Seminar on management of

fluid & electrolyte

disturbance, and Dehydration
Prepared by:
•Mezemer belete(C2)
•Michael Mulat(C2)
•Mubarek (C2)
Moderator:Dr.Tesfa G/Meskel
CONTENT
• Normal body fluid composition
• Sodium
• Potassium
• Calcium
• Maintenance theraphy
• Deficit theraphy
Physiological considerations in infants and
children
TBW

Total body water (TBW) as a percentage of body weight varies with

age.
Premature infants have higher TBW than term infants.
From the end of the first year to puberty ,TBW is
60% of body weight.
FLUID COMPARTMENTS

 The ICF & ECF

 By 1 yr of age, the ratio of the ICF volume to the ECF
volume approaches adult levels.
 The ECF volume is approximately 20–25% of body
weight .
 ICF volume is approximately 30–40% of body weigh
ELECTROLYTE
COMPOSITION

Sodium and chloride are the dominant cation

and anion, respectively, in the ECF.
Potassium is the most abundant cation in the
ICF.
Proteins, organic anions, and phosphate are
the most plentiful anions in the ICF.
Cont…
ICF (mEq/L) ECF (mEq/L)
 Sodium 43 140
 Potassium 140 4
 Chloride 3 104
 Bicarbonate 10 24
 Phosphate 107 2
 Protein 40 14
 Magnesium 7 1.1
 Calcium high 2.5
OSMOLALITY
 The ICF and the ECF are in osmotic
equilibrium
 The plasma osmolality is normally 285–295
mOsm/kg
 The effective osmolality can be calculated as
follows: Effective osmolality = 2 × [Na] +
[glucose]/18
Regulation of Osmolality
The plasma osmolality is tightly regulated and maintained at 285-295
mOsm/kg.
Osmoreceptors in the hypothalamus sense plasma osmolality.
An elevated effective osmolality leads to secretion of antidiuretic
hormone and permitting resorption of water into the hypertonic renal
medulla.
ADH secretion virtually disappears when plasma osmolality is low,
allowing excretion of maximally dilute urine.
This resulting loss of free water (i.e., water without Na+ ) and corrects
plasma osmolality.
 SODIUM
Body content and physiologic function.
Sodium is the dominant cation of the ECF

principal determinant of extracellular osmolality.

Sodium is therefore necessary for the maintenance

of intravascular volume.
Normalvalue between 135- 145meq/l
Cont…
Intake
Sodium is readily absorbed throughout the gastrointestinal tract.
glucose enhances sodium absorption due to the presence of a co-
transport system
excretion
The kidney regulates sodium balance and is the principal site of
sodium excretion
 Sodium excretion occurs in stool and sweat.
HYPERNATREMIA
Is a sodium concentration >145 mEq/L, although it is sometimes defined
as >150 mEq/L.
Causes of Hypernatremia
excessive sodium
Improperly mixed formula
Excess sodium bicarbonate
Ingestion of seawater or sodium chloride
Intravenous hypertonic saline
Hyperaldosteronism(HPN)
Cont…
water deficit
DI(if not drinking)
Increased insensible losses
Premature infants
Radiant warmers
Phototherapy
Inadequate intake
Ineffective breast-feeding
Child neglect or abuse
Cont…
water and sodium deficits
Gastrointestinal losses
Cutaneous losses
Renal losses Osmotic diuretics (mannitol)
Diabetes mellitus
Chronic kidney disease (dysplasia and
obstructive uropathy)
Polyuric phase of acute tubular necrosis (urea)
Post obstructive diuresis(urea)
CLINICAL MANIFESTATIONS.
Brain hemorrhage is the most devastating consequence of
hypernatremia

