
are calcium , magnesium and potassium). Increase an·ion h. fl
. · . c 1e y reflects
increased tn unmeasured anion. Albumin normally compr om1ses · most
of the AG : So !or every 1 gm/di decline in serum albumin a 2 mE /l
decrease 1n anion gap will occur. q
Importance of Anion Gap (AG)

A) AG in metabolic acidosis: Anion gap is most useful to establish
etiological diagnosis of metabolic acidosis. Mos_t important causes
of normal anion gap (hyperchloremic) acidosis is diarrhoea. While
important causes of increased anion gap acidosis are lactic
acidosis , ketoacidosis and CRF.
Increased anion gap acidosis is characterized by two factors :
(1) Low HC0 and (2) Increased anion gap. It is important to
3
remember that, fall in HC0 3 = rise in anion gap.
8) AG in diagnosis of mixed disorder: If high AG metabolic acidosis
is associated with (a) normal HC03 or (b) AG excess> HC03 deficit,
think of superimposed metabolic alkalosis.
5. Serum Potassium .
Normal value: 3.5 to 5.5 mEq/L
Low K+: Metabolic or respiratory alkalosis, diarrhoea, proximal RTA.
I f ·i re Type-4 RTA, OKA or
High K+: Metabolic acidosis due to rena 81 u ' ..
respiratory acidosis.
6. Pulse oxymetry . . N . rmal value : 96 -

. f rt ·a1 haemoglobm. o
Measures o 2 saturation o a_ en marked tissue hypoxia (less
5
100%. Less than 90% saturation su_gges!ful for hypoxemia screening,
than soo;0 Pa0 ). Pulse oxymetry is us . can occur with 1OOo/o 0 2
2
but tells nothing about PaC02· Hy~p~e~
. r~ca~p~n~ia~:::.:..::;_;...------
~
saturation. ...,
Diagnosis of acid base disturbances: step-by-step an al s icS
Step-1 : Is there an acid base disorder?
Look at PaC0 2 a1 ' CO •
norm al ra ge. I' ab o ~1
is no acid base dis ae !
Step-2 Is there acidosis or alkalos is?

Look at th e pH ( or. al 121 s · s •'• ss
If pH is < 7. 35, r's gges;.s ac·a sis I 2 · J~ s T. · a.
If pH is > 7.45 i s ~.;;;I

e .... s a l~ al s b I 2~. ~ 2 e ·
Step-3 What is the pri,m ary acid base d i so rder?

Determine hep · a y e·ec• ·
a If th e pH is lo .· (< 7.35), ' e as a . ·~s
may be either
1. Metabolic acidosis : C a I •· ~ C ,;
11. Respiratory acidosis : Ch arac e ·ze ·.., PaC 2

b. If the pH is high (> 7.45) the pa ien has al a ae . ·a.
which may be either
i. Metabo'fic alkalosis.: Cha.racterize · " . high iHC03
ii. Respiratory alkatosis: Charactefiized by lo PaC02
Step-4 Calcul:ate the expected compensation
Determine whether the actual value matches ~.ith the
expected compensation. atching of both confirms diagnosis
of primary disorder.
Step-5 :Determine the presence of mixed acid baSe disorder
Whether disorder is simple or mixed is judged by fi steps :
a Check direction of changes
'/ As per •rule of same direction• in simp,fe acid base
disorders HCO and PaCO changes from normal in the
3 2 _ . cfi ......_-+ion
same direction. If these changes are m opposite fc:;\#u
it suggests mixed disorder.
CH. 7 : Diagnosis and Treatment of Acid Base Disorders 209
b. Compare expected compensation with actual value. If actual

value is either more or less as compared to the calculated
expected compensation, it suggests mixed disorder.
c. Check the anion gap (AG)
In certain mixed disorders pH, PaC0 and HC0 are
2 3
normal and the only clue to an acid base disorder may be
an increased anion gap. So AG is called "foot print" of
metabolic acidosis. Hyperchloremic metabolic acidosis
leaves no "fo<?t print".
d. Compare fall in HC0 3 with increase in plasma anion gap.
i. In high AG metabolic acidosis, rise in the plasma AG
(AG - 12) matches ~ith fall in serum HC0 3 ( 24 -
HC0 3 ), (Rise in AG= Fall in HC0 3 ).
ii. If increase in AG exceeds the fall in HC0 3 (Rise in AG
> Fall in HC0 3), it suggests co-existing metabolic
alkalosis.
iii. If increase in AG is lesser than the fall of HC0 3
(Rise in AG< Fall in HC0 3 ), it suggests loss of HC03
(diarrhoea) causing non-AG metabolic acidosis.
Step-6 Clinical correlation and to establish etiological diagnosis
EXAMPLES OF ACID BASE DISORD.ERS

Case 1 A 15 year old boy is brought from exa.mination hall in
apprehensive state with complain of tightness of chest.
pH 7.54, HC0 21 mEq/L, PaC0 2 21 mm of Hg
3
Analysis : pH is high so patient has alkalosis. Low PaC02 is suggestive

of respiratory alkalosis. HC03 is also low suggestive of
compensation (follows "same direction rule").
Expected acute compensation (fall ,jn HC03 ) in respiratory
alkalosis will be
Fall in HC0
3
=0.2 x fall in PaC02 = 0.2 X (40 - 21)
= 0.2 x 19 = 3.8
j
21 O CH. 7 Diagnosis and Treatment of Acid Base Disorders
So expected HC03 will be 24 - 3.8 =20.2 mEq/L, which almost

matches with actual HC0 3 , which is 21 mEq/L, suggestive of
simple acid base disorder.
So patient has primary respiratory alkalosis due to anxiety.
Case 2 A patient with poorly controlled IDDM missed his insulin

f~r 3 days.
pH 7.1, HC0 3 8 mEq/L, PaC02 20 mm of Hg

Na 140 mEq/L, Cl 106 mEq/L and urinary ketones +++
Analysis: pH is low so patient has acidosis. Low HC0 3 is suggestive of

metabolic acidosis. PaC0 is also low suggestive of
2
Expected compensation (fall in PaC02 ) will be
PaC0 2 = HC0 3 X 1.5 + 8 = 8 X 1.5 + 8 = 12 + 8 = 20
So expected PaC0 2 will be 20 mm Hg, which matches with
actual PaC02 , suggestive of simple acid base disorder.
Anion gap is 26 (AG = Na - (Cl + HC03 ) = 140 - (106 + 8) =
140 - 114 = 26, which is high, suggesting high AG metabolic
acidosis. Presence of urinary ketones suggests presence of
diabetic ketoacidosis.
So patient has' high anion gap metabolic acidosis due to OKA.
Case 3 A patient With severe diarrhoea, co~plains of difficulty in
breathing.
pH 7.1, HC0 14 mEq/L, PaC02 44 mm of Hg & K 2.0 mEq/L
3
Analysis : pH is low so patient has acidosis. Low HC03 is suggestive
of metabolic acidosis. PaCO is expected to reduce due to
compensation. However aciual PaC02 is high, which is
sugge.stive of presence of associated respiratory acidosis.
ve·ry low K+ causing weakness of respiratory muscles is the
cause of respiratory failure leading to respiratory acidosis.
So this· patient has mixed disorder, metabolic acidosis with
respiratory acidosis.
case 4 ABG of patient with CHF on frusemide is as follows :

pH 7.48, HC0 3 .34 mEq/L, PaC0 48 mm of Hg
2
Analysis : pH is high s~ patient has alkalosis. HC0 is high suggestive

3
of metab~l1c alkalosis. PaC0 2 is high , suggestive of
Expected compensation (rise in PaC0 )will be
2
Rise in PaC0 2 = 0.75 x rise in HC0 = 0.75 X (34-24)
3
=0.75x10=7.5
So expected PaC0 2 will be 40 + 7.5 = 47.5 mm Hg , which
almost matches with actual PaC0 2 , which is 48 mEq/L
suggestive of simple acid base disorder.
So patient has primary metabolic alkalosis due to diuretics .
Case 5 Following sleeping pills ingestion, patient presented in drowsy

state with sluggish respiration with respiratory rate 4/min.
pH 7.1, HC0 3 28 mEq/L, PaC0 2 80 mm of Hg, Pa0 2 42 mm
of Hg
Analysis: pH is low so patient has acidosis. High PaC02 is suggestive

of respiratory acidosis. Low Pa0 2 -hypox~mia, supports
diagnosis of respiratory failure-acidosis. HC03 is also high
suggestive of co~pensation ~follows "same direction rule").
Expected acute compensation (rise in HC0 3 ) will be
Rise in HC0
3
=0.1 x rise in ~aC0 2 =0.1 X (80 - 40)
= 0.1 x 40 = 4 mEq/L
So expected HCO will be 24 + 4 = 28 mEq/L, which matches
3
with actual HC0 , suggestive of simple acid base disorder.
3
so patient has primary respiratory acidosis due to respiratory
failure, due to sleeping pills.
Case 6 ABG of patient with shock on ventilatory support since last 4
hours is pH 7.48, HC0 14 mEq/L, PaC02 22 mm of Hg.
3
212 CH. 7 Dlogno11lo And Trr:rntrn'Jn of A lrJ Bw ~ I r.> 'j<, ·,,
Analysis: pH is high so p ti nt ha
of respiratory lkalo i . If ltin f ven Ha
rate nd high tid al volum e, it can cau .,, r
HC0 3 is also low suggestive f com e
direction rule") .
Expected acute compensation (fall in HCO'j 11ilf ,)~
Fall in HC0 3 :::: 0.2 x fa ll in PaC0 2 = 0.2 X 4 - 22
= 0.2 x 18 =3.6 mEq/L
So expected HCO will be 24 - 3.6 = 20.4 m Ea/ L. B• 'a
value of HC0 is 3low (14 Vs 20.4 mE q/L , "I , .IC s .. ,. _
3
presence of additional metabolic acidosis sh ck a
lactic acidosis).
So patient has mixed disorder, respirato y aJkal si
metabolic acidosis.
Case 7 Known case of COPD develops severe vomiting.
pH 7.4, HC0 3 36 mEq/L, PaC02 60 mm of Hg
Analysis : pH is normal so patient has either no disorder or has mixed
acid base disorder. However .
abnormal value of HCO3 and
PaC0 2 is suggestive of presence of mixed disorders. High
HC0 3 suggests presence of metabolic al'kalosis (which can
occur due to vomiting). High PaC02 is suggestive of respiratory
acidosis (which can occur due to COPD). Metabolic alkalosis
·is expected to increase the pH, while respiratory acidosis is
expected to decrease the pH. Normal pH can be explained as
an end result of opposite changes caused by both primary
disorders. So patient has mixed disorder, respiratory acidosis
with metabolic alkalosis. ·
Case 8 A case of hepatic failure has persistent vomiting.
pH 7.54, HC0 3 38 mEq/L, PaC0 2 44 mm of Hg
Analysis : pH is high so patient has alkalosis. HC03 is high suggestive
of metabolic alkalosis (due to vomiting). PaC02 is high,
suggestive of compensation (follows "same directjon rule·).
Expected compensation (rise in PaC0 ) will be

2
Rise in PaC0 2 = 0.75 x rise in HC0 = 0.75 X (38-24)
3
= 0.75x14=10.5
So expected PaC0 2 will be 40 + 10.5 = 50.5 mm Hg. But actual
value of. PaC0 2 is lesser than expected PaC0 (44 vs 50.5 mm ~
2
Hg), which suggests presence of additional respiratory alkalosis
(hepatic failure can cause respiratory alkalosis).
So patient has mixed disorder, metabolic alkalosis with
respiratory alkalosis.
Diagnosis and Treatment of Simple Acid Base Disorders
Diagnosis, causes and treatment of simple acid base disorders are discussed ·
II
below. (
~
METABOUC ACIDOSIS
Definition
It is characterized by faU in 1p lasma HC03 and fall in pH (below 7.35). The
PaC0 2 is reduced secondari'ly by hy.perve~tilation, which minimizes the fall
in pH. ,
Pathophysiology
Metabolic acidosis can result from
1. Loss of the base- HC0 3 via the GI tract or kidnevs (diarrhoea,
proximal RTA).
2. Over production of metabolic acids in the body {ketoacidosis or lactic
acidosis).
3. Ingestion. or infusion of acid or potential acids (salicylates or NH 4 CI).
4. Failure of H+ excretion by ·k idney (renal failure).
214 CH . 7 Diagnosis and Treatment of Acid Base Disorders
Etiology
Calculation of anion gap (AG) is extremely helpful in narrowing etiological
diagnosis. AG= Na - (Cl+ HC0 3 ) = 12 ± 2 (normal value).
On the basis of AG causes of metabolic acidosis can be divided into two
groups, as summarized in Table No. 7.6.
Table No. 7.6 : Causes of Metabolic acidosis
Normal Anion Gap Increased Anion Gap
1. Loss of HC0 3 1. Metabolic disorders:
Diarrhoea, CA inhibitors Lactic acidosis, OKA
U reterosigmoidostomy Alcoholic ketoacidosis
Proximal RT A
2. Failure to excrete H 2. Addition of exogenous acids
Distal RTA Salicylate/methanol poisoning
3. Addition of H 3. Failure to excrete acid
NH 4 CI infusion Acute/chronic renal failure
Clinical Features
Clinical presentation in metabolic acidosis is chiefly due to
A. Manifestations of underlying disorder
'
B. Manifestations of metabolic acidosis
Metabolic acidosis can cause changes in pulmonary, cardiovascular,
neurological and musculo-skeleton system.
(a) Pulmonary changes : Kussmaul's breathing (deep, regular, sighing

respiration) suggests presence of metabolic acidosis. This
hyperventilation is more due to increase in tidal volume rather
than to respiratory rate.
(b) Cardiovascular changes: If there is severe acidaemia (pH< 7.2),
there is increased susceptibility for cardiac arrhythmias, decreased
response to inotropes and secondary hypotension may occur. The
reduced blood pressure in such patients is due to depressed
myocardial contractility and arterial vasodilatation, both induced
by the low pH.
CH . 7 : Di" no I , n Trnatrnent of Acid Ba e Di order"' 215
(c) Neurological changes : ft rang es from headache, confusion

lethargy, and drowsiness to coma.
(d) Other changes : Chronic acidaemia , as with renal failure can
cause rickets in children and osteomalacia in adults. '
severe acidosis can cause nonspecific symptoms such as anorexia
• • I
nausea, vomiting and muscle weakness, especially in infants and

young children.
Diagnosis
History
proper history elicitation provides clue for presence of metabolic acidosis
and underlying etiology. Kussmaul 's breathing is the most important
diagnostic presentation. Pre-existing diabetes , renal failure and recurrent
renal stone provides clue to the presence as well as cause of acidosis. Lactic
acidosis can be suspected in patients with hypotension , shock, cardiac failure
and septicemia.
Investigations
Arterial blood gases
Low HC0 , low pH, and compensatory fall in PaC0 2 will confirm the
3
diagnosis.
To establish etiolog·l cal diagnosis
Anion Gap = Na - (Cl + HC0 3 ), blood sugar, serum K+, renal function
tests, serum lactate, level of salicylates and urinary examination tor
pH, ketones, and oxalate crystals are very useful investigations.
Urinary Anion Gap (UAG) = Urinary {Na + K - Cl) = 80 - NH 4
Urinary Anion Gap {UAG) reflects the ability of the kidney to excrete
NH 4 CI.
Normally UAG is zero or has positive value. UAG is useful for
differentiation between gastrointestinal and renal c.aus~ ~f
hyperchloremic acidosis. If the caus·e of metabolic acidosis ~s
gastrointestinal HC0 loss (diarrhoea), the urinary anion g~p ~s
3
negative ( 20 to -50 mEq/L) because of increased NH4CI excretion in
response to acidosis. In metabolic acidosis due to renal tubular
CH . 7 : Diagnosis and Treatment of Acid Base Disorders
216
acidosis or renal failure (with impaired NH 4CI excretion) the urinary anion
gap is positive (25 mEq/L).
Treatment of Metabolic Acidosis
Treatment of metabolic acidosis includes

1. ·s pecific management of underlying disorder
As a rule treat underlying disorder meticulously. It is the most important
measure and may be the only required treatment for mild to moderate
acidosis.
2. Alkali therapy
Bicarbonate administration should be reserved only for selective
patients with severe acidaemia. Treat.m ent o_f all acidaemia with
NaHC0 is not only unnecessary but _can also, be detrimental.
3
3. Correct volume and electrolyte deficits
Alkali Therapy in Metabolic Acidosis
NaHC0 3 should be administered judiciously
(A) Why to treat r'0etabolic acidosis ?
Exogenous alkali is often required for the prompt reduction of severe
acidaemia and associated detrimental effects: Kussmaul's breathing,
cardiac arrhythmias, hypotension, impaired response to pressure
·agents, hyperkalemia etc, are the life thr9"atening complications
(B) Why alkali therapy is given in selected patients, and aimed for· only
partial correction ? ·
Disadvantage and risk of NaHC0 therapy : ·
3
1. Hypernatraemia and volume overload especially in CHF or renal
failure
2. CNS acidosis and ~ypercapnia
3. Hypokalemia and hypocalcaemia
4. · Overshoot or rebound alkalosis in organic acidosis (i.e. ketoacidosis,
lactic acidosis) due to conversion of accum~lated organic anions
(lactate, acetoacetate) into bicarbonate.
H. 7 : Di n is and Tre tment of Acid Base Disorders 217
5. Stimula_Hon of phosphof ructokinase activity enhances lactate

production and worsens acidosis.
So t reduce possible complications only partial correction of severe
acidaemia is desirable.
c Indications of alkali therapy :
1. When blood pH drops below 7 .15 to 7 .20. Such a severe acidaemia
can be life threatening.
2. When HC0 3 falls below 1O mEq/L. Low HC0 needs prompt
3
treatment because ·
a. Small additional fall in HC0 3 can cause a large fatal drop in pH.
b. Respi ratory compensation requires heavy muscular work. Such
compensatory hyperventilation for prolonged period can cause
fatigue of respiratory muscles especially in elderly and debi\itate'd
patients. If fatigue occurs ventilation fails, PaC0 2 rises and the
patient develops superimposed respiratory acidosis.
3. Treatment of hyperkalemia with metabolic acidosis.
Bicarbonate therapy is useful mainly in hyperchloremic (normal AG)
acidosis, but is controversial in increased AG-organic metabolic acidosis.
(D) What should be the goal of treatment?
NaHC0 should be administered judiciously with an aim to return
3
blood pH to a safer level of about 7 .2 and bicarbonate must be
increased to 8 to 1O mEq/L. Patient with acute normal AG acidosis
(i.e. diarrhoea) needs early bicarbonate therapy and goal of therapy
is:...:.::_:_:.:.::.:..:..:.:.::;:..:...:.:.:~
to maintain HCO a~=-.~- -
at 15mE..q/L. In lactic acidosis bicarbonate should
.
be started lat~ and discontinued ea~ly.
(E) How much bicarbonate is needed to achieve the goal?
There is no simple prescription as several factors affect the acid
base status (i.e. rate of acid production and bicarbonate loss,
respiratory compensation, ECF volume status, and treatment of
etiology).
Amount of HC0 3 required =
{Desired HC0 - Actual HC0 3 ) X 0.5 X body weight in kg
3
->
218 CH . 7 : Diagnosis and Treatment of Acid Base Disorders
¥ @.!cept in cases of extreme acidaemi~ Na~C0 3 should be administered

/J' as an infusion over a period of severar minutes to a few hol:l rs, rather
than a bolus.
,---------
(F) Precautions taken during NaHC0 3 administration
1. As NaHC0 is highly irritant, establish proper large l.V. line for
3
infusion.
2. Avoid l.V. bolus of NaHC0 3 , except in an emergency.
3. Correct hypokalemia, before correcting acidosis as intracellular
K+ shifting can cause life-threatening hypokalemia.
4. NaHC0 3 should be given with caution in circulatory overload.
5. Never treat just acidosis, treat its etiology simultaneously.
¥ e. Avoid mixing of calcium with NaHC0 3 to avoid precipitation.
7. · Avoid mixing of NaHC0 3 with inotropes. CA..~~)
Alternative alkalinizing agents
Disadvantage of infusion of bicarbonate is production of C0 (HC0 +
2 3
H+ ~ H2 C0 3 --? H2 0 + C0 2 ), which can aggravate acidosis. Experimentally
promising, Carbicarb generates bicarbonate rather than C0 2 while buffering
hydrogen ion (C032- + H+ --? HC03). In experimental lactic acidosis, Carbicarb
increased blood and intracellular pH with little or no rise in the carbon dioxid~
level. However clinical experience with Carbicarb is limited, and is not
commercially available for clinical use.
Another carbon dioxide consuming, sodium free solution buffer THAM,
also limits C0 2 production and increases pH. However THAM is not
documented to be clinically more efficacious than bicarbonate. In fact
serious side effects of THAM (hyperkalemia, hyperglycemia, ventilatory
depression etc.) markedly limits its usefulness. .
CH . 7 Diagno si and Treatme n of Ac id Ba se Diso ders 219
Metabolic acidosis in specific situations
(A) Increased anion gap acidosis
(1) Lactic acidosis

It is the most serious, as well as the most common cause of
metabolic acidosis in hospitalized critical patients. The most
common cause of lactic acidosis is shock (cardiogenic or septic).
Suspect lactic acidosis in any patient with shock, hypoxemia or
sepsis with increased AG acidosis. ·
Table No. 7.7 : Causes of lactic acidosis
Type A Type 8
Shock (cardiogenic or septic) Diabetes mellitus
Respiratory failure Hepatic failure
Carbon monoxide or Severe infection
cyanide poisoning Toxins-Ethanol , Methanol
Severe anaemia Drugs : Biguan ides
Type A - Characterized by impaired tissue oxygenation.

Type B - No hypoxia, but mitochondrial respiration is impaired.
Diagnose lactic acidosis in increased AG acidosis by exclusion of

ketoacidosis, intoxication and renal failure. Serum lactate levels
confirm the diagnosis. Its normal value is 1 mEq/L, which
increases to at least 4-5 mEq/L, but is commonly 10-30 mEq/L in
lactic acidosis. Lactic acidosis occurs due to increased production
and decreased utilization of lactate.
Treatment of lactic acidosis :
Goal of the therapy is adequate tissue oxygenation as well as
detection and treatment of the underlying causes. Improvement of
tissue oxygenation can be achieved by high-inspired oxygen
fraction, ventilator support, repletion of ECF volume, after load
reducing agents, and inotropic support by dopamine and
dobutamine. Avoid vasoconstricting drugs such as noradrenaline,
as they can worsen tissue hypoxia.
220 CH. 7 Di agn osis and Trea tment of' Acid Base Di so rd ers
In lactic acidosis alkali is used judiciously, because alkali therapy

is known to stimul ate the phosphofructoklnase activity, exacerbating
lactic acidos is vi a enhanced lactate production. Administration of
NaHC0 3 is started late (in severe acidosis with pH < 7.1 ) and
discontinued early. Early bicarbonate haemodialysis is effective as
it corrects acidosis without the risk of volu.me overload or
hypernatraemia.
The drug under evaluation agent, Dichloroacetate stimulates
pyruvate dehydrogenase (PDH) activity and thereby limits lactate
production from pyruvate. Although the effect of dichloroacetate
in experimental lactic acidosis is impressive and there is fall in
plasma lactate concentration and rise in bicarbonate leyel, clinical
studies have failed to demonstrate· a substantial advantage over
conventional management.
(2) Diabetic ketoacidosis
It is due to overproduction of acetoacetic acid and hydroxybutyric
acid by liver due to relative or absolute insulin deficiency. Insulin
administration is the cornerstone of treatment of diabetic
ketoacidosis.' Adequate replacement of water, sodium and
potassium is also mandatory: Alkali therapy should not be
administered /OUtinely b.ecause i_nsulin and supportive therapy
will regene_rate. bicarbonate from . resolution of retain.ed ketone
bodies. Moreover, alkali therapy may even delay recovery by
augmenting hepatic ketogen~sis. Bicarbonate ·is in~icated. in patient
with marked acidaemia (blood pH < 7.1 ), wher~ decreased
myocardial performance can worsen tissue perfusion. The goal
of therapy is to raise the pH to a relatively safe level of 7 .15 to
7.20. Bicarbonate administration is also indicated in patients with
severe hyperkalemia.
(3) Alcoholic ketoacidosis
It occurs after abrupt discontinuation of alcohol consumption,
and is ·usually due to vomiting, prolonged starvation, and volume
depletion. Correction of hypoglycemia ·with dextrose infusion will
correct hypoglycemia, stimulate Insulin secretion and inhibit
glucagon secretion, and thereby promote the regeneration of
CH.7 Diag nosis
· and Treatment of Acid Base Disorders 221
~icarbo~at~ fro'.11 the metabolism of retained kelones. Correction of

ypovo em1a with saline infusion Will suppress counter regulatory
h ormones that enha nee -. k etoacidosis. Hypokalemia
hypop hosp h ataemia and hy . '
after 12 to 24 hour . pomagnesaemia may occur! especially
. . s, which may need correction. Supplement
thiamine
. k ,together with glucose t o avo1.d t h e development
. . .of
W ernic es encephalopathy.
(4) Salicylate (Aspirin) poisoning
It is cha.racterized usually by respiratory aikalosis .or mixed
metab~l1? acidosis with respiratory alkalosis. Respiratory
alkalos.1s is caused by direct stimulation of the respiratory centre
by sal1cylate , w hereas the accumulation of lactic acid and
ketoacids largely accounts for metabolic ·acidosis. Presentation
varie s with severi ty of poisoning. Hyperventilation and CNS
disturbances are the usual manifestations.
Treatment : Initial therapy includes gastric lavage, reducing drug
absorption by administering activated charcoal and correction of
hypovol emia by saline (and not by NaHC0 3 ) . Subs·equently forced
alkalin e diuresis (high uri ne flow with pH > 7.5) is the mainstay
of t re at men t. Increase in pH converts salicylate to more
imperm eabl e salicylic acid and thus prevents CNS damage. Thus,
unless blood is already alkalinized by respiratory alkalosis, infuse
NaHCO infusion. Add 88 mEq/4 amp. of NaHC0 3 (25 ml of 7.5°/o
NaHCO 3 contains 22 mEq NaHC0 3 ) in one litre of 5°/o dextrose
3 .
and infuse it at the rate of 10-15 ml/kg/hour. Therapy should be
planned meticulously to avoid hypokalemia, hypoglycemia and
hypovolemia. Bicarbonate haemodialysis should be used to
remove salicylate in patient with refractory acidosis, severe CNS
symptoinS. progressive clinical deterioration, pulmonary oedema
and renal failure.
(5) Renal failure
ARF and CRF can result in an increased anion gap acidosis due
to retention of sulphate, phosphate and organic anions. In CRF,
especially in children, bicarbonate supp~ementat~on is required
to prevent renal rickets or osteomalac1a resulting from bone
buffering. Correction of severe acidosis with alkali therapy in renal

failure patients carries risk of volume overload. In such patients
dialysis can correct acidosis safely and effectively.
(8) Normal anion gap (hyperchloremic) metabolic acidosis

1. GI loss of bicarbonate
Diarrhoea is the most common cause of normal AG acidosis. Severe
acidosis often occurs in patients with diarrhoea due to cholera.
Correction of hypovolemia and hypokalemia are the most important
measures. Correction of acidosis with NaHC0 3 is required only in
selected patients with severe acidosis.
2. Renal tubular acidosis
RT A is a group of renal disorders characterized by defect in H+
excretion, bicarbonate absorption or both.
a. Classic distal (type1) RTA is characterized by hypokalemic
hyperchf oremic metabolic acidosis and is due to selective
deficiency in H+ secretion in distal nephron. Despite acidosis
urinary pH is always above 5.5. Nephrocalcinosis,
nephrofithiasis and bone diseases are the most important
clinical comp'licat ions of distal RTA. In distal RTA,
1
supplementation of bicarbonate (1-3 mEq/kg/day) or its

precursors such as citrate is necessary since acid
accumulates syste m fcally. Generally, potassium salt is
1
1
administered, which wm correct the potassium deficit as well.

ll Proximal (type 2) renal tubular acidosis is characterized by
hypokalemic hyperchloremic metabolic acidosis due to a
selective defect in the proximal tubule's ability to reabsorb
filtered HC0 adequately. During early stage, when HC03 is
3
> 18 mEq/L, urine is alkaline. But when plasma HC0 3 level
drops to 15-18 mEq/L, bicarbonaturia disappears, and urina~
pH can be acidic. Treatment of low HC03 in proxi~al RTA ts
sometimes hazardous and unnecessary except in severe
cases. The most important aspect of treatment of proximal ~TA
is to search the underlying treatable disorders (i.e. mufttp!e
myeloma, vitamin D deficiency and the use of c~rbo~tc
anhydrase inhibitors). If aJkali therapy is needed dose is qutte
larg.e (10-15 mEq/L). Also supplement potassium adequately to

avoid hypokalemia. When large dose of alkali is ineffective or not
well tolerated, the addition of thiazide diuretics may be helpful.
METABOLIC ALKALOSIS
Definition
Metabolic alkalosis is ~haracterized by increase in the serum HC0 , high
3
pH and compensato~y increase in PaC0 due to alveolar hypoventilation.
2
Increased HC0 3 and increased Paco is also a feature of chronic respiratory
acidosis, but the differentiating featu~ is low pH.
Pathogenesis
There are two steps involved in the development of metabolic alkalosis :
1. Generation of metabolic alkalosis and 2. Maintenance of metabolic
alkalosis
1. Generation of metabolic alkalosis : Mechanism of primary rise in
the plasma HC0 3 can be one or more of the following :
a. The loss of hydrogen ion from upper GI tract (vomiting) or urine
(diuretics)
b. Addition of alkali: Administration of HC0 3 or its precursors as
citrate (multiple transfusion of citrated blood)
c. Disproportionate loss of chloride .: .The loss of fluid with a h~gh
Cl/low HCO concentration (cond1t1on referred to as contraction
3
alkalosis)
2. Maintenance of metabolic alkalosis : Under normal circumstanc~s
the excess in bicarbonate generated by any of these processes. 1s
rap1'di y excre t e d ·1n the uri·ne · To maintain
. metabolic
. alkalos1s,
.
.1mpa1rmen
. t.m rena 1 b'1carbonate excretion
. is required. Three important
factors maintaining metabolic alkalos1s are
a. Volume /chloride depletion
b. Hypokalemia
c. Aldosterone excess
Etiological and differential diagnosis . . .

. f tabolic alkalosis are loss of gastric fluid (1.e.
Mos~ .1mport~nt ~auses o m:radrenal states. The most useful factors to
vomiting), d1uret1cs and hyp . lk . re ECF volume, blood pressure,
determine etiology of metab~l1c a ados1s a potassium Urinary chloride
1
urinary chloride concentration, an serum .. .
concentration differentiates metabolic alkalosis in ~wo maier grou.f~) saline
responsive and saline resistant metabolic al~alos1s (Table No. · ·
Table No. 7.8 : Cause of Metabolic Alkalos1s
SALINE RESPONSIVE SALINE RESISTANT
(Urine Chloride < 15 mEq/L) (Urine chloride > 20mEq/L)
ECF Volume Depletion Normal or Increased ECF Vol.
Vomiting I Gastric suction Hypertensive
Diuretics Hyperaldosteronism
Hypercapnia correction Cushing syndrome.
No ECF Vol. Depletion Normotensive.
NaHC03 infusion Bartter's syndrome
Multiple transfusion Severe K+ _d epletion
Clinical features ·
Metabolic alkalosis rarely causes specific manifestations. Common features
are:
(a) CNS symptoms : Alkalaemia can increase neuromuscular excitability
leading .to paresth~sia, ligh~ · ~e~pache, and carpopedal spasm.
(b) CVS symptoms : Hypotension. and cardiac ·arrhythmias are common
presentations.
(c)
Other symptoms : Weakness, _musGle cramps and postural dizziness
due to hypovolemia; muscle w·eakness · and polyuria due to
hypokalemia.
(d)
Respiratory abnormalities : In ·moderate to severe metabolic alkalosis
. '
compensatory hypoventilafion rhay cause hypoxia in the patient with
preexisting lung disease. .. .
Diagnosis
• Increased HC0 3 , pH and compensat(?r)r increase in Paco
• Expected increase in PaC02 = 0.75 )(. Rl!!e in HC0 2
• Serum potassium and chloride are usuaUy ·1ow 3
-
CH. 7 : Di ag nos is and Trea tm ent of Acid Base Di sorders 225
• Urinary chloride estim ation i very use-ful ·for etiological diagnosis .
Treatment of metabolic alkalosls

A. Treatment of underlying cause
B. Saline (chloride/volume) responsive alkalosis
1. Aim of therapy is adequate correction of volume, chloride and K+ deficit
2. I. V. isotonic saline with KCI or lsolyte-G are preferred infusions.
3. Treatment with H2 inhibitors or proton pump inhibitors will reduce
gastric acid secretion and will minimize further H+ loss and,
therefore, will prevef')t or reduce metabolic alkalosis due to vomit_ing
or nasogastric suction.
4. Diuretics induced metabolic alkalosis in oedematous patients is
difficult to treat. It needs dose reduction, KCI . supplementation ,
spiranolactone or carbonic anhydrase inhibitors.
5. Avoid or disc:ontinue exogenous source of alkali such as NaHC0 3
inf~s.ion.s. , Ringer's l~ctate, acetate or ~itrate.
6. In rare cases with s~vere metabolic alkalosis diluted HCI can be

given l.V. to lower the plasma HC0 3 concentration. Although
relatively · diluted, 0.:1. N_ hydrochl_pric ·acid _(HCI) infusions are
corrosive and can produce thrombophlebitis. So it must be infused
slowly ihto large veins like ·subclaviari or·_ femoral veins: ·
7. Dialysis therapy m.ay be he.lpful in·ocd:isional patient~ ~ith severe
metabolic alkalosis, volume overload, and renal failure.
C. Saline (chloride/volume) resistant metabolic acidosis
. '
It needs specific treatment of ·underlying ca.uses (surgical ~reatment

of pituitary tumor 0 ·r adrenal adenoma in Cushing's syndrome) or
supportive treatment such as spiranolactone, correction of
hypokalemia, and sodium restrictionj
RESPIRATORY ~.QIP.OSIS
Definition
Respiratory acidosis is a clinical disorder characterized by an elevation
in the Paco (hypercapnia) leading to reduc'tion in pH and variable
2
compensatory increase in the plasma HC0 3 .

Respiratory acidosis occurs when the effective alveolar ventilation (CO
excretion by lung) fails to keep pace with the rate of co2 production.
2
Renal (metabolic) Compensation
Kidney responds by increasing H+ secretion so that urine becomes acidic

and plasma HC0 3 rises gradually.
Acute Every 10 mm of Hg rise in PaC0 2 causes 1 mEq/L rise in HCO
3
and 0.1 fall in pH
Chronic : Every 10 mm of Hg raise in PaC0 2 causes 4 mEq/L raise in HC0
3
and 0.03 fall in pH
Serum HC0 3 usually does not exceed 38 mEq/L due to compensation. If
HC0 3 is > 38 mEq/L, think of concomitant metabolic alkalosis .
Re.s piratory acidosis vs. metabolic alkalosis
Increased PaC0 2 and increased HC0 3 characterize both disorders, but

pH is low in respiratory acidosis and pH is high in metabolic alkalosis.
Relation between high PaC02.(hyp~~capni~) and low Pa02 (hypoxemia)

. / .
1. In most cases, hypoxem.ia.oc;:c~rs ~arlier and is more prominent than

hypercapnia. Alveolar diffusion of C0 2 is 20 times as quick as 0 2 .
2. All patients with hypercapnia who are breathing room air are hypoxic.
3: In chronic hypercapnia, hypoxemia is the primary stimulus to
res pi ration. So rapid and excessive correction of hypoxemia with
uncontrolled oxygen can cause extreme hypercapnia, which can lead to
neurological symptoms.
Causes
Respiratory acidosis can be due to airway obstruction, pulmonary
diseases, muscle fatigue or abnormality in ventilatory control as
227
CH. 7 Diagnosis and Treatment of Acid Base Disorders
Table No. 7.9: Causes of respiratory acidosis

CNS depression Air way
Drugs (anesthesia, sedative) Obstruction, asthma
Infection, stroke
Neuromuscular impairment Alveolar diseases
Myopathy, myasthenia gravis, COPD , pulmonary oedema,
polymyositis, hypokalemia ARDS , pneumonitis
Ventilation restriction Miscellaneous
Rib fracture , pneumothorax, Obesity, hypoventilation.
haemothorax.
Clinical features
1. Features of the underlying primary disorder.
2. Features of hypercapnia and hypoxia :
Hypercapnia causes neurological features, which vary as per the
severity and duration. Acute , severe hypercapnia may cause anxiety,
headache, dyspnea, confusion , psychosis, hallucination, and coma.
Mild to moderate chronic hypercapnia may cause sleep disturbances,
loss of memory, daytime somnolence, personality changes, impairment
of co-ordination, tremor and myoclonic jerks. Increased CSF pressure
may cause papilloedema.
Lipid soluble C0 crosses blood brain barrier rapidly, compared to
2
HCO . So tall in CSF pH is greater in respiratory acidosis as compared
to m~tabolic acidosis. So CNS manifestations are more with
respiratory acidosis and less with metabolic acidosis.
Treatment
Treatment varies as per the severity, rate of onset and underlying etiology.
A. General Measures
1. The major goal of therapy is to identify and treat the underlying
cause promptly.
2. Establish patent airway and restore adequate oxygenation.
3. If a patient with chronic hypercapnia develops sudden increase
in PaC0 , search for the aggravating factor. Vigorous treatment
2
of pulmonary infection , bronchodilator therapy and removal of secretions

can offer considerable benefits in such patients.
8. Oxygen Therapy
Role of oxygen therapy in respiratory acidosis is like a "Double edged
sword" and therefore needs careful titration. In acute respiratory acidosis,
major threat to life is hypoxia and not hypercapnia or acidosis, so oxygen
supplementation is needed. In chronic hypercapnia, 0 2 therapy should
be instituted cautiously and in the lowest possible concentration. Since
hypoxemia may be the primary and only stimulus to respiration,
injudicious therapy can lead to further reduction in alveolar ventilation
and aggravate hypercapnia drastically.
C. Mechanical Ventilatory (MV) Support

1. Patient selection : In acute respiratory acidosis, the early use of
ventilatory assistance is more appropriate. While in chronic
respiratory acidosis, a more conservative approach is advisable
because of the .great difficulty often encountered in weaning such
patients from ventilators.
2. Indications : Need of mecflanical ventilation is judged more on
the clinical condition of the patient, and not on absolute PaC0
2
value. Important indications of mec~anic~I ventilation (MV) are
a. Unstable, symptomatic or progressively hypercapnic (PaC0
2
> 80 mm of Hg) patients
b. If the patient exhibits signs of musde fatigue, start MV before
respiratory failure occurs
c. Refractory severe hypoxia or apnea
d. Depression of respiratory center {e.g. drug overdose)
3. .Rate of correction of Paco and p_o st hypercapnic alkalosis : In
patients with chronically e~evated PaCO rapid correction of
hypercapnia with MV can lead to sudden, s2ubstantial alkalaemia
and marked rise in pH. This leads to post hypercapnic alkalosis,
which can be detrimental. To avoid post hypercapnic alkalosis
correction of hypercapnta should be done gradually.
CH. 7 Diagnosis and Treatment of Acid Base Disorders 229
4. Target PaC0 2 on MV: In patients with chronic respiratory acidosis

on MV, the target PaC0 2 is usually the patient's prior stable leve_l,
not a "normal" PaC0 2 of 40 mm of Hg. While in acute respiratory
acidosis, the target PaC0 should be the normal level.
2
o. Alkali Therapy
Avoid alkali therapy except in patients with associated metabolic
acidosis, severe acidaemia (pH < 7.15) or severe bronchospasm (as
alkali therapy restores the responsiveness of the bronchial musculature .
to beta-adrenergic agonists).
RESPIRATORY ALKALOSIS
Respiratory alkalosis occurs when hyperventilation reduces the PaC0 2
(hypocapnia) and leads to increased pH. It occurs when respiratory
disturbance causes excessive pulmonary C0 2 excretion (hyperventil~tion)
that exceeds metabolic production of C02 by the tissues.
Diagnosis
Low PaCO ( < 35mm of Hg ), High - alkaline pH ( > 7.45 ) and
compensat5ry low HC0 3 . Low PaC0 2 and low HC0 3 occurs even in
metabolic acidosis, but pH will be acidic (< 7.35).
Calculation of compensation
Acute : Every 1o mm of Hg fall in PaC02 causes 2 mEq/L fall in HC03 and
0.1 rise in pH
Chronic : Every 1O mm of Hg fall in PaC02 causes 5 mEq/L fall in HC0 3 and
0.03 rise in pH
The serum bicarbonate usually dose not fall below 15 mEq/L, unless a
concomitant metabolic acidosis is present.
Etiology
Respiratory alkalosis is the most frequently encountered acid base
disorder, since it occurs in normal pregnancy and high altitude residence.
Causes of respiratory alkalosis are variable. It can occur due to benign
causes (e.g. anxiety or pain induced hyperventilation), iatrogenic causes
(e.g. excessive mechanical ventilatory support) or may be due to an
underlying serious illness (e.g. sepsis, hepatic failure or brain tumor).
Important causes of respiratory alkalosis are summarized in Table No. 7.1o.