Frequently do have features of hypernatremic DHN

Hypernatremia is associated with hyperglycemia and mild

hypocalcemia
TREATMENT.
As hypernatremia develops, the brain generates idiogenic osmoles to
increase the intracellular osmolality and prevent the loss of brain
water.
The goal is to decrease the serum sodium by <12 mEq/L every 24 hr
monitoring of the serum sodium is crucial
Normal saline is preferable to lactated Ringer solution to correct
hypernatremic DHN
 If there is hypernatremic DHN, 1st priority is restoration of
intravascular volume with isotonic fluid .
Cont….
• Sever hypernatremia with sodium intoxication can be treated
Peritonel dialysis(volume overload)
D5W(sodium overload)
diuretics
HYPONATREMIA
Causes of Hyponatremia
pseudohyponatremia (measured OSM is Nl)
hyperosmolality
Hyperglycemia , Mannitol
HYPOVOLEMIC HYPONATREMIA

Extrarenal losses
• Gastrointestinal (emesis, diarrhea)
• Skin (sweating or burns)
• Third space losses
• Renal losses : Thiazide or loop diuretics , Osmotic diuresis ,
Postobstructive diuresis Polyuric phase of acute tubular necrosis
• Lack of aldosterone effect (high serum potassium)
• Absent aldosterone
• Urinary tract obstruction and/or infection
Cont…
Euvolemic hyponatremia
• Syndrome of inappropriate antidiuretic hormone
• Nephrogenic syndrome of inappropriate antidiuresis (Nl ADH)
• Glucocorticoid deficiency
• Hypothyroidism
• Water intoxication
• Iatrogenic (excess hypotonic intravenous fluids)
• Feeding infants excessive water products
Hypervolemic hyponatremia

• CHF
• Cirrhosis
• Nephrotic syndrome
• Renal failure
• Capillary leak due to sepsis
• Hypoalbuminemia due to gastrointestinal disease (protein-losing
enteropathy)
CLINICAL MANIFESTATIONS.
• Brain edema
• Symptoms of DHN
• Serum sodium concentration is less than 130 meq/L
TREATMENT.
• Monitoring & avoidance of rapid correction of hyponatremia especially in
chronic cases
• All symptomatic cases should be treated with hypertonic saline(3% Nacl).
• hypovolemic hyponatremia : restore the intravascular volume with NS
first.(suppresses ADH)
• hypervolemic hyponatremia is difficult to treat: cornerstone of therapy is
water and sodium restriction because these patients are volume-
overloaded.
• Diuretics
Cont…
• Isovolumic hyponatremia:excess of water and a mild sodium deficit
• limiting water intake may help for asymptomatic
• symptomatic hyponatremia due to water intoxication, hypertonic
saline is required
• Na + ,K+ -ATPase maintains the high intracellular [K+ ]
• Insulin , an increase in PH , . β-Adrenergic agonists increase {K+}
movement into the cell
• Decrease in PH, an increase in plasma osmolality , α-Adrenergic
agonists and exercise cause net movement of [K+] out of the cell
• The serum [K+ ] increases by approximately 0.6 mEq/L with each 10
mOsm rise in plasma osmolality
• K+ is necessary for the electrical responsiveness of nerve and muscle
cells and for the contractility of cardiac, skeletal, and smooth muscle
intake
• Recommended in take 1-2mEq/kg
• 90% normally absorbed by intestines(small)
• Colon exchanges body potassium for luminal sodium
• Regulation of intestinal losses- minimal effect on potassium
homeostasis
• Renal failure,aldosterone and glucocorticoid increase colonic
secretion of [K+]
excretion
• Sweat, colon-minimal loss
• After acute [K+] load >40% move intracellulary
• Eventually excreted through kidney
• Frealy filtered at the glomerulus , >90% reabsorbed before reaching
• Distal tubule and collecting duct, the principal site for [K+[ regulation
• Aldosterone- principal hormone regulating potassium excretion
• -cortical collecting duct
• . Glucocorticoids, ADH, a high urinary flow rate, and high Na +
delivery to the distal nephron also increase urinary K+ excretion
hyperkalemia
• because of the potential for lethal arrhythmias—is one of the most
alarming electrolyte abnormalities.
• typically is considered to be >5.5 mEq/L
• Severe hyperkalemia {k+] >7 mEq/L-neads immediate attention.
• Pediatric hyperkalemia is due to one or a combination of the
following mechanisms:
• ●Excessive increase in potassium intake
• ●Transcellular movement of intracellular potassium into the
extracellular space
• ●Decreased renal excretion of potassium
etiology
• Spurious hyperkalemia or pseudohyperkalemia:-
common in children b/c of difficultie in obtaining blood sample
-hemolysis, prolonged tourniquet application,fist clenching
-serum [K+] usually 0.4mEq/L greater than the plasma
Analysis of a plasma sample usually provides an accurate result
Clinical Manifestations
Asymptomatic patients- most children with mild tomoderate
hyperkalemia.
Mostly diagnosed when serum electrolyle are obtained for monitoring
or electrolyte abnormalities are suspected.
-may have ECG changes
Symptomatic patient:-
-muscle weakness- ascending begin in the leg and progressing to
trunk and arms
-symptoms of cardiac conduction abnormlities: palpitation,sycope or
asystole
Cardiac conduction abnormalities
• Based on the level of extracellular potassium and rate of change in
the extacellular level different ECG changes are seen
• ECG changes begin with peaking of the T waves. Followed by ST-
segment depression, an increased PR interval,flattening of the P
wave, and widening of the QRS comlex
• Can eventually progress to ventricular fibrillation
• Asystole also may occur
Diagnosis