Table No. 7.1 o: Causes of respir.atory alkalosis
1. Hypoxemia .. . . . .
a Pulmonary disease : Pneumonia, interst1t1al f1bros1s , embolt and oedema
b. CHF, hypotension or severe anaemia
c. High altitude residence
2. Pulmonary diseases
. 3. Direct stimulation of the medullary respiratory center
a Psychogenic or voluntary hyperventilation , pain , pregnancy
b Hepatic failure , gram-negative septicemia
c. Salicylate intoxication
d. Rapid correction of metabolic acidosis
e. Neurological disorders , accidents, pontine tumour
Clinical features
The clinical features of respiratory alkalosis vary with severity, rate of
onset and underlying disorders. It may be the only clue of underlying
sepsis, hepatic failure etc. and carrie~ a bad prognostic sign in critically
ill patients. The mortality increases in direct proportion to the severity of
hypocapnia. PaC0 2 below 20-25 mm of Hg constitutes is a grave prognostic
sign.
Common features are light headache, tingling of the extremities, circumoral
anaesthesia, cardiac arrhythmias and infrequently tetany or seizures.
Headache, shortness of breath and chest wall tightness or pain occurs
with psychogenic hyperventilation.
Treatment of respiratory alkalosis
1. Vigorous treatment. of the underlying cause.
I
2. Mild alkalosis with few symptoms needs no direct treatment.

3. As hypoxemia is the common cause of hyperventilation, 0 2
supplementation is essential along with etiological diagnosis and
treatment.
4. In absence of hypoxemia, hyperventilation needs reassurance and
rebreathing in a paper bag.
s. Pretreatment with acetazolamide minimizes symptoms due to
hyperventilation at high altitude.
FLUID THERAPY IN CHI LDREN
EAsoNS FOR SPECIAL

SUBSEQUENT FLUID
A coNSID ERATlO s 231 THERAPY
INDICATIONS OF l.V. FLUID 244
Aim s
THER APY 233 244
Rate of infusio n 245
MAI NTENANCE FLUID A D Selection of I .V. fluid
ELECTROLYTE 245
lSOTON lC DEHYDRATION 246
REOUIREME TS 233 HYPOTONIC DEHYDRATION 248
Calculations 233 HYPERTONIC DEHYDRATION 250
Modifying factors 234 ORAL REHYDRATION THERAPY 252
Ideal maintenance fluid 235 Introduction and a dva ntag ~ s 253
Mainte nance fluid Pharmacological basis 254
for neonates 237 Composition of ORS 256
ASSESSMENT O F Standard WHO ORS 257
DEHYDRATI ON 237 Low Sodium ORS 258
TYPES OF DEHYDRATION 238 Rice based ORS 258
1.V. FLUID TH ERAPY 2l0 Low Osmol arity WHO ORS 259
INITIAL TREATMENT 2 0 Admi nistration of ORS 260
Importance and g\Jidelines 2 0 Monitori ng of ORS
Selection of l. V. ftuid s 2 the rapy 261
Rate of infusion 2 4
Fluid th erapy ln children needs better understanding and more careful

planning as co mpared to dults because in children fluid requirement is
higher and th ey are more prone to dehydration.
0. Why ·ftuid th erapy in children needs special consideration ?

A. Fluid balance is more delicately balanced in young infants and children
and needs special consideration for the following reasons :
1. Greater insensible losses
· · · ared to
Higher basal metabolic rate and larger surface area comp .h
total body weight in young infants favour greater fluid loss wit
higher risk of dehydration.
2. Greater urinary loss . d
. ·s less as compare
ln neonates renal ability to concentrate unne 1 tes are more
to adults (600 Vs 1,200 mOsm/~g), so n~o~~d deficit state.
vulnerable to fluid loss in form of urme, even m
23 2 CH . 8 Fluid Th era py in Child re n
3. Thirst mechanism
It is tile most e'ffective way to correct' negative fluid balance in
older cll il dren and ad ults. Youn g infants are unable to express
their need fo r fluid even during fluid loss, so they are more prone
to dehydration.
4. Larger turnover
Larger turnover in infants needs due consideration. An infant
exchanges about 1/2 of tot~I ECF volume per day as compared
to 1/7 in an adult.
5. Fluid overload
As compared to daily requirement of I. V. fluids (100 ml/kg)
circulatory volume is relatively small (80 ml/kg), so fluid overload
can occur easily in young childre~.
Example· :
For 5 Kg. Child :
Fluid need = 500 ml, · Circulatory Volume = 400 ml
For 50 Kg. Adult :
Fluid need =2,000 ml, Circulatory Volume = 4,000 ml
6. Smalle·r total ·volume of fluid required
As total volume of fluid required in children is smaller (requirement
in m·I) compared :to adults (requirement in litres), meticulous
calculation is required to avoid.under or over hydration, especially
in preterm babies, sick neonates and children with renal failure.
7. Volume and distribution of body water
Neonates have relatively larger water content. The water content is
.around 80°/o of body weight as compared to 60°/o in adolescents
and adults. ECF volume is half of ICF volume in adults. In contrast
ECF and ICF volume are almost equal in neonates.
Q. How to infuse I. V. fluid safely ?

A.. To avoid overload it is important to give l.V. fluids slowly and continuously
over the desired ti.me . .To .prevent accidental fluid overload a special
CH. 8 : Fluid Therapy in Children 233
r. v. set incorporating an additional chamber can be used. Desired volume

is charged in such calibrated chamber and is given at a required rate.
Here accidental fast infusion will allow only small volume infusion and
hence protects against fluid overload. Use of microdrip set will ~llow
more accur~te fluid infusion. In micro.drip l.V. set 1 ml= 60 drops. Special
syringes which are operated electronically are available, which can infuse
fluid at the rate of even 0.5 ml/minute.
a. When to give I. V. fluid ?
A. Oral fluid rep lacement is always a safe and preferred mode. The
indications of I. V. fluid therapy are shock, severe dehydration,
uncontrolled vomiting or diarrhoea, inability to drink, paralytic ileus-
abdominal distension, impaired sensorium and serious complications.
Q. What are the aims of parenteral fluid therapy ?
A. Aims of parenteral fluid therapy are :
1. To correct fluid and electrolyte deficit
2. To provide maintenance requirements
3. To replace ongoing losses
Maintenance fluid and.electrolyte requirements
Q. How do you calculate maintenance fluid and electrolyte requirements

of the child ?
A Marntenance
. requrre ·
. ments are calculated on the basis of caloric
requirements, bo dY wer'ght and surface area. ·
a. From caloric requirements : d I t ofyte
This calculation
.
is
requirements are dire Y?a~~ ~lated
d n the fact that fluid an e ec r
to metabolic rate and caloric
intake as shown in Table No. 8.1.
. of ca Ioric expenditure
iabfe No. 8.1 : Calculation
Body weight Caloric expenditure per day
Upto 10 kg 100 Kcal/kg 1o k
11-20 kg I 50 Kcal for each kg above g
1 OOOK
1500 ca 20 Kcal for each kg above 20 kg
Kcal++
Above 20 kg
234 CH. 8 : Fluid Therapy in Children
For every 100 Kcal metabolised, 100 ml of water, 2.5 mEq sodium
and 2 mEq potassium are recommended. So each litre of
maintenance solution -should contain 25 mEq of Na and 20
mEq of K+.
b. ·From body weight:
Maintenance requirements calculated as per the body weight is
easy to remember and convenient to calculate.
1. Water requirement :
For 1st 1O kg body weight = 100 ml/kg/day
For 11-20 kg body weight = 1000 ml + 50 ml/kg/day
Above 20 kg body weight = 1.500 ml + 20 ml/kg/day
Example : A 25-kg child will require
10 kg. x 100 + next 10 kg x 50 + rest 5 kg x20
= 1,000 + 500 + 100
= 1,600 ml of total ·fluid
2. Sodium:
3 mEq/kg or 2-4 m'Eq/100 nil of fluid (as 0.45°/o, 0.33% or
0.2°/o NaCl, which contains 7.5 mEq , 5 mEq and or 2.5 mEq
sodium/100 ml of fluid respectively) .
. 3. .Potassium :
2 mEq/kg or 2-4 mEq/100 ml of fluid.
4. Calorie requirement :
100 Kcal for first 1O kg.
50 Kcal for next 1O kg.
20 Kcal for remaining weight (above 20 kg.)
Q. In which conditions are the normal requirements modified ?

A. Modification in normal requirements are :
Decreased requirement : With oligo-anuria, meningitis due to
excessive ADH release and high humidity atmosphere.
lncre.ase~ requirement: With. G.I. losses, heat stress, hyperventilation,

loss in third space, adrenal insufficiency and abnormal renal loss.
Q. Whicl1 1.V. fluid is an ideal maintenance fluid for children and why?
A. lsolyte-P is an ideal 1.V. fluid for younger children because .
;. It provides uniform administration of fluid and electrolytes all
throughout the period. ·
\
2. It's electrolyte conce,ntration (Na 25 mEq/L and K+ 20 mEq/L)

matches with the ideal maintenance requirements.
Let us calculate maintenance requirement of fluid and electrolytes
for 1O kg. child as a sample. For 10 kg. child requirement of water
is 100 x 10 kg. = 1,000 ml, sodium requirement is 2.5 mEq/100
ml x 10 = 25 mEq and potassium requirement is 2.0 mEq/100 ml
x 10 = 20 mEq - . .
So 1O kg child needs 1,000 ml water+ 25 mEq sodium + 20 mEq
potassiu ·m, which is exactly identical to the elecfrolyte
concentration of lsolyte-P.
3. It contains 28 mEq/L of acetate which will get converted into
bicarbonate by liver and will co'rrect' associated metabolic
acidosis.
4. It will also supply magnesium and phosphate.
5. It contains ·so g/L of glucose which provides caloric requirement
of the child . .
As lsolyte-P provides calories arong with total requirements of
fluid and electrolytes, it is an ideal maintenance I. V. fluid.
Q. Why lsolyte':'P is ~ot an ideal ~a-if'.ltenance I. V. fluid tor aider children?

A. In children as weight increases, water requirement reduces rapidly
(100 ml/kg for 1st 1O kg reduces to 50 ml/kg for next 1O kg and only 20
ml/kg subsquently). However, sodium requirement rem?ins almost
static (2.5-3 mEq/kg). So. children with g_reater weight will need I. V.
fluid With greater sodium _ concen~ration as ~hown in the table.
236 CH. 8 Fluid Therapy in Children
first 1O kg 10-20 kg 20-30 kg For total 30 kQ'

Requirements
Water (ml) 1,000 500 200 1,700 -
. 25 25 25 75
Na (mEq)
Na Cone. (mEq/L) 25 50 125 44
This example suggests that a 30 kg child will need total 1_ ,700 ml fluid ,
-
the Na concentration of which should be 44 m Eq/L. As lsolyte-P contains
only 25 mEq/L sodium , sodium concentration is lower than required for
children with weight greater than 15-20 kg and may lead to hyponatremia.
Therefore lsolyte-P is not an ideal maintenance I. V. fluid for older children.
Conclusions :
1. For a child upto 12-13 kg. weight lsolyte-P is ideal.
2. ~or a child with 15-20 kg. or more weight needs lsolyte-P +
additional Na supplementation or I. V. fluid with higher Na
concentration.
Q. What problems can occur if maintenance ·fluid therapy is provided
exclusively with below mentioned I. V. fluids ?
A. a. 5°/o-dextrose : As it provides only water and glucose but no
electrolytes, child is at risk of developing hyponatremia and
hypokalemia.
b. Isotonic saline or DNS : Normal requirement of sodium in children
is roughly 30 to 50 mEq/L (30 mEq/L in young children with lesser
weight i.e. 1O kg, while 45 mEq/L in older children with greater
weight i.e. 30 kg), sodium concentration of isotonic saline or DNS
is 154 mEq/L (which is 3 to 5 times greater than normal requirement).
So maintenance fluid therapy exclusively with it will lead to
hypernatremia. Moreover it does not contain any potassium,
therefore hypokalemia can occur. So it is not a preferred fluid for
maintenance fluid therapy in children.
c.- Ringer's lactate : Ringer's lactate contains 130 mEq/L of sodium,
4 mEq of potassium and does not contain any glucose. As sodiU
concentration of RL is 3-4 times greater than the requirement
children, ·so RL as maintenance fluid will lead to hypernatre
Moreover potassium concentration is very Jess (4 mEq/L Vs t
required concentration of 20 mEq/L), so the child will be prone to

develop hypokalemia. As RL is free of dextrose chi)d is prone to
develop hypoglycemia and starvation ketosis. So RL is not a
suitable agent for maintenance fluid therapy in children.
a. Which maintenance fluid should be given to a ful\ term neonate ?

How much?
A. 10°/o dextrose with calcium gluconate (1-2 ml/kg/dose 6 houriy or
100-200 mg for every 100 ml) is the fluid of choice. (10°/o calcium
gluconate, 10 ml ampoule contain 4 mEq = 224 mg calcium) The
amount of 10°/o dextrose administered is 60-80 ml/kg on the first day
with 10°/o increment everyday till it reaches to 160-180 m\/kg/day.
Infant receiving phototherapy requires 25°/o increment in daily fluid
requirement. No electrolytes are required for the first two days. Later
on Na 3 mEq/kg/day and potassium 2 mEq/kg/day are added. So at
this stage 1 /5 (0.2°/o) isotonic saline with added potassium chloride
or lsolyte-P are suitable 1.V. fluids.
Assessment of dehydration
Q. What should be asked, looked and felt to evaluate dehydration ?

A. Ask Look Feel
Stool detail Sunken eyes Anterior fontanelle
Vomiting Alertness Skin turgor
Thirst Dry mouth & tongue Pulse, Heart rat.e
Urine output Breathlessness Temperature ·
Q. How to assess severity of dehydration ?

A. Clinical features of dehydration.
Mild dehydration -
Thirst, mild oliguria and no detectable signs. .. . - • /' .
. .
Moderate dehydration .
. .. . l"ghtly sunken 'eyes
More thirst, oliguria, restlessness, weak~es.s, _s 1 . ·.
and anterior fontanelle, tachycardia.
238 CH. 8 Fluid Therapy In Children
Severe dehydration
Marked tachycardia, low BP, greatly sunken eyeballs and anterior
fontanell e, loss of ski~ turgor, severe oliguria or anuria, restlessness
and apatf1y. ,
·In addition pallor, cold clammy skin, weak or even nonpalpable radial
pulse, circulatory collapse, drowsiness, coma, hyperpyrexia and
cyanosis may occur.
Q. Which are the misleading signs in assessment of dehydration in children?
A. Misleading physical signs in dehydration are :
1. Obese infants may be markedly dehydrated with no signs except
tachycardia.
2. The degree of dehydration is often over-estimated in marasmic
infants.
3. In hypernatremic dehydration, ·the skin and circulatory changes
may be deceptively inapparent with predominant neurological
signs.
4. A raised blood urea may be an indicator of dehydration more
severe than it appears on physical signs or may give a clue to an
underlying renal disease.
Q. What is the appro'.ximate fluid deficit in dehydration ?
A Table No: 8.2 : Fluid deficit in dehydration
Severity of Weight loss in Approximate
Dehydration young infant older children fluid deficit
Mild 5% 3% 40-50 ml/kg
Moderate 5-10% 6% 60-90 ml/kg
Severe 10-15% 9% 100-11 O ml/kg
> 15o/o deficit is rarely compatible with life.

Types of dehydration
0. What are the different types of dehydration ?
·Why and how to differentiate it ?
A. Depending upon the proportion of salt and water loss, dehydration can
l,
CH. 8 Fluid Therapy in Children 239
Table No,, 8.3 : Types of Dehydration

Dehydration rsonatremic Hyponatremic Hypernatremic
Incidence 70% 20% :10%
S.Na. (mEq/L) 130-150 < 130 > 150
Types of Proportionate Loss of Na Loss of water
loss water & Na in excess in excess
loss of water of Na
ECFvolume Moderately Severely Decreased
decreased decreased
ICFvolume Maintained Normal or Decreased
increased
Common Diarrhoea, Diarrhoea, Large salt or
etiology vomiting , vomiting or solute intake,
Fasting excessive inadequate
perspiration water intake
with hypotonic
fluid intake
H/O thirst Normal Normal Excessive

Skin Cold Cold Cold or hot
temperature
Skin turgor Poor Very poor Fair
Skin feel Dry Clammy Doughy

Mucous Dry Slightly moist Parched
membrane
CNs status · Lethargic Drowsy/coma Hyper-irritability

Pulse Moderately
Rapid, . Very rapid-
weak thready rapid
BP Moderately low
Low Very low
Initial lsolyte-P or
0.9% NaCl or 0.9% NaCl or
Selection of D-5%, Isotonic
Ringer's hypertonic
l.V. flu.id saline if shock
lactate NaCl
l
be hyponatremic, isonatremic or hypernatremic. As clinical presentations

and amount and type of fluid to be replaced varies iri different types of
dehydration it is important to differentiate it. Table No. 8.3 provides
differential diagnosis in dehydration.
1.V. f luid t herapy
Q. How to plan out fluid therapy in dehydration ?

A. Parente ral rehydration therapy can be discussed in 3 stages.
1. Init ial t reatment to tide over crisis and stabilize patient
2. Subsequent therapy is planned to replace deficits
3. Final stage is to switch over to oral therapy with an aim to
establish normal nutritio
Initial Treatment
Q. What are the goals of initial fluid therapy ?

A. Aims of initial fluid therapy are :
1. To treat shock
2. To achieve haemodynamic stability
3. To improve tissue perfusion
Q. How to plan out initial fluid therapy in dehydration ?

A. Guidelines for initial fluid therapy are :
1. In shock stage, initial treatment remains the same in iso/
hypo/hypernatremic dehydration. Subsequent treatment differs
as per the clinical and biochemic~I status.
2. If shock is present du(ing first hour 20-30 ml/kg isotonic saline
· or Ringer's lactate is infused. Same dose is repeated if
nec~ssary till pulse is well palpated.
3. After one hour if shock does not improve 1O ml/kg, 5°/0
albu~in or plasma may be given. As both remain entirely in
int.r avascular comp.a rtment, even lesser volume improves
circulation better.
J
4. If patient is asymptomatic and/or dehydration is isotonic or

hyponatremic, one half of the calculated fluid for 24 hours
should be administered in the first 8 hours. The remaining half
should be administered in the remaining 16 hours.
Total fluid required= fluid deficfr +maintenance fluid.
5. Ongoing losses should be assessed frequently and should
be added to replacement of deficit and maintenance fluid and
electrolytes. In febrile child there is additional 12°/o need of
maintenance fluid which should also be calculated and added.
6. Establishment of normal urine output (2 ml/kg/hour or 50
ml/kg/24 hours) suggests adequate tissue perfusion and
reflects adequate fluid replacement. An urine output less than
0.5 ml/kg/hour suggest pathological oliguria and requires
assessment to rule out inadequate hydration, development
of renal failure or other causes.
7. Along with fluid therapy , specific treatment for the underlying
etiology should also be started as early as possible.
Selection of fluid
To correct shock and to increase tissue perfusion the fluid which
rapidly expands volume of extracellular fluid, especially plasma,
will be ·most preferred (see Chapter No. 4). Till u.rine output is
established isotonic saline is the fluid of choice. On failure, 5°/o
albumin may be required to treat shock.
In patient with shock, once urine output is established Ringer's
lactate is the preferred I. V. fluid because : ·
1. It's composition is most physiological so avoids fluid
electrolyte distur~ances even with rapid infusion.
2. · Lactate in RL gets converted .into ·bicarbonate so corrects
associated metabolic acidosis, especially in cases of
diar~hoea.
However, AL is av~ided in ~evere shock because impaired

hepatic conversion of lactate can lead to lactic acidosis, rather
than correction of acidosis. RL is also avoided in vomiting
induced .dehydration where associated metabolic alkalosis gets

aggravated by·conversion of lactate to bicarbonate.
Q. Should we use lsolyt~-P in initial treatment ?,

A. No. Though lsolyte-P is freely available and the most widely
used fluid in pediatric practice, lsolyte-P should never be
used in t he initial treatment of shock, as it has definitive
disadvantages.
1. Sodium content of lsolyte-P is just 1/6 of Isotonic saline
(25 mEq/L Vs 154 mEq/L of Na in isotonic _saline) hence
it's ability to expand the compromised intravascular
~olume and shock will be very poor.
2. Due to low sodium concentration, lsolyte-P can lead to

hyponatremia and may worsen the general condition.
3. lsolyte-P being rich in potassium (20 mEq/L) increases
risk of hyperkalemia specially when renal functions are
compromised. So use of lsolyte-P can be dangerous with
unknown renal status or till the urine output is
established.
Q. Can we use 5o/o-dextrose in the initial phase of shock ?

A. No. 5%-dextrose should not be used to treat the initial phase of
shock because ·
1. 1 litre of D-5o/o increases just 83 ml of intravascular
volume (which decides blood pressure), so it is useless
to select 'this fluid in the initial treatment.
2. ·It does not contain any electrolytes, especially sodium,
so it will lead to gross electrolyte disturbances. If ?-5°!0
is selected as a sole agent for fluid replacement, it can
be life threatening.
3. Rapid infusion of So/a-dextrose (> 0.5 gms/kg/hr) w!ll
cause osmotic diuresis, which is undesirable and 15
detrimental.
CH . 8 : Fluid T erapy in C ildren _4
0,.. Why dextrose contajning fluid should be avoided in the initial

treatment of shock ?
A. rn severe dehydration large volume of fluid at rapid rate is

required. Rapid infusion of dextrose con•aining fluids i.e. lsolyte-
P , 5o/o-dextrose etc.) can cause hyperglycemia and subsequent
osmotic diuresis vhich leads to fluid loss and impairs correction
of dehydra ·ion. Ho vever dextrose In water can be given I. V. at
the rate of 0.5 gm/Kg body\ eigh r without causing glycosuria.
Exceptions o this rul e are infants and sic, and malnourished
children .1ith less glucose storage. As they are more prone
to de 1elop h .poglycemia even the iini t.ial fluid should contain
glucose.
Q. Why Ri · ge 's lac at and 'iso onic saline are preferred fluids
for initi f ti r ·py o d h dr ion induced shock ?
A. Because O'i f sodiur 1 concen tration RL i 30 mEq/L and
1
1
I e e Uuids :have maximum ability

mongst an c ·s , o· · o e, pand intravascular volume and
o to t ; e l ·oc · . .r o eo er, both fluids are gl,ucose free so
there i . no tit ot
1 . o i i Jr sis., unlike dextrose containing
fluids on rap:·d in f . ion , nd, ther,e fore are pre.ferred ·f or the
1
initial treatm:ent. of shoe .

a. How to select appropria ·e I V. fluids in treatment of severe
dehydration due to diarrhoea ?
A. Sel·e ction of LV. nu.ids are as folio 1s :
1 . Preferr ed so'luUon :
1
Ringer's lactate
2. Acceptable solutions :
Isotonic saline, 0.45o/o NaCl (half strength saline)
3. Unacceptable solutions:
So/o-dextrose, lsolyte-P
244 CH. 8 · : Fluid Therapy in Children
a. In severe .dehydration how much 1.V. fluid should be given

and how rapidly ?
A. _ The fluid deficit in severe dehydration is about 1 Oo/o of body
weight i.e. 100 ml/kg , which should be infused as follows :
Infant s
rnfan t sh ould be given I. V. fl _
uid at the rate of 30 ml/kg in first
hour, followed by 70 ml/ kg in the next 5 hours, thus providing
a total of 100 ml/kg in 6 hours.
Older c hild ren
Older children should be given l.V. fluid at the rate of 30 ml/
kg within first 30 minutes , followed by 70 ml/kg in the next
2.5 hours, thus providing a total of 100 ml/kg in 3 hours.
After the first 30 ml/kg l.V. infusion, a strong radial pulse
should be easily felt. If it is still very weak and rapid, a second
infusion of 30 ml/kg should be given at the same rate.
Q. After initial treatment with Ringer's lactate, how is the

subsequent fluid therapy planned in patient with diarrhoea ?
~· After initial stabilisation with AL, most of the children
with good oral acceptance are treated with oral
rehydration solution (ORS). l.V. fluids are continued in
exceptional cases of nonacceptance of ORS. Type of I. V. fluid
selected subsequently depends on the type of dehydration
and it's magnitude. In absence of deficit lsolyte-P is preferred.
Subsequent treatment
Aim of subsequent therapy is to :
1. f1eplace fluid and electrolyte deficit :
2. Correct ongoing losses
·.
3. Provide maintenance requirement ·-
Q. How rapidly is the replacement of fluid and electrolytes desirable

for the subsequent treatment?
A. Fluid and . sodium defici_t is corrected slowly in the first 24 to 48

hours, w hile ~ota~sium deficit in 3 to 4 days. ~sually potassium
sup pl e~entat1on ts started after first 24 hours. However, early
potassium replacement is necessary with proven hypokalerriia
o~ when severe hypokalemia is expected as in severe vomiting
with hypochloremic alkalosis, prolonged diarrhoea or diabetic
ketoacidosis. Sodium bicarbonate should be given if serum
bicarbonate is below 15 mEq/L. Amount of sodabicarb req~ired
(in mEq/L) == 0.4 x body weight (kg) x (desired HCO - measured
3
HCO)
Q. How to select I. V. fluids for subsequent treatment ?

A. The fluid selected is on the basis of underlying etiology and the
sodium status of the child. Ringer's lactate is preferred in patient
with diarrhoea induced dehydration while isotonic saline is the
suitable initial fluid to treat vomiting induced dehydration.
On the basis of sodium status of a child fluid deficit is classified
as lsonatremic, Hyponatremic or Hypernatremic dehydration. Table
No. 8.4 provides guidelines about amount of fluid and N~ deficit,
which enables us to select the right fluid for replacement. Clinically,
patients with hyponatremic dehydration are haen:'odynamically
most unstable, while those with hypernatremic dehydration are
least unstable.
After proper calculation, sodium concentration in th.e fluid to be
infused is determined and accordingly fluid is selected. lmpro~er
selection of fluid may cause either hypernatremia or hypona~remia.
If NaHCO .. is given to treat acidosis, sodium replaced with _the
same sho~ld be considered in the calculation. 100 ml of. · ~
7 5
NaHCO contains 90 mEq of sodium. Sodium concentrfationdo

3 . N0 a 5 I rea y-
the available I. V.. fluids is mentioned. m Table . · . · · f different
made fluid is not suitable or available, proper combination °
suitable I. V. fluids can match the need.
' ..
Table No. 8.4 : Deficit in moderately severe dehydration
Type of Range Water Sodium Potassium Chloride

Dehydration of sodium ml/kg mEq/kg mEq/kg mEq/kg
Isotonic 130-145 100-120 8-10 8-10 8-10
Hypotonic < 125 100-120 10-12 8-10 10-12
Hypertonic > 150 100-120 . 2-4 0-4 4*
* indicates excess chloride at beginning of therapy.
Table No. 8.5 : Sodium concentration (mEq/L) of l.V. fluids
Type of 0.9°/o Ringer1s 0.45°/o 0.33°/o lsolyte 25ml

Fluid NaCl lactate NaCl NaCl p 7.5°/o
NaHC0 1
Na Con. 154 130 77 57 25 22.5/
(mEq/L) · Amp.
Treatment plan as per the type of dehydration is discussed belo~.

t Isotonic or lsonatremic dehydration
2. Hypotonic or Hyponatremic dehydration
3. Hyp~rtonic or Hyp~rnatremic dehydration
ISOTONIC OR ISONATREMIC DEHYDRATION

(Serum sodium 130-145 mEq/L)
This is the commonest type of dehydration (70°/o), with balanced loss of
sodium and water. Most of the infants with diarrhoea, who ar~ ~reast-fed
(intermedi~te solute l~ad) are. likely to have isotonic dehydration.
Therapy is planned in ·such a way that only two third of the approximate
losses ·of sodium and water are replaced during the first 24 hours of
treatment. The most commonly used initial .fluid during shock is isotonic
0
saline or Ringer's lactate and for subsequent therapy 0.45°/0 or 0.33°!
NaCl with glucose is preferred. But water requirement relative to the solute
is higher in infants as compared to that in older children. oue to this reason
fluids lower in sodium content are usually administered to infants.
o. In a given-child how to calculate the need of fluid volume and sodium,

and how the selected fluid is to be infused ?
A. For a 10 kg child with moderate degree isotonic dehydration we' can
calculate as follows : !
1. Volume deficit in moderate dehydration is 1Oo/o = 100 ml/kg

Volu me deficit = 10 kg x 100 ml/kg = 1 000 ml
70°10 of deficit = 700 ml
2. Maintenance volume = 100 ml/kg x 1O kg = 1 000 ml
So total fluid to be replaced = 700 + 1,000 = 1 700 ml
3. Sodium deficit= 10 mEq/kg x 10 kg = 100 mEq
70°10 of deficit = 70 mEq Na
4. Maintenance sodium = 3mEq/kg x 1O kg= 30 mEq
So total sodium need =70 30 = 100 mEq
So child needs 1,700 ml I. V. fluid containing 100 mEq Na.
These needs can be provided by selecting proper I. V. ·fluids
considering its Na concentration (calculation based on Table No.
8.5) as follows
a 1,000 ml 0.45o/o N Cl + 700 ml lsolyte-P
( 77 + 18 = 95 mEq Na )
h 500 ml RL + 1,200 ml lsolyte-P (65 + 30 =95 mEq Na)
c. 700 ml 0.45°/o NaCl + 1,000 ml 0.33°/o NaCl (53+51 = 104
mEq Na)
Additional supplementation should be made to correct ongoing losses,
to correct potassium deficit (after 24 hours or once the child starts
voiding) and bicarbonate supplementation for treatment of acidosis if
needed.
Remarks : Never use lsolyte-P (Na-25 mEq/L) or 5%-~extrose as
initial fluid . to correct isotonic dehydratio~ as it w!ll
lead ~~
hyponat.remia. _So avoid hypotonic fl':1ids induced iatrogen
hyponatremia.-
HYPOTONIC OR HYPONATREMIC DEHYDRATION
It occurs in 20°/o_of dehydration with serum sodium less than 130 mEq/L. In
this con dition relatively greater loss of sodium occurs than water. Fluid loss
comes mai nl y from ECF (lntravascular + Interstitial) compartment rather
than IC F. Due to severe ECF depletion patient is haemodynamically more
unstab le with more chan ces of circulatory collapse.
Patient also develops hypotonic dehydration when combined sodium and
water loss is replaced with low solute-hypotonic fluids like plain water,
frui t juice, 5o/o-d ext rose or lsolyte-P. Excessive loss of sodium ih stool is
especi ally seen in cholera and bacillary dysentery. Sodium concentration
of choleric stool is 90-140 mEq/L. Hyponatremic dehydration also occurs
if there is excessive perspiration or excessive diuresis with abnormally
high renal sodium loss. Most widely used fluid in treatment is isotonic
saline or DNS , Ringer's lactate or 0. 45°/o NaCl with glucose, with necessary
addition of NaHC0 3 with potassium .
Practical Guidelines
(Also see Hyponatremia Chapter No . 3)
1. Avoid rapid correction of hyponatremia.
2. Hypertonic sa line used judiciously only in severe hyponatremia (s.erum
Na < 120 rnEq/L) , water intoxication or convulsions.
3. High risk of volume over load and CHF with hypertonic saline infusion.
4. Avoid hypotonic solutions, as there is a very ·high risk of inducing
symptomatic hyponatremia. .
Q. How to calculate deficit and select fluid infusion in hyponatremic
dehydration ? · ·c
. . · ·1ar to isonatrem1
A. Treatment of hypotonic dehydration 1s s1m1
dehydration. But as these Patierits are haemodynamically dmor~
0 0
unstable rapid corrections of losses are fequired and, therefore, . ?0
require ;eduction in the calculated deficit. (Unlike 30% re.duction ~s
deficit in isotoniC dehydration). Moreover extra loss of sodium, neke d
to be calculated and added a fact which is often forgotten or over _oo e.d
Extra sodium loss is corr~cted over 3-4 days, which prevents. rapi
correction of hyponatremia and circulatory overload.
sample calculation: For 10 kg child with moderate (10°/o) hyponatremic

dehydration with serum sodium 120 mEq/L,
A. Volume requirement= Deficit + Maintenance fluid volume.
B. Sodium requirement= (1) Deficit+ (2) Maintenance Na need + (3)
Extra sodium deficit (correct only 1/3 deficit per day)
A. Volume requirement:
1. Volume deficit= 10°/o x 1Okg=1,000 ml
2. Volume maintenance= 100 ml/kg x 1o kg= 1,000 ml
Therefore Total required volume= 1,000+1,000 = 2,000 ml
B. Sodium requirement:
1. Sodium deficit= 12 mEq/kg x 1okg=120 mEq
2. Maintenance sodium = 3 mEq/kg x 1O kg = 30 mEq
3. Extra sodium deficit =
(135-current sodium) x 0.5* x body weight (kg)
= (135-120) x 5/10 x 10 = 15 x 5 = 75 mEq
1/3 of extra sodium deficit = 25 mEq
. .
* (because of dehydration 0.5 and not 0.6 as the usual factor
for Na+ space has been used)
Therefore total sodium requirement =120 mEq + 30 mEq + 25 mEq
= 175 mEq
So total need : Water= 2,000 ml and Sodium = 175 mEq
Possible combinations of fluids that can provide these needs are:
1. 1,000 ml 0.9°/o saline/ONS + 1,000 ml lsolyte-P
(154 + 25 = 170 mEq Na)
33010
2. 1,000 ml Ringer's lactate + 1,000 ml 0 · NaCl
(130 + 51 = 181 mEq Na)
3. 2,000 ml 0.45°/o NaCl+ 25 ml 7.5°/0 NaHC03

(154 ~ 22 = 176 mEq Na)
250 CH. a : Fluid Therapy in Children
During subsequent days 0.45°/o or 0.33°/o NaCl with dextrose is

sufficient to meet with the requirement, provided there is no further
l.oss.
HYPERTONIC OR HYPERNATREMIC DEHYDRATION
·(also see Hypernatremia Chapter No. 3)
1. It occurs in 1Oo/o of diarrhoea dehydration with serum _Na > 159 mEq/L.
2. This type of dehydration is dangerous with higher morbidity due to
the risk of brain damage from hyperosmolality or its treatment.
3. Common etiologies are excess salt or solute intake, poor water intake
and diabetes insipidus.
4. Haemodynamically more stable, characterized by intense thirst, shrill
cry or mewing sound, muscle weakness and tachycardia. Rapid
correction of hypernatremia can cause neurological symptoms like
irritability, confusion, twitching · and convulsions.
5. Large water and potassium deficit, slight deficit of sodium with low
serum calcium.
Treatment:
1. Hypernatremic dehydration is frequently iatrogenic .so ·prevention is
always better. Use of WHO formula of ORS containing Na 90 mEq/L
should be avoided in infants.
2. Do not. correct hypernatremia and water deficit rapidly. Don't allow
l.V. infusions to run rapidly. It can cause cerebral oedema and
convulsions. Gradual correction over a period of 48 hours or more is
safer. Avoid. 5°/o-dextrose infusion, which can lower serum sodium
rapidly.
. - .
3. Usually 60-75 ml/kg/24 hours of 5°/o dextrose, containing 25 mEq/L of

sodium (i.e. lsolyte-P) is ·the preferred l.V. fluid.
4. While calculating maintenance fluid requirement, reduce it by 25°/o
due to high ADH generation with greater water r_
e tention by kidney.
5. Few hypernatremic dehydration patients, who present with hypotension
or shock, will require initial resucitation with 1.V. isotonic saline (even
with hypernatremia). However, once volume expansion occurs, it will
be detrimental to provide further l.V. isotonic saline.
CH. 0 FlulcJ· Thorn.rJY In Chlldr n 2~ 1
6. In case of hypernatremia caused by salt poisoning, there shou ld b

sign of over hydration and volume expan sion . Excretion of r Ja should
be enhanced by using a loop diuretic to augm ent urinary r Ja Josses
and by replacing urin~ output with free water.
1. If the serum Na concentration is greater than 180 mEq/L or patient
has renal or cardiac compromise because of the electrolyte imbal ace,
dialysis may be required to correct the abnormalities. In this case,
peritoneal dialysis may be preferable to haemodialysis·, since the
correction occurs relatively slow.
Q. Why exce.ssive l.V. solute ·.supplementation should be avoided during

the treatment of dehydration, especially in infants ?
A. Treatment of dehydration exclusively with isotonic saline or Ringer's
lactate will lead to excess solute load. Because infants cannot
effectively co~ce~trate urine beyond 600 mOsm/kg (as compared
to 1 ,209 m.Osm/kg of adult c~p_acity.), larger volume of water is
re.quired for urin~ry . excretion. of e.xcessive solute. So excess renal
solute locid will cause obligatory. urinary free water loss in this infant
~
and will aggravate or prevent correction of .d~hydration. This may lead

• • ' I
to hypertonic dehydration. .. ' i ·,\

! -;. '
Q. Why· undiluted cow's· milk or skimmed milk should be avoided during

initial treatment of dehydration in infants ? · ~ ·
A. Because of ·greater solute load cow's .milk will cause . free water loss
three times great.er as compared .to human milk, while boiled skimmed
milk leads. to four times · f~ee water loss. Similarly, even oral
supplementation of ~igh Na leads to excess water loss because of
p·oor concentrating capacity in inf~nts. Excess solute loss. induced
free water loss can lead to .hypernatrem.ic ·dehydratio.n and, therefore,
should be avoided. So, for infants ·under six months of age, dilute
milk to half strength (1 :1) to prevent this problem, tili hypernatremia
is· corrected. ·
FLUID THERAPY IN RENAL DISORDERS

a. Why fluid therapy in patient with renal diseases needs special
consideration ?
A. As renal ability to adjust fluid and electrolyte imbalance is re~uced
with renal impairment, ability of children to tolerate changes '~ the
total body water or alteration in the electrolyte balance will be
compromised.
Roughly 2/3 of any daily m·aintenance fluid prescription is to replace
urinary water losses. So in oliguric or anuric child infusion of normal
maintenance fluid can exacerbate or precipitate volume overload and
administration of maintenance electrolyte therapy can lead to serious
electrolyte disturbances. So to avoid these complications fluid and
electrolyte therapy in presence of renal diseases needs special
modifications.
In oliguric patients fluid volume required is roughly 1/3 of the normal
requirement. This fluid volume is to replace insensible losses chiefly
through the sweat and stool which is electrolyte free with negligible
loss of Na and K. Hence electrolyte free fluid is usually selected to
replace insensibf e losses. ·
However precise fluid therapy is planned after considering hydration
statu~, urine output, clinical and biochemical status., and type of
coexisting renal disorder.
ORAL REHYDRATION 'THERAPY (ORT)

Use of Oral Rehydration Therapy (ORT) has changed the outcome.of millions
of children suffering from diarrhoea around the world. ORT is a wonderful
discovery, which has save~ more lives than any other treatment modality in
the last century. Oral rehydration solution (ORS) is a simple, inexpensive
glucose and electrolyte solution promoted by WHO to treat dehydration.
Q What is oral rehydration therapy (ORT)? , .
A. ORT is a method to provide fluid, electrolytes .and calorie
supplementation ORT includes:
1· Oral rehydration solutions (e.g. Standard WHO OAS, Low sodium
ORS, Low osmolarity WHO ORS)
2. Improved/modified ORS (e .g. Rice based ORS, Amino acid and/

or maltodextrin containing ORS, Zinc ORS etc)
3. Home made electrolyte solution: Mixing 40 gram sugar and 4
gram salt in one liter of water
4. Home available solutions i.e. Lemon sarbat, buttermilk with salt
and sugar, coconut water, thin rice kanji, dal water etc
a. What is the difference between ORT and ORS?
A. ORT includes all variety of solutions (including ORS) which are
effective in treatment of rehydration and usually contains salt-sugar
along with water.
Balanced solution of glucose and electrolytes, made as per the
recommendations to treat dehydration are ORS. e.g. Standard WHO -
ORS and low sodium ORS and low osmolarity WHO ORS : ·
Q. Which fluids are not acceptable as o ·RT?
A. Fluids, which are not acceptable as ORT, are:
1. Plain water
2. Glucose. water without salt or sweetened drinks
3. Salt water. without sugar or dextrose
4. Fluids consume(f in ·very small qua~tities e.g: tea
-~ - ~" '
Q. Why sweetened drinks should be avoided . as· oral ' fluid therapy for
dehydration?
A. · Sweetened drinks· such as sweet te·as, soft' drinks and commercial
fruit drinks shou'1'd be avoi.d.e d '-bec'a use they la.ck . necessary
electrolytes. Moreover, they are often hyperosmolar owing to a high
concentration of sugar (i.e. contain- more' than 300 mOsm/L). So they
can cause osmoti.c diarrhoe~, worsening dehydration and
hypernatrer:nia.
0. What are the advantages of using ORS? . .
A. ORS is safe,· easily available . everyYJhere, .simple to use and an eff

ective method to co'rrect - dehydration,'\~hich does not require skilled
medical supervision. Hence ORS is . used as the first line of treatment
for rehydration unles.s contraindicated~ qRS is likely tQ be. s~ccessful
in up to 95~/o_ of cases of mild to moderate dehydration. . ·
1 '¢•
25a! C~. 8 Fluid Th erapy in Children
ORS avoids LV. Uuid infusion , which needs a skilled person to

establish a venous Hne especially in inf ants and also avoids the risk
of pulmonary oedema or el·e ctrolyte imbalance which are likely to
occur vith the I. V. fluid therapy.
Q. o , ORT wor,ks?
A Basic principles of oral rehydration therapy (ORT) are as follows:
1. In diarrhoeal state , absorption of ·sodium and water by intestinal
vall is impaired.
2. ORT is based on the observation that glucose (or d~xtrose)
absorption through intestinal wall remains unaffected in infective
diarrhoea due to cholera or viruses.
3. With active absorption of glucose by small intestine, sodium is
carried with it on 1: 1 molar basis by a co-transport coupling
mechanism. Glucose- sodium absorption enhances water
transport across the mucosa of the intestine.
4. It should be noted that gluc~se qoes not co-transport water but
sodium absorption leads relative increased cb'ncentrate of sodium
across the intestinal wall whi~h pulls water.
Q. What are the. WHO criteria for acceptable ORS formulations?
A For optimal absorption the composition , of the rehydration solution is
critical. Criteria for desirable characteristics . . of .. solution after
~
preparation are ..
listed .in Tabl,e No.
.
8.6~ ., .-.
{
. ...
Table No 8.6 : Criteria for acceptable ORS I• : •
. . - '
Substance . Desirable con~entration

Glucose At least equal that of s~diurn but
Should not excee~L111 . mmol/L
Sodium Within the range.·of '60·90 mEq/L
. '
Glucose sodium ratio At least 1 :1 and should' not exceed 2: 1

. :
Potassium Within the ranQe of 15·25 mEq/L

Citrate Within tne ~ange of 8·12. mniol/L
Chloride
T otaf Osmolarity
vyithin the· range Of
.
Within the range of 200-31 o·roosm/L
so-so.mEq/L
.
r
a. Can we use glucose free , salt solution for ORT in patients with
secretory diarrhoea?
A. No. Without glucose, sodium and therefore water also will not get
absorbed by intestine. Hence unabsorbed fluid will remain in the gut,
which will be added to the volume of stool passed by the patient.
Q. Whether simple mixture of salt sugar and water is a complete
formulation in correcting diarrhoeal deficit?
A. No. Solution containing only salt and sugar is incomplete formula as
it does not restore potassium deficit and does n.ot correct metabolic
acidosis.
Diarrhoeal stool contains large amount of potass!um so diarrhoea
can lead to hypokalemia which can cause muscular weakness,
lethargy, anorexia , and abdominal distention. Potassium
supplementation is needed to correct potassium deficit, especially in
a child who suffers repeated attacks of diarrhoea.
As diarrhoeal fluid is rich in bicarbonate it leads to metabolic acidosis
in addition to electrolyte imbalance and fluid loss. Infants are more
prone to metabolic acidosis as their renal function is not fully developed
and they have higher metabolic rate. ORS .contains citrate, which
corrects metabolic acidosis _ by J?roviding bicarbonate.
Q. Is it necessary to check serum electrolytes in patients with diarrhoea
prior to starting ORS?
A. No, it is not usually helpful. Knowing the levels of serum electrolytes
rarely changes the management of children with diarrhoea. Indeed
these values are often misinterpreted leading to inappropriate
treatment. Adequate volume of ORS usually corrects electrolytes
disturbances such as hypokalemia, hyponatremia, and hypernatremia
effectively.
a. Can ORT be given if the child is vomiting? ·
A. Yes. As hypoglycemia can be cause of vomiting, ORS will correct the
same and will help in reducing vomiting.
Q. Can ORT be given in patient with severe dehydration?
A. Yes. ORT can be given before l.V. fluid can be administered, if child is
thirsty and oral intake is possible. However, I. V. fluid is preferred in
severe dehydration for ~apid correctio11 of dehydration.
256 CH . a Flu id Therapy in Children
Q. What are the causes of failure of ORT?