• Hx—potassium intake , Rfx transcellular shift of K+,medication , signs

of renal insufficiency
• Initial laboratory- creatinine,BUN, assessment of acid base status
Treatment
The plasma K+ level, the ECG, and the risk of the problem worsening
determine the aggressiveness of the therapeutic approach
URGENCY of theraphy
#emergent theraphy: patient who are at risk for life threatening cardiac
conduction disturbances
Onset of action is immediate
>patient with clinical sign and symptoms
>asymptomatic patient with K+> 7mEQ/L
>K+ level b/n 6-7 , but at risk for continued rapid rise
• NON-EMERGENT
> . K+level below 7 and not atrisk for rapid increase. Treatment focus
on lowering potassium level over 6-12 hours
>.adjunctive intervention for these receiving emergent therapeutic
intevention

• The first action is to stop all source of additional K+

• If the K+ is > 6.5 mEq/L, an ECG should be obtained
•
• Goal of treatment
• (1) stabilize the heart to prevent life threatening arrhythmias
• (2) to remove potassium from the body
• Rapid measures to counteract adverse cardiac effects
• calcium infusion –calcium gluconate(10%) 0.5ml/kg (max 20ml) over
5 minute. And it should be given over 30 minute in patient receaving
digitalis
• Bicarbonate , most effacious in a patient with metabolic acidosis
• Insulin and glucose therapy-he effect of insulin begins in 10 to 20
minutes and peaks at 30 to 60 minutes
• The major adverse effect is hypoglycemia, and serum glucose level
should be measured one hour after the administration of insulin even
when glucose is administered.
• Inhaled beta-adrenergic agonists
Therapies removing potassium from the bod:- diuretics, cation echnage
resin , and dialysis
we use furosemide, a loop diuretic, at a dose of 1 mg/kg intravenously.
hypokalemia
• Common in children , with most cases related to gastroetritis.
• Most reference laboratories establish the lower pediatric limit of
normal serum potassium between 3 and 3.5 mEq/L
• However, symptoms are unlikely to occur in most healthy children
until serum potassium is below 3 mEq/L.
• Severe <2.5mEq/L
• Mderate 2.5-3 mEq/L
• Mild 3-3.5mEq/L
• Pediatric hypokalemia is due to one or a combination of the following
mechanisms:
• ●Decreased potassium intake
• ●Increased intracellular movement of potassium
• ●Excessive loss of potassium via the gastrointestinal (GI) tract, kidney,
or skin
Clinical Manifestations
• Symptoms generally do not become manifest until the serum
potassium is below 3 mEq/L unless there is a rapid significant fall in
serum potassium.
• Clinical findings include:
• ●Muscle weakness and paralysis
• ●Cardiac arrhythmias and electrocardiogram (ECG) changes
• ●Polyuria due to impaired urinary concentrating ability
diagnosis
• The presence of hypertension suggests excess mineralocorticoid
effects or levels
• The combination of hypokalemia and metabolic acidosis is
characteristic of diarrhea and distal and proximal RTA
• . A concurrent metabolic alkalosis is characteristic of emesis or
nasogastric losses, aldosterone excess, use of diuretics, and Bartter
and Gitelman syndromes.
• If a clear etiology is not apparent, the measurement of urinary K+
distinguishes between renal and extrarenal losses.
•
• TTKC=[k]urine/[k]plasma X (plasma osmolality/urine osmolality)

• A TTKG >4 in the presence of hypokalemia suggests excessive urinary

losses of K
Treatment
Treatment is influenced by:-
K+ level, l, clinical symptoms, renal function, the presence of
transcellular shifts of K+ , ongoing losses, and the patient's ability to
tolerate oral K+ .
, intravenous K+ should be used very cautiously
Oral K+ is safer, but not as rapid in urgent situations
 A typical PO starting dose is 1-2 mEq/kg/day, with a maximum of 60
mEq/day in divided doses
The dose of IV potassium is 0.5-1.0 mEq/kg, usually given over 1 hr.
. The adult maximum dose is 40 mEq
Potassium supplementation commonly comes in five preparations:
potassium chloride, potassium phosphate, potassium acetate,
potassium citrate-citric acid, and potassium bicarbonate.
• Correction of concurrent hypomagnesemia is important because it
may cause hypokalemia. Disease-specific therapy is effective in many
of the genetic tubular disorders
Maintenance Therapy

• Maintenance intravenous (IV) fluids are used in a child who cannot

be fed enterally
• replacement fluids if they have continued excessive losses
• If dehydration is present, the patient also needs
to receive deficit replacement
• Maintenance fluids are most often necessary in preoperative and
postoperative surgical patients
• a healthy adolescent can easily tolerate 12 or 18 hr without oral
intake.

10/01/23 51
• Maintenance fluids are composed of a solution of water, glucose,
sodium (Na +) and potassium
• This solution has the advantages of simplicity, long shelf life, low
cost
• Goals of Maintenance Fluids
• Prevent dehydration
• Prevent electrolyte disorders
• Prevent ketoacidosis
• Prevent protein degradation
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• The glucose in maintenance fluids provides approximately 20% of the
normal caloric needs of the patient
• Maintenance fluids do not provide adequate calories, protein, fat,
minerals, or vitamins
• Maintenance therapy replaces the ongoing daily losses of water and
electrolytes occurring via physiologic processes
(urine, sweat, respiration, and stool)

10/01/23 53
Hypocalcaemia

Preterm newborn – serum calcium <7 mg/dl or ionized calcium <1 mmol/l

Term newborn – serum calcium <8 mg/dl or ionized calcium <1.1 mmol/l

 Children – serum calcium <8.5 mg/dl or ionized calcium <50 % of serum calcium
Clinical Features

• may often be asymptomatic.

• Acute case often results in symptoms due to neuromuscular irritability or cardiac
arrhythmias.