A. Causes of failure of ORT to correct dehydration are :
1. Abdominal distension and paralytic ileus , where ORS is
contraindicated.
2. Inability to drink due to stomatitis , drowsiness , convulsion ,
stuporous or comatose child.
3. Severe continuous vomiting.
4. Glucose malabsorption.
Q. When is I. V. supplementation required along with ORT ?
A. Situations where 1.V. fluid supplementation is required are :
1. Severe continuous vomiting despite small frequent feeding.
2. Severe dehydration , shock or circulatory collapse.
3. Worsening diarrhoea and an inability to correct dehydration inspite
of proper ORT.
4. Severe electrolyte disturbances and severe acidosis.
5. Convulsion and abdominal distention.
Q. What are the compositions of most widely used ORS?
A. Most widely used ORS are:
1. Standard WHO ORS (high sodium • 90 mEq/L) formula
2. Low sodium ORS (sodium 50 m.Eq/L) formula
3. Low osmolarity WHO ORS (sodium 75 mEq/L) formula
Composition of these ORS formulas a.re summarized in Table No 8.7
and 8.8.
Table No 8.7 : composition of ORS (mEq/L)
Composition Standard tow sodium Low osmolarity
WHO ORS ORS - WHO ORS
.. ;-
Sodium 90 50 75
I
Potassium 20 20 20
Chloride 80 40 65
I
Citrate 10 10 10
1:
Glucose 111 150 75
~ Osmolarity 311 330 245
. c
CH . 8 Fluid Therapy in Children 257
Table No 8.8 : Content of ORS (grams/L)
Ingredients Standard Low sodium Low osmolarity

(grams/L) WHO ORS ORS WHO-ORS
Sodium chloride 3.5 1.25 2.6

Potassium chloride 1.5 1.5 1.5
Sodium citrate 2.9 2.9 2.9
Dextrose 20 27 13.5
Q. Why W.HO recommends use of trisodium citrate instead of sodium
bicarbonate o prepare ORS?
A. Sodium bicarbonate and trisodium citrate both can effectively corrects
metabolic acidosis resulting from diarrhoea. However WHO has
recommended use of risodium citrate due to following advantages:
1. Longer shelf lif e/stabilily
2. No soiling .of th sachet
3. Better taste and 1
lesser cost.
O·RS : Practlc ~ ·1 Recommenda.'tions
A. Standard WHO ORS tormul

Standard WHO o ·R s as 1 i ntroduced in late sixties when cholera
induced diarrhoea ·as very common. n has contributed substantially
to the dramatic global reduction in mortality ·f rom diarrhoeal disease
during the period.
Indications: Preferred treatment in diarrhoea due to cholera, initial
rehydration in moderate to severe dehydration or in hyponatremic
dehydration.
Limitations:
1. When used for common (non cholera) diarrhoea minimal risk of
hypematremia (40-50 mEq/L Na loss in stool Vs 90 mEq/L Na in
ORS),
2. The high sodium Standard WHO ORS should not be used as the
sole fluid intake for maintenance fluid therapy because of the
risk of hypematremia.
258 CH . 8 Fluid Th erapy in Children
3. Similarly infants need more water than electrolytes so if they are

provided only standard WHO ORS , there is a risk of hypernatremia.
Q. In ·practice inspite of extensive use of standard WHO ORS,
hypernatremia is not usually seen. Why?
A. Simultaneous intake of no or low sodium containing fluids such as
water or breast milk prevents hypernatremia. Moreover once
rehydration and volume expans_ ion occurs· the kidney can effectively
regulate sodium concentration (except in infants) which also prevents
significant hypernatrem ia in most of the cases.
B. Low sodium, maintenance ORS
Currently low sodium (50-60 mEq/L) and high glucose containi ng ORS
is available in market. The total osmolarity of this so lution is 330
mmol/L compared to 311 mmol/L osmolarity of standard WHO ORS.
Q. Why low sodium ORS was introduced after standard WHO ORS?
A. Diarrhoea commonly occurs du.e to organism like E.Coli, Shigella
and Rotavirus. Comparative sodium ·loss occurring in common diarrhea
is less (40 -50 mEq/L), ·compa:red to sodium loss occurring in cholera
(100- 120 mEq/L). So, if dehydration due to common diarrhea is
corrected solely with standard WHO ORS (with sodium concentration
90 mEq/L), these patients may develop hypernatremia. Hence there
was need to introduce low sodium ORS to replace common low sodium
containing diarrhoeal losses.
Indications:
1. It is an ideal rehydration solution for the treatment of non-cholera
· · diarrhoea. .
2. It can be used as a sole agent as maintenance fluid therapy with
no risk of hypernatremia in the patients with diarrhoea.
3. For infants (who needs more fluid and less electrolyte) ideal
solution for treatment of dehydration and as a maintenance
solution.
C. Rice based ORS
0. What·is the physiological basis and advantage of rice based ORS?
A. Above mentioned oral rehydration and maintenance solutions, although
effective in rehydration, do not decrease stool volum·e because of the
CH : 8 : Fluid Therapy in Children 259
relatively high osmolarity of the glucose which they contain. Rice

powder provides adequate glucose to sodium pump, without increasing
the osmolarity of the rehydration solution.
This rice based ORS is not only as effective in correcting dehydration
as glucose based ORS , but also offers the additi<?nal advantage of
reducing the amount and duration of diarrhoea by 30°/o. Rice based
ORS also provides calories and protein which helps in regeneration
of infected intestinal mucosa. So rice based ORS reduces morbidity,
cost of treatment and has increased acceptability.
a. What is the composition of commonly available rice based ORS?
A. Composition of rice based ORS is same as standard WHO ORS
formula except that dextrose in standard WHO ORS is replaced by
precooked rice powder.
D. Low Osmolarity WHO ORS
WHO and UNICEF reviewed all published studies related to standard
and low osmolarity ORS in 2001 and subsequently in 2003
recommended new, improved low osmolarity WHO ORS formula for
treatment of diarrhoeal dehydration.
Q Why improved low osmolarity ORS form~lation is introduced by WHO?
A Goals of introducing new improved low osmolarity ORS are
1. To provide single formulation around the world, which can be used
in all cases of diarrhoea .and in all ages.
2. To reduce risk of hypernatremia/ hyponatremia.
3. To reduce volume of diarrhoea and its frequency.
0. What are the additional advantages of improved, new, Lo~ osmolarity
WHO ORS? .
A. Low osmolarity (245 mOsm/L) ORS is least as safe and effective as
standard WHO ORS (osmolarity 311 mOsm/L) for prevention and
treatment of detiydration from all types of diarrhoea. Its addition~!
advantages are
1 · It reduces stool volume output by about 25°/o as compared to·standard
WHO ORS formula.
2. It reduces incidence of vomiting by about 30°/o
3. It reduces incidence of unscheduled I. V fluid support by 33o/o.

Caution: Use of low osmolarity WHO ORS in adults with cholera is some
times associated with an increased risk of transient , asymptomatic
hyponatremia. So careful monitoring is advised.
Q. Can we still use the standard WHO ORS or should we discard it and
only use the new low osmolarity WHO ORS?
A. One should not hesitate to use standard WHO ORS , which is highly
effective in the treatment of dehydration. However because of added
advantages, WHO and UNICEF now recommend to use new low
osmolarity WHO ORS where feasible.
Q. How to administer ORS?
A. Practical guidelines
1. ORS is needed for rehydration , replacement of ongoing losses
and to provide maintenance requirement.
2. Do not add salt or glucose in prepared ORS solution. It will make
the fluid hyperosmolar and will aggravate the diarrhoea and
dehydration.
3. ORS should be given in a small amount at short intervals (small
sips or with teaspoon every' one or two minutes). Large fluid
volume can stimulate gastrocolic reflex resulting in a quick
passage of stool or vomiting.
4. A child should never be kept on ORS fluid alone for more than
24 hours. Fasting has been shown to prolong diarrhoea. This may
be due to undernutrition of the bowel mucosa, which delays the
replacement of mucosal cells destroyed by the infection. Early
refeeding should begin within 6 hours. A full diet should be
reinstituted within 24 to 48 hours, if possible.
5. ORS, if required, can be given through nasogastric tube.
a. How to modify ORT as per severity of dehydration?
A. Individualize ORT considering the status of dehydration as follows:
1. No dehydration, besides diarrhoea:
Avoid high osmalirity fluid such as undiluted juices and offer low
· sodium maintenance oral rehydration solution "ad libitum"·
CH . 8 Fluid Therapy in Children 261
2. Mild dehydration
a 50 ml/kg body weight ORS within 4 hours (or 1o ml/kg/hour ORS
for 4 hours).
b. Reassessment at 4 hours interval. Increase the amount and rate
if diarrhoea continues or rehydration is inadequate.
c. Allow early breast feeding 'ad libitum ' in infants , plain water should
be given in others.
d. If diarrhoea persists , provide extra ORS or maintenance solution
(i.e. 5-10 ml/kg or equal to diarrhoea volume) after each stool.
3. Moderate dehydration
Treat with 100 ml/kg weight ORS within 6 hours (or 15-20 ml/kg/hour)
preferably under direct observation. Reassessment is done at 4 hours
interval and further planning is same as discussed in mild dehydration.
4. Severe dehydration
It needs l.V. fluid therapy (30 ml/kg of body weight in first hour and 20
ml/kg/hour in next 2 hours).
5. Maintenance therapy
It is started after complete rehydration is achieved. In addition to
maintenance requirement, provide 10 ml/kg extra ORS for each loose
stool passed.
Q. How to monitor a patient on ORS?
A. Thirst, pulse volume and rate, urine output and presence of oedema
or rales at the lung bases should guide oral fluid therapy. Mother
should be asked to look for urination and number of stools and should
consult doctor if child does not pass urine for 6-8 hours, fails to drink
ORS or develops persistent vomiting or bloody diarrhoea.
CHAPTER
NINE
FLUID TH·ERAP Y IN
SURG ICAL PATI ENTS
1
NEED FOR SPECI L Colloids 269

CONSIDER Tl N 262 Volume of fl uid re placement 271
PREOPERATIVE FLUID Bl ood transfusion 274
TH E RAP 263 POST-OPERATIVE FLUID
C rrection of hypovolem ia 264 THERAPY 278
C rrectio n of anaemia 265 Goals of fluid therapy 278
Correction of otller facto rs 266 Post-operative fluid
INTRAOPERATIVE administration 278
FLU ID THERAPY 267 Post-operative electrolyte
Crystalloids 268 problems 282
Fluid and electrolyte management is an important aspect for the care of
surgical patients.
Proper fluid and electrolyte state is helpful in reducing morbidity and
mortality in certain surgical patients. So understanding , analyzing and
providing proper fluid therapy to a patient requiring surgical treatment is
very important.
Q. Why fluid therapy in surgical patients needs special consideration ?
A Jn surgical patients, multiple factors modify the normal physiology of
fluid and electrolyte palance of t;>ody and, thereto.re, need special
consideration. Important factors to be considered are :
1. Acute Stress : Physical and mental stress which occurs before,
during and after surgery leads to increased sympat~etic stimuli,
which leads to tachycardia, vasoconstriction and stress.
2. In surgical patients secretion of ACTR is increased. Increased
ACTH stimulates adrenal glands to secrete (a) large amount of
hydrocortisone to fight with acute stress and (b) aldosterone which
leads to sodium retention and urinary loss ·o f potassium.
During major surgery hypovolemia also leads to inc~eased
aldosterone secretion. This increased secretion for the first 2-3
postoperative days leads to decreased sodium requirement. T.his
fact should be remembered while calculating postoperative
requirements.
CH. 9 : Fluid Therapy in Surgical Patient 263
3. Post operative pain and stress leads to increased ADH secretion

from posterior pituitary gland in first 2-3 post operative days. This
increased ADH secretion leads to water retention, which can lead
to reduction in urine output to as low as 500 ml in the first post
operative day. Therefore, it is important to remember that
maintenance fluid required on the first post-operative day is lesser.
4. Fluid deficit, which occurs due to preoperative oral fluid restriction
(NPO), needs consideration and replacement pre- or intra-
operatively.
5. Abnormal blood as well as fluid loss which occurs before, during
and after various surgery needs proper attention ~nd careful
calculati.on to decide type, volume and rate <?f fluid to be infused.
6. Patient who is hypovolemic prior to surgery is -very likely to
become hypotensive during surgery and anaesthesia. Hence
hypovolemia should preferably be corrected prior to surgery.
7. Surgical stress or direct dan:1age· can affect kidney, brain, lung,
skin or GI tract. These organs are very useful in maintaining normal
fluid, electrolytes and acid base .balance. So fluid therapy in such
surgical patients needs special consideration.
Fluid therapy in surgical patients can be discussed under three headings :

. .
(A) Preoperative, (B) lntraoperative and (C) P9stoperative.
PREOPERATIVE FLUID THERAPY

·Preoperative evaluation and correction of existing fluid arid electrolytes
disorder is very important for better outcome in surgical patients. However,
in emergency conditions complete correction is not possible, Bu.t it is always
better to correct fluid deficit partly by rapid fluid replacement and to correct
life threatening disorders than none at all.
Preoperative fluid therapy can be dis~ussed under three headings :
(1) Correction of hypovolemia
(2) Correction of anaemia
(3) Correction of other disorders.
264 CH. g Fluid Therapy in Surgical Patient
Correction of Hypovolemia
Q. Why to correct l1ypovoleml preoperatively?

A. Any degree of liypovolemia jeopardizes 0 2 transport a~d increases
. the risk of tissue hypoxia and the development of organ failure. Greater
the degree and duration of hypovolemia, greater the risk. Therefore, it
is important to correct hypovolemia preoperatively as quickly and
effectively ?S possible. Moreover, uncorrected hypovolemia is
compensated by increased vascular resistance anq heart rate due to
normal baroreceptor reflexes pre operativ~ly. But on induction of
anaesthesia these reflexes are · interrupted ·and compensation is lost
and so patient may develop severe hypotension or even ARF. If fluid
deficit is not corrected preoperatively, hypotension is more likely intra
operatively and postoperatively. So it is important to correct fluid
deficit preoperatively.
Q. What are the causes of hypovolemia in su_rgical patients ?

A. Vomiting, nasogastric s.uction, bl_o od loss, third space losses, fever,
hyperventilation,_diuretic the~apy, . d. i .arrh~e~ or preoperative bowel
preparation are important _yause~ of. hypovolemia in surgical
patients. · . · .
Q. What is "third space lo~s~·. and its causes ?

' ·. .
A. Internal redistribution of ECF due to sequestration of fluid in body is

called third space loss. The volume of such sequestrated fluid can be
as much as 4-5 litres or even more and· it .will decrease the circulating
blood volume and produce signs of hypotension or ·shock. Massive
, ascites, crush injuries, acute ·intestinal ·obstruction, acute gastric
dilatation, acute peritonitis, acute paricteatltis, acute severe cerlulitis,
post operative swelling of bowel wall arid' mesentery are important
causes of third space losses. ·
a. How to decide the volume of fluid deficit p~e operatively ?

A. It is impossible to decide the fluid deficit exactly, but rough estimate
can be made by judging severity of dehydration with clinical signs (also
refer Chapter No. 2).
CH. Flu id h r r, y In urc lcnl f it nt 2 'J
Rough guidelines are :

Mild dehydration= 4°/o body weight fluid deficit.
Moderate dehydration= 6-8°/o body weight fluid deficit.
severe dehydration = 10°/o body weight fluid deficit.
(i.e. severe dehydration in 50 kg= 50 x 10°/o = 5 litre fluid deficit.)
a. To correct fluid deficit in pre operative period which fluid to give ?

How fast to give ?
A Choice of proper fluid for replacement depends on nature o'f loss,
haemodynamic status and concentration or composition al abnorm ality.
0.9% saline , Ringer's lactate , colloids and whole blood are most wid ely
used. Rate of fluid administration varies considerably depending on th e
severity and type of fluid disturbance , the presence of continuing losses
and haemodynamic and cardiac status. In severe deficit rate of initial I
fluid replacement may be 1000 ml per hour, and gradually reducing th e 1 I
rate as the fluid status improves. Elderly patient requires slower and
more careful correction with appropriate monitoring. Ii
a. How to monitor fluid therapy ? I
A. Improvement in tachycardia and blood pressure, absence of orthostatic
hypotension and achieving urine output> 30-50 ml/hour (in absence of
diuretics) suggests correction of fluid deficit.
Correction of Anaemia
0. Why to correct anaemia in surgical patients ?
A. Correction of anaemia is important
1. To establish haemodynamic stability in surgical patient with
blood loss.
2. For proper tissue oxygenation in intra operative and postoperative
period.
3. To cope up with possible operative blood loss.
4. Proper post-operative recovery and healing. Inadequate tissue
oxygenation due to severe anaemia can cause problems like
acidosis and impaired wound healing.
266 CH. 9 Fluid Therapy In Surgical Patient
Q. When to correct anaemia and why ?

A. In elective surgery correction of anaemia by blood transfus,ion should
be done 48 to 72 hours prior to surgery.
Stored blood is low in 2, 3 diphosphoglycerate (2, 3 D.P .G.) levels,
espedally when blood is collected in ACD (Acid Citrate Dextrose)
bag/bottle rather than CPD (Citrate Phosphate Dextrose). Restoration
of this low 2, 3 D.P.G. levels in the body may take about 48 hours.
2, 3 D.P.G. is necessary to allow oxygen to dissociate from haemoglobin
and make it available to the tissues. So if blood transfusion is given
timely in early preoperative period it will ensure maximum availability of
oxygen during and after surgery.
Q. How to correct anaemia ?
A. Packed cell is always preferred to correct anaemia, as it avoids volume
overload. If whot'e blood needs to be given, it is safer to give slowly and
along with diuretics.
Correction of other factors
a Fluid overload : Surgical patients usually do not present with
· volume overload, although it is not an uncommon problem in
hospitalized patients. Over aggressive fluid therapy or returning of
fluid collected in third space into ECF compartment during recovery
of the basic disease are important ~auses of overhydration. In
patients with CHF, renal failure or cirrhosis of liver, fluid overload is
commonly seen. Diuretics, salt restriction and fluid restriction are
needed to correct fluid overload preoperatively. In patients with
severe renal failure, dialysis may be necessary._
b. Hypokalemia : Important causes of hypok~lemia in surgical
patients are GI losses (e.g. vomiting, nasogastric aspiration,
ureteroenterostomies), potassium free I. V. fluids or parenteral
nutrition, excessive renal excretion due to diuretics or mannitor,
continuous obligatory renal k>ss of potassium (more than 20 mEq
per day), metabolic alkalosis. (e.g. vomiting).causing·increased renal
excretion of potassium and Intracellular shift of pota.ssium etc. So
hypokalemia is likely to occur frequently in the surgical-patients, I
II
CH. 9 : Flu ld Th rnp y In Surglc I Pn tl ont 267
except in shock or acidosi s whicl1 inte rferes with normal renal

excretion of potassium.
Pati ents ~itt1. hypoi<a lemi a are at ri sk of developing cardiac
arrhyth.m1as mtraop eratively ; and res piratory difficulty after
extubat1on and paralytic ileus postoperatively. So hypokalemia
needs correction.
c. Hyperkalemia : Hyperkalemia is more serious but less frequently
encountered abnormality in surgical patients. Important causes of
hyperkalemia are release of significant quantities of intracellular
potassium into extra cellular space in response to severe injury
(crush syndrome) or surgical stress, acidosis and the catabolic state
or potassium rich fluid infusion especially in oliguric or anuric renal
failure. Dangerous hyperkalemia (serum potassium > 6 mEq/L) is
rarely seen if renal function is normal.
Failure to recognize and treat hyperkalemia preoperatively can lead
to serious life threatening bradyarrhythmia or cardiac arrest leading
to death.
INTRAOPERATIVE FLUID THERAPY

. •''
Proper fluid therapy intraoperatively will avoid hypovolemia and

hypotension. It also maintains prope(tissue perfusion and oxygenation.
. ' I . .
To avoid hypoten.sion it is important to diagnose and·treat the underlying

causes of hypotension : Important causes of hypotension intra
operatively are loss of blood, fluid depletion (intraoperatively fluid
loss + maintenance requirement), third space losses, evaporative
·1osses from viscera or wound itself, hypoxia, vasodilatatory effect of
anaesthetic ·agents and spinal or epidural anaesthesia.
0. Which fluid to give intraoperatively, crystalloid or colloid ?
A. Whether intraoperative fluid replacement should be done with colloid or
crystalloid is a dispute. If one were clearly better than the other, there
would not be any controversy. There is no human data that demonstrates
that any particular solution (colloid or crystallold) is better than another
in terms of outcome. There is, however, good data to suggest that to
avoid tissue hypoperfusion, you need to give enough of whatever you
choose and you need to give It promptly with proper monitoring. For
CH. 9 : Fluid Therapy in Surgic al Patient
268
rapid restoration of tiaemo?ynamic function a colloid does the job more

effectively than a crystallo1d.
Crystalloid
Crystalloid is the most commonly used agent intraoperatively because it is

least expensive, readily available and reaction free. But since it passes
readily through the semipermeable membrane, it cannot remain confined
to the the intravascular compartment. So it has a short lived haemodynamic
improvement effect. Larger volume of crystalloid is needed for correction of
hypotension, which can lead to excess salt and water retention leading to
peripheral and pulmonary oedema. If the goal of fluid therapy is to replenish
interstitial dehydration, then the crystalloid will be the treatment of choice.
Q. Which l.V. fluid should be given intraoperatively?

A. Ringer's lactate is most widely used l.V. fluid but selection of intraoperative
I •
fluid needs to be individualized depen~ing upon age, vital data, basic

etiology and type of surgery required, associated illness (e.g. OM) and
current fluid and electrolyte status.
' .
. .
Basic guidelines for selection are :
1. Ringer's lactate is used to replace the intraoperative fluid losses.
Since Ringer's lactate is the most physiological fluid with
composition similar to body fluid, .it is the ideal fluid for replacement
wit~ additional advantage of correction of acidosis.
2· ls.otonic saline is often used intraoperatively, especially when
Ringer's lactate is contraindicated or .when large volume of fluid
needs to be replaced rapidly i.e. hypovol.emic shock.
3
· ~o/o-de~trose is used as initial fluid replacement. which replaces
ins~nsible fluid loss and maintenance fluid deficit during starvation
penod. Losses during starvation are poor in salt. .So/o-dextrose is
,I
selected to correct this deficit as it not- only corrects intracellular
dehyd ra t'ion but also provides calories. I
1
Caution : Rapid replacement with dextrose containing fluid should

never be done. Dextrose more than 25 gm. per hour (or 500ml of
5°/o-dextrose per hour) causes hyperglycemia and glycosuria with
resultant osmotic diuresis. This 'diuresis prevents correction of fluid
deficit, especially in hypovolemia or in patient with shock.
4. lntraoperative fluid repl~cement in specific situations.
(a) Paediatric patients : lsolyte-P is the preferred solution as it
avoids sodium overload. It should be avoided in oliguric patient
till urine output is establ!shed because .it contains high potassium
(20 mEq/L). Newborn babies require 10°/o-dextrose to prevent
hypoglycemia. · . · :
(b) Diabetes :· 5o/o-dextrose with insulin infusion is infusea under
careful monitoring to avoid hypoglycemia intraoperatively.
During emergency surgery with uncontrolled.diabetes isotonic
saline is preferred with close blood glucose monitoring.
( c) Hypertension : 5o/o-dextrose is given in hypertensive patients.
It is preferable to avoid isotonic saline. If needed, Ringer's
ractate can . be giv·e n·· in ~ ·, opHmum , amount ca·r efulry.
(d) · Oedemato'us 'patients·(due to ·~HF., · cirrhosis o·r renal !ailure):
Ringer's lactate is usually . contraindicated an.d isotonic saline
is usually avoided or given very'judic·iously. In such patients
5°;0 -dextrose is given l.V. slowly in· least possible· amount.
(e) TURP and neurosurgery : Avoid 5%-dextrose in p~tients
. undergoing TURP ar:id neuro~urgical . operat~ons.
(f) 1.v. fiui.d s containing large amount of K+, Mg++ or Ca++ sh_ould
be avoided intraoperatively for fear of specific i~nic overload.
Colloids
lntraoperative colloids are used selectively ' ~hen rapid restoration of
plasma volume is needed to correct severe. -~cute hypotension. ·
Advantages
( 1) As colloids do cross semipermeable membran~ and remain in
not
the intravascular compartment., they are more ~Uective than
crystalloids in treating hypotenslon.
270 CH. g Fluid Therapy in Surgical Patient
(2) Increase in the plasma volume is for a prolonged period as compared to

crystalloid.
(3) Smaller volume of colloids improve the haemodynamic status. Avoid
excessive salt and water administration ," thereby reducing chances of
minimum peripheral oedema.
(4) Better haemodynamic stability so higher systemic oxygen delivery indirectly.
Disadvantages
(1) Much more expensive than crystalloid.
(2) Rapid and larger infusion can cause pulmonary oedema.
(3) Higher risk of hypersensitivity reaction and bleeding (especially with
dextran).
(4) Glomerular filtration rate is decreased , so excretion of nitrogenous end
products is reduced.
Indications
lntraoperatively colloids are used to treat sudden hypotension due to major
blood loss till blood is awaited, or to avoid blood transfusion. Colloids when
giv.en along with crystalloids (Ringer's lactate, or 0.9o/a isotonic saline), will
correct interstitial dehydration and increase urine flow which allows excretion
of nitrogenous end products.
Precaution
Before infusing colloids sample for blood g.rouping and cross-matching
should be collected because colloids may ,interfere with blood group and
crossmatching.
Colloids available
Albumin-5°/0 or 25%, Dextran (e.g. Lomodex-70), Gelatin Poly~ers (e.g.
Haemaccel), Hetastarch and Plasma are tlie most widely used colloids . .
<1) Albumin : Very effective in increasing intravascuJar volu~~. deple~ion
secondary to intraoperative blood loss. But as cost is prohibitively high,
it is not used in day to day practice.
H. Flu id Therapy in Surgical Patient 271
De ' tran-40 ~~ {e.g. Lomodex) : Effective but expensive plasma

expander. It is known to cause hypersensitivity reaction so needs to
be administered cautiously under medical supervision. Contraindicated
in patients with bleeding disorders or severe cardiac or renal failure.
(3) Gelatin Polymer (e.g. Haemaccel): It is a purified protein of animal collagen
origin , and is an effective plasma expander. Advantage of gelatin polymer
is that it does not interfere with blood transfusion and cross matching.
However hypersensitivty reaction including anaphylactic reactions may
occur after infusion.
(4) Hetastarch : It is a synthetic colloid derived from corn starch. It is less
expensive than albumin and has great advantage of being nonantigenic,
so it is safer as compared to dextran.
(5) Plasma : It is the most physiological plasma expander, which not only
corrects intravascular volume but also corrects certain bleeding disorders.
It carries the risk of transmitting hepatitis and other infective diseases.
Volume of Fluid Replacement
Q. How much fluid to give ?
A. There is no fixed ready-made formula, which can calculate fluid volume
in all patients. After proper consideration of all existing parameters fluid
volume is calculated for each patient individually. Infusion of this fluid
should be carried out under careful observation to avoid under or over
hydration and may need modification as per the clinical situation.
Factors to be considered :
Age, weight, hydration status, vital data, preoperative a~d intraoperative
urine output, cardiac and renal status and type of fluid to be replaced
should be considered while calculating fluid volume.
Guidelines for calculation :
In adult patients with no preexisting fluid deficit, amount of intra operative
volume can be roughly calculated as below :
(1) correction of fluid deficit due to starvation.
Plus (2) Maintenance requirement for period of surgery.
Plus (3) Loss due to tissue dissection or haemorrhage.
272 CH. g : Fluid Therapy in Surgical Patient
(1) Volume to be replaced for starvation fluid deficit=

duration of starvation (hours) x 2 ml/kg body weight
· This deficit is usually replaced with 5%-dextrose. The deficit (fasting)
may be replaced by giving half of the calculated volume in 1st hour and
the other half over next 2 hours in addition to the intraoperative fluid
replacement.
(2) ·Maintenance volume for intraoperative period=
duration of surgery (hours) x 2 ml/kg body weight
or Rate of infusion = 2 ml/kg body weight per hour.
(3) Usual fluid required to correct intraoperative fluid loss due to tissue
dissection or haemorrhage depends on the type of surgery (Table No. 9.1 ).
Table No. 9.1 : Fluid loss in different types of surgery

--
Type of surgery Fluid volume (ml/kg/hour)

(A) Least Trauma Nil
(8) Minimal Trauma 4
(C) Moderate Trauma 6
(D) Severe Trauma 10
(A) Least surgical trauma
1
In surgery with least trauma, ther.e is minimal loss of blood or fluid. It

includes ophthalmic surgery, cystoscopy etc. Here no additional fluid
replacement is necessary. They need only hypotonic maintenance fluid,
2 ml/kg/hour (usually 5°/o-dextrose). ·
(B) Minimal surgical trauma

Surg_ery with minimal tissue trauma includes tonsillectomy, nasal septal
repair and plastic operations. They should receive 4 ml/kg/hour fluid
;~~lacem~nt for surgi~al trauma. In addition, as mentioned, m~intenance
uid .requirement dunng surgery is 2 ml/kg/hour. So such patient should
receive total of 6 ml/kg/hour balanced salt solution for the duration of
surgery. .
CH . 9 Fluid Thorapy In Surulou l PatI rit 273
(C) Moderate surgical trauma

Surgery with moderate tissue t raum a in c lud es h e rni a re p a ir,
appendicectomy , procedures on extremiti es , thoracotomy eto. Such a
patient should receive 6 ml/kg/hour fluid repl acement fo r surgical trauma,
plus 2 ml/kg/hour maintenance fluid requirem ent. So total intraoperative
need will be 8 ml/kg/hour of Ringer's lactate or isotonic saline.
(D) Severe surgical trauma

It includes total hip replacement, bowel resection for in tes tin al
obstruction, radical mastectomy, radical neck dissection etc. Such
patients should receive 1 o. ml/kg/hour fluid replacement for surgical
trauma plus 2 ml/kg/hour maintenance fluid requirem(3nt. So such a
patient should receive total 12 ml/kg/hour Ringer's lactate or isotonic
saline as fluid replacement.
Sample Calculation
If 40 years male, weighing 50 kg, NPO for 1O hours needs to be
subjeCted for appendicectomy (duration of surgery one hour), calculate
how much ·fluid to give ? ·· : · · · ···
. ~ ' • • ' : ~ f- ! , . ' ...
Total fluid required= . ..

r I
i ~
r I
f •
f.' I\
(1) Correction of starvation deficit

= Duration of starvation in h~urs' x2 ml/kg
= 1o·x 2 x 50 · ' ·
= 1,000 ml _ , ..
(2) Mainte~:arice rie~d du~ing op~rative per~od . ·
= Duration of ~urg~ry in hours-x ~ 1')11/kg
= 1 X 2 X 50 •' r ' '
= 100 ml ..: - . . ~\ '\ :.
(3) Correction of operative loss .

Appendicectomy involves moderate .s-Urglcat "trauma so .~eed
= 6 ml/kg/hour
= 6 x 50 x 1
=300 ml
So total intraoperative fluid requirement= 1 + 2 + 3

= 1,ooo ml+ 100 ml+ 300 ml= 1,400 ml.
Blood Transfusion
lntraoperative blood transfusion is often life saving and should be used

judiciously.
Advantage
It is the most physiological way to replace blood loss. As blo?d remains
entirely in intravascular compartment, it is the best agent to correct
hypotension secondary to blood loss. Blood transfusion has added advantage
to ensure adequate tissue oxygen delivery. As compared to crystalloid it is
very effective and as compared to colloids it is less expensive and safe in
treatment of intraoperative hypotension.
Disadvantage
Blood of same group may not be reaqily available and needs time for
crossmatching before it can be supplied and transfused. Moreover blood
transfusion has definite risk of transmitting infections like hepatitis, Al OS,
malaria, etc. and, therefore, should be used judiciously.
Q. How to estimate intraop.erati~e blood Joss ?

A Many a times it is extremely difficult'to estimate blood loss. A simple
and only way to estimate blood loss during a surgical operation is to
weigh the sponges before and after use. The difference in gram is
equivalent to the volume in ml of blood they have absorbed. Add to this
the volume of blood in .the operating·roqrri suction bottle. Then increase
the total by one half to approximate the actual blood loss.
0. How to decide need of blood transfusion ?

A. F~ctors to be
. considered
..
for intraoperative
..
_blood transfusion are :
'
(1) Preoperative haemoglobin or haematocrit.

(2) Percentage loss of blood volume.
(3) Others : Vital data, hydration status, age, associated IHD etc.
(1) Preoperative haemoglobin (Hb) or haematocrit

In normal adult patient oxygen carrying capacity is unaffe·cted till Hb is
as low as 8 gm/di and haematocrit 25°/o, provided there is no hypovolemia .
Therefore , patient with normal Hb and haematocrit can tolerate bloo·d
loss well, but preoperatively anaemic patient needs blood transfusion
even at lesser expected intraoperative blood loss.
For example :
lntraoperative reduction of Hb by .2 gm/di can be tolerated well if
preoperative Hb is 12 gm/di or above. But patient with preoperative Hb
1O gm/di or less will need blood transfusion ~ ·
(2) Percentage loss of blood volume
An important fact~H to decide need of blood transfusion is percentage
loss of blood volume.
Total blood volume in body varies according to body weight (Total blood
volume is 90 ml/kg in new born, 80 ml/kg in infants, 70 ml/kg in child
and adult male, and 65 ml/kg in adult female). So only from volume of
blood loss, possible reduction in Hb and the need of blood ·transfusion
cannot be predicte~. . r •
A perfect method to predict the need of blood transfusion is percentage

loss of bloo.d volume.
' .
For example : Loss of 500 .ml in 70 kg body weight iri adult male (where
total blood volume in ml = 70 x wt= 70 x 70 = 4,900 ml) is the loss less
than 1Oo/o of total blood volume, which is not a significant loss and m·a·y
not require blood transfusion. But 500 ml blood loss in a 2o·kg boy with
total blood volume of 1,400 ml (70 x 20 kg = 1,400 ml) is roughly 30°/o of
total blood volume, which can be life threatening, if not treated timely
with blood transfusion.
(3) Other factors
(a) Vital data : Emergency surgery in hypoten·sive patient needs blood
transfusion even with lesser blood loss.
(b) Hydration status : Patient with ~ncorrected hypovolemia
preoperatively needs blood transfusion with lesser loss.
(c) Young adults tolerate blood loss better than old people.
(d) Patient with IHD needs greater haemoglobin for proper oxygenation.
Q. How-to estimate newer/subs~quent Hb status after intra operative blood

loss?
A. Hb status after blood loss is calculated by following 3 steps
Step 1 :
To convert volume of blood lost into loss as o/o of preoperative Hb
0 /o reduction of Hb = 1.25 x volume of blood loss
weight
Step 2:
To convert o/o reduction of Hb into reduction of Hb in gms/dl
Reduction of Hb in gms/dl = preoperative Hb x 0/o reduction
I ' 100
Step 3:
Hb status after blood loss
= Pre operative Hb gms/dl .. reduction o·f Hb gms/dl
Example: - '
If patient with 50 kg weight, with 14 gms/ dl· preoperative Hb, ·loses 800 ml
of the blood, what will be the subsequ.ent Hb status ?
Step 1 :
0
/o reduction of Hb = 1.2s· x volume of blood loss
weight
= 1.25 x 800 = 20%

50
Step 2:
Reduction of Hb in gms/dl = preoperative Hb x /o reduction
0
100
= 14 gm x 20 = 2.8 ·gms/dl
100
CH. 9 : Fluid Therapy in Surgica l P tl ent 277
step 3:
Hb status after blood loss
== Pre operative Hb gms/dl - reduction of Hb in gms/dl
::14-2.8
== 11 .2 gms/dl
If surgeon can predict intraoperative blood loss, by this method Hb status

~ubsequ~nt to loss of blood can be calculated. It will be a useful guideline
in arranging blood to be transfused intra-operatively.
Q. When not to give blood transfusion?

A. 1. It is unnecessary to replace blood loss of less than 500 ml in adult
with normal preoperative haemoglobin or
2. Loss of 10°/o of estimated blood volume is well tolerated and usually
doesn't require blood transfusion. Such losses are usually replaced
with crystalloids like Hinger's Lactate or 0.9% Isotonic saline.
As large volume (about 75°/o) of ,crystalloid leaves the circulation
into the interstitial space, the volume of crystalloids required to
replace blood loss is larger than the volume of blood lost.
As a rule blood loss needs to be replaced with three times
volume of crystalloids.
0. When to give blood transfusion intraoperatively _?

A. 1. Blood loss > 20010 of blood volume definitely needs replacement,
without considering preoperative haemoglobin status.
2. Replacement of blood loss between 10°/o and 20°/o of total blood
volume is a matter of clinical discretion. If Hb status after l~ss ~f
blood is expected to be less than 1O ~midi, blood transfusion 1s
usually given.
3. In adult patient when intra operative blo~d toss is 500 ml to 1,000
ml, usually single unit of blood is required.
4. Blood transfusion is necessary if haemoglobin is likely to fall
below 8 gm/di after blood loss.
278 CH . g : Fluid Therapy in Surgical Patient
a. What is the maximum allowable blood loss and how to calculate it ?

A. Amount of loss of blood , which ·does not require- blood transfusion is
maximum allowable blood los$ (MABL). How.much fall of ~aematocrit can
be safely allowed is determined after considering hydration status,
associated illness (i.e. IHD), preoperative Hb - haematocrit etc. Maximum
allowable blood loss may be calculated as a proportion using the patient's
starting haematocrit (starting pt hct) and the lowest accept_able haematocnt
(usually 25°/o) :
MABL = (starting pt hct - 25 ) x estimated blood volume
starting pt hct
Example:
In a adult male with 60 kg weight and 35°10 haematocrit what will be
maximum
t1' .
allowable blood loss ?
Estimated
. . volume in a adult male = body weight in kg x 70
blood
Maximum allowable blood loss = ( 35 - 25 ) x 60 x 70 = 1 ,200 ml
35
· .So if intraoperative blood loss exceeds 1,200 ml,. blood transfusion is
required.
. POST-OPERATIVE FLUID THERAPY
The administration of fluid and electrolytes during the post operati.v e period
depends upon the clinical judgement of the patient's status. No equation or
formula is perfect in planning fluid therapy.
Goal of_fluid therapy . . .

The aim is to maintain reasonable blood pressure (> 1Oona mm of Hg), pulse
rate of less than 120 per minute and an hourly urine flow between 30 and 50
ml along with normal temperature, warm skin, normal respiration and sensorium.
Q. When and how long to give postoperative I. V. fluid ?

A. Whether a patient n~eds postoperative IV fluids or not and for how
long depends upon type (minor or major) and nature of surgery (surgery
on limbs, abdominal surgery, etc.)
CH. 9 : Fluid Therapy In Surgical Patlont 279
.The patients who are subjected to short operative procedures and, who
do not require handling of intestine or viscera, with little morbidity will
require only maintenance I. V. ·fluid to correct de·ficit due to NPO state.
After 4-5 hours oral fluid is restarted and I. V. fluid is not needed.· Th.is
group includes operations like hernia, minor orthopedic operations on
limbs , minor plastic surgery, etc.
On the other hand, patient with major surgery like intesti'nal resection
with anastomosis or total colectomy, where.intestinal ·viscera need rest,
requires postoperative l.V. fluid for a few days. After ens~ring normal
movement of intestine oral fluid intake is restarted.
In most of the major surgeries where handling of intestine is not required
J • •
1.V. fluid is required for only 24 _

to 48 hours e.g. cardiac surgery, coronary
bypass surgery, total hip replacement, etc.
Q. What are the causes of hypovolemia in postoperative·patients ?

A Important causes of .postoperative· hypovolemia are :
1. · Inadequate correction of sfar\tatlon (NPO) or intr'aoperative period

maintenance fluid deficit. · ·; ·~ " · --~ ·. ·· ·
2. Empirical and not meticulo~sly calqulated : replacement. of intra-
ope~ative fluid l<?ss.
3. lntraoperative blood loss replaced with equal volume of crystalloid.
The fact often overlooked is th9t vo,ume..of bl9od lost should be
replaced with three. times volume of crystalloid. .
4. Fluid loss from nasogastric aspirations, drains and fistulas is
not replaced. I •
5. Third space loss : Several litres of fluid .m ay be sequestered into

the . interstitial space, peritonec;il or . pleura.~ cavitie_s and bowel
lumen.
6. Excessive loss due to hypermet.abolism, hyp~~entilation or pyrexia.
7. Delay in operation due to . long OT list, , especially in summer.
a. In early postoperat_ive pe~iod i~ there is hypotension and
· dispropo~ionate anaemi.a, think ~f Internal Q,l~edlng unless proved
otherwise ..
~ tu d T nwpy In JJ(UI ;: I Putlont
hr Id I . , n.Jl rJ oru d bf:, fore writing po"'top rati 1e
A Bef (t=l pr ,_;' ribin rr ti I J I. V, fluid onG h uld alway conn jd r

, poin. :
I d tr, hydration r-·t tu and urine output
z n i , n tur J f - urgery anrJ blood J o .~
a ur f fluid and bJ od replaced intraope ratively.
z Or Jn u pu , n a tri a piration, fluid lost at Nound injury site
r p - ra i / ~ it .
i - rsn f ""ta . , a ociat ·d illness (HT, OM and IHD) and associated
e:f&;ctr Jyt~ and acid base disorders, if any.
2. n jdt:)r in""'ensible loss due to atmospheric temperature, pyrexia,
nyp :p/ , ntHation etc.
z - urati,on f,o r which LV, fluid needs to be given.
ri - the routine postoperativ~ orders of l.V. fluid for first three days?
.,,., ,;:;n,,J~Q.,J prr~ cription of postoperative LV. fluid in NPO patients is :
1. · Fir 24 hours of surgery-: ·· · · ·,

2 Utr - 5o/o·dextrose or 1.5 litres 5o/o~dextrose + 500 ml isotonic
fin•~I
2, . econd po t operative day =

2 fitr of 5o/{; .. dextrose + 1 litre 0.9o/o Saline.
o, Third po t operative day :
,;milar ff uid + 40-60 mEq potassium-per -day
·mcmb~ r that th ese ·are only guidelines, which may require
rnr diti .,ation depending upon the clinical situation.
hy rndintenarice LV, fluid on th~ first postoperative· d$y has less
~· ang it, total volume J lee er 7 ·
, ~' · rauv,7 pain and tress lead to increased secretion of ·ADH and
r n , Tho ref ore aft r .an op·eratlon of moderate .severity, salt
r- nd .1 r · r-tainad by the kidney under the Influence of these
CH· 9 . : Fluid Therapy in Surgical Patient 281
hormones. So to avoid overloadin 1 .

lesser or even no sodium and.
1
°
9 either salt or water, l.V. fluid with
of
need a normal individual . .m ess~r volume t,han routine maintenance
~$prescribed.
Q. When, on first postoperative d . . . . ·
. . ay, saline contammg fluid is preferred?
A. To infuse salt free LV. fluid on first · . . .
all patients. Early saline· inf . .postop~rati~e day is not a routine in
. us1on is required m :
(1) Elde.rly patients ~ith salt losing nephropathy.
(2) Head injury or neurosurgical operations.
(3) Patient on treatment ·with diuretics and mannitoL
(4) To replace nasogastric aspiration and drain output.
(5) In most of the major surgery, saline is given to replace third space
losses.
0. Why usually potassium is avoided in 1.V. fluids for. ·the first two
postoperative days ? . .
A. For the first 2-3 postoperative days, potassium is avoided due to
following reasons :
1. Patients may have oliguria or azotemia. So till urine output is
• I
established and normal renal status is ensured, potassium

supplementation can be risky.
2. Post operative tissue trauma may release potassium from

intracellular to extracellular compartment, whjch may cause
hyperkalemia.
3. lntraoperative or postoperative transfusion of stored blood or
haemolysed blood may add large amount of potassium, so it is
unsafe to start potassium early.
4. Postoperative metabolic acidosis wmshift ~ntracellular pota~siu~

extracellularly, so there is no need of potassium s.upple~entat1on in
early pos.t operative period.
A b dy has large store of potassium intracellularly hypokalemia
5.
w~I ~ot ocC.u r. if potassium is avoided for first 2-3 postoperative
days.
282 CH . 9 Fluid Therapy in Surgical Patient
Q. How to infuse IV fluid postoperatively?

A. It is a wrong method to infuse total 1.V. fluids wi.thin 8 to 12 hours in
postoperative period and not giving any infusion in rest of the period .
. Maintenance fluids should be administered at a steady rate over an 18
to 24 hour period. If given over a short pe~iod, r~nal ex?retion .of th~
excess salt and water may occur. But as the normal lo~ses co~tinue
over the full 24 hour period, body will be deprived of their fluid need
during the remaining period. 'For the same reason, fluids ·of different
composition are alternated and additives to l.V. fluids are evenly
distributed in the total volume of fluid given.
Q. Which fluids should be given to replace additional losses in postoperative

patients?
A. Simple guidelines for replacement are as follows :
(1) Prolonged vomiting or nasogastric suction : Fluid of choice is normal
saline. If urine output is adequate , potassium is added to it after
second day. After initial two days even lsolyte-G can be given in an
amount same as upper GI loss, provided u_rine output and. renal
status is normal.
(2) Fluid loss due to small bowel fistulas causing diarrhoea :
Ringer's lactate is the ideal fluid for replacement and may need
additional bicarbonate and potassium supplementa.tion to treat
metabolic acidosis and hypokalemia.
(3) Loss of blood : If volume is less, replacement is done ~ith three
times yolume of isotonic saline or Ringer's lactate. But if the loss is
gre.ater, it needs blood or colloids for replacement.
Post Operative Fluid Electrolyte Problems

Special consideration in post operative patients are :
1. Volumeexcess
Over e~thusias~ic excessive infusion of -intraoperative fluid or ~load
transfusion, or large volume of blood loss replaced exclusively with
three times volume of crystalloid can cause volume excess. Excessive
absorption of irrigation fluid during TURP will lead to volume excess.
CH. 9 Fluid Therapy in Surgical Patient 28;3
Volume _excess due. to blood will present chiefly ·with pulmonary

con~estion . .E~cess1ve saline will cause weight gain, periorbital
_ pu~fin~ss, ~oarseness or_ dyspnoea on exertion. Excess of .hypotonic
f~Uld. like 5 Y0 ~d.extr?se will ~ave chief presentation of hyponatremia
like mental confusion, d .ro~si_ness or ~arely ~oma or convulsions.
2. Hyponatremia _ ·
Hyponatremia in post operativ~ period is d~e to :
a Stress induced increase in ADH, -which causes ·retention of water
in excess of sodium.
b. Catabolism· induced release of water from glycogen, fat or protein
breakdown.
c. Post operative fluid supplementation exclusively with 5°/o-dextrose
or excessive infusion of 5°/o-dextrose. f .
d. Water administration consistently which exceeds water losses.

e. Erroneous replacement of gastrointestinal losses with sodium
free fluids .
. f. · Post TURP syndrome and SIADH in neurosurgical patients.
If any [>ostoPerative patient on 1.V. fluid therapy becomes drowsy,

weak, confused or gets convulsions, always rule out hyponatremia.
Hyponatremia is usually treated with water restriction and diuretics.
3. Hypernatremia · : ·
Hypernatremia is an uncommon problem, which occurs due to (1)
excessive· infusiOn of isotonic salirie, (2) pure water loss replaced
with isotonic saline, (3) post head injUry or neurosurgery, (4) diabetes
insipiduS or (5}' excessive pure water loss in severe hypergly~emia
due to osmotic diuresis. Treatment of cause and gentle correction of
hypernatremia with 0.45% NaCl - half strength saline is the usual
treatment.
I
I
I
284 CH. 9 Fluid Therapy In Surgical Patient
4. Post-operative oliguria
a Hypovolem'ia is the most important cause of postoperative oliguria.
Dry tongue, decreased skin turgor, sunken eyeballs, low volume
pulse with tachycardia, postural hypotension and concentrated urine
favours hypovolemia as etiology 'of oliguria.
b. Always rule out retention of urine in the oliguric patient, by proper
clinical examination, and in few patients with diagnostic dilemma
by sonography or by urinary catheterization.
c. Postoperative acute renal failure, which may be due to either
hypovolemia, septicemia or nephroto.xic drugs. .(i.e. NSAID,
aminoglycosides, etc.)
5. Hypokalerilia
Hypokalemia is the most common electrolyte abnormality in
postoperative patients.
I. Important causes of hypokalemia in .surgical patients are :
a. Gastrointestinal loss : Direct loss of potassium as in
diarrhoea or indirect loss in vomiting or prolonged nasogastric
a~piration cau~ing metabolic alkalosis, which promotes the
renal excretion of potassium. '
b. Post operative infusion of mannitol or diuretic~.
c. Prolonged . administration of p~tassium free l.V. fluid or
parenteral nutrition. The ability of kidney to reabsorb potassium
is incomplete and, therefqre, even in hypokalemic patients,
renal loss of potassium .is more than 20 mEq/day. So prolonged ·'
admjnistration of potassium tree pa~enteral fluids or parenteral
nutrition poor .in potassium can lead to hypokalemia. ·
IL Extreme weakness is the commonest presentation of hypokalemia
with rare occurance of respiratory distress secondary to involvem~nt
of respiratory muscles. Muscular hypotonla is the outstanding
physical sign. It is important to remember that hypokalemia can
~ead to paralytic lieus in surgical patients. Patient on digitalis thera~y
is more prone to develop cardiac arrhythmias due to hypokalemta.
I, '
,o I 11
' ' '

. CH ...9 . F.. I 'd .. ; . . . .... , . :·· . . .
Th . ·. ' ..
~
::~~~~~~~~~----=· :·.:.:::.ra~p:y~in~su:"r~gl:ca~l:P~:·.t~~.:.>~·~··:. ·~·,
0
" . UI
/ ' . . . , 10nt. ·.285 .
oral potassium (K+) supplem . .. ·.

Ill. . . entat1on ,18
upplernentat1on. 1n treatment of hyp ksafer than
. ·1·v·potass1um.
5 0
of hypokalerrna
· v
with I · · potassiu alem1a. Rapid correction .
tiyperka Iemta, which is more dangerou mththerapy can cause ··
8
Chapter No. 3). .· · an hypokalemia (see
. • Hyperka · mia
6
1. Hyperkalemia is an uncomm .
due to crush syndrome sevoen . P.?~toperative problem. It occurs
· ' re 1n1ury s · 1
state and metabolic acidosis. ' urgica stress, catabolic
2. Elevation of serum potassium above 6 m · ·' . . . . · ··

of potassiUm by the normal 'ki Eq/Lmayst1mulateexcretion
hyperkalemia. . ·. dney and prevents severe
3. Life thre.atenin9. hyperkalelnia usually occurs in oliguric or anuric

~enal .f~1lure. Life threatening ·hyperkalemia is seen in adrenal
insufficiency. · ··
4. Most important signs of hyperkalemia' are evident to the
?ardiovascular system. Serum potassium > 7 mEq/L impairs
intracardiac impulse conduction leading to bradyarrhythmia,
hypotension and may be followed by diastolic cardiac arrest.
5· Any hyperkalemic patien~ showing wide ORS complex, peaked

T waves or other ECG evic:lenCe of cardiac toxicity should be treated
immediately. Life threatening hyperkale~ia is ~sually treated with
injection calcium gluconate, injection sodium bicarbonate, glucose
and insulin; KayeXalate (orally or by retention enema),
haemodialysis or peritoneal dialysis. .
' "
''
CHAPTER
TEN
FLUID THERAPY IN SPECIAL

SURGICAL P-R OBLEMS
TURP SYNDROME 286 Pathophysiology of burns 295

Definition and risk factors 286 Initial fluid resuscitation 296
Presentation 287 Fluid selection 296
Pathophysiology 288 Fluid volume 296
Hypotension during TU RP 288 Rate of administration 297
Prevention 289 Role of colloids 299
Treatmen t 290 Role of blood transfusion 299
NEUROSURGICAL PATIENTS 290 Monitoring 300
Importan ce of fluid therapy 290 Subsequent Buid therapy 302
Selection of I. V. fluids 291 Fluid therapy after 48 hours 303
~ Guidelines for ICP
Other guidelines for
292 Diuretics in burns
Electric burns
305
305
neurosurgical patients 293 URETEROSIGMOIDOSTOMY 306
BURNS 29 4 Indications 306
Importance of fluid therapy 294 Pathophysiology 306
Goal of fluid therapy 294 Treatment 307
Indication of I. V. fluid therapy 295
Role of nasogastric tube 295
In this chapter we will discuss fluid therapy in important surgical disorders
like TURP, neurosurgical patients , burns and ureterosigmoidostomy.
TURPSYNDROME
Transurethral resection of prostrate (TURP) is the second r:nost common
surgical prqcedure (after cataract extraction) done in men over the age of
65 years. Transurethral resection of prostrate (TURP) syndrome is one of the
commonest and dreaded complication of urological endoscopic surgery.
0. What is TURP syndrome?

A. TURP syndrome is a distinct clinical entity characterized by a
constellation of sign-symptoms secondary to neurological,
cardiovascular and electrolyte imbalance resulting from the absorption
of the irrigation fluid through prostatic veins or breaches in the prostatic
capsule during TU RP.
CH. 10 : Fluid Therap . S .
~----~~~----------------~~:y~m~· :p:e:c:a~IS~u:rg~ic:a:l:P:ro~bl~e::ms~2~8:.
1
7
0. Which
.
patients are·at greate . k
r ns for TURP syndrome? .. .
A· patients are at greater- risk f ·
d · o developing TURP
expose to a resection time 1 syndrome when
. . anger than 60 min t
weight 1s more ~eavier than 30- ram· . . u es, res~cted prostate
30 litres, e.spec1ally when TURP~s and irngant v~lurne 1s greater than
. f 11 d perfo~m~d by an inexperienced hand
a. Why 1s 1 e water carries mor .
d . ·
irrigation fluid ? · e risk co~pared to glycine as
A. Although sterile water is less expen · -~ · ·

with it it is extremel h . sive a~d TU~P can be tjone safely
' · Y. ypot?nic as _compared to glycioe. So distilled
wadter carlrf1e~I greater nsk of haemolysis, difutional hyponatreniia, shock
an rena a1 ure. - ·
a. Why glycine is the preferred irrigation fluiq for TURP ?

. .
A.· Glycine is used because its refractive ·index allows good vision for
prostatic resection. Moreover, as 1.5°/o glycine is isotonic solution it
does not change the tonicity of the blood and so avoids haemolysis (as
seen with distilled water) , but it does dilute the blood electrolytes. It is
important to remember that rapid absorption of glycine ·is toxic due to
its adverse effect on heart and retina.
0. What are the common signs and symptoms of TURP syndrome ?
A. When TU RP is done under spinal or an epidural anaesthesia, the
patient is conscious , so TURP syndrome can be diagnosed early.
Characteristic f ea tu res of TU RP syndrome are .dizziness, he~d~ch~,
mental confusion , nausea , vomiting, visual disturbances, shortness of
breath , restlessness , tight feeling in the chest and throa~, brady~ardia
• 1• d even
and hypertension. In severe cases 1t can cause convu s1ons an .
coma. If not treated promptly the· patient may develop cyanost~,
hypotension and even cardiac arrest. Diagnosis of TUAP syndrome ~
1
difficult and often delayed when TURP is done under g~nera

anaesthesia. .
-- · . dycardia is the very
Unexplained hypertension and refra~tory brall rents· undergoing
important warninQ sign of TURP syndro~e- S~~ P~~ frequent blood
TURP should be closely monitored with E a .
pressure monitoring.
288 CH . 1o Fluid Therapy in Special Surgical Problems
Q. What is the pathophysiology of TURP syndrome?

A. Pathophysiology of TURP syndrome is mentioned below.
t Circulatory overload : The average rate of fluid absorption through
venous network of prostatic bed during TURP is 20 ml/min. so
usually about 1 litre of fluid is absorbed in one hour. But when
greater fluid is absorbed , increased blood volume leads to
circulatory overload, increased systolic and diastolic blood pressure
and may lead to heart failure. This volume overload and elevated
blood press ure drives fluid from the vascular to the interstitial
compartm ent causing pulmonary and cerebral oedema.
2. Water intoxicatio n : It is a neurological disorder caused by increased
watP.r con te nt of the brain leading to somnolence , restlessness,
and in th e severe cases , seizures and even coma. Papilloedema is
o'fton een. These symptom s of water intoxication appear when
arum . odium level falls 15-20 mEq/L below normal level.
3. Hyponatremia: It is chiefly due to dilution of serum sodium through
exce ive abso rpt ion of irrigation so lution which is devoid of
electrolyt es. The early symptoms of hyponatremia are irritability,
restlessness and mental confusion, while seizures and coma can
occur in se vere form. When serum sodi um falls below 120 mEq/L
hypotension and bradycardia occurs.
Q. How to a sess the volume of the absorbed irrigation fluid ?

A. Tho following. equation allows the rapid estimation of the absorbed
Irrigation fluid volume.
Volum e abso rbed ={ preoperative serum Na x ECF } - ECF
. In litre · postoperative serum Na
ECF I 20°/o of body weight, so ECF = 0.2 x weight (in kg).
0. Wh -.t r the causes of hypotension during TURP?

A. C f hypotension during TUAP are:
1, P eneral anaesthesia or high spinal anaesthesia.
2 Hyp v lemia due to intraoperative blood loss or use of diuretics
r r ' per tively.
CH. 10
Fluid Therapy in Sp~cial Surgical Problems
289
3. Fluid overload, if cardiac failure occurs. ... _: . . . . .

Bladder perforation may . . ·
4. . . bl . cause hypotens1on, but usually there is
an increase in ood pressure. · · ·
5. Sepsis.
6. lntraoperative myocardial infarction.
prevention of TURP Syndrome
a. How do we prevent TURP· syndrome? .1
A. Following measures are useful in prevention of TURP ·syndrome :

1. Early diagnosis and prompt treatment tan prevent onset of severe
or life threatening form of TURP syndrome.
2. Pati ents with pre~xisting hyponatremia are at greater risk of
developing TURP syndrome. So patients on salt restric.ted diet or
diuretic therapy, who are at risk of develop_
ing hyponatremia, need
correction before surgery.
3. Hydrostatic pressure of irrigation fluid at prost~tic bed .determines
the rate of absorption of fluid. The ideal height of irrigation fluid is
60 cm so that approximately 300 ml fluid is obtained per minute
during resection for good vision. So avoid fluid height greater than
60 cm above the patient.
· 4. Restricting duration of TURP to one hour, staged TURP when
more duration of resection is required, preservation of prostatic
capsule and avoiding distention of bladder helps in .prevention of
TURP syndrome. Continuous flow irrigation system reduces
incidence of TURP syndrome as compared to intermittent flow
system.
5. Avoiding 50;0-dextrose preop.eratively, reducing v?lume of
preoperative maintenance fluid therapy, prophylactic ~se. of
frusernide, use of PCV instead of whole blood and close momtonng
of serum sodium are important -measures to prevent T_URP
syndrome.
290 CH. 1o Fluid Therapy in Special Surgical Problems
Treatment of TURP Syndrome · ··
· ·Early and prompt treatment of ~U RP ·syndrome will prevent its serious

1
CNS and cardiac complications. ·
1. Termination of surgery : When TURP syndrome is "diagnosed
surgical procedure is terminated as early as possible . .
2. Diuretics and fluid restriction : About 66o/o !of cases are correG.ted
with just diuretics, fluid restrictions and observation. Frusemide 1mg/
kg or 15o/o mannitol will increase water excretion and reduce the
circulatory OVE?rload. . ..
: 3. Hypertonic salin~ :. Co~rection of severe and . symptomatic
hyponatremia should. be done with slow administration . of 3°!o
hyperto~ic saline with I. V. frusemide. Hypertonic saline must be
given slowly, preferably. in divided doses, with monitc»rfng of serum
sodium level. Rapid administration of s·aline leads to pulmonary
oedem.a and central pontine myelinoly~is. lri general TURP
syndrome can be corrected with 200 ml of 3o/o saline. · ·
Other supportive measures ·:
. .
I
a. Oxygen : Oxygen administr?tion for pulmonary oe~ema .
b. : .S~izures . : It should be treated with diazepam, barbiturate
or dilantin .
. c. i l.V. ·calcium:
.. .To treat acute cardiac disturbances
. during
. surgery.
'· ·· d. · Blood transfusion : Blood loss or anaemia should be corrected
· · · · - . with packed.red cells .
. .. .
FLUID THERAPY IN NEUROSURGERY
fluid in .the neuro~urgical patients is a c.linic.al challenge

The manage.rnent.of _
because.: . . . . . . . . . . .
1.:·· · Blood ·loss is difficult to measure. -

2· Inadequate fluid replacement to avoid increased intracranial pressure
(ICP) will lead to dehydration and cardiovascular instability.
CH. 1 O : Fluid Therapy in Special Surgical Problems 291
3. Overhydration with hypoosmotic solutions will increase cerebral

oedema. · .. ·
4. Diuretics used to red.uce brain bulk can cause intravascular velum~·
shift and electrolyte disturbances. : · · , . .. ·
Q. Why over enthusiastic volume depletion is hazardous ? .

A. Hypovolemia is hazardous even in neurosurgical patients because :
1. Hypoperfusion can impair -cardiovascular performance.
2. Haemoconcentration has adverse effect in the presence of focal
cerebral ischemia. . .
3. Induction of anaesthesia in a "patient :with in'travascular volume
depletion can' be hazardous dt.ie to ttie risk of hypotension. In volume
depleted patients blood·pressure is maintained by vasoconstriction.
But anaesthetic agent induced inctease capacity of the vascular
system - vasodilatation can cause sudden, severe hypotensi9n i.n
' . . . ;. I '·
such volume depleted patients. · · · ·

. ' '
So it ·is necessary to administe.r iso-osmoti~ flui~s· in a~ a~ount

sufficient to normalize the infravascular volurtle before the i~~uction
t 1 I I ''
of anaesthesia. ' .. '
So we have to. maintain euvolemia in n~uros~rgical pati_en.ts ... R.estriction

of fluids to half of the maintenance requirement is ~noug~ tq . control
intracranial pre$sure (ICP).
. h fl .d should be given to neurosurgica·I patients·? Why .?
Q. Wh IC UI S . . .. .
. . . . : . Movement of water across the blood brain ba·~ner is
A. Basis of selection · . the blood to brain total osmqlarity, so type
. determined by the change in. rt t determinant of. ICP and fluid to
·d mains an 1mpo an ·-·
of th~ I. V. flu1 re ~uld remember that-the osmolality of norma 1
flow m parenchyma. One sh · . . .. . . . · .· ·
. b t 285 mOsm/L - . .. . . . .
. pIasma IS a 0~ . . .- d so/c hetastarch are ISO
. line .50/o·albumm ·an o
Safe I. V. fluids : Isotonic sa ' . effect on-the brain's water content
to hyperosrilotic, so they have ~1~~~se Isotonic saline with 308 mosm/
or ICP. So these fluids are safe om . . ~d easily available; so it is:used
. "d . I as well as cheap a . . . . ·.
Losrnolality 1s 1 ea . . atients. . ... ·
most widely in neurosurgica1P
Cautious use : Osmolarity of Ringer's _lactate is · 27 4 mOsm/L and

5°/o-dextrose is 278 mOsm/L. As both of them are hypotonic, they can
increase. ICP and cerebral oedema. So these fluids should be avoided
or should be used judiciously. ·
Q. '/\/hy 5o/o-dextrose is avoided in neurosurgical patients?

A. 5%-dextrose is avoided because :
1. It is hypo-osmotic (278 mOsm/L), hence it accelerates ICP and
cerebral oedema.
2. fn pati ent with acute ischemic brain damage, dextrose produces
hype rg_ly~emia and the anerobic 9xidation of glucose prod_
uces more
lactic acid and free radicals, which further damages t~e brain.
. "
3. · Surgical stress itself raises and maintains blood glucose levels

to an acceptable level during surgery.
Q. When to give dextrose intraoperatively and why ?

A. With perhaps the exception of neonates , to avoid hyperglycemia
neurosurgical patients should not be given glucose solutions
intraoperatively. However patients with longer intraoperative period may
require dextrose supplementation to avoid hypoglycemia. Most of the
healthy adults can withstand withholding of dextrose during surgical
procedures upto 4 hours; thereafter dextrose administration should be
guided by blood glucose measurement and should be maintained at
near low normal range.
Guidelines of fluid management of increased intracranial pressure
A. In acute phase : In acute phase mannitol is the mainstay of therapy
for increased ICP. Mannitol is impermeable to the blood brain barrier
· , · and therefore drains water out of the oedematous brain irito the plasma.
It is most effective in oedematous brain tissue with a defective blood
brain barrier, in the acute phase. Prolonged administration of mannitol
-should be avoided as equilibrium is rapidly established in the brain
and it becomes less effective. If the ICP is markedly raised, restrict
fluids give l_.V. mannitol but be careful to avoid dehydration, electrolyte
imbalance, renal dysfunction and hypotension.
CH. 1o : Fluid Therapy in Special Surgical Prob~ems
293
I
I
I'
8. Maintenance therapy: Fluid restriction and diuretics are the mainstay

of maintenance therapy for ICP. Frusemide and acetazolamide can be
used to improve water clearance. The initial aim is to produce
isovolaemic hyperosmolality, i.e. elevate serum osmolality without
reducing the intravascular volume. Hence tree water loss is replaced
w~th isotonic soluti~ns. The best fluid for this purpose is isotonic saline
with added potassium chloride (KC!). Whole blood or albumin solution
can a!so be u.sed to advantage if required. Diuretic therapy helps in
reducing the nsk of rebound cerebral oedema after stopping mannitol.
Other guidelines for fluid management in neurosurgical patients are

1. Ai m is to keep patient normovolemic and normo or slightly hyper
osmolar, at the same time ensuring normal sodium balance. Watch for
brain related disorders like SIADH and cerebral natriuresis (cerebral
salt wasting syndrome).
2. In general do not replace overnight the fluid deficit unless the patient
has inadequate oral intake , vomiting or excessive urine loss. Remember
that blood loss is difficult to quantify and third space losses generally
are not significant during neurosurgery.
3. When large volume of fluids are required in addition to isotonic saline
use of hetastarch solution or albumin can maintain iso-osmolality, so
this avoids increase ICP without deterioration in blood composition.
4. To assess hypovolemia in neurosurgical patients clinical signs
including hypotension, tachycardia, inability to t~lerate an~s~het~c
agents and a 1 o mm Hg or greater inspiratory expiratory variation in
systolic blood pressure with positive pressure ventilation is us~ful. I,
CVP is helpful to guide fluid replacement and to prevent overhydrat1on.
5. Monitor intraoperative levels of Na+, K+, osmolality, glucose ~nd
haematocrit frequently. Administer insulin if serum glucose concentration
exceeds 250 mg/di.
. FLUID THERAPY IN BURNS

Fluid management in burns patient is controversial and no universal formula
will suffice in every clinical situation. So proper understanding is necessary
in order to make a right choice amongst the various fluid regimens.
Q. Why proper fluid therapy is important in patient with burns ?
A. Proper fluid therapy is important in burns patient because of following
reasons :
A. Hypovolemia can lead to
1. Shock or shock induced renal failure which' can be life
threatening.
2. Rapid conversion of viable but ischemic deep-dermal burn
to non viable full thickness burn, which can increase mortality.
B. Acute loss of protein (especially in first 24 hours) due to leaky
capillaries in the burns tissue causes hypoproteinemia, which
accentuates oedema formation in burns as well as non burns area.
Proper fluid therapy is important for its prevention.
C. Over aggressive fluid therapy can lead to
1. Massive tissue oedema leading to decrease in tissue
oxygenation and further ischemic insult to already damaged
cell.
2. Increased tissue pressure caused by oedema can further
compromise blood flow, again potentiating tissue damage and
increasing risk of infection.
3. Oedema formation in the chest will result in increase in the
work of breathing because of increased chest wall stiffness.
So objective of proper fluid therapy is to
1· Restore and maintain adequate tissue perfusion and oxygenation.
2· Avoid organ ischemia.
3· Preserve heat injured but viable soft tissue.
4
· Minimize the degree of tissue oedema, so as to avoid chest wall
oedema and upper airway obstruction.
5
· Avoid detrimental effect of over resuscitation.
1
CH. O : Fluid Therapy in Special Surgical Problems 295
Fluid therapy in burns is broadly discussed und h d'

er 3 ea ings.
A. Fluid resuscitation in first 24 hours
B. Fluid therapy from 24 to 48 hours
C. Fluid therapy after first 48 hours
Q. Which patient of burns needs intravenous fl .d . .
u1 resusc1tat1on ?
A. Indications of intravenous fluid resuscitation are:
1. Adults with more than 15-20o/o burns.
2. Child with more than 10°/o burns.
3. Electric burns with haemochromogens in the urine.
4. Th e extremes of age or elderly patient with preexisting cardiac or
pulmonary disease, where compensatory response to even minor
hypovolemia is reduced.
Q. Why, when and how long to put nasogastric tube in patient with burns ?
A. Burns of 20°/o or more body surface area (BSA) is associated with
paralytic ileus. So to reduce the risk of aspiration nasogastric tube is
inserted and low suction is performed to maintain gastric
decompression. It is advisable in more than 20% burns, patients with
inhalation injury or those who develop nausea, vomiting and abdominal
distension due to adynamic ileus. After 48 hours patients should be
reevaluated for the possibility of nasogastric feedings. Once the
adynamic ileus resolves most of the patients can be fed within 3 days
of injury. Prolonged ileus can occur with large burn.s, hypok~lemia, over
use of narcotics and is also a hallmark of underlying sepsis.
Q. Why type and volume of fluid selection ~iffers on different post

burn days?
A. To answer this question we need to understand the basic pathophysiology
of burns.
.. . Burns in1·ury causes an increased capillary leak,
a. Initial losses · · · ECF fl 'd f
. I of sodium and protein nch u1 rom
leading to oss artment into area of burns. It leads to significant
intravascufl~rcc;~~sue injured due to burns. Moreover when burns
oedema o( o 25°/c) in~reased capillary permeability occurs
1s large > 0
throughout the body, even in unburned tissue resulting in total bod

oedema. Loss of sodium and protein rich fluid is at its greate:i
during the first 8 to 12 hrs. Large amount of loss of intravascular
fluid in the immediate post burn period can lead to hypotension and
shock.
so due to this basic pathophysiological characteristic during initial
period of fluid resuscitation sodium rich l.V. fluid in · large
quantity is requi.r ed.
b. Subsequent losses : The rate of loss of fluid and plasma volume
decreases substantially by 18 to 24 hours.
c. Losses after 24 hours : As loss of ECF fluid is significantly less
after 24 hours , volume of fluid requirement is less and should
contain less sodium.
A. Initial fluid resuscitation
Q. Why Ringer's lactate (RL) is the most preferred fluid for initial
fluid resuscitation ?
A. Ringer's lactate is the most popular and appropriate resuscitation
fluid because :
1. RL with a sodium concentration o·f 130 mEq/L replaces large
quantity of sodium and water lost from the intravascular space into
the burn wound.
2. Composition of RL is most physiological, so large volume can be
used without causing electrolyte derangements.
3. It is free of glucose so safe in view of early glucose intolerance . . ·
4. Lactate in RL is converted into bicarbonate, which .helps in
correction of metabolic acidosis, commonly found in burns patients.
Q. How much fluid should be given in first 24 hours in patients with burns ?
· te
A. Numerous formulas have been proposed for calculating the appropna
amount of resuscitative volume. But it is important to remember that
given formulae are only a guide and not a regimen to be followed blindly.
The most famous formula is Parkland formula, where estimat~d
15
requirement of Ringer's lactate for the first 24 hours-post burns
10
CH. : Fluid Therapy in Special Surgical Problems 297
calculated based on patient ·

weight and 0/o of body surface area (BSA) of
b urns.
Volume required (ml) = 4 x o/c0 BSA ·

Burn x Body Weight (kg)
As per recommendations of so · ·
fluid therapy should be 2 ml ~e of the centers the volume of initial of
is infused to minimize vol pel r Yo ~SA per weight (kg). Smaller volume
. b ume oadmg. If necessary, fluid volume can be
increase su sequently .
ft is important to remember that 24 hours period for resuscitation is

calc~fa~ed from the time of burn accident and not from the time of
adm1ssron or treatment:
Q. How is the fluid administered in first 24 hours?

A. . It is important at an early stage to secure largebore intravenous lines
for initial rapid fluid resuscitation. Out of total fluid requirement for the
first 24 hours, half is g,i ven within first 8 hours post .burns and
remaining half is given over the next 1,6 hours. This is because fluid
loss is most severe. during the first eight hours, so larger volume is
needed to compensate for the plasma loss in the burn wound. As most
of loss has subsided after the first 12 hours, less volume is needed
subsequently.
Calculated fluid should be infused at constant ·flow rate. Bolusing large
amount of intravenous fluid should be discouraged, $ince boluses of
fluid only increase the patient's oedema.
Q. In which patients wit!1 burns, fluid requirement is altered significantly?

A. Patients who characteristically require large resuscitation fl~id ~olume
are those with high voltage electric injury, inhalation injury, druretrc u~e,
. . . d those who requ1re
delayed resuscitation, burnt while drunk an
escharotomy. .
. e the least possible
Volume sensitive patients who should receiv n years age, those
50
resuscitation fluid volume include those older th~ ling cardiopulmonary
younger than 2 years of age and those with preexis
diseases.
298 CH. 1o : Fluid Therapy in Special Surgical Problems
a. What is the status of hypertonic saline for initial resuscitation of bums ?

A. Because of increased sodium concentration, volume of hypertonic
saline required for initial resuscitation is small as compared to that of
Ringer's lactate. So it results in less tissue oedema.
Increased osmolality of hypertonic saline {513 mOsm/kg of 3°/o NaCl
as compared to 308 mOsm/kg of isotonic saline) generates increased
osmotic pressure, which shifts intracellular water to fill intravascular
volume, and therefore it is effective in treating shock.
Increased osmotic pressure of intravascular volume due to hypertonic
saline counteracts osmotic pressure of the burnt tissue. So hypertonic
saline by decreasing net fluid flux into the burnt area, reduces tissue
oedema and the need for the escharotomy. Urine output is normally
high er with the hypertonic solution because of the natriuresis.
Benefit of hypertonic saline is seen in young patients with more than
50°/o burn s or in the presence of significant inhalation injury to maintain
ECF volume but to avoid massive oedema. Elderly burns patient with
limited cardiac reserve with high risk of developing pulmonary oedema
also gets benefited by resuscitation with hypertonic saline in order to
decrease total volume of fluid administration.
Hypertonic saline is used selectively and sparingly because margin
of safety is low. It requires extensive monitoring and is found to be
associated with higher incidence of acute renal failure. During the
use of hypertonic saline , serum sodium should not be allowed to
exceed 160 mOsm/L.
Q. Why electrolyte-free fluids are avoided for initial resuscitation of

patients with burns ?
A. Electrolyte-free fluids (i.e. solo-dextrose) are avoided for initial fluid
resuscitation because :
1· Endocrine response to burns injury commonly induces
hyperglycemia, so glucose containing fluid should not be used.
2· ~lectrolyte-free fluid is used to replace evaporative loss, which
is modest in early phase due to hypovolemia and vasoconstriction
and therefore such replacements are not required.
CH. 10 : F luid Thera
PY in Specral
. Surgical Problems 299
3. To correct hypovole .
is much Iarge as compared
mia, amount
to RLof- el ec trolyte-free fluid required
signific~nt ad~~t~~~n
oe d ema More .
whe~s1~!~nomf ored_tiss~e
so it will r 1 •
tfhe initial period
o such s d" so 1um 1s
· 0 may lead to
h yponatremia 1um free fluid
However children a re an exc r
h
ave unusu~lly low glycogen s~~/on to this rule. Since children
hyp_oglycem1a, glucose cont . . ag~ a_nd are at risk for profound
period. aining fluid is needed even in th e early
0. Why should colloids b .