• Tetany and seizures

• Rickets,basal gaglia calcifications,cataracts, skin and dental changes

• Trousseau’s Sign
• Chvostek’s Sign
• Evaluation
Serum ionized calcium, phosphate, and Plasma 25-hydroxyvitamin D (25 OH D)
Serum albumin, serum PTH, U/A
Serum alkaline phosphatase
Serum electrolytes, creatinine
Arterial blood gases

Maternal vit D, ECG, wrist X-R

Evaluation cont…
Treatment

Acute symptomatic cases –

An intravenous infusion of calcium is the most effective intervention.
• Calcium gluconate (10% 2 ml/kg can be administered slowly, over a 10 minute (can be repeated
every six to eight hours.)
• To maintain normocalcemia, a continuous intravenous infusion of calcium (50–75mg Ca/kg/24
hours) is preferable
Asymptomatic patients,
• Oral therapy should be the first line of therapy with 50 to 100 mg Ca/kg/day divided every four to
six hours
Hypomagnesemia should be corrected when present.
Treat underlying causes
 Asymptomatic patients,
• Oral therapy should be the first line of therapy with 50 to 100 mg Ca/kg/day divided every
four to six hours
 Hypomagnesemia should be corrected when present.
 Treat underlying causes
Hypercalcaemia

• defined as serum calcium >10.3 mg/dl.

• Severe hypercalcemia is defined as serum calcium >14 mg/dl (3.75 mmol/l).

Etiology
• Hyperparathyroidism

• Hypervitaminosis D

• Drugs

• granulomatous disease

• Malignancy

• Thyrotoxicosis

• immobilization
Clinical feature
• Gastrointestinal: nausea, vomiting, constipation, poor feeding

• Cardiac: hypertension, arrhythmias, shortened QT interval

• Neurological: hypotonia, poor activity, psychiatric disturbances,

coma

• Renal: polyuria, polydipsia, nephrocalcinosis, nephrolithiasis, distal

renal tubular acidosis, acute renal injury

• Ocular: conjunctival and palpebral calcification

Others: Weakness, anorexia
• Renal: polyuria, polydipsia, nephrocalcinosis, nephrolithiasis, distal
renal tubular acidosis, acute renal injury

• Ocular: conjunctival and palpebral calcification

Others: Weakness, anorexia
Treatment
The four main strategies in management of hypercalcemia are
to

• decrease intestinal calcium (Ca) absorption

• increase urinary Ca excretion

• 200-250ml/kg/day fluid and iv furosemide 1mg/kg QID

• decrease bone resorption

• remove excess Ca with the help of dialysis.

Maintenance Water
• Water is a crucial component of maintenance fluid
therapy because of the obligatory daily water losses
• These losses are both measurable (urine, stool) and
not measurable (insensible losses from the skin and
lungs)
• The goal of maintenance water is to provide enough
water to replace these losses.
• urinary losses are approximately 60% of the total

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Intravenous Solutions
• These solutions are available with 5% dextrose (D5), 10% dextrose
(D10), or without dextrose
• Except for Ringer lactate (lactated Ringer, LR), they are also available
with added potassium (10 or 20 mEq/L)
• A balanced IV fluid contains a base (lactate or acetate), a more
physiologic chloride concentration than NS
• additional physiologic concentrations of electrolytes such as
potassium, calcium

10/01/23 72
10/01/23 73
Glucose
• Hypotonic fluids increase the risk of
hyponatremia; hence, isotonic fluids with 5% dextrose are
recommended as standard maintenance fluid except in neonates
• Maintenance fluids usually contain D5, which provides 17
calories/100 mL and nearly 20% of the daily caloric needs.
• This level is enough to prevent ketone production and helps minimize
protein degradation

10/01/23 74
Selection of Maintenance Fluids
• An isotonic fluid (NS, LR, PlasmaLyte) with 5% dextrose and KCl (10-20
mEq/L is usually added to NS) is recommended for maintenance IV
fluids
• Subsequent maintenance fluids have the addition of 5% dextrose and
10-20 mEq/L KCl based on the serum K + and the clinical setting
• Electrolytes should be measured at least daily in all children receiving
>50% of maintenance
fluids intravenously