A. Colloid infusion i· ~thavo1ded in first 24 hours ?
· s e1 er ineffecr .
and hence avoided as me t. ive or destructive in early period
n 1oned below ·
1. It is not more effective than . . .
volume during this period Ret cr~~tallo1d in ~estoring the plasma
no greater than the equai I en ion of.colloid within circulation is
vo ume of Ringer's lactate
2. Colloid is more expensive as well as not more effective
crystalloid. . than
Due to initial profound capillary leak 0 like . I

s~ift extra~~~~~~?s~:~!'.n1 r:~
3. . .
colloids infused will into the
exacerbat~ _rat~er than improving the total body oedema and will
make mobll1zat1on of oedema more difficult at a later stage.
4. Early c~lloid infusio~ significantly increases extravascular lung
water with resultant higher late pulmonary complications or mortality
especially with inhalation injury. .
0. Why Blood transfusion (BT) is usually avoided initially ?
When and why is blood transfusion indicated in burns ?
A. Initial period : During the first 24 hours plasma loss and hypovolemia
leads to significant haemoconcentration and resultant increased blood
viscosity. Administration of blood at this stage may further compromise
poor peripheral perfusion and so BT is usually avoided initially. However
in patients with prior anaemia or associated severe injuries with blood
loss, PCV is infused to correct anaemia. Whole blood transfusion is
usually avoided to prevent the sequestration of albumin and plasma
proteins in extravascular space.
Subsequent period : Burns leads to red cell destruction and decreased

half-life leading to early destruction, so anaemia is common in post
burn period. Allowing anaemia to persist results in · continued poor
peripheral flow, poor wound healing and stress hypermetabolisrn
induced hyperdynamic heart. So in a patient with haematocrit less than
40, BT is begun on the third day, with an aim to maintain the haematocrit
arou nd 35.
Q. Ho w to manage large thermal burns unresponsive to "adequate
resu scitati on" ?
A. Unrespon siveness to resuscitation may be due to an underestimation
of the severity of the injury, cardiac depression or vasoconstriction. Some
patients respond to fluid volume in excess of predictions. "Early"
introduction of colloid-containing solutions into the resuscitation (at 12-
18 hours instead of the more usual 24 hours mark) or use of cardiotonic
drugs (dopamine or dobutamine) may be useful. Fluid resuscitation of
these patients requires invasive monitoring (i.e. CVP monitoring).
Q. How to manage patients with delayed or inadequate initial resuscitation?
A. These patients usually present with refractory shock, oliguria,
hypotension, acidosis and disturbed sensorium and carry very high
mortality. These patients require the use of greater than predicted fluid
volume, cardiotonic drugs and correction of the acidosis.
Q. Why and how to monitor the fluid resuscitation ?
A. As no resuscitation formula is a "license" to put the patient on auto
pilot, monitoring the burn patient is an important part of resuscitation.
Careful and precise monitoring and necessary adjustment in regimen
is very important for adequate fluid resuscitation in an individual
patient.
1. Sensorium : Anxiety and restlessness may be the early signs of
hypovolemia and hypoxia that require correction.
2. Blood Pressure : The released catecholamines maintain systolic
pressure even in presence of hypovolemia. So blood pressure
recording is a relatively insensitive monitor for adequacy of
resuscitation. Moreover because of peripheral vasoconstriction
and extremity oedema blood pressure recording is difficult.
CH. 1 O : Fluid Therapy in Special Surgical Problems 301
Measurement of blood pressure .in the burnt limb can be even

misleading because auditory blood pressure signal may be
progressively attenuated as oedema develops beneath the burns
wound.
3. Pulse Rate : The pulse rate is a more useful and better indicator.
Pulse rate less than 11 O/min in a young adult is usually suggestive
of adequate resuscitation. When the rate exceeds 120/min
hypovolemia should be suspected. Even cold clammy,extremities'
suggest hypovolemia and demands stepping up of fluid resuscitation.
But pulse rate is a less reliable indicator in elderly patients.
After 24 hours tachycardia can be due to hyperdynamic circulation
secondary to wound inflammation and may not be necessarily due
to hypovolemia.
4. Urine Volume : A urinary catheter is essential for measurement.
Urine output is the best guide to adequate tissue perfusion and is
useful in the assessment and readjustm,ent of volume administration.
1
A urine output of 0.5 o 1 ml/kg/hour or 30-50 ml/hour

.
in an adult.
and 1 ml/kg/hour in a child is considered adequate. The fluid infusion
r te should be adjusted if the hourly urine output falls below or
exceeds by more than 33°/o fo r 2 to 3 hours.
Urine output can also increase spuriously in patients with glycosuria,
hypertonic saline or dextran infusion owing to clearance of an
osniotic load. So increased urine output in such conditions does
not reflect volume status accurately. On the contrary such spurious
increase in urine output may worsen severely depleted intravascular
vo\un1e.
5. Haen1 atocrit : Normal haematocrit value is about 40-50°/o in a
mate and 36-44°/o in a female. ·M ajor burn shock is accompanied
rked haemoconcentration reflected in an elevated
b y a ma . · lt
haematocrit or haemoglobin and adequate resusc1tat1on resu s
in a gradual fall in this parameter to_ n~rmal ~r subnormal levels.
matocrit or haemoglobin 1n the f1rst 24 hours suggest
S.ub norma hae . . . . .
· t" g' anaemia or coex1st1ng· 1n1ury induced blood loss.
preexts in
CH. : Fluid Therapy in Special Surgical Problems
302 10
Urine sodium : Because of sodium loss into the interstitial space

6.
d hypovolemia, the kidney conserves sodium. So before
ansuscitation urinary sodium falls precipitously (less than 20
re . 11 • •
mEq/L sodium on "on spot urine examination). As the volume is

restored, urine sodium value will rise (> 20 mEq/L on a "spot"
sample) indicating improvement in the plasma volume.
7. Metabolic acidosis : Significant metabolic acidosis is seen initially

in major bu rns and its gradual clearance reflects improved
perfusion.
a. Invasive monitoring : The use of invasive monitoring should not
be taken lightly, since the risk of mechanical damage and line
sepsis is especially high in burn patients and should only be
used with specific indications. CVP or Swan-Ganz catheter to
measure pulmonary capillary wedge pressure is useful in elderly
patients with preexisting cardiac or respiratory diseases, massive
burns complicated with inhalation injury and those who do not
respond initially to resuscitation.
8. Subsequent Fluid Therapy (from 24 to 48 hours}
Q. How to plan out fluid therapy between 24 to 48 hours?
A. As the capillary permeability reduces significantly after 24 hours, the
rate of extravascular fluid loss is considerably less than that seen in the
first 24 hours. So lesser fluid volume is required in second 24 hours.
Since burn tissues are saturated with sodium, they do not attract sodium
and inturn water. So in the second 24 hour period, as a rule no sodium
containing fluid is infused.
Electrolyte-free, 5°/0-dextrose should be given in an adequate volume to
ma~ntain urine output and to provide adequate replacement for
maintenance need and to cover evaporative water loss.
Similarly. even capillary protein loss is sealed at this stage, so colloids
can be given safely to restore plasma volume and to maintain cardiac
output.
Q. How much fluid to be infused between 24 to 48 hours ?
A. During the second post burns day the volume of fluid infused per
hour should be roughly reduced by 25 to 50o/o. Further modification is
1
CH. 0 : Fluid Therapy in Special Surgical Problems 303
general~y do~e by closely monitoring the urine output. If the urine

utput 1s satisfactory sub . .
o . . , sequent reduction 1s made gradually in
stepwise fashion.
ouring the first 24 to 48 hours after burns, if the urine output is less
but other parameters suggest adequate perfusion, it can be due to
increased ADH and aldosterone secretion and selective reduction in
the r~nal blood flow. In such a situation low dose dopamine (2-3 mg/
kg/min) may be useful rather than pushing excessive intravenous
fluids.
Fluid infused is chiefly 5°/o-dextrose but if sodium supplementation is
needed, RL or 0.45°/0 saline can be added depending upon clinical
status.
a. How much and which colloids are infused ?
A. The amount of colloids infused after 24 hours depends on the degree
of burns. Volume required is roughy 0.3 to 0.5 ml/kg/0/o of burns (0.3 ml
for 30°/o to 50°/o burns, 0.4 ml for 50°/o to 70°/o burns and 0.5 ml/kg/0/o for
more than 70°/o burns).
Amongst colloids infusion albumin is often preferred, the only drawback
is that it is very expensive. Pentastarch, dextran, haemaccel or low
weight molecular dextran may also be used. Colloids and crystall~ids
must be infused at a constant rate.
C. Fluid therapy after 48 hours
a. Which fluids are required after 48 hours and why ?

A. Fluid requirement after initial 48 hours of resuscitation is the sum
of normal maintenance requirements plus replacement of abnormal losses
(including evaporative water loss and continuous loss of plasn:ia).
• Maintenance requirement contams · ch'1efl Y water ' sodium (3 mEq/
kg) and potassium (2 mEq/kg).
the wound surface at
• Significant evaporative loss oc_curs from S to replace this
this stage which contains chiefly wat~r.
0
ferred Volume
loss salt free solution 5°/o-dextrose is pre ·
required is 1 ml/kg/ 0/o burns approximately.
• Plasma loss occurs into burns tissue in deep burns and wound
surface in superficial burns, which is replaced by dextrose saline
plasma or albumin with an aim to maintain serum albumin > 2.s
gm/di.
·• Correct anaemia by packed cell infusions maintaining haematocrit
> 35°/o.
Urine output, haematocrit, serum electrolytes, blood sugar and renal

function test are monitored during fluid therapy. Fluid selection
needs to be modified as per the electrolyte status. Adequate urine
output (30-50 ml/hour) in absence of osmotic diuresis suggests
adequate fluid replacement. High urine output with high specific
gravity is a clue for osmotic diuresis and it generally indicates the
need for more fluid administration in absence of glycosuria.
Q. How much fluid is required after 48 hours ?

A. Maintenance and evaporative fluid loss is calculated as outlined in
Table No. 10.1, while loss of plasma needs to be determined by clinical
criteria and frequent serum albumin estimation. While calculating volume
of intravenous fluid, volume of oral fluid intake needs to be deducted.
Table 10.1 : Calculation of fluid requirements after 48 hours
1. Maintenance Calculation for a 50 kg patient

100 ml/kg for each kg 1-10 kg 1-1 0, 100 x 10 = 1 ,000 m I
50 ml/kg for each kg 11-20 kg 11-20, 50 x 10 = 500 ml
20 ml/kg for each kg over 20 kg 2·0-50, 20 x 30 = 600 ml
.2,100 ml
2. Evaporative water loss (50 kg patient with 40°/o BSA burn)

1 ml/kg/ 0/o burns= 1 x 50 x·40 = 2,000 ml
So total da.ily requirement is (1 +2)
Maintenance _ 2,100 ml
Evaporative water loss _ 2,000 ml
4,100 ml
CH. 10
Fluid Therapy in Special Surgical Problem·s 305
a When should we use diuretics in a patient with burns ?

A. Oliguria during the resusc·t t" · ·
1a ion period (first 48 hours post burns) is
co~monly due to inadequate resuscitation and is almost never an
in~1cator ~f _acut~ renal failure. It should be treated with increased
fluid ~dm1nistrat1on, not by fluid restriction or administration of
diuretics.
Hovi1ever diuretics are required in a patient with high voltage eiectric

inj ury, deep burns involving muscle and in a patient with ~ssociated
crush injury. All these patients have heavy load of haemochrom.ogens
in the ir urine and are prone to develop acute renal failure unless a
brisk urinary output (75-100 ml/hour) is maintained. One ampoule
(12.5 gm) of mannitol is added to each litre of intravenous fluid until the
desired level of urine output is achieved and urine is clear of pigments.
Diuretics are also required in patients with extensive burns who remain
oliguric in spite of receiving fluid volume far in excess of estimated needs.
Q. Why and how does fluid therapy di'ffer in a patient with electric burns?
. gement of hig: h voltage electric injury is a difficult challenge
A. Mana · . . d 1·
because significant and extensive deep muscle. m1ury may un er me
norma 11 oo k .1ng sk'in · so proper estimation of seventy and extent of burns
becomes impossible in most of cases.
. . · titrated more aptly to the urine output than to a
The resusc1~at~onl l~o underestimate the fluid requirements significantly.
formula that IS 11,ke .Y . d mage deep tissues and muscles and can
· · 1ury can a .
Severe electric. m f . 1 re due to precipitation of urinary
te renal a1 u d'. I
lead to acu 1tubules such patients require ad 1t1ona
ns in the rena · . (
haemochromoge diuretics to achieve high urine flow 75-
. I nt and even
fluid supp eme t acute renal failure. .
100 ml/hour) to preven
306 CH. 1o : Fluid Therapy in Special Surgical Problems
FLUID THERAPY IN URETEROSIGMOIDOSTOMY ·

(Urinary diversion) .
Q. Why and when urinary diversion is required ?
A. Urinary diversion (implantatio~ of the ureter into the sigmoid colon or
into the short loop of ileum) is required to treat patients with obstructive
uropathy due to a locally invasive tumor, surg!cal removal of the bladder
-for carcinoma or less often neurologic bladder dysfunction.
Pathophysiology of fluid and electrolyte disturbances
The most conventional method of urinary diversion is uretero-
-sigmoidostomy. Urine containing chloride, sodium and ammonium is
diverted to the sigmoid colon, which acts as a reservoir. Exchange of
urinary electrolytes with that of plasma by the colonic mucosa is
responsible for the fluid and electrolyte disturbances as mentioned below
1. Hyperchloremia and metabolic acidosis: Luminal urinary chloride

is reabsorbed by anion exchange pump of colonic mucosa with
resultant secretion of HC0 3 in exchange, leading to both
hyperchloremia and metabolic acidosis.
The colonic mucosa can directly absorb ammonium (urinary as
well as colonic) which will aggravate metabolic acidosis.
2. Hypokalemia : Urinary diversion will lead to increased fluid
delivery into the colon, which stimulates potassium secretion
into the lumen. This loss of potassium will cause hypokalemia.
3. Diarrhoea : Due to irritation of colonic mucosa by urine, patient
may develop diarrhoea.
0. Which method of urinary diversion can reduce fluid and elec.trolyte
disturbances and why?
A. These complications are due to the larger capacity of sigmoid colon
and longer urinary contact time in ureterosigmoidostomy.
So to decrease these complications, iliac loop is used to form
uretero-ilial connection. The ilial loop serves as a conduit and not as a
reservoir. Thus the contact time between urine and intestinal mucosa
is minimized and so is the likelihood of acidosis.
CH. 1 O : Flu!d Therapy in Special Surgical Problems 30?
10.1
Treatment
The treatment of hyperchloremic metabolic acidosis needs administration
of alkalizing agents or blockers of chloride transport. As fluid and electrolyte
abnormalities are usually chronic and persistent (unlike acute infective
diarrhoea), fang term planning with oral agents is desirable, although basic
principles are same as described in diarrhoea (Chapter No. 4).
Alkalinization with oral sodium bicarbonate is effective in restoring normal
acid base balance. However oral administration of bicarbonate may not be
tolerated well due to formation of considerable intestinal gas. Sodium citrate
and citric acid solution (Shohl 's solution) used together is an effective
alternative. If excessive sodium administration is a problem (as in cardiac
diseases), and if potassium supplementation is desirable, potassium citrate
may also be used. f n patients with persistent hyperchloremic metabolic
acidosis, where sodium loads are undesirable, chforpromazine or nicotinic
acid may be used to limit the degree of the 'acidosis. These agents used
alone do not correct the acidosis, but they limit its development and thus
reduce the need for alkalizing agents. Chlorpromazine or nicotinic acid inhibit
cAMP and thereby impair chloride transport. Chlorpromazine may be usually
given in a dose of 25 mg three times a day. Nicotinic acid may be usually
given in a dose of 400 mg three to four times a day.
HYPokalem1a . . d ran occurs in patients with
and total body potassrum ep 1e 1 • •
· · usually assocrated with
ureterosigmoidostomies. Hypokafem1a rs . b h
hyperchloremic metabolic acidosis. So treatme~t m_~st .rn~~~=tab~li~
replacement of potassium and correction of metabolrc acr .osis. ere life
a ·d nt of potassium, sev
c1 osis is corrected without replaceme ·t hypokalemia is
threatening hypokalemia can occur. On_ the_ c~nt~~?;;a~ to h erkalemia.
corrected without treatment of metabolic acrdosrs, it c YP
CHAPTER
ELEVEN
EVALUATION AND PRESCRIBING

FLUID THERAPY
EVALUATION AND APPROACH PLANNING AND PRESCRIBING
TO DIAGNOSIS 308 FLUID THERAPY 313
Clues from history 308 Goals 313
Cl in ical sig ns and Clinical approach 313
symptoms 308 Estimating the requirements 314
Investigations and Guidelines for l.V. fluid
interpretati on 309 administration 315
After all detailed discussion of fluid therapy in various clinical conditions in

previous chapte rs here we have summarized how to approach a given patient
and to plan out fluid infusion, considering individual need.
Evaluation and approach to diagnosis
A. . Clues from the history
1. Vomiting or gastric outlet obstruction causes loss of water,
metabolic alkalosis (loss of HCI) and loss of potassium and sodium.
2. Diarrhoea resul ts in loss of water, sodium and potassium but
tends to result in acidos is if the volume loss is severe.
3. Burns provides loss of plasma and ECF (water, protein and sodium).
The magnitude of fluid loss depends on the extent and depth of
the burns.
4. Sweating, if excessive, causes appreciable loss of both sodium and
water, and can cause hypovolemia and shock.
5. Diuretic therapy, especially with salt restriction, induces a state
of mild to moderate salt depletion , hypovolemia and hypokalemia
with no clinical consequence. However such patients are prone to
hypotension during general anesthesia or fluid loss.
6. Past history of renal, cardiac, hepatic or respiratory disease .
can contribute in etiology and type of fluid loss.
8 · Clinical signs and symptoms
1· Excessive thirst with dry tongue, decreased skin turgidity,
restlessness, cold clammy extremities reflects hypovolemia.
_.....I
CH. 11 : Evaluation and Prescribing Fluid Therapy 309
2. Blood pressure and pulse - postural hypotension and tachycardia

are frequently the earliest sign of decreased intravascular volume.
Hypotension indicates a need for sodium containing fluids, colloids
or blood.
3. Urine flow rate per hour reflects tissue perfusion and is an
important indicator of hydration (in absence of glycosuria, osmotic
diuresis or diuretic therapy)
4. Oedema, basal rales and weight gain indicates water retention.
5. Jugular veins, central venous pressure (CVP) and pulmonary
artery wedge pressure (PAWP) measurements are very important
parameters to assess volume status and to administer intravenous
fluid safely and adequately in critical patients especially with cardiac
problem (see Chapter No. 2).
C. Useful investig:ations
1. Blood investigations :
Most useful blood tests are full blood count and haematocrit, serum
electrolytes , blood urea, serum creatinine, serum protein, blood sugar,
etc. Selected patients may need arterial blood gases and pH (ABG),
plasma osmolality and plasma vasopressine (ADH) test.
2. Urine tests :
Urine specific gravity and osmolality, and spot urinary sodium
are most useful tests.
3. Other investigations :
X-ray chest (PA) and ECG.
D. Interpreting laboratory values/Investigations

. . f fluid an·d electrolyte
It is important to remember that diagnosis 0 de on laboratory
abnormalities and its management should never be ~~ always be done
values alone. Interpretation of laboratory values shou
along with clinical background. It d water
.d r e to assess sa an
1. Haematocrit : Provides useful gui e ';emoJysis). In salt and water
depletion (in absence of blood loss or h
CH. 11 Evaluation and Prescribing Fluid Therapy
310
depletion (hypovolemia) the plasma volume decreases and the

hematocrit rises. An increase in haematocrit should be considered
as need for saline infusion.
2. Serum Sodium Concentration
a. I n p u re water de p I et ion (de hydration) serum sod i urn
concentration increases and leads to hypernatremia (e.g.
diabetes insipidus).
b. A decrease in serum sodium concentration i~ mostly due to
water excess and not sodium deficit. Water excess due to
iatrogenic administration of only electrolyte free l.V. solutions
· (i.e. 5°/o-dextrose) or stress-induced antidiuresis is seen
frequently in surgical patients.
c. Hyponatremia associated with tachycardia, hypotension, low
JVP and oliguria is indicative of salt and water depletion and
needs saline infusion.
/
d. Hyponatremia in euvolemic patient, without tachycardia or
hypotension is most commonly due to in appropriate ADH
activity-SIADH (rule out myxoedema, hypokalemia,
glucocorticoid deficiency and renal failure before diagnosing
·SIADH)
e. Hyponatremia in an oedematous patient (e.g. CHF, cirrhosis
of liver, nephrotic syndrome and renal failure) suggest water
as well as salt retention and so usually needs restriction of
water and salt.
3. Serum Potassium Concentration
It represents only a small fraction, about 1°/o of the total body
exchangeable potassium. So severe potassium depletion may be
reflected in only minor hypokalemia. While in the state of
~otassium excess even a small addition of potassium can result
in severe and dangerous hyperkalemia. Serum potassium
concentration is increased in acidosis and decreased in alkalosis.
It. ·
is '':11Portant to monitor serum potassium and avoid hypokalemia
spe.cially in patients with cardiac ·disorders, hepatic, and surgical
~atie~ts with paralytic ileus and hyperkalemia in patient with ren
1mpa1rement.
4. Arterial bl
oo d gases and pH : Change in pH and pnmary
.
well as secondary (compensatory) changes in HC0 3 and PaC
CH. 11 Evaluation and Prescribing Fluid Therapy 311
in simple (primary) acid base disorders are summarized in ·Table No.

11.1.
Tabfe No. 11.1 : Characteristics of simple acid base disorders
Respiratory Respiratory Metabolic Metabolic
Acidosis Alkalosis Acidosis Atkalosis
pH Decreased Increased Decreased Increased
Prima ry changes tPaC0 2 tPaC0 2 tHC0 3 tHC0 3
Secon dary changes tHC0 3 tHC03 tPaC0 2 tPaC0 2
Metabolic acidosis : It is the most common acid base disorder in

the hospitalized patients , characterized by low HC0 3 and low pH.
fn patien ts with metabolic acidosis it is very important to determine
_the anion gap . Anio n gap= Na - (chloride+ bicarbonate)
Norm al anion gap is 12. Important causes of normal anion gap (or
hyp erchloremi c) metabol ic acidosis are diarrhoea and distal renal
tubular acido si s (RTA). Whil e important causes of high anion gap
metabolic acido sis are ketoaci dosis , lactic acidosis, chronic renal
failure and sa licyl ate poisonin g.
Metabolic alka losis : I is characterized by increased HC0 3 and
high pH . Most co mmon cause of metabolic alkalosis are vomiting
(or nasog as tric aspiration) and diuretics.
Respiratory aci dosis : It is characterized by increased PaC02 and
low pH . Respirato ry failure due to various causes leads to
respiratory acidosis .
Respiratory alkalosis : It is characterized by decreased PaC02 and
high pH. It occurs during pregnancy and at high altitud_e in a normal
individual or it can be a marker of underlying grave diseases (e.g.
septicemia· or hepatic failure). .
ful parameter in different1af
5. Plasma osmolality is a very use
diag.nosis of hyponatremia
Plasma osmolality =2 x Na + Glucose + B. Urea
18 . 2 ·8
312 CH. 11 : Evaluation and Prescribing Fluid Therapy
Plasma osmolality in hyponatremia :

Low : True hyponatremia
Normal or high : Hyperlipidemia, multiple myeloma, hyperglycemia
renal failure, mannitol infusion and absorption of glycine during TURP.'
6. Blood Urea Nitrogen (BUN) : Serum Creatinine ratio is 1O:f
normally. Hypovolemia leads to selective rise in BUN/S. Creatinine
ratio, frequently to greater than 20:1, due to excessive renal
reabsorption of urea. This selective rise in the BUN is called
prerenal azotemia.
7. Urine analysis
a. Urinary osmolality (Uosm) : It is helpful in differential
diagnosis of both hyponatremia and hypernatremia. In
hyponatremia Uosm is low but if Uosm is inappropriately high,
think of SIADH.
In hypernatremia Uosm should exceed 600-800 mOsm/kg.
But if Uosm is below that of plasma in the hypernatremic
patient think of primary renal water loss due to diabetes
insipidus (ADH lack or resistance).
b. Specific gravity : It reflects osmolar concentration of solutes
in urine. But if urine contains significant amount of abnormal
solute , such as protein, glucose, radio contrast media, mannitol
or carbenicilline , specific gravity is high (can reach to 1.030 to
1.050) despite a normal urinary osmolality (280 mOsm/kg).
Specific gravity of urine varies in a relatively predictable way
with urinary osmolality, provided urine is normal: For every
35 mOsm/kg increase in osmolality, specific gravity will rise
by 0.001 roughly. Thus a urinary osmolality of 280 mOsm/kg
is associated with a specific gravity of 1.008 approximately.
So when facilities are not available instead of urinary
• osmolality, urine specific gravity may be used. .
c. Urinary electrolytes : They are extremely useful for diagnosis
of fluid electrolyte imbalance and useful guide for fluid therapy.
Spot urinary Na excretion usually reflects renal perfusion and
its normal value is> 40 mEq/L. In renal hypoperfusion, urinary
Na is usually below 10-20 mEq/L. Exceptions to this principle
CH. 11 : Evaluation and Prescribing Fluid Therapy 313
include s_alt wasting renal diseases, adrenal insufficiency and

use of diuretics.
During ~luid therapy rising value of urinary sodium suggests
correction of both hypovolemia and renal hypoperfusion.
Measurement of ur_inary chloride concentration is more useful
in monitoring fluid therapy of vomiting and ketoacidosis.
Planning and Prescribing Fluid Therapy.·

A. Goals
1. To correct life threatening imbalances (shock and hyperkalemia)
as top priority.
2: To replace electrolyte and water deficits.
3. To provide water, electrolytes and nutrients for maintaining the
daily needs of the patient.
4. To avoid creating new disturbances as a result of improper therapy.
5. To prescribe I. V. flu id in a proper order which can be easily
understood and eas ily followed.
6. To select proper l . V . fluid with . correct compositi0.n and to
determine proper rate of infusion.
B. Clinical approach to fluid therapy

1. Fluid-electrolyte therapy is simplified if approached
systeniatically. To arrive to a plan of treatment in any situation,
answers to these questions are needed :
a. What imbalance (deficit I excess) are present now and what
is their probable magnitude ?
b. What additional losses can be expected during treatment ?
c. What are the daily maintenance requirement of fluid and

electrolytes ?
. . . . ?
d. Which problem of the patient gets maximum pnonty ·
2. · r"1ties must be established in the treatment of fluid and electrolyte

P r10 t'
disorders. Therapy must be first directed towards the correc ion
314 CH. 11 : Evaluation and Prescribing Fluid Therapy
of abnormalities that constitute the greatest threat to the patient's

life. These are :
a. Treatment of shock : It needs immediate correction of the
intravascular volume.
b. Correction of hyperkalemia : It carries a significant risk of fatal
cardiac arrhythmias and needs urgent treatment.
c. Correction of blood loss.
d. Avoid the complication of too rapid correction or over correction.
e.g. CHF due to rapid correction of saline, central pontine
myelinosis due to rapid correction of hyponatremia and
overzealous treatment of acidosis with l.V.- NaHC0 3 carries a
risk of seizures because of the rapid flux of PC0 2 into the
cerebrospinal fluid (CSF) with resultant accentuation of CSF
acidosis.
3. Consider renal , cardiac and hepatic status and its severity while
determining individual requirements. Usually these patients require
downward adjustments in sodium and water requirements to
minimize oedema and ascites formation.
C. Estimating total requirement
Calculation of total requirement is based on sum of (1) Present
imbalances (deficit or excess), (2) Expected additional losses and (3)
Maintenance requirement.
1. Present imbalances (deficit or excess)
Requirement for its correction is calculated with the help of
det.ailed history, examination and investigations as mentioned and
recorded properly.
· · 2. Expected additional losses during treatment

Consider following losses and calculate requirements for its
correction and record it properly.
a. Nasogastric suction.
b. Increased insensible losses from fever, high grade environ~ental
~emperature and hyperventilation. .
CH. 11 : E I
va uation and Prescribing Fluid Therapy 315
c. Third space losses of .E . .

patients burns or t CF or plasma tn post operative
' rauma and losses from drains and fistulas.
d. Increased renal loss of w t
(mannitol, low molec a e_r and salt from osmotic diuresis
u1ar weight dextran).
3. Maintenance body requirement
In a normal adult usual maintenanc e required
. .1s :
Water : 2 to 2.5 litres/24 hours.
Sodium : 3 mEq/kg/day
Potassium: 2 mEq/kg/day
Based on these requirements determine the need for the following

a Electrolyte-free water
b. Sodium , potassium and other electrolytes
c. Acid base adjustment
d. Blood and plasma products.
Sum of the all these calculated requirements and deficit will give us
total requirement of the patient. It also gives us exaqt idea about
magnitude of problem , which helps in deciding priority of treatment.
D. Guidelines for I. V. fluid administration

Proper selection and administration of prescribed I. V. fluid includes :
1. Selection of proper I. V. fluid for infusion
2. Safe and proper administration of intravenous fluids
3. Monitoring fluid therapy and reassessing subsequent requirements
4. Specific treatment for primary etiology respons.ible for fluid
electrolyte imbalances
1. Selection of fluid for inf~sion _

Select type and volume of readily available solutions in such a
way that it meets the total requirements of water, electrolytes,
calories and acid-base balance (refer Chapter No. 2,3 and 4).
. 316 CH. 11 : Evaluation and Prescribing Fluid Therapy
2. Guidelines for I. V. fluid infusion

a For safer and proper administration write orders clearly
mentioning total volume of fluid to be infused, type of fluid and
sequence of its administration by numbering bottles (1,2,3 etc.)
b. "Rule of Ten" provides simple and reasonably reliable method
for calculating drop rate (for routine I. v. set where 1 ml = 15
drops) for 1.V. fluid infusion in 24 hours.
As per "Rule of Ten" :
Volume of 1.V. fluid (L)/day x 1O = Drop rate/min.
c. Calculation for microdrip l.V. sets (where 1 ml = 60 drops) :
Volume of 1.V. fluid (in ml/hour) =drop rate per minute.
d. Except in cases of shock, when a physician will be in attendance,
limit infusion rates to < 500 ml/hour
e. Limit potassium infusion to 1O mEq/hr to avoid cardiac arrest.
3. Mon it or i n g f I u id therapy and reassess in g s u b sequent
requirements
For proper monitoring of fluid therapy assess clinical signs and
symptoms of hydration and record daily input/output chart and
weight in the fluid balance chart. During fluid therapy monitoring,
the clinical status will determine which investigations are to be
repeated and their frequency .
At end of each day reevaluate patient; compare it with previous
status to know the extent of correction of fluid imbalance and to
determine subsequent requirement depending.upon current status
of the patient.
On~e patient starts improving and resumes oral therapy decrease
parenteral therapy as soon as possible.
4. Specific treatment for primary etiology
Determine the primary etiology responsible for the fluid and
electrolyte disorders (i.e. diarrhoea, vomiting, burns, diuretic
therapy, diabetic ketoacidosis, diabetes insipidus, SIADH etc.) and
provide specific .treatment for the same.
CHAPTER
TWELVE
PARENTERAL NUTRITION THERAPY

INTRODUCTION 317 Acute renal failure 346
Definition 317 Liver disease 348
Basic principles of nutrition 318 Pancreatitis 350
EN vs. PN 320 Inflammatory bowel disease 352
Indications of PN 322 Short bowel syndrome · 352
NUTRITIONAL REQUIREMENTS 324 Gastrointestinal fistulae 355
Fluid requirements 324 Burns 355
Energy requirements 324 ADMINISTRATION 356
Carbohydrate 327 Selection of macronutrients 356
Fat 328 Delivering PN .. 357
Protein 332 PPN vs. CPN 358
Disease specific amino acids 335 Multiple bottle vs. 3 _
in 1 361
lmmunomodulators: 336 Continuous vs. Cyclic PN 362
Glutamine 336 Designing PN formula 363
Omega 3 fatty acids 337 Calculation of requirements 363
Arginine 337 Preparation of prescription 364
Electrolytes, trace elements Selection of an optimal
and vitamins 337 formula 366
NUTRITIONAL ASPECTS Initiation of PN 370
OF SPECIFIC DISEASES 340 Monitoring of PN 370
Perioperative nutrition 340 Termination of PN 372
Critical illness 341 COMPLICATIONS 372
Cancer 343 Mechanical 373
Cardiac disease 343 Metabolic 373
Pulmonary disease 344 Infectious 376
INTRODUCTION
Parenteral nutrition (PN) is one of the most sophisticated forms of
intravenous therapy used currently. Appropriate use of parenteral nutrition
provides life saving therapy for patients who could not otherwise be
nourished.
Definition . .
Parenteral nutrition (PN) is pharmacological therapies where nutrients,
Vitamins, ·electrolytes and medications are delivered via the venous route
to those patients whose gastrointestinal tract is not functioning and are
unable to tolerate enteral nutrition. ·
PN is an effective means of sustaining life and promoting recovery in
critically ill patients incapable of ingesting, absorbing, or assimilating
. .
·31 a CH. 12 · : Pare~teral Nutrition Therapy _. ·
nutrients. Similarly PN is a .life supporting therapy even for non-critically ill

patients who have pre-existing malnutrition and for non-stressed but
hospitalized patients who are unable to take oral intake for 5 to 7 or more
days.
Basic Principles of Nutrition
1. Avoid malnutrition. There is no disease process that benefits from
starvation.
2. If the bowel works, use it. Whenever feasible, enteral nutrition
(EN)is preferred over parenteral nutrition. But safe and adequate
administration of nutrition is more important than the route of
administration. ·
3. Avoid overfeeding: Overfeeding the patient is associated with
significant complications including hyperglycemia , hepatic
steatosis (fatty infiltration of liver) with hepatic dysfunction,
elevated blood urea nitrogen , and excessive C0 2 production.
4. The route , timing and type of nutritional ·formulation are more·
important than the specific amounts of nutrients supplied.
5. During acute stress, the body mobilizes endogenous amino acid
and energy stores . It is not possible to make catabolic patients
anabolic. The role of nutritional support is to limit protein wasting
and to supply essential and conditionally essential nutrients.
Q. Why it is important to avoid malnutrition?
A. Malnutrition should be avoided because of its detrimental effects.
1. Malnutrition leads to increased morbidity and even mortality. It
leads to increased susceptibility to infection, poor wound healing,
fistula formations, delayed callus formations, pulmonary
complications (impairment of respiratory muscles leading to
.reduction of vital capacity and hypoxic ventilatory response)
decreased tolerance to radiotherapy and chemotherapy, reduce
enzyme synthesis, and impaired oxidation of drugs by the liver.
2. A longer recovery period and increased duration of hospitalization
3. Poor quality of life.
......
CH : 12 : Parenteral Nutrition Therapy 319
a. What are the goals of parenteral nutrition? ·

A. The goals of PN remain supportive. Principal goals of nutritional
support are:
1. To maintain or improve the nut~itional status by providing all

nutrients (proteins, carbohydrates, lipids, electrolytes, minerals,
trace elements and vitamins) for ongoing· metabolic functions.
2. To minim.ize the deleterious ·effects o{
catabolism by maximizing
protein synthesis, limit_ing body protein breakdown and ·reducing
the rate of weight loss. ·
. .
3. To boost up the immune function and to improve wound

healing.
4. To improve the cardiac and respiratory function by restoring the
glycogen storage in cardiac and diaphragmatic muscles.
5. To maintain or correct acid-base and electrolyte disturbances.
6. To accelerate rehabilitation and improve the quality of life.
Q. How to plan parenteral nutrition?

A. Planning of parenteral nutritional therapy is summarized in ~able No.
12.1.
Table No. 12.1 : Planning of parenteral nutritional support
1. Selection of' Patient: Nutritional support is recommended ·only when
potential benefits (improvement in prognosis and quality of-life) exceed
the risks.
2. Calculations of nutritional requirements: Calculate the requirements of
fluid, energy, glucose, lipids, proteins, minerals and vitamins ·tor the ·
individual patients (along .with disease specific modifications).·
3. Select and establish appropriate route of administration . .
4. Prescribe parenteral nutrition: Convert nutritional req~irem~nts to
prescription. Prepare 6r select an optimal formula to deliver nutrients.
5. Administration, monitoring and avoiding co~plic~tions of parenteral
nutritional support.
320 CH. 12 Parenteral Nutrition Therapy
Q. Why enteral nutrition (EN) is preferred over parenteral nutrition (PN)?

A. Enteral nutrition is strongly preferred if the gastrointestinal (GI) tract
(from the jejunum distally) is functional and accessible without
contraindications to its use. The potential benefits of enteral feeding
are:
· 1. Maintains mucosal protection: Provides nutrients, which are
needed in the intestinal lumen to maintain the structural and
functional integrity of GI tract. Enteral feeding prevents atrophy
of intestinal mucosa; and maintains or preserves mucosa! protein
concentration , digestive enzyme function and GI lgA secretion.
Intact mucus membrane prevents bacterial translocation, and
therefore prevents possible risk of sepsis.
2. EN supplies· gut-preferred fuels (glutamine, glutamate and short
chain fatty acids), unlike standard PN.
3. More physiological. The liver is not by-passed. So hepatic ability
to takeup, process and store the various nutrients for later rel.ease
on neural or hormonal command is maintained.
4. Prevents cholelithiasis by stimulating gall bladder motility.
· 5. Fewer serious complications and it also avoids known and
potential complications of PN.
6. Less costly and easier to maintain than .PN.
Because of potential advantages of EN, whenever possible,
provision of even "token" enteral supplementation is'
recommended to patients receiving total PN support.
0. When is enteral nutrition contrajndicated?
-
A. . Cont~dications of enteral nutrition are: .
1.\./f31 causes: Severe diarrhoea, paralytic ileus, intestinal obstruction,
severe GI bleeding, severe acute pancreatitis and high output
~rnal fistula.
2Vcardiac causes: Haemodynamic instability, low cardiac output,·
~ ~
hypotensive patients on moderate to large dose of alpha agonists

or in circulatory shock. Fnteral feeding in haemodynami_g,gl4£-
unstable patients carries potential risk of gastrointestinal ischemia.
. ----
CH. 12 : Parenteral Nutrition Therapy 321
3. Lack of access: Unobtainable safe access to gastrointestinal tract.

4. Complications of enteral ·feeding: The patients with complications
of enteral feeding (i.e. pulmonary aspiration, severe diarrhoea,
and intestinal lschemia or Infarct precipitated by enteral feeding
in patients with ischemic bowel syndrome) should not be fed by
enteral route.
a. \1Vt1at are the advantages of parenteral nutrition over enteral nutrition?

A. Potential advantages of PN ove r-EN are: ----
1. Ensured, desired volume delivery . of nutrients without the
concerns of gastrointestinal intolerance or compliance with
transnasal feeding tubes.
2. Improved metabolic, electrolyt~, and micronutrient management.
3. Better acid-base manipulation.
)
4. Drug delivery · capabilities (histamine H2 blockers,
,...__ ___/
metoclopramide, insulin, heparin etc).
So, PN not only delivers nutrition but -also regulates fluid,
electrolyte and acid-base homeostasis.
Q. What are the contraindications of parehte.ral nutrition? ·
A. Contraindications of PN .are broadly discussed in two groups: ·
A. General contraindications.
1. If enteral nutrition meets .or exceeds the calculat~d nutritional
requirements.
2. Patient with good nutritional status w.ho requires short-term
suppo,rt.
3. Severe liver failure, cardiac f_
a ilure, she.c k and blood
dyscrasias.
4. Fluid-electrolyte imbalances
B. Disease specific contraindications.
1. Avoid excess use of carbohydr~tes in pati.ents · w_ ~th
.
compromised pulmonary function a nd in patients with·
322 CH ; 12 Parenteral Nutrition Therapy
- ventilator support during weaning period, as it may result in

production of large amount of carbon dioxide.
2. Avoid lipid administration_, if the triglyceride l~vel is more
than 350 mg/di or in patients with severe s.epsis, moderate
degree of jaundice, low platelet count (< 50,000 to 60,000/
mm) and ARDS or severe respiratory disease.
3 . . In patients with hepatic encephalopathy and severe renal
failure modified amino acids are preferred over standard amino
acids.
It is important to remember that parenteral nutrition is · not to be
undertaken lightly. It is ·potentially hazardous and can be dangerous
in inexperienced hands. ·
Q. Which facto'rs should ·be considered while determining indications of
nutritional support?
A. Following factors should be considereq for determining the indications
of PN: .
V Age and pre.mo~bid state (healthy. or otherwi.se). .
2JNutritional status including endogenous fuel (fat) and protein
(muscle) stores, weight loss and serum albumin yalue.
3.v»uration Qf st~ryation and degree o! the anticipate,d i,nsult.
4. Underlying disease, its severity and concomitant medical therapy.
5. Gastrointestinal function and the likelihood of r~uming normal
intake ·soon. · ·
------
Indications of Parenteral Nutrition
Parenteral nutrition therapy is indicated to prevent the adverse effect of
malnutrition and to prevent or correct specific nutrient deficiencies when
the gastrointestinal tract cannot be used efficiently or safely tor a prolonged
period . ._PN is expensive and has potential far serious comg!jcatio!l_S. At
the same time use of PN can reduce total hospitalization costs due to
faster recover; and reduced complications _of the underlying condition.
/?_~. b~n.efits ?f PN sh<?Ufcfbe weighed against the pote_ntial .risks bef~~
: ~ :1 m1~1atmg PN. Important indications of PN are summarized m Table
1f 1'2.2. '
d
CH. 12 Parenteral Nutrition Therapy
323
Table No. 12.2: Indications of parenteral nutrition

A. Gene1~ndications '
1. \)fi C\deguate oral or enteral nutrition for at least 7-1 O days
2. re existing severe malnutrition with · inadequate oral or enteral
nutn -1on
B. Anticipated or actual inadequate oral or enteral ·intake
1. Conditions that impair absorption of nutrients
a~rocutaneous fistula
b. ~~bowel ~yr:idrome. \ 1 •
c. ~all bowel obstruction 1
d. ·~cts of radiation or chemotherapy

2. Need _!9f bowel rest
a. (/Sev~re pancreatitis .
b. ~mm·atory bowel disease ·'
c. ~chemic bowel
d. v(e'ytonitis · · - ' '
e. J?fe and post operative status

3. Motilit_)Ydisorders
a. ·~rolonged ileus
4. lnabili~o achieve or maintain enteral -_access
a. vfijlBmodynamic ·instability . .
b. ~c;§.5ive gastrointestinal bleeding . . .
c . ..JJ"']9cceptable aspiration risk . . ·
d. ~yperemesis gravidarum, eating disorders
C. Significant multiorgan system disease
Significant renal, hepatic, and pulmonary diseases or critical illness
(multi . organ failure, severe head injury, burns etcT, which prevents
adequate oral or EN
When to start parenteral nutrition?
Even in critical patients, decision to start PN is never an emergency.
Risks of adve.rse effects of e.N-dec+-a.a-se.s-i-f-p.atient is
~aemodynamically stable, electrolyte abnormalities are corrected, and '
there are no blood glucose disturbances prior to starting PN. At times
adequate Lnitialth.e_r_ap_y of critical illness may sufficiently improve clinical

'siatus ." s~ as to permit oral or EN, and patient may not require PN.
However, early PN is beneficial in patients with preexisting malnutrition,
critically ill patients, acute severe necrotizing pancreatitis and high nutrient
losses from wound or fistulas. '·
NUTRITIONAL REQUIREMENTS
Basic nutritional requirements include balanced amount of fluid ,
carbohydrates, fat, proteins, minerals, trace elements and vitamins.
Fluid Requ'.remen.ts . '3.r -nJ / !e_Q. ( f+•.d ~~ f

The total flurd requrrement rn an adult patient can be ca1f!u1ated
'IE/l ~:i.>l
b\ra~ 'J_!)
abnormal losses to normal daily requirement (35 ml/kg or 1500 ml for 20
~g weight + 20 ml/kg for additional weight). Volume of fluid delivered by
enteral route should be subtracted from the estimated total fluid
requirement. Significant minerals are lost with enteric fluid loss. So extra
amount of these nutrients, as well as fluid, must be added to the parenteral
solution.
Energy Requirements
PN should provide adequate energy to patients. Energy required can be
estimated by any one of the three methods (Table 12.3).
1. By applying a simple calculation based on calories per
kilogram of body weight.
2. By using Harris-Benedict (HB) equation to calculate resting energy
expenditure (fil=E), plus additional calories' for activity and illness
or
3. By measuring energy expenditure with indirect calorimetry.
r ·
Table 12.3 : Methods for estimating energy requirements (kcal)
1. Simple body weight based calculation:

• REE (kcal/day) = 25 x weight
2. Harris-Benedict Equation:
• REE (Man) = 66 + (13.7 x W) + (5.0 x H) - (6.7 x A)
• REE (Women) = 655 + (9.6 x W) + (1.8 x H) - (4.7 x A)
3. Indirect calorimetry:
• REE (Man) = (3.9 x V02) + (1.1 x VC02) - 61
W = weight iri kg H = height in cm A = age in years.
1. Simple body weight based calculation

Energy requirements can be estimated roughly by multiplying actual
body weight in kilogram (for obese patients ideal body weight) by 25
Kcal, which needs correction as per physical activity and associated
illness. (Table No. 12.4)
2. Harris-Benedict equation
Whil e calculating REE by Harris-Benedict equation, for
undernourished patients , actual body weight should be used, and for
obese person ideal body weight should be used. To calculate total
energy expenditure (TEE) from REE, it is necessary t9 correc~_f~r
physical activity (activity factor - AF), associated illness (disease
factor - DF) , and temperature (Thermal factor - TF) as per Table No
12.4.
So, TEE = REE X AF X DF X TF
Table No 12.4 : Guidelines for adjustment in energy requirements
.._ AF==Activity Factor DF=Disease Factor TF=Thermal Factor

1.2 Bed rest 1.25 General surgery 1.1 38°C
1.3 Out of bed 1.3 Sepsis 1.2 39°C
1.6 Multiorgan failure 1.3 40°C
1.7 30-50°/o Burns 1.4 41°C
1.8 50-70°/o Burns
2.0 70-90°/o Burns
3. Indirect calorimetry
Both of above methods do not provide precise estimates of actual
energy expenditure, especiaJly for the markedly under weight, over
weight and critically ill patients. For accurate determination of energy
expenditure in critical patients, indirect calorimetry should be
measured with the instrument metabolic cart.
Most of the time, simple weight basep calculation and HB Equation
over estimates the energy expenditure'·. Remember, it is better to err
on the side of giving too few, rather than too many calories -1.o__fue
p~nt because of the com lications of over feedi~g . .
Q. How to provide energy requirements to a patient on PN?
A. Approximate proportion of different macronutrients (carbohydrate, fat
and protein) in parenteral solution for energy supplementation is as
~ I lows:
50 - 70%
~ o - 30%- Carbohydrate
Fat
(1 gram dextrose
(1 gram lipid
=
=
3.4 kcal)
9 kcal)
1 - 20% Protein (1 gram protein = 4 kcal)
Usually only non protein calories are utilized for energy content of
PN, applying the th eory that protein will be used for anabolic process
rather than as an energy source . ·
In clinical practice , usually . a mixture of glucose and triglycerides is
given in a 'ratio of approximately 60 to 70°/0 glucose and 30-4._~o_ of
fat. This mixed fuel nutrient in stressed atients significant! reduc s
. 0 2 production an , erefore , reduces the respiratory work of
~eathing. · ·"
0. Why it is -important to avoid over feeding?
A. ?ver feeding is associated with the following significant complications:
1. ~.n~o_ntrolled hyper.gl~cerl].ia will produce gly~osu~ia,. ~smotic. .
d!~.resis, and non-ketot1c hyperosmolar dehydration a~Q-·'-~ ~e
cases, coma.
2. Hyperglycemia increases risk of nosocomical infections.
3. Excessive calories can increase oxygen consumption, carbon
dioxide production, minute ventilation, and the work of breathing,
which can fatigue patients with impaired lung function.
,_
CH. 12 Parenteral Nutrition Therapy 327
4. Over feeding can lead to hepatic steatosis (fatty infiltration of

liver), which may lead to hepatic dysfunction.
carbohydrate
Dextrose is the least expensive and most commonly used - primary source
of calories· in the PN. ·
A. Caloric Value, Preparations And Requirements
Each gram of hydrated dextrose monohydrate supplies 3.4 kcal.
Commercially made formulas are available in concentration ranging
from 5°10 to 70°10. Most of central PN (CPN) formulations use dextrose
in 50°10 to 70°10 concentration, which subsequently gets diluted to 15
to 30°10 concentration, when it is mixed with other macronutrients.
Usually 50-?0o/o of total energy requirement is provided in the form of
dextrose.
B. Functions And Advantages
1. Low cost: Dextrose is the least expensive macronutrient, and
hence, most commonly used.
2. Supplies Calories: Parenteral carbohydrate provided in the form
of dextrose is a vital source of fuel. Certain tissues, such as
erythrocytes, white blood cells, and renal medulla, require glucose
(because they lack the enzymatic machinery to oxidize fatty
acids), whereas brain tissue prefers glucose as a fuel. So,_
minimum 100 to 150 gram dextrose per day is required to mset
with this demand.
3. Nitrogen sparing effect: Adequate carbohydrate supplementation
has an important nitrogen sparing effect. Providing calories as
glucose stimulates insulin secretion, reduces muscle protein
breakdown, and decreases hepatic glucose release. Thus dextrose
decreases the need for skeletal muscle to provide amino acid
precursors for gluconeogenesis. Glucose oxidation is also
stimulated, thus sparing the oxidation o~ amino acids.
C. Disadvantages
1. Low calorie supply: Dextrose is a poor source of calorie (3.4
kcal/gram of dextrose vs. 9.0 kcal/gram of fat). So to meet with
the total calorie requirements, patient either needs larger fluid
328 CH. 12 : Parenteral Nutrition Therapy
volume (if we use diluted dextrose solution), or needs highly

concentrated dextrose solution (which can cause thrombophlebitis).
2. Increased C0 2 production (high respiratory quotient): As
~arbohydrates produce more co (as compared to lipids), it
2
increases t~e work of respiratory muscles to eliminate C0 2 and,
therefore, is not preferred as an only source of calorie in
respiratory compromised patien.ts.
3. Thrombophlebitis: Concentrated dextrose solution (above 10%)
has high osmolarity (Table No 12.5), so it can cause
thrombophlebitis, requiring central line for administration.
Table No 12.5 : Osmolarity (mOsm/L) of dextrose solutions
Concentration 5% 10% 20% 25°/o Plasma

Os mol arity 252 505 1010 1262 280
D. Admini stration Of Dextrose Infusion And Monitoring

The amount of oxidation of infused dextrose is directly proportionate to
the rate of dextrose infusion , until a threshold level is reached. The maximum
rate of dextrose oxidation is approx imately 5 mg/kg/min (7.2 gram/kg/
day) , and is not inc re ased by insulin administration . Providing excess
amount of dextrose does not increase dextrose oxidation but could have
adverse consequences (hyperglycemia , fatty liver and excess C0 2
production). Dextrose infusion should be monitored closely, with an aim
to maintain blood sugar between 120-180 mg/di. Administer regular insulin
if necessary. Initially capillary blood glucose should be monitored at every
4-6 hours .
Fat
Lipid emulsion provides an IV source of fat , calories, including the essential
fatty acids linoleic and linolenic acids.
A. Contents Of Lipid Emulsion
Fat emulsion contains long chain triglycerides derived from so~abean
oil or combination of soyabean and sunflower oil. It also contains _egg
yolk phospholipids as an emulsifying agent and glycerin to achieve
isotonicity with plasma.
B. Caloric Values, Preparations and Requirements

Fat is the richest source of calories; one gram provides 9 kcal (vs.
dextrose provides 3.4 kcal/g and protein provides 4.0 kcal/g). The
lipid emulsions are available as 10°/o (1.1 kcal/ml), 20°/o (2.0 kcal/ml)
and 30°/o (3.0 kcal/ml) solution and have low osmolarity (260 mOsm/L).
The optimum percentage of calories that should be infused as fat is
unknown, but 20-30°/o of total calories (or about 50°/o of non-protein
calories) are reasonable for most patients. Limit the total dose to 2.0
gm/kg/day. A minimum of about 5°/o of total calories as a lipid emulsion
is necessary to prevent essential fatty acid deficiency in patients
receiving continuous PN. Underfeeding obese patients with lipid
calories facilitates mobilization of endogenous fat store and may
improve insulin sensitivity and glucose control.
c. Functions and Advantages
1. Calorie supplementation: IV lipid emulsion is calorie dense
(9 kcal/g), so it is the other major calorie fuel, which provides
energy effectively. Providing mor"e energy in a given volume (as
compared to IV dextrose fluids), is an important advantage of
lipid emulsion in critically ill, volume overloaded patients.
2. Glucose sparing, avoids hyperglycemia: Lipid emulsio
provides portion of total calorie requirement, and thereby
allows lower rate of dextrose infusion and reduces the potential
adverse effects of infusing excess glucose for calories.
3. Protein sparing: IV fat emulsion is as effective as IV dextrose in
providing energy. Adequate caloric supplementation spares protein
by conserving body nitrogen economy and supporting protein
metabolism.
4. Less C0 2 production (lower respiratory quotient): As compared
to carbohydrates, lipids produce less C0 2 and, therefore, are
preferred in respiratory compromised patients. Respiratory
quotient (RQ) of fat is the least (RQ of fat 0.7 vs. 0.8 of protein
and 1.0 of carbohydrate). Respiratory quotient is the ratio of C02
production to 0 2 consumption.
So, IV lipid emulsion has the advantages of better glucose
tolerance, less hyperinsulinemia, less production of C0 2, and
' I
'I
less fatty infiltration of liver. Therefore, lipid emulsion is

increasingly utilized in patients with hyperglycemia, diabetes
mellitus, respiratory failure and liver disease. ·
s. Prevention of essential fatty acid deficiency: PN administration
without lipid emulsion beyond 2 weeks is not advisable because
of the risk of essential fatty acid deficiency. Lipid emulsion assist
in wound healing, in the production of ABC and in prostaglandin
synthesis.
6. Reduced risk of thrombophlebitis: Hypertonic solutions are irritant

to veins, thus increasing the risk of thrombophlebitis. Osmolarity
of lipid .e mulsion is low (260 mOsm/L), almost same as that of
plasma. So addition of lipid emulsion reduces the osmolarity and,
therefore, reduces phlebitic potentials of parenteral admixtures.
In addition, l!pid emulsion exerts a protective effect qn the vascular
endothelium. For the same reason, lipid emulsion is an important
component of solutions for peripheral PN (PPN).
D. Adverse Effects and Disadvantages
High cost as compared to dextrose is the major disadvantage of lipids.
Adverse effects of lipid administration are: ·
1. Increased triglyceride levels: Infusion of lipid emulsion causes
increase in plasma triglycerides, cholest~rol, phospholipids and
concentration of lipoproteins. At very high infusion rates,
enzymatic removal system for free fatty acids becomes saturated
·and therefore hypertriglyceridemia can ?ccur.
2. Sepsis: Lipid emulsion carries a risk of. infection when
administered separately over a prolor:iged tir:ne.
3. Fat embolism: Lipid is less stable when infu_sed along .wit.~
amino acids and glucose, as a combined "three-in-on~ solution ·
Destabilized fat particles have potential to coalesce into _larger
droplets to form fat emboli. For the same reason three-in-one
solution has a shorter storage life and improperly mixed or delay
in use of solution carries risk of fat embolism.
CH . 12 : Parenteral Nutrition Therapy 331
4. Rare Complications· Im .
dyspn~a, cyanosis ·naumediate or early adverse reaction includes
an d back pain or thrombocyto
' sea or voem~tmg,
·· headache, flushing, chest
prolonged administration inclu! ma. 0 .elayed complications with
syndrome, pancreatitis and del~y~e:atic dysfunction, fat overload
Most adverse effects are rath . d gastnc emptying.
rrp1"d s er ue to h
per se. Hypertriglyceridemia
.
ypertnglyceridemia than due t
rate faster than lipid clearance. Thus oi~~iu~~sdue ~o
infusion of lipids at ~
rat~s. and serum triglycerides are mo~ito:ed arel infused at proper infusion
of hp1ds are avoided. regu arly, most adverse effects
E. Contraindication
Lipid emulsion shoi.Jld be avoided in . . .
(serum triglycerides > 350 mg/di) (2) ~:t1~nts with (1) hyperlipidemia
evidence of intravascul ' . ac1 o~1s (p~ < 7.3), (3) anemia, (4)
patients at risk f d ~r ~oagulat1on , (5) impaired circLilation, (6) any
~ eve oping fat embolism. Lipid emulsion may not be
necessary at all in obese patients .
F. Administration and Monitoring

.IV lipid
. emulsion , when used to prevent essential fatty acid d
. ef'1c1ency,
·
IS given only 3 to 4 days a week , and when used as a calorie source
is given daily. The lipid can be administered . IV either by piggyback
infusion or as 3 in 1 admixture of fat , dextrose and protein in one
container. Lipid emulsions also provide rich media for the growth of
bacteria and fungi. Scrupulous hand washing prior to handling lipids
is mandatory to reduce the risk of touch contamination.
Since most complications are associated with rapid IV lipid infusion
(in excess of 1.0 kcal/kg/hr or 0.11 gram/kg/hr), the rate should not
exceed 0.7 kcal/kg/hr. Usually lipid emulsions should be administered
slowly over 12 hours. However avoid very slow infusion of lipids, and
bottles and tubing hung alone after 12 hours should be discarded.
Three-incone PN containers and tubing should be changed every 24
hours. In patients with lipid infusion, triglyceride le~~I should be
monitored at least weekly. If level is over 400 mg/di, hp1d should be
cut back ·or preferably discontinued.
G. Modified Preparations
Preparations containing mixture of both long chain triglycerides (LCTs)
together with medium chain triglycerides (MCTs) are currently
available commercially. Medium chain fatty acids can serve as an
energy source during stress, when glucose and long chain fatty acids
are poorly tolerated. These modified preparations have potential
advantages of undergoing more rapid elimination from plasma, more
complete and carnitin as well as insulin independent metabolism, and
a triglyceride lowering effect. So the modified preparations are well
tolerated as an energy source and shown to improve nitrogen balance.
Protein
Amino acids are the primary source of protein supplementation for body
requirement in PN. Amino acids are essential for synthesis of protein and
therefore are the essential component of parenteral nutrition.
A. Calorie Value and Preparations
The calorie supplied by amino acid solution is 4 Kcal/g. 6.25 gm of
protein contain 1 g nitrogen. The standard amino acid solution contains
approximately 40-50°/o essential amino acids (N=9) and rest 50°/o
nonessential amino acids (N=10) plus semi essential (N=4) amino
acids. Crystalline amino acid solutions used in PN are of high biological
quality. The concentration of amino acid in standard commercially
made solutions ranges from 3 to 15°/o. Thus 10°/o solution of amino
acids contains 100 grams of protein per liter.
B. Requirements
Approximately 15 to 20°/o of total energy intake should come from
protein. To minimize protein catabolism a sufficient amount of
nonprotein calories (as carbohydrate and fat) must be administered
simultaneously. A Calorie to nitrogen ratio of 100 - 150 : 1 will be
satisfactory for normal patients. The protein requirement for an
average adult is about 0.8 - 1.5 gm/kg/day, provided total calorie intake
is adequate. Lower protein intake is recommended in patients with
chronic renal insufficiency, not treated by dialysis and certain patients
with hepatic encephalopathy. Protein requirement is higher (1.5 - 2.5
gm/kg/day) in massive burns severe trauma h · · pro t em

- t emem1a, ·
losing enteropathy '_ , ypopro
treatment. In critical~r il~ep~ropath~' or in. patients receiving dialysis
Y patients with sepsis, large amount of nitrogen
I
losses resu ts from abnormal metab . . .
protein requirement in ho . . ~lism. General guidelines for
No. . . spitahzed patients are summarized in Table
12 6
Table No. 12 ·6 : Recommended daily protein intake
Clin ical Condition Protein requirements
(G/kg ideal body wt/day)
Normal 0.8
Metabolic stress (illness/injury) 1.0 - 1.5
Acute renal failure (undialysed) 0.8 - 1.0
ARF receiving dialysis 1.2 - 1.5
Critically ill patients 1.5
Compensated cirrhosis 1.0 - 1.2
Hepatic encephalopathy < 0.5
Acute sepsis 1.7
For critically ill patients optimal protein intake is approximately 1.5 g/
kg/day. This amount of protein intake can decrease the degree of
nitrogen loss in catabolic patients, mostly by enhancing visceral
protein synthesis and to a lesser extent by diminishing peripheral
protein catabolism. Delivering additional amount of protein does not
further reverse this trend and does not yield a positive nitrogen
balance. On the contrary, if excess protein (>1.7 g/kg/day) is provided,
it results in excess ureagenesis rather than contributing to protein
anabolism.
C. Functions and Advantages
1. Calorie supplementation: 1 gram of protein provides 4 kcal energy.
At steady state protein oxidation equals protein intake and,
therefore, calorie requirement should be estimated as total calories
rather than as nonprotein calories. However, some clinicians
calculate only nonprotein calories as energy content of TPN,
applying the theory that the protein will be used for anabolic
process rather than as an energy source.
L
2. Protein synthesis: The main function of protein is growth and

maintenance of cells and tissues in steady stage.
3. Reduces rate of protein catabolism: In critically ill patients protein
catabolism exceeds protein synthesis and leads to net protein · 1oss.
The administration of adequate amount of protein along with calories
decreases the loss of body protein, but does not prevent- the loss
completely.
D. Contraindications and Adverse Effects
1. Hepatic insufficiency: Infusion of standard amino acids in SUGh
patients may cause metabolic alkalosis, prerenal azotemi~,
increased level of ammonia, stupor or coma.
2. Renal failure: Patient with impaired renal function may develo·p
marked rise in BUN.
3. Metabolic or respiratory alkalosis may be exacerbated because
of the excess acetate ions in amino acid solutions.
4. Infusion at excessive rate may cause nausea, vomiting, headache,
flushing, chills or fever.
5. Administration of excess protein or insufficient calorie
supplementation results in the production of increased amount of
urea. Renal loss of excess nitrogen leads to loss of water and
m~y cause hypertonic dehydration (especially in young children},
unless extra water is provided.
E. Monitoring
In stable patients receiving amino acid infusion, the adequacy of protein
support can be assessed by analyzing nitrogen balance.
Nitrogen Balance = Nitrogen intake - Nitrogen loss
Nitrogen Loss = {[24-urir:ie urea nitrogen {G) +4] x 6.25}
Positive nitrogen balance suggests anabolism or nitrogen retention.
Nitrogen loss greater than nitrogen intake {negative nitrogen balance)
suggests net nitrogen loss. While infusing amino acids, if rising BUN
exceeds 100 mg/di or in a patient with hepatic encephalopathy there is
clinical worsening with rising ammonia level, dose of standard amino acid
needs to be reduced or discontinued.
Diseases Specific Amino Acids . . . .

Modified. ~pe~ialized solutions with adjusted amino acid contents are available
tor spec1f1c disease state. . . . . . . ..
1. For Hepatic Encephalop.athy :
PN soluti~ns rich i.n bra11ched chain amino acids (BCAAs) (Pr~viding
up to 50 : 0 of ammo acids ·as leucine, isoleucine, and v~line) are
commercially available~ Compared -with non-branched chai~ amino
aci.ds (Non-~~AAs), which are metaboli.zed by liv~r," BCAAs are
uniquely ox1d1zed in skeletal muscle and adipose tissues and,
therefore, do not directly contribute to he.patic urea production. · ·
In addition, BCAAs compete with aromatic. amino acids (thought to
contribute to hepatic encephalopathy) for the carrier, which is
responsible for their transport into:· the brain. Thus BCAAs potentially
decreases the passage -of aromatic amino acids across the blood
brain barrier. BCAAs may also improve . the efficiency with which
protein is utilized. BCAAs appear to benefit patients by. reducing the
grade of encephalopathy and possibly improving survival when used
in patients suffering from chronic (not acute) hepatic encephalopathy~
In such patients, protein ·administration should be reduced to 1.0 gm/
kg/day. Because of increased cost and arguable efficiency, BCAAs
should not be used as the first line treatment for hepatic
encephalopathy. Once the encephalopathy resolves, the less costly
standard amino .acid solution should be used. Patients with liver
disease but no ·encephalopathy can tolerate the less costly standard
amino acid solutions.
2. For Renal Failure Patients -
PN solutions containing large amount of essential amino .adds are
recommended for'patients who have acute renal failure. The nitrogen
in essential amino acids is partially recycled to produce non-essential
amino acids. So the metabolism of essential amino acids· produces
less rise in the BUN concentration than metabolism of non-essential
amino acids. For this reason amino acid solutions ·designed for use in
renal failure are rich in essential amino acids. Between 67°/o and 1OOo/o
of the total amino .acids in these formulas are composed of the eight
essential ·amino acids and histidine, which is believed to be essential
in patients with renal ~ailure. ~owever, superiority of these specialized

solutions for renal failure patients, over the mixture of essential and
non-essential amino acids has not been established.
3. For volume overloaded patients, a modified amino acid solution with

15% concentrated amino acid base solution provides higher calorie
and protein supplementation in lesser volume. The disadvantages of
this product are similar to those of branched chain solutions, its
expense and lack of evidences for its efficiency.
Special Formulas - lmmunomodulators

These formulas are designed to modify the inflammatory response and to
enhance resis tance to infection by reducing gut bacterial translocation
and enhancing the gut associated lymphatic tissues. In recent meta-
analysis of trials of "immune enhancing" enteral diet (glutamine, arginine
and omega 3 fatty acids), was found to reduce the risk of infection ,
ventilator days and hospital length of stay without influencing mortality.
Glutamine
Glutamine is the most abundant amino acid in the free amino acid pool in
blood and skeletal muscles. Glutamine is a non-essential amino acid as it
is synthesized in the body (primarily by skeletal mu·scles). Glutamine is
essential for cell proliferation. During stress, in critically ill patients, plasma
level of glutamine decreases, inspite of its increased release from muscle.
·Low level of glutamine, inspite of its increased release, is due to its
increased consumption by proliferative cells, where demand exceeds
supply. During stress rapidly growing tissues like intestinal mucosa and
lymphocytes use glutamine as a primary source of fuel, sparing glucose
for other tissues. As requirements of glutamine increases during stress,
glutamine is labeled as "conditionally essential" amino acid.
Glutarnine supplementation can improve gastrointestinal tract structure
and function. Glutamine supplementation increases mucosal cell
proliferation, xylose absorption and decreases permeability of gut. It helps
to maintain mucosal integrity and prevents translocation of bacteria and
endotoxins to circulation. Glutamine is useful in patients with inflammatory
bowel disease, short bowel syndrome, extensive burns, multiple trauma
CH. 12 : Parenteral Nutrition Therapy · 337
and septic shock. ~s glutamine is associated with positive effects on nitrogen

bala~ce and pr.ote 1.11 synthesis, it is useful In catabolic states. In established
sepsis , glutamme 1s believed to Improve Immune function. .
Enteral feeds containing glutamine are commercially ava'ilabl GI t · ·
• • e. u amine 1s
unstable in so 1ution, and therefore not present in standard PN c ti
· t · · IV . . . . urren y
glutamine co~ ainmg solution is available commercially (as Dipeptiven
20°/o or Glamin from Fresenius Kabi).
Omega 3 Fatty Acids
Because of anti-inflammatory and · immunomodulatory effects, omega 3

fatty aci ds have a protective effect (by reducing inflammatory tis~ue
damage , capillary permeability and improved immunological resistance).
At present there is no precise guidelines for the use of omega 3 fatty
acids. However supplementation of omega 3 fatty acids may reduce the
catabolic response to burn injury, trauma and radiation by reducing the
synthesis of prostaglandin that enhances. the inflammatory response.
Omega 3 fatty ac.i ds seems to decrease disease activity and reduce
steroid requirements in treatment of ulcerative colitis, and prevent
recurrence of Crohn's diseases. In oncosurgical patients omega 3 fatty
acids helps in prevention of infection, in achieving weight gain by favo~rably
modifying variety of biochemical parameters. Parenteral omega-3 fatty
acid preparation is available commercially (Omegaven, Fresenius Kabi).
Arginine
Arginine is an amino acid with important roles in nitrogen an~ ammon~a
metabolism, in generation of nitric oxide and ha·s· potent1~1. role m
immunomodulation. supplementation with large quant1t1es of argm~ne may
improve cellular responses, and reduce the incidence of infection an~
wound complications after major surgery. However, paren.teral
administration of large dose of Arginine (more than 15 grams/da.y) is not
recommended.
Electrolytes, Trace Elements and Vitamins . .
ents and vitamins for PN m normal
Requirements of electrolytes, trace e 1em lue needs to be adjusted
adult are summarized in table No. 12.7. These va
according to the clinical situations.
Table No.12.7: Recommended daily parenteral requirements of nutrients
Nutrient Requirements Nutrient Requirements
Electrolytes Fat Solutble Vitamin
Sodium 80 - 100 mmol/day Vitamin A 33000IU

Potassium 60 - 150 mmol/day Vitamin D 200IU
Magnesium 8 - 12 mmol/day . Vitamin E 10IU
Phosphate 15 - 30 mmol/day Vitamin K 150 ug
Calcium 2.5 - 5 mmol/day
. Trace Minerals Water Soluble Vitamins
Chromium 1 o - ·20 ug Thiamine (B 1) 3mg

Copper 0.3 - 13 mg Riboflavin (82) 3.6 mg
Iodine 130 ug Niacin (83) 40mg
Iron 1 - 2 mg Pantothenic Acid (85) 15 mg
Manganese 0.2 - 0.8 mg Pyridoxine (86) 4·mg
Selenium 50 - 100 ug Folic Acid (89) 400 ug
Zinc 3 - 12 mg Cobalamin 812 5 ug
Vitamin C 100 mg
Biotin 60ug
I
E~ectr~l_vtes
As electrolytes are essential to perform critical metabolic activities, it is
must in all_PN formulas. As sodium influences intravascular volume status,
it is restricted in patierits who are at risk of volume overload (those with
cardiac, liver and renal failure) and given liberally when volume expansion
is desired (those w{th GI losses). The requirement of electrolytes to replace
GI secretion can be predicted from approximate. composition of GI
secretions mentioned in table No. 12.8.
Table No. 12 ·8 : Approximate electrolytes of GI secretion
Nam~ol/L Kmmol/L Clmmol/L HCOmmol/L

Gastric Juice 60 9 90 0
Bile 150 10 90 70
Small Bowel 100 5 100 20
Colon 40 100 15 60
Potassium requirement increases in patients with increased renal loss of

potassium, in those · who receive amphotericin B therapy, and in severely
malnourished patients while initiating PN. Na and K ·cations are usually
added to PN solutions as chloride or acetate salt after phosphate
requirements is met. The choice of the salt form has an impact on acid
base balance. Acetate is further metabolized to bicarbonate by the liver,
which provides an alkaline buffer and therefore is a preferred salt in patients
with metabolic acidosis. L9.rge chloride loss (such . as nasogastric
aspiration) can lead to development of metab_ olic alkalosis. In such. patients
Na and K is provided preferably as chloride s~lt for PN ..
Sodium bicarbonate is incompatible for use in PN, as it forms .insoluble
coprecipitates (particularly calcium and magnesium). Bicarbonate salts
should never be infused through a common intravenous line with PN.
Trace Elements
Trace elements are essential in small amounts for efficient ·substrate use
and other supportive functions. Deficiency ·of trace elements develops
quickly ·in stressed patients or ih patients with increased GI losses.' On
the other hand, stable patients do not develop evidence ·of deficiency,
even though trace ·e lements are not supplemented for 2 months.
Commercially preparations are available as injections in a vari'ety of
combinations, which provides required trace elem_ ents.. Most trace element
mixtures contain chromium, copper, manganese, and zinc, but they do
not contain iron and iodine. Iron is given as needed to stable patients as
iron dextran. Some mixtures contai~ selenium,.and others do not Because
of risk of fatal cardiomyopathy caused by selenium deficiency, ·selenium
supplem~ntation is recommended for patients r~ceivi_ng lor-Jg t.erm PN.
The requirements of many trace elements for PN are lower than for oral or
EN. This is because the gut absorbs only a portion of a nutrient supplemented,
which sometimes is even less than 1Oo/o (e.g. chromium). However it is
important to remember that paranteral requirements of some of the trace
elements are higher than actual body requirements. These increased
requirements are because of increased urinary losses, as they are delivered
via systemic rather than portal circulation (and therefore not captured by
liver).
Vitamins
Vitamins are essential for normal metabolism and therefore are important
part of PN. Requirements of trace elements for PN are generally lower
than in EN, but the reverse is true for vitamins.
Parenteral requirements of vitamins are higher than oral or EN requirements
because of following reasons.
1. Vitamins supplemented orally are generally absorbed to a much
greater extent than most trace elements.
2. Vitamins get degraded during preparations and storage. Example
Vitamin A, riboflavin and vitamin K are degraded by light and thiamine
. ·. is degraded by sulfite ions used as preservative for amino acid
·· solutions.
3. Vitamins are lost partially due to adherence to tubings and delivery bags.
Usual recommended dose for water soluble vitamins is four to five times
th~ p ormal requirements, and minimal daily requirements for the fat-soluble
vit~r;r:iins. Commercially available aqueous multivitamin preparations will
provide normal daily requirements for most vitamins with the exception of
vitamin-K. It is important to remember that vitamins and trace elements
are added to PN shortly before the use because of the concern about
stability.
NUTRITIONAL ASPECTS OF SPECIFIC DISEASE

1· Perioperative Nutrition
~alnourished patients undergoing surgical procedures are at a high
nsk for postoperative morbidity and mortality, when compared with
well-nourished patients.
---- - - -- - -
CH. 12 Parenteral Nutrition Therapy. 341
Preoperative Parenteral Nutrition

Preoperative PN in severely malnourished patients (weighf los.s > 10
to 15°/o, serum albumin <2.8 gm/di o"r score ·af less than · 83.5 ·an the
n~trition r~sk index) reduces the rate of postoperative- complications
and improves outcome. Preoperative PN also reduces non-infectious
complications (e.g. pulmonary emboli an·d delayed wound healing).
So, preoperative PN is recommended in moderately or .severely
malnourished patients undergoing major gastrointestinal tract surgery,
provided the operation can be safely postponed. Effective pr~operative
restorati_on of ma.lnutriti.on by PN requires at least 7 to 14 days and
should be contfnued post operatively. Patients with mild malnutrition
did
. not .benefited from PN ' but had more infectious complications
(such as pneumonia or wound infection) than .patients receiving a
regular diet.
Postoperative Parenteral Nutrition
The routine use of PN in the immediate postoperative period carries
. an approximately 10°/o increased risk of postoperative complications.
So, PN should not be given routinely in postoperative patients. Short
term (9 days or less) administration of glucose soh..Jtions does not
compli.cate recovery after major surgery. So, post~perative PN is
indicated in
1. Patients unlikely to resume oral feeds within 1O days. ·Ttie PN is
commonly used · because of paralytic ileus postoperative or
concern about disrupting a new bowel anastamosis. PN is.initiated
usually within 3 days after surgery.
2. Immediate nutritional support' may be appropriate in patients as
a continuation of preoperative nutritional support for malnutrition.
3. In previously severely malnourished patients undergoing
emergency surgery. ·
4. In previously well-nourished patients who have suffered major
trauma or burns.
2. Critical Illness
Nutritional considerations
Critical illness refers to a wide spectrum of life threatening medical
or surgical conditions usually requiring ICU care. Metabolic alterations

in these patients include hypermetabolism, hyperglycemia with insulin
resistance, accelerated lipolysis and net protein catabolism. So,
critically ill patients tolerate starvation for a much shorter period and
are prone to develop malnutrition. Some patients may be malnourished
prior to development of critical illness.
EN is the preferred route of feeding even in critically ill patients
requiring nutritional support. In severely catabolic patients (severe
head injuries, burns and major abdominal trauma) early PN is
recommended if enteral nutrition is not possible for 5 to 7 days. Early
· nutritional support
.
(within the first 48 hours) improves .survival and
reduces infections and length of hospital stay.
Nutritional requirements
Nutrition support cannot fully prevent or reverse the metabolic
alteration and disruption in body composition associated with critical
illness. Nutritional support in these patients is supportive (as opposed
to therapeutic), it can slow down the rate of net protein catabolism.
Their energy expenditure is often lower than values obtained from
classical equations and tables. In most of the patients, energy
expenditure does not exceed 2000 Kcal/day.
Table No.12.9 : Nutritional requirements in critical and .stable patients
Critically ill patients Stable patients
Protein 1.2 to 1.5 g/kg/d 0.8 to 1.0 g/kg/d

Carbohydrate Not >4 mg/kg/min Not> 7 mg/kg/min
Lipid 1 g/kg/d 1 g/kg/d
Total calories 25 to 30 kcal/kg/d 30 to 35 kcal/kg/d
Fluid Minimum needed to deliver 30 to 40 ml/kg/d
adequate macronutrients
3. Cancer
Mal~utrition and weight loss often contribute to the de.ath of cancer patients.
Mallgn~ncy per se or its treatment (such as chemotherapy, radiotherapy
or surgical tre~~ment) can lead to anorexia, nausea, vomiting or diarrhoea,
severe ~ucos1t1s, and GI complications such as dysphagia, ileus, intestinal
obstruction, malabsorption, short bowel syndrome, and fistulae, which
can lead to malnutrition.
Role of PN
a. PN should not be used routinely in patients undergoing .major cancer

operations or along with chemotherapy and radiotherapy .-
b. PN is provided only if clinical improvement with quality survival is
expected.
c. PN is indicated in cancer patients if chemotherapy or radiotherapy is
likely to cause GI toxicity, which will prevent oral/enteral intake for
more than a week. Immediate morbidity is reduced if glutamine
supplement is added to the PN solution.
d. PN is unlikely to benefit patients with rapidly progressive malignant
diseases who fail to respond to the treatment and in terminal stages
of malignancy where further anticancer therapy is ineffective.
4. Cardiac Disease
The use of PN should be reserved for those very few cardiac patients
having postoperative complications that prevent the use of GI tract.
In cardiac surgery patients, EN should be deferred until the patient is
haemodynamically stable. Patients requiring PN after cardiac surgery
carries the risks of volume overload, hyponatremia, metabolic
alkalosis and uremia. To avoid fluid overload in CHF, use maximally
concentrated PN solutions. Fat emulsion can provide greater calories
(9 kcal/gm) with smaller volume. Cardiac patients with anasarca and
HT need fluid and salt restriction. In patients receiving diuretics,
requirement of potassium, magnesium and zinc increases.
5. Pulmonary Diseases
There is a strong association betwee·n malnutrition and lung fun.ction
In fact .it i's often said that , "death from starvation is death.. fro~
pneumonia". · · ·
1. Effect of malnutrition on lung function: If calorie intake is
inadequate in critically ill patients with pulmonary disorders,
protein is catabolised to provide energy. So, skeletal m_ uscle
protein is utilized as a source of calories, reading ,to catabolic
muscle wasting. So, in such malnourished critical· patients
respiratory muscle strength .decreases, .which can precipitate or
aggravate respiratory failure. So, malnutrition can i_ ncrease
morbidity of respiratory disorders , especially respiratory failure
by impairment of respiratory muscle function, decreased
ventilatory drive and decreased response to hypoxia. Malnutrition
induced muscle weakness also adversely affect weaning from
mechanical ventilators. Moreover impaired immune function
associated with malnutrition reduces pulmonary defense
mechanism and increases susceptibility to infection.
. .
2. Effect of pulmonary diseases on nutritional status: Advanced
pulmonary diseases leads to malnutrition and weight loss, due to
increased work of breathing and poor food intake. Patients with
chronic pulmonary disease, who are <90°/o of their ideal weight
have a higher~ .year~ mort?lity, independent of pulmonary status.
3. Effect of nutritional support on lung function: Nutritional repletion
improves diminished respiratory muscle function. Ventilation drive
returns to normal with refeeding and weaning from ventilator
improves.
Nutritional require~ents
Nut~ition given by enteral route is preferred. But if gastrointestinal fu.nction
is impaired for a prolonged period, PN is indicated. Patients with ARDS,
COPD , respiratory failure and patients on mechanical ventilators need
special consideration for their nutritional requirements.
1. The recommended energy intake for patients with chronic

pulmonary disease is 1.7 times their resting energy expenditure.
2. Avoid excess calories from dextrose so as to prevent excessive
co2 production and increased work of br~athing.
3. Lipid is the preferred ' source of additional energy in critically ill
patients with respiratory disorders, as it ·provides more energy
with less production of' CO 2 and therefore reduces the work of
breathing. However excessive or too rapidly infused lipids ·have
been associated with alteration of pulmonary function resulting
in impaired gas exchange.
4. 'Avoid overfeeding: The over production of C0 2 is chiefly due to
overfeeding so energy intake should be kept at or below estimated
needs. As excess supplementation of dextrose and lipids is
harmful, balanced supplementation of dextrose and lipids (70:30)
is ·safe to provide required calories.
5. The use of a low carbohydrate formula, which contains m,ore fat
C!-nd less carbohydrates (50:50) is beneficial in weaning of patients
trorn the ventilator. However, routine use of such a formula in
. amb.L:Jlatory patients with chronic lurig diseases is not ' required .
. 6. It is . ~ wrong concept that, calorie requirements increases in
mech.anically ventilated patient. Ventilatory support provides rest
to respiratory muscles and such. patients are bed ridden, and
hence, .their calorie requirement is lesser than normal.
7. Recommended ·protein or amino acids intake is at lea·st 1 ·gm/kg/
day~ ·Amino acids also increase respiratory drive and the sen·s itivity
of the respiratory centers· to C0 2 •
8. In ARDS patients, administer fluid restricted nutrient formulation,
if haemodynamic status necessitates.
9. .Avoid hypophosphatemia, hy.pocalcemia and hypomagnesemia,
whic~ can r~duce r~spi~~tory muscle strength. These
abnormalities can occur due to refeeding syndrome; so PN should
be · initiated gently in s~verely malnourished patient's with
respiratory disorders. · ·
6. Acute Renal Failure

The acute loss of excretory renal function not only affects water,
electrolyte and acid base meta.b.olism, but also has a pro!ound eff~ct
on protein metabolism and nutnt1on. The hallmark of ARF 1s excessive
protein catabolism and sustained negative nitrogen balance, which
can lead to malnutrition. Energy metabolism is not grossly affected
by renal dysfunction and is more determined by associated
complications. Patients with ARF given parenteral calories and amino
acids have lesser infectious complications and better chances of
leaving the hospital than those A.RF patients given only calories. So,
protein intake in critically ill patients should not be limited in c;in attempt
to avoid initiation of dialysis. Nutritional , requirements of ARF are
variable as per the ·underlying cause and associated complications of
ARF, type and frequency of dialysis and degree of malnutrition, rather
than only on the degree of renal dysfunction.
Initiation of Parenteral Nutrition
When to initiate PN in patients with ARF is an important question .to
be answered. Avoid PN during the acute phase of ARF (i.e. within
first 24 hour after trauma, surgery etc). Infusion of large quantity of
amino acids or carbohydrate during this period will increase oxygen
requirements and may aggravate tubular injury. If the patient is likely
to resume diet within 5 days, nutritional support is not required. In
patients with moderate ·to severe catabolism receiving PN, early
dialysis may be necessary to control uremia aggravated by PN. PN
may lead to or aggravate fh.~id over-load in oliguric patients. Such
patients may need dialysis or continuous renal replacement therapy
(CART) to maintain fluid balance.
ARF patients with mild catabolism can be fed orally. Moderate to
severely catabolic patients with ARF need nutritional support, and in
. such patients enteral nutrition is the preferred route. However total or
supplementary PN is indicated if enteral nutrition is not adequate, or
in patients with GI dysfunction, hypercatabolism or multiple organ
dysfunction.
~-------------~-==::::::::__~
Nutritional Requirements
" ARF Treated Conservatively (n di _

{"· on alytlc therapy)
1. AdjusVrestrict fluid Intake . _. . .
overload in ofiguri ti as per the urine output to avoid volume
need sodium restr~ t~.a ents. ~ost of the ollguric patients also
ic ion. Maximally d PN .
are infused through . . concentrate solutions
a_central hne in oliguric patients.
2. Avoid hyperkalemia h .
by restricting potas '. ypermagne.sem1a and hyperphosphotemia
sium, magnesium and phosphorus.
3. Energy re.quirements are variable as per the clinical status
of the patient.
a. Ene~gy required for uncomplicated _ARF is similar to that

required by a .n?rmal individual (25 Kcal/kg/day).
b. E~~rgy ~equir.ement increases, (25 to 35 . Kcal/kg/day) in
critically 111 patients with ARF (e.g. sepsis, burns, multiorgan
failure). ·
4. Protein requirements are variable as per clinical status

Protein requirement fs 0.8 gm/kg/day for uncomplicated ARF and
approximately 1 .5 to 1.8 gm/kg/day
.
for complicated, hypercatabolic
.
ARF and in malnouri~~ed patients .. Avoid greater supplementation

of protein because it will stimulate the _production of urea and
aggravate uremic complications.
Infusion of balanced solutions containing essential amino acids
and hypertonic dextrose, in predialysis period, can reduce
accumulation of BUN, may delay the need of dialysis and
significantly improve survival.
B. ARF treated with renal replacement therapy