10/01/23 75
Replacement Fluids
• The gastrointestinal (GI) tract is potentially a source of considerable
water loss.
• GI lossesare often associated with loss of potassium, leading to
hypokalemia.
• children with diarrhea usually have a metabolic acidosis ,
• Emesis or losses from an NG tube can cause a metabolic alkalosis

10/01/23 76
• The losses are usually replaced every 1-6 hr,
depending on the rate of loss
• Diarrhea is a common cause of fluid loss in children and can result in
dehydration and electrolyte disorders
• Each 1 mL of stool should be replaced by 1 mL of this solution.
• The volume of stool should be measured, and an equal volume of
replacement solution should be given

10/01/23 77
10/01/23 78
• Loss of gastric fluid , through emesis or NG suction, is also likely to
cause dehydration
• Electrolyte disturbances, particularly hypokalemia and metabolic
alkalosis, are also common
• These complications can be avoided by judicious use of a replacement
solution
• The associated urinary K + loss is an important cause of hypokalemia
in this situation

10/01/23 79
10/01/23 80
• Urine output is normally the largest cause of water loss
• Diseases such as renal failure ana SIADH secretion can lead to a
decrease in urine volume
• continuation of maintenance fluids produces
fluid overload
In contrast diabetes mellitus, and diabetes insipidus increase urine
production.

10/01/23 81
• The approach to decreased or increased urine output is similar
• The patient receives fluids at a rate to replace insensible losses.
• This is accomplished by a rate of fluid administration that is 25–40%
of the normal
maintenance rate
Most children with renal insufficiency receive little or no potassium
because the kidney is the principal site of K + excretion
.

82
10/01/23 83
Deficit Therapy
• Dehydration most often caused bygastroenteritis, is a common
problem in children.
• Most cases can be managed w oral rehydration
• The 1st step in caring for the child with dehydration is to assess the
degree of
dehydration
DHN is common child due to common AGE,high surface areto volume
ratio,inability to talk thier fluid
need

10/01/23 84
Clinical Evaluation of Dehydration

10/01/23 85
• Clinical assessment of dehydration is only an estimate; thus the
patient must be continually reevaluated during therapy
• Hypernatremic dehydration is likely in any child
with losses of hypotonic fluid and poor water intake
Hyponatremic dehydration occurs in the child with diarrhea who is
taking in large quantities of low-salt
fluid, such as water or formula.

10/01/23 86
• Physical examination findings are usually proportional to the degree
of dehydration
• tachycardia in children with intravascularvolume depletion;
diaphoresis may also be present
• Tachypnea in children with dehydration may be
present secondary to a metabolic acidosis
AKI because of volume depletion is the most common etiology of renal
insufficiency in a child with volume depletion,

10/01/23 87
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Fluid Management of Dehydration
• No DHN– Mx plan A
• Fluid – in addition to the usual fluid intake
give ORS: 10ml/kg or
50-100ml for those below 2yrs per loss

100-200ml for children > 2yrs

Feeding - frequent breast feeding
-cow’s milk or formula
- continue other foods if he started
Return/follow up-see him in 5 days if sign are improving
10/01/23 89
b.Some DHN– plan B, loss is estimated to be 5%(average)
Treat with ORS
Volume is 75ml/kg
Give over 4hrs
Continue breast feeding
If vomiting, wait for 10minutes
After 4hrs, reassess and classify DHN
10/01/23 90
 c. Severe DHN-
• treatment plan C,loss estimated to be 10% of body
weight
• Start IV immediately
• Ringer’s lactate or NS ORS 5ml/kg/hr
• Volume is 100ml/kg

Infants (below 1st give Then give

12months of age) 30ml/kg over 70ml/kg over 5hrs
1hour
Children>12month Over 30minutes Over two and half
s of age hours
10/01/23 91
Monitoring and Adjusting Therapy
• All calculations in fluidtherapy are only
approximations

10/01/23 92
reference
• William 21 edition
• Uptodate
• Who guidiline