1. . In AR F patients treated with haeniodialysis, pe~itoneal dialysis
or continuous haemofiltration, an extra amino acid sup~ly of ·
02
gm/kg/day should be added to the recommend~d require~e~ts.
This amount will compensate the protein loss, which occurs ~ring
dialysis therapy.
348 CH. 12 : Parenteral . Nutrition Therapy
I
I
2. After regular dialysis is established: a. conventional mixture Of
essential and nonessential am_ino acid 1_s used. .
3. Water soluble vitafnin supplementation is requir~d f~r batients
treated with dialysis. Vitamin C should be given cautious Y ecause
it is a precursor of oxalic acid and excess amoun.ts (> 250 mg/
I
day) can result in· secondary oxalosis. In patients with .acut.e ren~I
I·
failure, requirements of vitamin A, D and E (but not vitamin K) is
incre.ased (unlike in patients with CRF), so ~hey should be
supplemented daily.
7. Liver Disease
Nutritional considerations .
i. The liver is a "work horse" for metabolic activity. Afthqugh the liver
constitutes only 2°/o of the body weight, it consumes approximately
20% of resting energy requir.enients. Liver plays vital roles in
metabolism, storage and distribution of nutrients. ft is the major site
for metabolism of (1) protein (e.g. synthesis of albumin and coagulation
factors), (2) carbohydrates (production of glucose and maintaining
euglycemia) , and (3) nitrogen (urea synthesis antj ammonia
cle~rance). So impaired hepatic function can lead to many metabolic
a~normalities including susceptibility to ~ypoglycemia,
hypoproteinemia, and increased prothrombin time etc~ Malnutrition is
common in advanced liver diseases, often due to excessive alcohol
I'
I and decreased food intake.
I
I
Guidelines for PN in patients with liver disease are similar to other
I
I
I
acute and chroni~ illnesse~. Aggressive PN support improves survival
in patients with hepatic failure.
Nutritional requirements
,I
Nutritional requirements in patients with liver diseases vary dep.ending
upon preexisting malnutrition, type_of disease ~ and severity of illness
and its complications. . . .
Energy requirements
In stable, compensated patients with cirrhosis of liver, non-protein
energy requirement is 25 to 35 kcal/kg/day. In cirrhotic patients with
d
c~mplications (post operative period, · sepsis, GI bleed and hepatic

failure), th~ energy requirement Is considerably high. (35 -,45 kcal/kg/
day ~f est1m~te~ dry body weight). Administration of adequate non-
prote111. calo.nes 1~ essential. for t.he optimum · use of protein supplied
(especially 1.n patients with protein · rest~iction).
In liver failure, glycogen rese~ve diminishes and therefore, the patients
are .prone to develo~ . hypoglyce. mia ~ Patients sho,uld be closely
monitored for glycem1c stat.u.s . . Adequqte administration of dextrose
can prevent hypoglycemia. However, over feeding should be avoided
to prevent complications like hepatic steatosis, liver dysfunction and
over production of C0 2 . IV lipid infusions are well tolerated by cirrhotic
patients. So there is no ·need to change the proportion of fat and
carbohydrate in PN· solution. The percentage· of calories as.fat should
be 25 to 35°/o and in no case should be more .than 40°/o.
Protein requirements
To provide optimum protein supplementat!on ..to cirrh~tic , patient is
the most important as well as the most difficult part of nutrition. If
too much ·protein is given, 'It may p'recipitate ·hepatic encephalopathy;
and if inadequate protein is ,' given, it may lead to malnutrftion.
Requirement of p·ratein v·c:tri~s with . . C.linical_·st~tu_s. · ·
a. Compensated cirrhosis ··
• • ' t
In stable _ .Patient~, protein requiremer;it shoul_d not exceed 1 gm/

kg/day. If the patient is malnourished anq repletion is - d~sired,
· protein supplementation can be .in?reas. ed by 20% ..!f the patient
is hospitalized and unstable, more protein may be needed~ but it
should -be given with caution.
b. ·Cirrhosis with encephalopathy
Protein sho.u ld . be restricted (0.5 gm/kg/day).· in patie.n ts with
hepatic encephalopathy (HE), and is avoided in com?tose P~.tients.
Administration of .branch chain amin? acids (BCAAs) is h~lpful
because ·they pr.o'mote_ bet.t ar nitrogen qalance and P..r $vent
formation of aroJJlatic amino acids (which is as~ociated wit~ the
development of "HE). But these specialized hepatic PN ~orniulas
are expensive and should be us.ed only in those patients ref~~ctory
to conventional treatment. Once the patient recovers from HE

protein should be restarted gradually. '
c. Vitamins and micronutrients
Vitamins and micronutrient deficiencies are frequently seen in
patients with liver diseases, especially in those with alcoholic
cirrhosis. Such patients require supplementation of vitamins (both
fat and water soluble) and micronutrients. Increased prothrombin
time is frequently encountered, requiring supplementation of
injectable vitamin-K.
d. Fluid and salt requirements
Cirrhosis affects the patient's ability to handle salt and water. In
patients with severe anasarca and ascites, salt and water
restriction is necessary.
8. Pancreatitis
If a patient with acute pancreatitis is provided oral or enteral feed in
to duodenum, it will stimulate secretion of pancreatic enzymes.
Pancreatic enzymes can cause auto digestion, inflammation, necrosis
and abdominal pain. So, the aim of EN (Enteral feeding in to jejunum
distal to ligament of Treitz) or PN is to provide adequate nutrition
without stimulating pancreatic enzymes secretion and to prevent
further damage to pancreas.
About 80°/o of patients with acute pancreatitis have a mild and self-
limiting disease and the patient is able to take oral diet within 7 days.
These patients do not require either tube feeding or PN. Roughly 20%
of the patients with pancreatitis, who develop severe disease, are
unlikely to eat within 7 days, and need either EN or PN. In acute
pancreatitis, parenteral nutrition is necessary in patients (a) who
develop paralytic ileus, pseudocysts, fistulae, pancreatic abscess or
pancreatic ascites, and therefore enteral nutrition is not possible; or
(b) if enteral feeding leads to exacerbation of abdominal pain. In
acute severe pancreatitis, as compared to EN, PN is superior and
!I
•'
I
I
more effective in providing rest to the pancreas as well as providing

the total nutritional requirements.
When to start PN? Patients with acute severe narcotizing pancreatitis
are highl~ catabolic, and if not provided adequate and timely nutrition,
are predisposed to malnutrition. In severe pancreatitis, survival
decreases as malnutrition becomes more severe. As per recent
reports, starting nutritional support within 48-72 hours of
hospitalization is beneficial. When PN was delayed beyond 72 hours
in these patients, complications and mortality rates were three times
higher compared to similar patients treated earlier.
Nutritional Requirements
Rough guidelines for nutritional requirements in acute severe
pancreatitis are:
1. Energy : 25 - 35 kcal/kg/day.
2. Protein : 1.2 to 1.5 gm/kg/day.
3. Carbohydrate : 4 - 6 gm/kg/day.
4. Lipid : up to 2 gm/kg/day.
Carbohydrate supplementation
Hyperglycemia occurs frequently in patients with pancreatitis,
requiring administration of insulin for proper glycemic control. So,
blood sugar should be measured every 4 -· ~ hourly.
Lipid infusion
In the absence of severe hypertriglyceridemia (>350 mg/di) or
thrombocytopenia, IV lipids appear safe . and effective, especially if
glucose intolerance is present. Lipids can safely provide ~O - 30o/o of
total calories, (without causing hypertriglyceridemia) and prevent
deficiency of essential fatty acids: Triglyceride level should be
determined prior to starting PN, should be monitored closely and
should remain below 400 mg/di. If triglyceride level exceeds 400 mg/
di, lipid infusion should be withheld. To avoid hypertriglyceridemia, IV
lipids should be given slowly over 10-12 hours. .
352 CH .. 12 Par~nteral .Nutrition Therapy
9. ·Inflammatory Bowel Disease .

The inflammatory bowel disease (180) primarily includes Crohn's
disease (CD) and ulc~rative colitis (UC). In patients . with IBD
malnutrition and nutrient deficiency results from decre~sed intake,
malabsorption, protein losing ,enteropathy, ario
drug .nutrient interaction
(i.e. treatment of UC with sulfasalazin~ can le~d to folate deficiency).
PN" does not increase the rate of remission-<x decrease the need for
surgery in patients with 180. PN and bowel rest s'hould not be used
routinely as primary therapies· for 180. PN is less effective than·steroid
therapy in treatment of CD. Bowel rest is not necessary to achieve
clinical remission. Qorrection of . dehydratio_ n and replacement of
various micronutrients are more important than bowel rest alone.
Indications of Parente.ral Nutrition
PN is indicated in selected patients with 180,
1. If a patient cannot tolerate oral or enteral feeds during acute
exacerbation.
2. If a patient develops paralytic ileus, mechanical bowel obstruction,
..
distal small bowel fistula and toxic megacolon, where more than
I . . .
7 days of starvation is anticipated. ·

3. Perioperative PN is indicated in patients who are severely
malnourished and in whom surgery may be safely postponed.
Patients of 180, who received surgical treatment following
preoperative PN for 5 days or more, had fewer postoperative
complications than those -who did· not receive PN·.
10. Short Bowel ~yndrome
, Massive resection of the small bowel ~ever~ly reduces t.he. area
ava.ilable for the absorption of nutrients and le.ads to d·iarrhoe~ and
malabsorption. These symptoms are severe if (1) more than .75% of
the small bowel is resected, (2) the ileocaecal V'3:1ve is removed, or
(3) the remaining bowel is disease_d with i~paired absorption. Common
causes of shott bowel synd.rome (SSS) are Crohn's diseases,
mesenteric vascular occlusion, malignancy and volvulus.
Pathophysiology and presentation ··

1.· Decrease in intestin al surface are a, a decrease in· intestinal transi·
time and/or dysfunction of the remaining bowel reduces intestina
absorption leading to
a. Large volume diarrhoea, hypovolemia and hypokalemia.
b. Malnutrition, weight loss and deficit of water and fat-soluble
vitamins.
2. Gastric acid hypersecretion due to .loss of .inhibitory hormones,
which are normally secreted by jejunum. ·
3. D-lactic acidosis: · Bacterial fermentati6'n of malabsorbed
carbohydrate in colon p·roduces · substantial ·amount of 0-lactic
acid, which can lead to high anion gap ''metabolic acidosis.
4. Nephroiithiasis: Normafly dietary oxalate is bc»und to intra\uminal
calcium and forms . an .ins6luble complex, which 'is excreted in
stool. In patients with SBS, calcium· is ·bound to unabsorbed fatty
acids. This leads to decreased bindi'ng of oxalate, which is
absorbed · in patients with intact co~on, · leading -to hyperoxaluria,
and.predisposes to oxalate stone formation (especially in presence
.of diarrhoea induced hypovolemia and reduced urine output).
• ~ / ' ; ~ ~' • ' ' '. I
Treatment of SBS
Before the advent ·of PN·, ": s~r~ival in .· a~~t·e .SBS 'tJas "v~ry poor. But
wi,th PN support, many patients surviye. ind.efinit.~ly. f\fter massive
bowel resection, adaptatio.n occurs via bowel . hyperplasia and
' hypertrophy' which b.~gins to occur · i. mme~iate~y after surgery and
may continue for atleast the first' two years. 'The process of intestinal
adaptation · is promoted by supplementin~g ~ ·uminal nl.ttrients. The
metabolic·
.
ancf nutrient therapy of SBS
·'' '
is di.
.
vide9
, .
into 3 phases. '
1. Immediate postoperative period . .

2. Bowel adaptation period.
3. Long term treatment.
1~ · Immediate postoperative period
a. Adequate replacement of lV . fluid, el'~ctro\ytes and other
nutrients.
354 . CH. 12 : Parenteral Nutrition Therapy
b. .Early PN is beneficial and can decrease mortality. It is

important to replace zinc loss, which is required for proper
wound healing but is lacking In standard PN formulas.
c. H2 receptor antagonists for control of hypersecretion
gastric acid. · of
2. Bowel adaptation period
a. As enteral feeding is necessary for bowel adaptation, it should
be started as soon as . the volume of faecal loss decreases
to less than 1000 ml/day.
b. In patients with SBS requiring enteral feeding, EN in bolus
form may cause ,diarrh.oea; so' slow continuous overnight tube
feeding is recommended.
c. The PN is. reduced gradually as enteral intake increases.
d. The nutrient supplementation should contain glutamine and
. m~dium chain triglycerides .to ..main~ain muc~sal healing.
3. Long term treatment . . .:
a.· Selection of treatmeht'is based upon severity of SSS. Patients
with severe type of SSS need· PN along with small enteral/
oral feeding, while · patients · with adequate adaptation and
absorption may not need PN.
b. Oral diet should .be advanced:,
slowly using small and frequent
feeding of solid food. . ~
c. The dietary managemen.t"of SSS depends on whether a
patient has a colon. Patients with intact colon should receive
a diet rich in complex c~rbohydrates. The .intact colon can
convert comple?< carbohydrates to short cha.in f~tty acids,
which stimulates sodium and water absorption and provide
additional calories. Diet should be low in fat and oxalate. In
patients with ·end jejunostomy, normal amounts of complex
carbohydrates are recommended.
d. Water as well as fat-soluble vitamins should be supplemented
adequately. If terminal ileum is resected or resection is gre.ater.
than 100 cm of ileum, injecti~n vitamin S12. should be given
monthly.
e. Patients with D-lactlc acidosis need restriction of

· carbohydrate containing diet and administration of non-
absorbable antibiotics.
11. Gastrointestinal Flstulae
Gastrointestinal fistulas result in diversion of intestinal contents most
commo.nly to skin (gastrointestinal cutaneous fistula). Common causes
of ?I .f1st~I~ are Crohn's diseases, injury to bowel, bowel surgery,
r~d1at1on lnJUry, abscess and foreign body penetration. High output GI
fistulas (loss gr·e ater than 500 ml of fluid daily) might cause substantial
loss of fluid, electrolytes; proteins, carbohydrates, vitamins and trace
minerals resulting in dehydration, acid base imbalance and malnutrition.
These losses together with food restriction to minimize symptoms,
and hypercatabolism resulting from sepsis cause profoun~ nut~ient
depletion and death, if not corrected.
Role of PN is supportive and should be provided to patients with GI
fistula with anticipated inadequate oral or EN beyond 7 to 14 days. In
patients with GI fistula, bowel rest and PN have contributed
significantly to the improvement in clinical outcome (lower mortality
rate, h~gher spontaneous fistula closer and hig~er. ~urgical closer
rates).
12. Burns
Nutritional cons_iderations
Malnutrition in patients with burns carries high risk of complications
such as infection and delayed wound healing. Important causes of
malnutrition are p) large loss of protein and micronutrients through
damaged skin surface, (?) large loss of heat through exposed surface
causes increased energy expen.d itu re and (3) post burn
hypermetabolism and hype'rc.atabol.i~m. Patients with ~~cond or third
degree burn~ are at risk of malnutnt1on and n~~d ~utnt1on support.
Nutritional requirements i ·
Early aggressive nutritional therapy improv~s survival i.n major b~r~s.

EN should be used in preference to PN in burn patients requmng
nutrition support. EN should be initiated as soon as possible in patients
with moderate/severe burns. Use·of PN should be reserved for those
few patients in whom EN is contraindicated or is unlikely to meet
nutritional requirements within 4 to 5 days.
356 CH. 12 .Parenteral Nutrition Therapy
Adequate calories must be provided to counteract the

hypermetabolism associated wit11 acute burn .injury. Current practice
is to provide 20 to 30 % extra calories or 30 to 35 Kcal/kg/day for
most of the patients wlt11 major burns. Severely burnt patien.ts also
require increased intake of protein ~ntil significant WOL;lnd healing is
achieved. Commonly recomme~ded dose is to give 1.3 to 1.5 gram
protein/kg/day. At least 15°/0 . of. total ca.lories .should be supplied by
fat but should not exceed 30 to . 35 °/o. Although the results of
preliminary clinical trials involving arginine, glutamine _and omega-3
fatty acids look promising, considerable controversy still remains.
' . .
:· ADMl~ISTRATION OF PARENTERAL N~~RITION
Selection of Macronutrients ·
A. Practical guidelin.es in selection ·of various solutions for different

patients are:
1. ·Indications of only·dextrose containing crysta'l loids, avoid PN
If patient is unable to take oral intake only for short period (les~
than a week), patient is not malnourished, and patient .is stable
(absence of critical illness or complications), there in no ·deed for
nutritional support. Dextrose infusions (100 to· 150 g/day) with
electrolytes and vitamins are the mainstay for. sho(t-term therapy
in patie·n·ts such .as postoperative patients. Usually 2 to 3 L of 5%
dextros·e ·solution · is infused: Dextrose administration provides
calories and has nitrogen sparing effecqdecreases urinary nitrogen
·1oss.es by . soo/o.i.n comparis·ori with the administration of saline).
2. r ose cont~ining ~~lutions,
Indications of amino ac.ids plus dext_
withhold lipid emulsion
Amino acids infusion is used as a protein supplementation, which
also acts as a body protein sparing therapy (because nitrogen
balance is better with amino acids than with isocaloric dextrose).
PN with combination of amino acid and dextrose will be sufficient
to meet with nutritional requirements if :
a. Patient needs PN, but Its expected duration is only for a

short period (less than 2 weel<S); and
b. Patient is not malnourished, is stable (absence of critical
illness or complications) and total caloric requirement is not
high. Withholding lipid emulsions will not make significant
difference to these patients
c. In patients where lipid emulsion is contraindicated (i.e.
hypertriglyceridemia). In these patients essential fatty acid
deficiency (due to long term PN with out lipids), is prevented
usually by infusing lipid emulsion once in a week.
3. Indications of PN with all three macronutrients (dextrose+ amino
acids + lipids)
These are the most widely used combinations for PN. Addition of
lipid emulsion provides additional calories, reduces osmolarity of the
solution and prevents essential fatty acid deficiency. If patients need
PN, three in one solutions are commonly recommended in the following
situations.
a. All patients who need PN for'"a prolonged period.
b. Patients who need PPN, high caloric supplementation but fail to
tolerate carbohydrates, patients who are critically ill and in patients
with hyperglycemia, diabetes mellitus and respiratory failure.
Delivering Parenterat' Nutrition

For proper supplementation of PN, it is important to understand
different basic aspects .of delivering PN, as classified below:
1. Routes of nutrient delivery . 1
Peripheral parenteral nutrition vs. Central parenteral nutrition
2. Systems of delivering PN
"Multiple bottle" system vs. Three-in-one solution
3. Duration of delivering PN
Continuous infusion of PN Vs Cyclic infusion of PN
.1. ,Routes Of Nutrient Delivery ·

A. Peripheral parenteral nutrition (PPN)
Peripheral parenteral. nutrition (PPN) is the method to delive r
all the required nutrients through peripheral veins. The goal
of PPN is to provide enough calo_ries and nutrition for a short
period (less .than 2 weeks) which can prevent malnutrition
and provide protein sparing nutritional support.
c·omposition: Osmolarity of formulas for PPN should be less
than 900 mOsm/L. Formulas for PPN contains low
concentrated dextrose (5-10°/o) and amino acids along with
concentrated, calorie dense lipids (usually as 20°/o ·lipid
emulsion), which can provide the patient's average basal
energy and protein needs. Lipid emulsion is an essential part
of PPN. Because of low osmolarity (260 mOsm/L), it reduces
the osmolarity of PPN, and therefore reduces the risk of
thrombophlebitis of peripheral veins.
Prerequisite : For PPN peripheral vein should be readily
accessible and the patient should be able to tolerate PN in
large volume.
Indications
1. Requirements of PN for short period (7-1 O days).
Postoperative patients requiring PN support are the most
suitable candidates for PPN .
2. Central venous catheter insertion is not possible, carries
a high risk or is contraindicated (e.g. patients with
coagulopathy).
3. Sepsis or bacteraemia in patients with CPN, to avoid
central vein catheterization for a few days.
Contraindications
1. In patients with high nutritional requirements (i.e.
hypermetabolism, preexisting moderate to s~vere
malnutrition or high risk of protein depletion) PPN is not
suitable, as it cannot provide enough nutrients.
2. ~atients Who need fluid restriction (oliguric patients and

111
oedematous patients due to cardiac hepatic or renal
failure). '
3. Critically ill patients who will not tolerate the high volume
of PPN required for providing their increased nutritional
needs.
Advantages
1· Easy and safe venous access.
2. Avoids morbidity and expense related to .central PN.
Disadvantages
1. Larger volume is required to provide even maintenance
nutritional requirements.
2. Difficulty in meeting with high nutritional requirements
(because volume required to provide the same is
prohibitively high in sick patients).
to avoid thrombophlebitis of pe'ripheral veins,
concentration of nutrients is low in PPN, so larger volume
is needed to fulfill the nutritional requirements (compared
to formulas of CPN).
Prevention of thrombophlebitis due to PPN .
Various measures, which can prevent or reduce
thrombophebitis are:
1. Addition of heparin (1 U/ml) and hydrocortisone (5 mg/
ml) to. the PPN formulas.
2. Placing a glycerin trinitrate transdermal patch on the skin
overlying the tip .of IV catheter.
3. Topical NSAID creams and gel may inhibit the local
inflammatory response.
4. Limiting the ·osmolarity of PPN to 600 mOsm/L.
5. Frequent change of infusion site.
360 CH . 12 : Parenteral Nutrition Therapy
B. Central parenteral nutrition (CPN)

CPN is the most ef'fective method to deliver all the nutrients
by central
. .venous catheter inserted in to either superior 0 r
inferior venacava.
Goal and indications: Goal of CPN is to provide maintenance
nutritional requirements and correct existing nutritional
deficits. CPN is mandatory to provide long term PN support
and to provide increased nutritional requirements to patients
who are moderate to severely stressed.
· Composition: As per the requirement of patients, composition
of solutions for CPN varies. Most of the solutions contain
concentrated forms of dextrose (50-70%) and amino acids
(8.5~10°/o), -which makes these soluHons hypertonic
(Osmolarity of CPN 1000~1900 mOsm/L as compared to
plasma .osmolarity 280 mOsm/L)._These hypertonic CPN
solutions are too irritant for a peripheral vein and, therefore,
should be infused only through a central vein. For safe and
adequate delivery of CPN, it is import~nt to establish central
vascu .l ar access with ·proper selection of type of catheter
and site of insertion.. .
Selection of catheter for .CPN: For CPN, catheter made up of
polyurathrene (for short term use) or silicon rubber (for long
term therapy - months to years) is selected ...
Sites for insertion of catheter for CPN
1. Short term central access: The traditional central venous
is .infraclavicular approach to the .subclavian vein, and
subseque~tly advancing th.e catheter. tip to ~he junction
of the superior venacava and right atn.u~. Thts approach
has the advantage of easy dressing maintenance, bet~er
patient comfort and mobility and, probably, a lower nsk
of infection than other sites. · d
2. Long term central acc.ess: ·~Tunneled" cathetedr ant
. t are more stable an sa e
implanted subcutaneous por s . ced
for long term ·use ..·"Tunneled" catheters are usua 11 ~pa
1
• • • • lar vein and fed into the

in the subclav1an onnterna 1 Jugu . d
superior venacava. A subcutaneous tunnel ts create '
so that the catheter exits from the skin several inches

· away from its venous entry site. The tunnel acts as a
barrier and reduces the risk of infection substantially.
3. Percutaneous Inserted central catheter (PICC): It is the
. latest development in long-term catheter technology. PICC
can be used for CPN therapy for .1 week to as long as 6
months. The catheter is inserted into a vein in antecubital
area of the arm and threaded into the subclavian vein
with the ·catheter tip placed in the superior venacava.
This type of catheter is fast becoming the preferred
·choice for intermedfate term therapy due to less
discO'mfort and reduced complication rates.
' . . .
2 . . Systems of . delivering parenter~I nutrition

.. '
PN may be delivered through "multiple bottle" system or "three

in one." (all in . o~e or ~otal nutrient admixtu.re) system.
A. Multiple Bottle System
In this system separate bags infuse various required nutrients.
11
Advantage of "multiple bo.ttle system is the flexibility and
ease of adjustment to 'rapidly changing parenteral needs,
particularly in critically ill patients.
Dis.advantages of ":multiple bottle" system ·are:
1. Need~ proper monitoring to ~void risks associated with
rapid adm.i nistration, such as hyperglycemia and
hyertriglyceridemia . .
. .
2. Higher risk of incom·patibility due to improper mixing of
.various nutrients. . . '
For reducing number·of connections and .to avoid transfusion
of . multiple bottles simultaneously, mixtµre .of amino acids
and dextrose .i,s infused by. one bag and lipid is infused
separately by : many cer:-iters.
B. 'Three in One'' System
Three in ' one (or "all . in one" or "total ·nutrient admixture") is
the most preferred Way of administering PN. Here all the
components of PN, including lipid emulsions, are placed in a

single bag. Three in one solutions are suitable for long term
cyclic or home therapy.
Advantages of three in one system are:
1. Convenience and time saving as infusion of all nutrients
is done by one bag.
2. Cost saving during preparation, handling and delivery
(require fewer bags and tubings and no need of extra
pump for lipid emulsion). ·
3. Less chances of infection due to less handling during
preparation and delivery (reduced connections and
reduced need of changing of bags).
4. Better assimilation and utilization of nutrients due to slow
rate of infusion.
5. Lesser chances of metabolic complications due to slow
continuous infusion.
Disadvantages of three in one system are:
1. Lack of flexibility in change of its contents.
2. Lesser stability due to addition o~ lipids.
3. Absence of transparent colour. Due to presence of lipids,
three in one solution is opaque, which impairs visual
inspection of the solution for particulate matter,
precipitation or fungal growth.
3. Duration of delivering parenteral nutrition
Continuous infusion of PN vs. Cyclic infusion of PN.
A. Continuous parenteral nutrition
· In most of the acute, critical and hospitalized patients, continuous
infusion of PN is recommended. Slow continuous infusion of PN
by infusion pumps avoids volume overload, side effects secondary
to rapid administration of carbohydrates and lipids (such as
hyperglycemic and triglyceridemia), and provides nutritional
requirements all throughout the day.
CH . ·12 Parenteral Nutrition Therapy 363
B. Cyclic parenteral nutrition

Cy lie PN is the method by which PN Is delivered over a period
of 8 t.o ·12 hours , typically at night wh en patient is sleeping. This
permits a free period of 12 to 16 hours each day for normal daily
. ~ct ivities. Cyclic infusion should not be attempted if glucose
intolerance or fluid tolerance is a problem, and is not suitable for
critically ill patients. Cyclic PN is effective and safe for stable,
chronically ill patients who require long-term nutrient support (e.g.
home parenteral nutrition).
Designing Parenteral Nutrition Formula
Parenteral nu_trition formula can be designed. by following 3 steps,
where requirements of PN of given patient is converted into
prescription and subsequently into commercially available formula to
be infused.
Step 1: Calculation of daily requirements of PN.
Step 2: Convert ·requirement into prescription.
Step 3: To prepare _PN solution as per prescription, or to select an
_optimal commercially available formula to deliver prescribed
nutrients.
Step 1: Calculation of daily requirements of PN
First step in preparing PN prescription is calculation of daily nutritional
requirements. Consider all factors (discussed previously) affecting
these requirements. · Sample calculation of the daily· nutritional
requirements for 60 kg patient, who is stable, euvolemic with good
urine output· and moderate stress, is summarized below: .
1. Fluid requirement: Approximately 35ml/kg.
So 35 (ml/kg) x 60 (kg) = 2100 ml/day.
2. Caloric requirements: Approximately 25kcal/kg.
So 25(kcal/kg) x 60 (kg) = 1500 kcal/day.
3. Protein requirements: · For stable patient 1 gram/kg body weight
So 1 (gm/kg) x 60 (kg) = 60 gram/day
1 gram protein provides 4 kcal, so 60 gm protein will provide 60 x
4 = 240 kcal.
4. Fat requirements: 30°10 of total calories.

So 30°10 of 1500 (kcal/day) = 450 kcal
1 gm of fat provides 9 kcal, so to provide 450 kcal, 450/9 = 50 gm
of fat will be required.
5. Carbohydrate requirement:
Total caloric requirements minus sum of protein and fat calories.
So 1500 - (240 + 450 kcal)
= 1500 - 690 = 81 O kcal.
1gram dextrose in solution provides 4 kcal. So to provide 810
kcal,
810/4 = 202.5 grams of dextrose will be required.
So, total daily requirement of the patient is 2100 ml fluid volume,
total calorie requirements 1500 kcal, 60 gram of amino acids, 50
grams of fat, and 202.5 grams of dextrose. Electrolytes, trace
elements and vitamins should be added as per requirement.
Step 2: .Convert requirements into prescription
Basic principle: Selection of concentration of the nutrients is inversely
proportionate to the volume of fluid to be infuse.d. Select greater
concentration of various nutrients, if patient needs fluid restriction
(e.g. in CPN). When patient needs PN and larger fluid vol~me is
permitted, nutrients in low concentration are se~ected to prepare PN
solution (e.g. in
PPN).
Method to convert requirements into prescription
The process to determine an individual formula is very complex. For
above calculated requirements (fluid volume = 2100 ml, amino acic
60 grams, fat 50 grams and 202.5 grams dextrose), prescription car
be prepared by following steps.
1. Determine volume of lipid emulsion
We will select 10% lipid emulsion (as volume restriction is not
necessary) to provide 50 grams of fat.
Amt of substance (gm)

Fluid volume required (ml) = · , x 100
Cone of substance (%)
50 (gram)
So, volume of lipid emulsion · (ml) =· , · , x 100
I =500 ml.
So, 500 ml of 10°/o fat emulsion is required.
Remaining volume .of fluid to . be infused 2100 ml - 500 ml ==
1600 ml. So, in 1600 "ml fluid volume· amino acid and dextrose
should be supplemented.
2. Dete.rmine vol~me of amino. acid infusion . : ..

Calculate volume of 10,% amino aci~ solution.to procure 60 gram
of amino acid.
. . . _ . . . . . Amt of substance (g) x· .

Fluid volume required (ml)'= ·_ ._ _ _ _ _ __ 10 0
. Cone of substance (0/o)
,. .
.- Iume
S o, vo · of ammo
·
· ac1'd (m I) = 60.1·0(gram)
(Yo 0
) .
x··100 '
-. .-_.
= 600 ml. ·
So, 600 ml of 10% amino .acid .sol_ution ~s required. . .
~ Remaining volume of fluid to. be infused = ~100 ml .- (500 ml +
600 -ml sum of lipi~ .and am,ino acid) =.21 o:o mL - 110.0 ml
= 1000 ml.
•
So, volume required for dextrose to be infused will be 1OQQ. ml.
' ' I ;
3. Selection of. ·dextrose infusion . . .

In remaining 1000 ml fluid vol.ume, ~grarn of . de~tro~e needs
to be infused. ·· .· · · · .
Amt of substance (g) .. ·.

Fluid volume required (ml) = - - - - - - - - x 100
Cone of substance (0/o)
202.5 (gram)
1000 (ml)= ---------~--- x100
Concentration of substance (0/o)
202.5 (gram)
Concentration of substance (0/o) = - - - - - - x 100
1000 (ml)
. = 20.25o/o = 20 %
So, 1000 ml of 20 % of · dextrose is needed to provide
calculated requirement of dextrose.
4. Prescription
Patient needs 500 ml of 10°/o lipid emulsion,
600 ml of 10°/o amino acid and
1000 ml of 20°/o dextrose.
St~p 3: To prepare PN solution or to select an optimal formula
for prescription
As per prescription PN solution can be prepared, but such facilities
are not available in most of the centers. So, rather than preparing
iailor made PN solution, one or combination of more than one solution
are selected from readymade commercially available solutions, which
almost matches with the prescription.
To provide adequate required nutrients, it is very important to select
proper readymade solution. To help the clinician in quick and proper
selection, PN solutions available commercially are classified in Table
No. 12.10, Table No. 12.11 and Table No. 12.12.
Table No. ·1 2.10 provides a bird's eye view on PN solutions classified
broadly as per their contents and route of administration. It also
provides information about different volumes in which these products
are available. Once tentative selection is made, table No. 12.11 and
table No. 12.12 provides all the details about the contents required by
the clinician in day-to-day practice.
Table No 12.1 O: Classification o·f commercially available PN products

Route From Fresenius Kebl From Clarls Llfesclence
Amino acid containing

PPN Aminoven 5 %, 500ml
Aminoven infant 6 %, 1OOml I
None
CPN Aminoven 1O %, 500ml
Aminoven infant 10 % 1OOml Celemin-10 Plus,.200 ml/500 ml
Amino acid and dextrose containing
PPN None Celemin -58, 200 ml/500 ml
CPN Aminomix 1, 1OOOmV1500mV2000ml PNA-10, 1000 ml

PNA - 12, 1350 ml
PNA - 16, 1800 ml
Lipid emulsion
'
.
PPN lntralipid 10 %, 100ml/ 500ml Celepid-10%, 500 ml I
lntralipid 20 %, 250ml/500ml Celepid-20%; 250 ml/500 ml

lntralipid 30, % 333 ml Celepid MCT-LCT-20%, 50mV250mV500ml
Three in One solutions

•,
PPN Vitrimix, 1OOOml Celemix 1000 ml

(750ml AA+ Dextrose & 250ml lipids) TNA Peri 2000 ml
. .
CPN Kabiven, 1OOOml/1500ml/2000ml Celemix G 1000 ml

TNA 2000 ml w
Diseases specific amino acids
Aminosteril N Hepa 8 %, 500ml Celemin-Hepa 8%, 500 ml

PPN
Nephrosteril 7 %, 250ml/500ml Celemin-Nephro.7%, 500 ml
lmmunomodulator solutions
Dipeptiven 20 %, 50ml/1 OOml . None

PPN
Omegaven 1O %, 50ml/1 OOml None
368 CH. 12 Parenteral Nutrition Tllerapy
i
I!
Table No. 12.11 : Composition of PN products marketed by Fresenius
Kabi in India
Calorie !Os molarity Route Dextrose Amino acids
-
Solution Vol. Lipids
(ml} (J<cal} mOsm/L (Grams) , (Grams) (Grams)
-
Dextrose 1000 400 505 PPN ·100 - -
10 %
Dextrose 500 400 1010 CPN . 100 - -
20 %
..
Aminoven 500 100 495 PPN - 25 - .
5%
Aminoven 500 200 990 CPN .. -. 50 -

10%
i
Aminoven 100 24 530 PPN - 6 -
infant 6 % I
..
Aminoven 100 40 885 CPN - 10 -
infant 10 %
Aminomix I 1000 1000 1769 CPN 200 50 -

--
lntralipid 500 550 272 PPN - - 50
10% ..
:
lntralipid 500 1000 273 PPN - '
- · 100
20% . ·-
- 100·
lntralipid 333 900 219 PPN -
30%
. Vitrimix 1000 1000 960 PPN 75 53 50

{750 + 250) ·-
Kabiven 1000 34 40
1000 1060 CPN 110
Aminosteri\ 500 160 no PPN - 40 -
N Hepa8%
Nephrosteril 500 140 645 PPN - 35 -
7%
Table No. 12.12 : Composition of PN products marketed by Claris Lifescience

I
Solution Vci. Calorie Os molarity Route Dextrose Amino acids Lipids

(ml) (~<cal) mOsm/L (Grams) (Grams) (Grams)
Celemine 10 500 400 1040 CPN - 100 -

Plus
Celemine5S 500 400 800 . PPN . 25 50 -

•,
PNA-10 1000 1200 1908 CPN 250 50 -

PNA-12 1350 1500 1811 CPN 300 . 75 -
PNA-16 1800 2000 1811 CPN 400 100 -
Celepid 10 500 550 300 PPN - - 50
Celepid20 500 1000 279 PPN - - 100
CelepidMCT 500 954 . 380 PPN - - 100

LCT20% . '
Celemix 1000 800 670 PPN 37.5 37.5 . 50
TNAPeri 2000 1525 818 PPN 159 60 .. 68
CelemixG : 1000. ·1040 . '1110 CPN 75 60 . 50 .

I ·' '
TNA 2000 2044 1158 CPN 240 80 80
Celemine · 500 320 770 PPN - 80 ' -

.. !
Hepa a%
Celemine 500 280 637 PPN - 70 -

Nephro7%
Initiation of PN
• A detailed medical ex~mination including history, physical exami
nation an~ laboratory studies, is necessary to establish nutri-
tional re~u1reme~ts as well as to select the need based PN solution
tor the given patient. ·
• To avoid adverse effects, PN should be initiated slowly with a
vohJmetric infusion pump; 50°1° of the goal on first day, 75o/o on second
day , and 100°10 o~ third to four.th day.
• Because PN solutions are hi~h in dextrose, infusion should be
initiated slowly. Slow infusion . will allow the pa.tient's pancreatic
beta cells to a~apt ~o · the . glucose by increasing insulin output.
Within 3 to 5 days of initiating PN, most of the adult patients
tolerate about 3L of solution per day without causing adverse
reactions.
• In severely malho"urished p'a tients·, PN may precipitate refeeding
syndrome, due to._ rapid fall in p.otassfum, magnesium and phosphorus
levels. So slow · initia.tion .and close monitoring of the patient's
electrolytes is necessary to avoid compromising the cardiac and
respiratory function. .. .
Monitoring of PN ,,·;-· ·
Every patients receiving PN sh9uld be monitored carefully for the_
prevention or early detection of cohiplications as well as to judge the
effectiveness of therapy .- Clinical :data: and laboratory studies used
routinely for monitoring patient re·ceiving PN is summarized in table
No. 12.13.
• Always obt~in a chest X-ray to .check catheter placement after insertion.
• Record vital signs at least every 4 hours. Temperature .elevation
is orie of the earliest signs of catheter related sepsis.
• Patients should be weighed daily at the same time each morning after
voiding, on the same scale. Weight gain may indicate fluid overload.
• Perform site care and dressing change at least three times a week,
or whenever the dressing becomes wet.
• Patients receiving PN should be monitored carefully to de.tect early
signs of complications such as fluid overload, electrolytes imbalance,
nutritional problems or allergic reactions.
Table No. 12.13 : Monitoring the patient. on parenteral nutrition
Clinical data monitored dally
History · Sense ~f Well being, strength to perform routine activity;

fever, history suggestive.of fluid overload or glucose and
electrolyte imbalance.
Vital signs Temperature, pulse, blood pressure and respiratory rate :
Fluid balance Strict input/output chart, weight. ··
Local care Inspection and dressing of site of vascular access
(rule out infection).
Delivery system : Inspection of solution for contamination, and watch for
proper functioning of infusion pump, catheter function and ti~ely
changing of tubing and bags.
Laboratory Data
Fingerstick glucose (HGT) Three times daily until patient stable

Blood glucose
Na, K, Cl, HC0 3 ,
Blood urea nitrogen
} Daily until glucose inf us.ion load and
.. patient stable, then twice weekly
Liver function studies
Serum creatinine, albumin l
P0 4 , Ca, Mg
Hb/Hct, WBC J Baseline, then twice weekly
Clotting, INR Baseline, then weekly

Micronutrient tests as indicated
• Monitor serum glucose levels every 6 hours initially, then once a day .
Watch for the symptoms of hyperglycemia such as thirst and polyuria:
• Monitor electrolyte and protein levels daily at first, and then twice a
week. Albumin levels may drop initially as treatment restores
hydration.
• Assess liver function with liver function tests, bilirubin, SGPT,
triglyceride, and cholesterol levels. Abnormal values may indicate
intolerance.
• Monitoring response to nutritional therapy. There is no single criterion .

which can reliably indicate effectiveness of PN. Improvement in clinical
status and visceral protein concentrations (e.g. Albumin, prealbumin
and transferrin) are most commonly used to monitor nutritional status.
Always consider patient's fluid status, organ function and presence
of infection while interpreting values of visceral protein. If nutritional
recovery is inappropriate, nitrogen balance study may be used to
guide changes in amino acid intake. Similarly, if traditional methods
of calculating calorie requirements are unsatisfactory, indirect
calorimetry is indicated.
Termination of PN
• PN is the temporary method of nutritional supplementation. The
ultimate goal is to restart oral/enteral foocj intake as soon as·
gastrointestinal function returns.
• The transition from PN to oral or enteral nutrition should be done
gradually to avoid the deterioration in nutritional status when PN is
discontinued. ·
• PN should not be discontinued abruptly. Reduce infusion rate to
50% for 1 to 2 hours before discontinuing PN. Such reduction will
minimize the risk of rebound hypoglycemia. If there is a need to
discontinue PN abruptly, a 10°/o dextrose solution may be adm'inistered
for a few hours .and then discontinued to prevent hypoglycemia.
\ . . .
• Once patient is able to take 60°/o of the total energy and protein
requirements orally or entera!ly, . PN may be stopped.
• For those receiving substantial amount of. electrolytes in the PN,·
oral or IV electrolyte supplemeritatioh m·ay be needed.
• - • •• l I
11
Complication~
.: :
Complications of PN have been widely reported. However, the incidence of

most complications is reduced with carefu~ management and supervision by
an experienced nutritional support team. Commonly encountered
complication.s are summarized in table No 12.14.
Table No. 12.14 : Complications of PN
Mechanical Metabolic/GI Infectious

First Malposition, Fluid overload --
48 Haemothorax Hyperg!ycemia
Hours Pneumothorax Hypophosphatemia
Air embolism, Hypokalemia
Blood loss, . Hypomagnesemia
Puncture of Refeeding syndrome
subclavian/
carotid artery
First Catheter displacement Hyperglycemic coma Catheter
Too Catheter thrombosis .. Acid base imbalance induced sepsis
Weeks Catheter occlusion Electrolyte imbalance Exit site
Air embolism infection
Three Fracture or Tear of Essential fatty Tunnel infection

Months catheter acid 'deficiency Catheter induced
Onwards Catheter thrombosis Vitamin or trace element sepsis
Air embolism deficiency Exit site infection
Blood loss PN metabolic
bone diseases
PN liver diseases
Hyperglycemia: The greatest danger from PN during the first 24 hours is

the hyperglycemia. This · may lead to osmotic diuresis and glycosuria
leading to excessive ·excretion of free water by the kidney, thus causing
hyperosmolar dehydration. It is best treated by prevention. Risk factors
for hyperglycemia are excess and rapid administration of dextrose,
metabolic stress, medication, obesity and OM. Hyperglycemia in a
previously normoglycemic patient should also raise suspicion of infection.
Slow administration (2 to 3 mg/kg/min) and decreased amount (100-150
g/day) of initial dextrose infusion, reduction in total calorie supplementation,
increased portion of lipid administration (to limit the required dextrose),
and if needed insulin administration can prevent hyperglycemia .. Glucose
is best maintained between 120 and 180 mg/di. Managing glucose is
374 CH . 12 : Parent eral Nutrition Therapy
usually done by adding up to 20 units of insulin per liter in the PN solution. If

tflis does not control t11 e llyperglycemla, then an Insulin drip should be started.
The insulin drip typica lly b gins at 2-5 units o'f insulin per hour.
Hyponatremia: In patients receiving PN hyponatremla is frequent!
encountered and is caused chiefly by excess administration of hypotont
fluid. OU1er causes of llyponatremia include adrenal insufficiency, CHFc
SIADH nd cirrhosis with ascites. Based on the etiology, hyponatremia i~
usually treated with fluid restriction or diuretics. If sodium intake is
in dequate , and clinical condition warrants, additional sodium may be
administered.
Refeeding syndrome: Patients who require parenteral nutrition therapy
are frequ ently moderate to severely malnourished. During a period of
starvation, the body adapts to less carbohydrate and more fat metabolism
for the energy requirements and, therefore, tolerance for carbohydrates
may be greatly impaired. Aggressive administration of PN in such
malnourished patients can precipitate the complication known as refeeding
syndrome, with severe hypokalemia, hypomagnesemia, and
hypophosphatemia as its hallmark. Carbohydrate refeeding ·s timulates
insulin secretion, which in turn increases cellular uptake of e_lectrolytes
and reduces its serum concentration, if replacement is inadequate.
Clinical manifestations: Refeeding syndrome occurs due to severe and
potentially dangerous electrolyte fluctuations leading to (1) fluid overload
and CHF (due to excessive fluid and sodium administration in ·patients
with decreased cardiac mass and c.o ntractility); (2) severe muscular
weakness and risk of respiratory failure (due to hypokaleniia and
hypophosphatemia); (3) glucose intolerance with hyperglycemia; and (4) _
cardiac arrhythmia, cardiac dysfunction and death.
Prevention: In high risk patients PN should be started gradually. o.nly
one-third of estimated basal energy needs should be given dur.ing. t~~ f~rst
24 hours and fluid overload should be avoided. Specifically, while initia~ing
the therapy, glucose intake should be less than 150 gm/day and sodium
less than 20 mEq/day. Total fluid should be less than BOO ml/day.
Potassium, calcium, magnesium and phosphorus should be carefully
monitored and replaced as necessary.
Hepatic abnormalities: Hepatic abnormalities · are the most common

gastrointestinal complications associated with PN, and are generally benign
and tempor~ry. Ho~ever other etiologies of hepatic dysfunction should be
rule~ o.ut, tncludrn.g patient's underlying hepatic disease, sepsis,
med1cat1ons, e.ssent1al f.atty acid deficiency, and carnitine deficiency. PN
related hepatic complications may be biochemical (elevated serum
transaminase, alkaline phosphate or bilirubin) or histological (steatosis).
Transaminase elevation generally occurs early in therapy (1 to 2 ·weeks
after initiation of PN) and often resolves without change in the program.
Bilirubin and alkaline phosphatase elevations usually appear slightly later
(2 to 3 weeks after therapy). Interventions recommended to pr~vent or
treat hepatic complications include avoiding excessive calories, providing
a portion (20o/o-40°/o) of calories as fat, and cycling the infusion (stopping
for at least 8-10 hours/day).
Catheter sepsis: Catheter related sepsis is the most common life

threatening complication (as high as 15%) in patients receiving CPN.
Central catheter~related sepsis is usually caused by entry of organisms
at the catheter exit site or contamination at tubing connections.
Staphylococcus and candida are the most frequent pathogens. Fever in .a
patient who has no other identifiable source of infection raises suspicion
of a catheter related infection. Whenever catheter related sepsis is
suspected, the following steps should b~ considered ~1) evaluate the
catheter insertion site and culture any drainage, (2) obtain blood cultures
from a peripheral vein and the central vein cath~ter and (3) begin ~mpiric
antibiotic therapy. Immediate catheter removal rs mandatory (as with any
central venous ca~heter) if there is a purulent d.ischarge or abscess. at the
insertion site or if the patient is in septic sh.ock without an apparent etiology.
Whenever the catheter is removed, the tip should be cultured.
376 suggested Readings
Suggested Readings
Adrogue & Madias , Management of life threatening acid base di~orders

N Engl J Med 338 (1) : 26 &33.8, (2) : 107, 1998.
Adrogue & Madi as , Hypernatremia, and Hyponatremi~, N Engl J Med

342 (2 0) ; 493 , ~ 342 (21) 1581, 2000. ' .
A.S.P.E.N . Board of Directors: Guidelines for the use of parenteral

and enteral nutrition in adult and pediatric patients,· JPEN, volume
26 No 1, supplement, 2002.
"Baily & Love's Short ·Practice Of Surgery-", 23rd Edition, Arnold

publicati on, 2000.
nsasics in clinical nutrition"; Lobos Sobotka, Second ·e dition, Edited

for ESPEN courses, House Galen, 20·00. ·
Brenner & Rector's "The Kidney", 6th. Edition, W.B.Saunders, 2000.
"Campbell's Urology", 8th Edition, sa·unders, 2002·.

' ~ • I
Cecil's "Text Book Of ·Medicine", Bennett & Plum,, 21-st Edition, W. B.

Saunders, 2000
"Glinical Pharmacol.ogy 11 , Laurence & Bennett, 8th .Edition, Livingsto~·s

& Churchill, 1997. . .
"Clinical physiology of acid-base · and electrolyte disorders", Rose &

Post, 5th Edition, McGraw-Hill, 2001.
"Critical care nephrology", Claudio Ronco & R.i naldo Bellomo, Kluwer
academic publishers 1998.
"Current diagnosis and treatment in Gastroenterology" ' Friedman,

McQuaid & Grendel!, second edition, Tata McGraw-Hill 2003.
"Current Medical Diagnosis & Treatment", Lawrence & Stephen, 42nd
Edition, McGraw-Hill 2003 .
Suggested Readings 377
Davidson's "Principles and Practice of Medicine'', ·18th Edition,

Livingston's & Churchill, 19991
Forfar & Ernie's "Textbook .of Pediatrics", 4th Edition, Livingston's &
Churchill , 1993. ·
Forfar & Ernie's "Textbook of Pediatrics", 4th Edition, Livingston's &

Churchill, 1993. · · · · ··
Goodman & Gilman's, "The· Pharmacological Basis of Therapeutics"',

International 9th Edition, McGraw-Hill, 1996. ·
Guyton & Hall; Textbook Of Medical Physiology, 9th Edition, Saunders,
1996.
Halperine & Gold~tain, F_luid, ~lectrolytes . and acid base. disorders,
3rd Edition, W. B. Saunders, 1999.
Hand book of Clinical nutrition, Third edi~/on, ~t Louis, .M osby-Year
Book, 1997.
Harrison's, "Principles of internal medicine", 15th edition M'c Graw-
Hill, 2001.
Joslin's diabetes mellitus 13lh Edition, Lippincott Williams & Wilkins,
2000.
Kyra Backer, Intensive care unit management of the stroke patient,
Neurological clinics, Volume 19, No-2, May 2000.
"Manual of Nephrology", Robert.W. Schrier, fifth edition, Lippincott
Williams & Wilkins, 2000.
Martin Dale's "The Extra Pharmacopoeia", 30th Edition,
Pharmaceutical's Press, London, 1993.
"Neurosurgery" , Robert H.Wilkins Setti, & S. Rengachari, 2nd Edition,
. McGraw-Hill, 1996.
Oxford Text Book Of Medicine, 3rd Edition, Oxford Medical Publisher,
1996.
.!
'• Suggested Readings
378
"Oxford text book of clinical nephrology"' 2nd Edition, Oxford university

press 1998.
"Principles & Practice of Pediatric Neurosurgery", A Leland Albright

Ian. F. Pollack P. David, Adelson, Theime, New York, 199 9 .
"Principles of Surgery", Schwartz, 7th Edition, McGraw-Hill, 19 99 .
Sabiston's , Text book of Surgery, "The Biological Basis of Modern

surgical Practice", 15th Edition, W.B. Saunders, 1997.
Sheila Sherlock's, "Diseases of the liver and · billiary system", 11th

Edition , Black Well Science publication, 2002.
Souba W W: Nutritional support. N· Engl J Med 336: 41-48, 1997.
Sutin et al, Intravenous fluid therapy .in neurological injury, Critical

Care Clinics, Vol.8, No-2, April 1992.
"Text book of critical care" by Shoemaker, 4th Edition, William C.

Shoemaker, 2000.
"Text book of Pediatrics by .Nelson", 15th Edition, :W .B. Saunders, 1996.
"The practice of Neurosurgery", George.T. Tindall, William & Wilking,

1996.
Index 379
Index
Note · p age numbers foll
followed by 't' indicat:~~~es~y 'f' indicate figures; Page numbers
A
Acid base balance Amino acids (Cont.)
. Henderson-Hasselbalch equation 197 also see solutions, special
Acid base disorders selection of 357, 358
clinical disorders in 200t branched chained 335
compensation (secondary in hepatic disease 335
changes)201,202t in renal failure 335
evaluation of 204 in ~olume over loaded patients 336
examples of 209-21 3 Anaemia
investigations and in surgical patients 265-266
interpretations 20 5 _206 Anion4
mixed disorders 202 Anion gap
clinical disorders in 203 t calculation of 207 .
definition of 202 '.n metabolic acidosis 207, 214, 21 4t
diagnosis of 208-209 m metabolic alkalosis 207-209
see specific causes
tripl e disorders 203
Anion gap, urinary
primary (simple) disorders 199, 200t
calculation of 215
Acid bas e regulation
Antidiuretic hormone ADH
buffers in 197
in central diabetes insipidus 90
renal regulation 198
in SIADH 73, 74t
respiratory regulation 198
in water regulation 56-57
Acid citrate dextrose (ACD) 266
Arterial blood gases 204-206
Acidosis
collection method 205
see metabolic acidosis
indications 204-205
see respiratory acidosis
interpretations of 206
see specific causes
precautions 205
Acute renal failure
Ascites in cirrhosis 148
see renal failure, acute
pathophysiology of 148
ADH treatment of 149-150
see antidiuretic hormone
Aspirin (salicylate) poisoning 221
Acute respiratory distress
Aspiration lung diseases 166
syndrome (ARDS) Atrial natriuretic peptide (ANP) 57, 73
fluid therapy in 161
B
parenteral nutrition in 346
Bartters syndrome 224t
Alcoholic ketoacidosis 220-221
Bicarbonate
Aldosterone 58, 96 also see specific cause
Alkalosis compensatory changes 201
see metabolic alkalosis
interpretation of 206
see respiratory alkalosis
rise in AG vs. fall in HC03 209
see specific causes
Bicarbonate therapy
Amino acids 335-336
See sodium bicarbonate
also see protein requirements
380 Index
Carbicarb 218
Bisphosphonate 116 . Carbohydrates 327-328
Blood transfusion tor tiae111etemes1s 146-147
administration 328
Blood transfusion for oalorlc value 327
hypovolemia 133, 133t, 134f
disadvantages 327-328
Blood transfusion for
surgical patients 274-278 functions and advantages 327
monitoring 328
Blood loss
;11 surgi al pati nt 274-278 requirements 327
in ha -rn ti m i -- 144-i 46 Calorimetry, Indirect 326, 326t
Bron l1itis .. nd br n llial asthma 162-163 Cancer
Bran ~1 h in d Amino acids 336 parenteral nutrition in 343
Buffe -- 1°7 Cardiac disease
Bun s flui therapy 294-305 parenteral nutrition in 343
cin s f 294 Catheters, for parenteral nutrition
I d transfusion 299, 304 care of 370, 371t
1.ral ulation of requirements 304t mechanical complications of 373t
lloids 299, 303 sepsis of 375, 373t
diuretics 305 site of insertion
electric burns 305
central venous catheter 360-361
importance of 294
percutaneous inserted central
indications of 295
catheters (PICC) 361
initial resuscitation 296-302
peripheral venous catheter 358-359
loss after 48 hours 303~304
tunneled catheter 360-361
monitoring of 300-302
Cation 4, 196
nasogastric aspiration 295
Central diabetes insipidus 90-92
parenteral nutrition in 355-356
Central parenteral nutrition 361-362
pathophysiology of 295-296
Central venous pressure ·
subsequent therapy of 302-303
(CVP) monitoring 48-49
c Children fluid therapy 231-261
Calcium
also see ORT
blood concentration of 112
dehydration, assessment of 237, 238t
regulation of 112, 113
Calcium chloride 237 dehydration, types 238, 239t
Calcitriol 113, 119 importance of 231-232
Calorie requirements 129-130, 233 initial I. V. resuscitations 240-246
~lso see in specific disorders aims of 240
in parenteral nutrition 327 325t guidelines of 240
calculations of 327, 325 t' rate of infusion 240, 244
Harris Benedict selection of fluids 241-243
. . equation 325, 325t indication of 1.V. fluids 233
ind~rect calorimetry 326 325t maintenance fluid, ideal 235
f twe1ght based calculatio~ 325 325t maintenance requirements
ac ors effecting 325t ' of calories 233, 233t
percent~ge distribution 326 of electrolytes 234
amino acids as % of 326 332 of fluids 234
carbohydrate as °I< f ' neonates 237
fat as % of 328-3;1o 326,327
renal disorders in 252
Carbamazepine 92t, 93
subsequent I. V. fluid therapy 244
Index 381
Children fluid therapy (Cont.. .. )

treatment of Dextrose solution 19-20, 36-37
hyperto~ic dehydration 250-251 also see carbohydrates
~ypot~rnc dehydration 248-249 in parenteral nutrition 356, 368t
isotonic dehydration 24 6 _247 in central PN 360
Chlorpropamide 92, 92t in peripheral PN 358
Chronic renal failure Diabetes insipidus
see renal failure, chronic central 90-93, 90f
Chvostek's sign 117 nephrogenic 93-95, 90f
Cirrhosis of liver 149-150 Diabetic ketoacidosis
parenteral nutrition in 349-35 1 also see hyperglycemic coma
Colitis, ulcerative diagnosis of 172
parenteral nutrition in 353 fluid and electrolyte imbalance 173, 175
Colloids fluids in 177-178
albumin 38-40 HC03 in 179-180
characteristics of 37 insulin in 176
dextran 40-42 metabolic acidosis in 220
gelatin polymers 42-43 monitoring of treatment 181
hetastarch 43-45 pathophysiology of 172-173, 174f
pentastarch 45 phosphate in 180
Congestive heart failure 159-160 potassium in 178-179
parenteral nutrition in 344 treatment of 175-181
Critical illness Dialysis
immune-enhancing PN for 336-337 for hypercalcemia 116
parenteral nutrition in 341-342,3l1.2t for lactic acidosis 220
Crohn's diseases for metabolic alkalosis 225
parenteral nutrition in 352 parenteral nutrition in 34 7-348
Cyclic parenteral nutrition 363 Diarrhoea
CV stroke also see fluid therapy in children
fluid therapy in 166-169 combined loss with vomiting 144
D fluid & electrolyte
Dehydration 86-87 disturbances 139-140, 141 t
also see hypovolemia treatment of 141-143
Delivery of parenteral nutrition 358-362 Dichiaro acetate 220
duration of Diuresis 87t, 88, 173, 191-192
continuous vs. cyclic 362-363 Diuretics 149, 189-190, 193
routes of Drop calculation for l.V. fluids 51-53
peripheral vs. central 358-361 E
systems of ECF volume disorders
multiple bottle vs. volume deficit 85-87
three in one 361-362 water and salt deficit 85-86
Designing PN Fonnula 363-369 pure water deficit 85-87
calculation of requirements 363-364 0/085
preparation of prescription364-366 volume excess 82-85
selection of an optimal formula 367-369 predominant water excess 83-85
Demeclocycline 75, 78t water and salt excess 82-83
Dextrose saline solution 24-25
382 Index
Edematous state Fluld replacement (intravenous) (Cont )

see oedematous state characteristics of 15-1 7 ...
Electrocardiogram classification of 18
in hyperkalemia 106t compllcatlons 'of 13
in /lypokalemia 98 compositions of 14t
in liyper/hyp I min 114, 118 disadvantages of 13 I
Electrolyt goals of 313 /
see ifi I ctrolytes guidelines of administration of 315-3 16
in p.._ r nt r I nutrition 338, 338t
indications of 13
I ~m normal 3t monitoring of 47-51
E1 pl I pat11y, hepatic 150-152 clinical 47-48
iet in 151 CVP and PAWP 48-51
drug t11erapy of 152
planning and prescribing.of 313-314
fluid · electrolyte
priorities in 313-314
management 151,151t
rate of 47
treatment of 150, 153, 151t selection of fluids 54, 131-133, 133t, 1341
solutions 18-31 ·
Energy requirement
see caloric requirements also see solutions
Enteral nutrition colloids 37-45
advantages 320 crystalloids 18-36
contraindication 320-321 special fluids 32-36
Equivalents 4 •' summary of 54
Exercise volume of 46
heat cramps in 169 · Fluid requirements
heat exhaustion in 170 also see specific etiology
heat stroke in 170-171 calculation of 314-315
Extracellular fluid disturbances in parenteral nutrition 324
classification of 59 Foot print in metabolic acidosis 209
F Frusemide 115, 149, 189-190, 193
Fat G
see lipid emulsion Gallium nitrate 116, 117t
Fluid
Gap anion
body compartments 1-2, 1f, 2 t, 2t see anion gap
body composition 5-6
Gastrointestinal bleeding (upper) 144-148
Fluid-electrolyte requirement
approach to 144.;.146
caloric requirements 129•130
resuscitation and fluid therapy 146-147
da~ly electrolyte requirement 129
risk assessment of 148
?a1ly water requirement 128-129
. in parenteral nutrition 324 338 338t
Gastrointestinal fistulae
Fluid loss ' ' parenteral nutrition in 355
distribution of aot, 801 Gastrointestinal losses
also see hypovolemia see diarrhoea, vomiting
Fluid replacement (intravenous) Gastrointestinal secretions
advantages of 12 electrolyte composition of 339t
aims of 12 Gelatin polymers (Haemaccel) 42-43
calculation of infusion rate 51 _53 Glucocorticoids 116, 117t
Index 383
Glutamine Hyperkalemia 104-112

in parenteral nutrition 336-337 . approach to 106
Glycosuria 173, 174f clinical features of 105
H diagnosis of 105-106
'l
H+ (hydrogen) 196-198, 200t, 206, 213 electrocardiogram 1061
Haematocrit etiology of 105t
in burns 301 treatment of 107-112
in haemetemesis 146-147 Hyperlipidemia 61
in hypovolemia 50, 309-31 O Hypermagnesemia 123
in surgical patients 27 4-275, 278 Hypernatremia 78-82
Haemetemesis 144-148 clinical features of 79
also see gastrointestinal bleeding diagnosis of 80, 80f, 80t
Haemoglobin etiology of 78-79
in surgical patients 275-277 treatment of 80-82
Harris Benedict equation 325, 3?5t Hyperparathyroidism 113"'.115, 117
HC0 3 see bicarbonate Hyperphosphatemia 122-123
Heart failure, congestive 159-160 clinical features of 123
Heat illness 169-171 etiology of 122t
heat cramps 169 management of 122-123
heatexhaustion(syncope)169 Hyperproteinemia 61
heat stroke 170-171 Hypertension, essential 160
Henderson-Hasselbalch equation 197 . Hyperventilation
Hepatic disorders · also see respiratory alkalosis
ascites in cirrhosis of liver 148-150 in metabolic acidosis 214-215
hepatic encephalopathy 150-152 in hypoxemia 226-227
parenteral nutrition in 335, 348-350 Hypocalcemia 117-120
Hetastarch 43-44 clinical features of 117-118
Home parenteral nutrition diagnosis of 118-119, 119t
see cyclic PN etiology of 117, 177t.·
Hormones treatment of 119-120
see specific hormones Hypoglycemia
Hydrochloric acid 225 in parenteral nutrition 373
Hydrogen see H+ Hypokalemia 96-104
Hypercalcemia 113-117 approach to 98-99
clinical features of 113 clinical features of 97
diagnosis of 114-115 diagnosis of 98-99
etiology of 114, 114t electrocardiogram in 9S
treatment of 115-117, 117t 1 etiology of 97t
Hypercapnia 226-228 prevention of 99
also see respiratory acidosis treatment of 99-104
Hyperglycemia duration of 101
in parenteral nutrition 373-37 4, 373t indications of 100
Hyperglycemic non ketotic coma 183-185 l.V. K+therapy of 102
clinical features of 183 K+supplements 101
diagnosis of 183 method of administration 101
monitoring 184 oral therapy 101-102
treatment of 183-185 precautions 100
384 Index
Hypomagnesaemia 124-127 Infection

clinical features of 125-126 In parenteral nutrition 375
etiology of 125t Inflammatory bowel disease
treatment of 126-127 parenteral nutrition In 352
Hyponatremia 59-72 Infusion rate calculations 51--53
clinical features of 61-62 Insensible loss 3
diagnosis of 62-63, 63t, 64f Insulin therapy
etiology of 60-61 ~n diabetic ketoacidosis 176
importance of 60 in hyperkalemia 108-109
summary of 72 Intracellular fluid
treatment of 65-72 composition of 3-4, 3t
basic principles of 66-67 volume of 1
example 71 lntraoperative fluid therapy 267 _278
goals of 65 Inverted sugar solution 21 .
method of correction 68-69-. Isotonic saline 22-23
monitoring of 70 I. V. solutions 18-32
rate of correction 67 also see solutions l.V. ·
risk of correction 66-67
K
selection of fluids 70 .
K+ (potassium) 95-96
specific treatment of 65 Ketoacidosis ·
Hypoparathyroidism 118t, :11 9t _
see diab.etic ketoacidosis
Hypoperfusion see alcoholic ketoacidosis
acid base abnormality in 215, 21 9
Keyxalate 108t, 11 O
Hypophosphatemia 120-121 . .
L
clinical features of 120 Lactic acidosis 219"'.220
etiology of 121 t also see metabolic acidosis ·
treatment of 121 Linoleic and linolenic acids
Hypotension 45-46, 130-13.3, 133t, 134f . in parenteral nutrition 328
see specific etiology ·
Liver Failure
Hypoventilation · parenteral nutrition in 348-350
~lso see respiratory failure
Lipid emulsion
in metabolic alkalosis 224 .
administration 331
Hypovolemia .
adverse effects/disadvantages 330-331
. clinical features of 4 5 _46
calorie values & requirements 329
~valuation of 45, 308-30 9
investigations 309-31 3 contents 328
shock in hypovolemia contraindication 331
functions and advantages 329-330 .
selection of
modified preparations 330-331
fluid 131-133, 131t, 133t 134f
treatment 131-134 . ' preparations 329
vs. dehydration 85-86 requirements 329
Hypoxemia 207' 226-227 M
I Macronutrients
lmmunomodulator soluti ons. · see carbohydrates; fat; proteins ·
. .
A rg1rnne 337 ,· Magnesium
Glutamine 336-337 blood concentration of 123
Omega 3 fatty acid 3 37_ distribution of 123
Index 385
Magnesium sulphate . 126-127 Neurosurgical patients

Malnutrition fluid therapy in 290-293 ·
see specific diseases340-356 Nitrogen balance 334 ·. ·
why to avoid 318 Normal body water 1-2
Mannitol 292 Nutrition
Measurements units of 4-1 O basic principles 318
Metabolic acidosis 213-223 EN vs. PN 320-322
clinical features of 214-215 Nutritional support
definition of 213 see parenteral nutrition
diagnosis of 215 Nutritional requirements
etiology of 214t amino acid 332-333
investigations in 215 carbohydrates 327
pathophysiology of 213 · energy 324-326
treatment of 216-218 fluid 324
alkali therapy 216-218 . lipid emulsion 328
general principle 216 0
specific causes 219-222 Oedematous status
Metabolic alkalosis 223-225 etiology and treatment of 8~-83
clinical features of 224 cirrhosis of liver 148-1 SO ··
definition of 223 congestive heart failure 159-160
• .., ~ I '
diagnosis of 224 Oliguria 189
; I '
etiology of 223-224, 224t Omega-3-fatty acids

pathogenesis of 223 in parenteral n,utrition 337 .
treatment of 225 Oral rehydration therapy (ORl) 2~?-261
Micronutrients definition of 252 ·
' '
see minerals; trace elements; vitamins oral rehydration solution (ORS) .
Milliequivalent (mEq) 4-8 administration,: method.qf 260
mEq to mg advantages of 253 · · · .
relationship 6-8 · composition .of 256, 2S6t
conversion 8, ·a t failure of 25q ., · ·
Millimoles (mmol) 4-6 formulations and types·255-254t
Milliosmoles/litre (mOsm/L) 9-10 Low Osmolarity'WHO_ORS 259
Mg see Magnesium Low .sodium ORS 258·
Mithramycin 116, 117t · · monitoring of 261
Molecular weight 5t requirements of 260
Mole9 principles of action 254
rice base ORS 258 ·· ·
N ' ~ j
Standard WHO ORS 257 ·
Na+ see sodium vs. ORT253
1
NaHC03 .
Osmolality 9-1 O •
see sodium bicarbonate Osmolality effective 1o

Nasogastric Osmolallty plasma i o
aspiration 135-138, 146, 204-225, 295 Osmolality, urine 87-89; 90t
Nephrogenic diabetes insipidus 93-94 vs. specific gravity urine 89 ·
Nephrotic syndrome 187-188 Osmolar disorders ·
see hypernatremia
Neurological disorders
: ..
see hyponatremia
fluid therapy In 166-169
386 Index
Osmolarity 9-1 O Par:nteral nutrition (Cont...)

Osmotic demyelination immunomodulator solutions
syndrome (ODS) 66-67 Arginine337 -
Osmotic diuresis 131, Glutamine 336
Overfeeding 326 Omega 3 fatty acids 337
Oxymetry, pulse 207 !ndirect calorimetry 326, 3 25 t
p in specific diseases 340-356
Packed red blood cells 147 acute renal failure 346-348 .
Pamidronate 116, 117t burns355-356
Pancreatitits (acute) 153-158 cancer343
classification of 153 cardiac disease 343
treatment of 154-158 cirrhosis 348-350
electrolytes and metabolic critical illness 341-342, 3 42 t
disturbances 156-157 gastrointestinal .fistulae 355
fluid therapy I. V. 155 inflammatory bowel disease 352
guidelines 154 liver disease 348-350
nutritional supports oral 157 pancreatitis 350-351
parenteral nutrition total perioperative 340-341
(TPN) 158, 350-351 pulmonary Diseases 344
Parkland formula 296-297 short bowel syndrome 352-354
indications 322, 323t
Parenteral nutrition
infusion technique
administration
see administration of PN
routes of nutrient delivery
initiation of PN 323, 370
Peripheral PN 358-359 introduction 317
central PN 360-361 monitoring of PN 370-372, 371 t
systems of delivering PN over feeding 326
multiple bottle system 361 planning of PN 319t
three in one system 362-363 requirements
duration of delivering PN calories 324-326, 325t
continuous PN 362 carbohydrate 327
. cyclic PN 363 electrolytes 337, 337t
advantage 321 fat 329
complications of 372-375, 3 73 t fluid 324
hepatic disorders 375 protein 332-335, 333t
hyperglycemia 373-37 4 trace Elements 339-340, 338t
hyponatremia 374 vitamins 340, 338t
refeeding syndrome 374 selection of solutions
sepsis 375, 373t dextrose solution 356
co~tr~indications 321-322 dextrose and amino acid
definition 31 7 . solution 356-357
designing PN Formula 363-369 three in one solution 361-362
calculatio f . termination of PN 372
prepar r n o requirements 363- 364
Pediatric fluid therapy
selecra ion of prescription 364- 366
see children, fluid therapy
~~an optimal formula
Pentastarch 45
goals319 Perioperative PN 340-341
PeripheraJ PN 358-359
Index 387
pH
importance of 195 Renal Disorder (Cont...)
regulation of 197-199 parenteral nutrition in 346-348
vs. H+ concentration 206 renal failure, acute 188-192
Phosphate oral 116 diuretic phase 191-192
Phosphate regulation 120 non ollguric phase 190
Plicamycin 116, 117t oligurlc phase 190-19'1
Polydypsia pri mary 89 prerenal 188-189
Polyuria 87-90 renal failure, chronic 192-194
definition of 87 glomerular diseases 192-193
diagnosis of 88, 90f tubulointerstitial diseases 193-194
etiology of 87t metabolic acidosis in 194, 221-222
Pontine myelinosis, central 66-67 . Renal failure, acute 188-192
Postoperative fluid management 278-285 Renal failure, chronic 192-1_94
Potassium 95-96 Renal tubular acidosis (RTA) 222-223
Potassium Chloride solution 35-36 Respiratory acidosis 225-229
Potassium containing solutions 16 clinical features of 227
Prerenal azotemia 188-189 . · compensation, renal 226
Preoperative fluid management 263-267 definition of 225
Preoperative PN 341 etiology of 227t
Protein supplementation in PN hypercapnia & hypoxia 226
advantages 333-334 and parenteral nutrition
adverse effect 334 treatment of 227-229
caloric value 332 alkali therapy of 229
content 331 general measures 227
contraindication 334 0 2 therapy 228
function 333 ventilatory support 228
in hepatic diseases 335 vs. metabolic alkalosis 226
in renal failure 335-336 Respiratory alkalosis 229-230
in volume over loaded patient 336 . clinical features of 230
monitoring 334 compensation of 229
modified Preparation 335-336 definition of 229
requirements 332".333, 333t diagnosis .of 229
Postoperative PN 341 etiology of 229, 230t
Pseudohyperkalemia 105-106 . treatmentof 230
Pulmonary arterial wedge .
Respiratory failure
pressure (PAWP) measurements 50
parenteral nutrition in
Pulmonary disease
Respiratory muscles
Fluid therapy in 161-166
parenteral nutrition in 344-345 effect of malnutrition
Respiratory quotient (RO) . .
R Resting energy expenditure(REE)-324-325,325t
Refeeding syndrome 374 Rhabdomyolysis 111 · .
Rehydration solutions, oral Ringer's lactate
see ORT/ORS pharmacology of 25-27
Renal disorders 186-195 burns 296
fluid & electrolyte management surgical patients 268-269
general principles 186-187 diarrhoea 142-143
nephrotic syndrome 187 children 243-244
3 88 Index·
colloids 267, 269-271

Rule of four 51-52 crystalloids 268-269
Rule often 51-52 volume of fluid replacement 271-274
~alicyfate (aspirin) poisoning 221 postoperative fluid therapy 278-285
,. diuresis 115-116
Sa ~ne . tant metabolic aJkalosis 224t, 225 electrolyte problems 282-285 ·
Sal~ne resp1sonsive metabolic alkalosis 224t fluid administration in 278-282
Saline res . goalsof278
Salt loosing nephropathy 87t
preoperative fluid therapy 263-267
Sepsis correction of anaemia 265-266
in parenteral nutrition 375, 373t
glutamine in 336 correction of hypovolemia 264-265
serum electrolytes 6 reasons of special consideration 262-263
serum osmolality 1O . Swan-Ganz catheter 50
Shock treatment of 131, 133, 133t, 134f Syndrome of inappropriate ADH
Short bowel syndrome secretion (SIADH) 73-78
parenteral nutrition in 352-354 etiology of 73
Sodium bicarbonate lnj. 32-~5 , 109, 216-218 pathogenesis of 73
Sodium containing solutions 15 pathophysiolgy of 74f
Sodium regulation 57-58 diagnosis of 7 4
Solutions (l.V.) (crystalloids) 18-31 treatment of 75-77
5%-dextrose 19-20 summary of 78
. dextrose with half strength saline 23 T
dextrose saline 24-25 Transtubular potassium
Inverted sugar solution s 21 gradient (TTKG) 107-108
lsolyte-E 31 -32 Tetany 118
lsolyte-G 27-28 THAM218
lsolyte-P 30-31 Third space fluid loss 264
Ringer's lact to 25-27 Three in one solution 361 -362
Solutions (speci I) Thrombophlebitis
amino acids solutions 332-336,370t in peripheral PN 359
dextrose solutions 327-328, 368 To al parenteral nutrition (TPN)
dextrose 25% 36-37 see parenteral nutrition
lipid emulsion 328, 332,367-370t Triglycerides
lmmunomodulator solutions monitoring in PN 331
Arginine 337 in pancreatitis 350
Glutamine 337
Trousseau's sign 118
Omega 3 fatty acids 337 TURP syndrome 286-290
pot~ssium chloride 35-36
clinical features of 287
s~1urn bicarbonate 32-35
hypotension during 288-289
Sp~c1f1c gravity, urine 312
Sp1ronolactone 149 pathophsiology 288
Surgical patients, fluid thera prevention of 289
?lood loss 27 4-278 PY 262-285 risk factors of 287
tntraoperative fluid th treatment of 290
erapy 267-278 u
blood transfusion 274 , n .
2 Units of measurements 4-9
Index 389
U reterosigmoidostomy(U rinary diversion)

pathophysiology 306-307, 307f ·
treatment 307
Urine chemistry
anion gap in 215-216
diabetic ketoacidosis 181-182
hyponatremia 62-63, 63t
importance of 312-313
osmolality 87-89, 9ot
osmolality vs. specific gravity 89
salicylate poisoning 221
SIADH73-78
..
vomiting 136t
v
Ventilation, mechanical 163-166
acid base disturbances in 164-165
CVP measurements 164
failure to wean due to electrolyte
disturbances in 165-166
Vitamins
in parenteral nutrition 340
requirements of 338t
Vitamin D (ergocalciferol) 120
Volume depletion 85-87
also see ECF volume deficit
' '
also see hypovolemia
'·
also see specific etiology
Volume excess 82-85
also see ECF volume excess
Vomiting 135-138
combined loss with diarrhoea 144
fluid and electrolyte
disturbances in 135-136, 136f
treatment of
fluid therapy 136-138, 1381
urine electrolytes 136t
w . )
Water
total body 1-3
disturbances 1-3
balance 2-3
regulation 56-57
requirements in PN 325
Water intoxication 82-85, 288
WHO-ORS 252-253, 257-259
390 Abbrevations
Abbrevations ·
Amino acids dDAVP desamino-D-arginine vasopressin

AA
Arterial blood gas D-5% Dextrose-5 %
ABG
Acid citrate dextrose OF Disease factor
ACD
Angiotensin converting enzyme DI Diabetes insipidus
AC El
inhibitor OKA Diabetic ketoacidosis
Antidiuretic hormone OM Diabetes mellitus
ADH
Activity factors D 2-5
AF
AG Anion gap DPG 2-3 Diphosphoglycerate
ANP Atrionatriuretric peptide ECF Extra cellular fluid
ARDS Acute Respiratory distress ECG Electro cardio gram
syndrome EN Enteral nutrition
AAF Acute Renal Failure ERCP Endoscopic retrograde
ATN Acute tubular necrosis cholangiopancreatography
BCCA Branched chain amino acids ESRD End stage renal disease
BP Blood pressure FFA Free fatty acid
BSA Body surface area FFP Fresh frozen plasma
BUN Blood urea Nitriogen GFR Glomerular filtration rate
CAD coronary artery disease GI Gastrointestinal
CAVH Continuous arterio venous HE Hepatic encephalopathy
haemofiltration HGT Fingerstick glucose
CBC Complete Blood Count HT Hypertension
CD Crohn's disease 180 Inflammatory bowel disease
CHF Congestive Heart Failure ICF Intracellular fluid
CNS Central nervous system ICP lntracranial pressure ·
COPD Chronic obstructive pulmonary ICU Intensive care unit
disease IDDM Insulin dependent diabetes mellitus
CPD Citrate phosphate dextrose IHD lschemic heart disease
CPK Creatine phospho kinase Intramuscular
IM
CPN Central parentral nutrition lntrathoracic pressure
ITP
CPP Cerebral perfusion pressure
IV Intravenous
CRF Chronic renal failure
JVP Jugular venous pressure
CART Continuous renal replacement Kg Kilogram
therapy Long chain triglycerides
LCTs
CVP Central venous pressure
LFT Liver function test
CVVH Con rmuous veno venous
LVF Left ventricular failure
haemofiltration MABL Maximum allowable blood loss
\
~·
Abbrevatlons 391
MC Ts edium chain triglycerides

mEq/L M. me equivalents per liter
moms Millie osmols
MV ~echanical ventil . tor
NPO r~.m per oral
NSA ID ~on steroidal anti-inflammatory drug
1
ORS ral rehydration solution

ORT ral rehydration therapy
PAWP ulmonary artery'wedge pressure
PCV I acked cell volume
PEEP 1 ositive end expi~atory pres~ure ·
PICC f?ercutaneous inserted central
datheter
PN Pkrenteral nutrition
PPN Pkripheral parenteral nutrition
P~rathyroid hormone
' I
PTH I
REE R~sting energy expenditure

I .
RL Ringer's lactate
RQ Respiratory quotient
RTA Renal tubular aCidosis
SBP ( Systolic blood pressure .
SBS Short bowel syndrome
TEE ; Total energy expenditure
TEN Total enteric nutrition
TF Thermal factor
1TG Triglyceride
\
; TPN Total parenteral nutrition
'
I TTKG Tran tubular potassium gradient
! TURP
)
Trans urethral resection of
I
),
; . prostate
, UAG Urinary anion gap
Ulcerative colitis 11,
Ve nti Ia ti o n-pe rf us ion

Practical Guidelines On Fluid Therapy 2nd Ed

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Practical Guidelines On Fluid Therapy 2nd Ed

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_ .... . . I ' "' ' .,. , '! . ,•' : ~ .. : ~ . . ": .

. - · -... _.·: ~tD~(Medicine)·,. D.N . ~· (Nephrology) ·.

- ·.' ... . ....

1. BASIC PHYSIOLOGY .................................................................................... 1 .

2. PRINCIPLES OF FLUID THERAPY AND

3. FLUID AND ELECTROLYTE DISORDERS ............................................... 56

4. FLUID THERAPY IN MEDICAL DISORDERS ......................................... 128

5. FLUID THERAPY IN DIABETES MELLITUS ........................................... 172

6. FLUID THERAPY IN RENAL DISEASES ................................................ 186

7. APPROACH AND MANAGEMENT OF ACID BASE DISORDERS ........... 195

8. FLUID THERAPY IN CHILDREN ............................................................. 231

9. FLUID THERAPY IN SURGICAL PATIENTS ............................................ 262

10. FLUID THERAPY IN SPECIAL SURGICAL DISORDERS ...................... 286

11. EVALUATION AND PRESCRIBING FLUID THERAPY ............................ 308

12. PARENTERAL NUTRITION THERAPY ................................................... 317

SUG.G ESTED READINGS ........................................................................ 376

INDEX ......................................................................................................... 379

ABBREVIATIONS ....................................................................................... 390

.:: .·;.\ .:· .. - ·~;·:' .. ' .-

BODY WATER 1 UNITS OF MEASUREMENT 4

Total body water:

Distribution of body fluid : ·':.

·· 2 ·... CH. -~ : > Baslc··. p~ysforo_gy ...... . ~ . . '

Table No. 1.1 ~ Di.stribution of fluid volume

Volume for 70 kg weight 42.0''L 28.0 L 14.0 L 10.5L ·- 3.5 L

So h.i~her amount of water ~s lost during exercise, abnormal perspiration,

Sodium 142.00 10.00

Table No. 1.3: Major ions in ECF and ICF .

Major Cation Sodium Potassium and Magnesium

Major Anion Chloride and Bicarbonate Phosphate, Sulphate and Protein

So to determine amount of any substance in one mole, we need to know

The atomic weight of Na+ is 23. So 23 mg is 1 mmol and 23 mg of Na+ in 1

Equivalent and milliequivalent :

6 CH. -1 : Basic Physiology

Table No·. 1.5: Normal plasma electrolyte concentrations

Electrolyte m'Eq/L mmol/L

Molecules must be quantified in moles (e.g. 'a mole of glucose') because

The relationship between mEq ·and mg ~

1. To convert from milligrams per deciliter (mg/di) to milliequivalerits

NaCl mEq/L = 154

. the end of both equations (Na

Salt mEq Cation or Anion/gm of salt mg of salt(mEq

Os·m otic pressure -and osmolality

·cH. 1 ·: · Basic Physiology

If a solute is di~solved rn 1- litre of .water (solvent), the ·concentration

So osmolality ·(mOsm/Kg), which is determined ~y . weigh~, of solvent is more

.· Under ·n ormal. circumstances, glucose accounts for only 5 mosm~kg in

BASIC PRINCIPLES OF FLUID THERAPY AND

INTRODUCTION 11 SPECIAL FLUIDS 32

'· ". ~S?... ii{afih~~i

:. · ' f .o r .proper ·fluid therapy it is necessary to know :

·.. \{'};f'6traHonai"ahd>adeqtiater·t1uid therapy "it is neces·s ary to answer following

_-:'. f;%~~~J~, :.:<.whe·n

~'.·fj1~~j~::,;~hii~ ;;4, id}.~ ~ive; ~~d ~hy :? , .·.· •. . , ·....

4. At which rate l.V. fluid is to be infused?

BASIC PRINCIPLES OF FLUID THERAPY

4. Hypoglycemia where 25°/o dextrose is life saving.

-- 6. Total parenteral nutritio~. ~

cardiac arrest and forced diuresis in drug overdose, poisoning, urinary

1. Mor :. exp nsivel needs strict asepsis.

1. l.V. fluid should be avoided if patient is able to take oral ·fluid.

· Table No .. 2.1.: Compos~tion of common 1.V. solutions (mEq/L) ....I.