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Pediatric Fluid & Electrolyte

Therapy/
Diarrheas

Rose Marie Cabio-Lorenzana M.D.


Pediatric patients, esp infants, are predisposed to
disturbances in hydration & acid-base balance

A. Larger surface area in relation to volume of his body,


thus incur more insensible loss and more renal
expenditure than adults.
B. Higher metabolic rate leads to higher proportional
turnover of body fluids esp. of the ECF(2X that of
adult)
C. Prone to more fluid losses via multiple routes
compared to adults
D. Immaturity of infant’s kidneys – less capacity to
concentrate urine
> infants – 800 mOsm/L
> older children & adults – 1500 mOsm/L
Distribution of Fluids
I.ICF – intracellular fluid – cellular water

II. ECF – extracellular fluid –


A. interstitial fluid
B. plasma water
C. transcellular water
Comparison of body fluid
components
Newborn 1-3 yrs old Adult
Total body
water % of 75%-80% 65% 55%-60%
body weight
ECF 45% 25% 25%

ICF 35% 40% 40%


Total body water, intracellular fluid, and extracellular fluid as
a percentage of body weight and a function of age.
•Compartments of
TBW
• - % of body weight,
• - in an older child or
adult
The concentrations of the major cations and anions in the
intracellular space and the plasma, expressed in mEq/L.
ELECTROLYTE COMPOSITION OF BODY FLUIDS

• Serum Interstitial Fluid Intracellular Fluid


•CATIONS
•Sodium (Na+) 140 mEq/L 138 mEq/l 9 mEq/L
•Potassium (K ) + 5 8 155
•Calcium (Ca )++ 5 8 4
•Magnesium (Mg ) ++ 4 6 32
• Total 154 mEq/L 160 mEq/L 200 mEq/L
•ANIONS
•Chloride (Cl-) 100 mEq/L 119 mEq/L 5 mEq/L
•Bicarbonate (HCO3-) 26 26 10
•Protein (Pr) 19 7 65
•Organic Acids 6 6 -
•HPO4- 2 1 95
•SO4- 1 1 25
• Total 154 mEq/L 160 mEq/L 200 mEq/L
Average electrolyte composition of body
fluids
Source of Na+(m K+ Cl- HCO3- H+
secretion mol/L) (mmol/L (mmol/ (mmo/L (mmol/L)
) L) )
Insensible 12 10 12 - -
sweat
Parotid/saliva 112 19 40 - -
Stomach 60 10 130 - 60
Small intestine
Duodenum 140 5 80 65 -
Jejenum/ileum 130 5 105 30 -
bile 140 5 110 35 -
Pancreas 140 5 55 90 -
Colon 50 20 40 30 -
Diarrheic 50 20-30 50 30 -
Regulation of Osmolality and Volume

•OSMOLALITY
> plasma Osmolality = 285–295
mOsm/kg
= 2 × [Na] + [glucose]/18
+ [BUN]/2.8
> sodium value X 2 = provides an
approximation of the osmolality.
> effective osmolality (tonicity) - determines the
osmotic force mediating the shift of water
between the ECF and the ICF
Regulation of Osmolality and Volume

•Hyperglycemia (DKA) - there is a shift of


water from the ICF to the ECF space
• -> causes dilution of the sodium in the
ECF space -> hyponatremia despite an
elevated plasma osmolality.
• [Na]corrected = [Na]measured + 1.6 ×
• ([glucose] - 100mg/dL)/100
Regulation of Osmolality
Mediators:
1) hypothalamic receptors
2) thirst mechanism
3) ADH(antidiuretic hormone)

> a change of 1% in Posm is sensed by the


hypothalamic receptors
Recommended Daily water requirements
Weight in kg Daily water requirements

3-10 100ml/kg

11-20 1000ml + 50ml for each kg >10

>20 1500ml + 20ml for each kg >20

Note: The Holliday-Segar method is not suitable for neonates,14days old or


conditions associated with abnormal losses
Modifications for specific water requirements(based on
Holliday-Segar method)
Conditions increasing water reqrmnt Conditions reducing water
reqrmnt

Abnormal water and electrolyte Edematous and antidiuretic


losses states
Fever(12% increase for every Hypothermia(15% decrease)
C>37.5 C)
Sweating(10%-15% increase) Sedated or paralyzed
patient(40% reduction)
Sustained hyperventilation or Compromised renal function
excessive muscular activity (255- and oligoanuria
50% increase)
Hypermetabolic states- severe Infants and children nursed
thermal injury, salicylate in high environmental
intoxication, and thyrotoxicosis humidity
(25%-75% increase)
Newborn and young infant on Enclosed incubator (25%-
radiant heat or phototherapy 50% reduction)
Volume depletion vs dehydration
Volume depletion dehydration

ECFV size ECFV sodium concentration

hypovolemia or shock hyponatremia/hypernatremia

sodium and water loss plasma–free water deficit


disproportionate to loss of
sodium

problems - due to SODIUM problems - due to WATER


control mechanisms control mechanisms

MGT– rapid fluid replacement MGT- slow careful infusion


CLINICAL FEATURES OF SODIUM OR OSMOLALITY
DISTURBANCE
• ISOTONIC HYPOTONIC HYPERTONIC
SKIN Cold and dry Cold and clammy Warm, velvety, doughy
Poor elasticity Very poor elasticity Normal to slightly poor
and turgor and turgor and turgor

LIPS and Dry Clammy or moist Parched; patient


- TONGUE Presence of hypersaliva- complains of extreme
- tion and shedding of tears thirst
- if serum sodium is 110 mEq/L
- or less
- CNS Lethargic Comatose; occasionally with Lethargic when undisturbed;
- generalized convulsions Hyperirritable when aroused;
- Focal or generalized seizures;
Increased muscle tone and
tendonreflexes;Meningismus

VITAL SIGNS N to low temp; Very low temp; Febrile temp;


N to low BP BP “in shock” BP normal
- Rapid PR Thready pulse N to slightly increased PR
-
Mechanism of brain edema during
correction of hypernatremia
• A rapid decrease of the
serum concentration during
treatment of hypernatremia
causes movement of water
into brain cells, leading to
cerebral edema. The
presence of idiogenic
osmoles in brain cells is
resp onsible for the osmotic
gradient.
TREATMENT OF HYPERNATREMIC .
DEHYDRATION

the serum sodium •Determine time for correction on


concentration should basis of initial sodium concentration
not decrease by • [Na] 145-157 mEq/L: 24 hr
>12 mEq/L every 24h •
• [Na] 158-170 mEq/L: 48 hr
Restore intravascular •
volume • [Na] 171-183 mEq/L: 72 hr
Normal saline: •
20 mL/kg over 20 min
• [Na] 184-196 mEq/L: 84 hr
(repeat until
intravascular volume •
restored)

Causes of Hypernatremia

I.EXCESSIVE SODIUM

II.WATER DEFICIT

III. WATER AND SODIUM DEFICITS


Causes of Hypernatremia

I. EXCESSIVE SODIUM
> Improperly mixed formula
> Excess sodium bicarbonate
> Ingestion of seawater or sodium chloride
> Intentional salt poisoning (child abuse or
Münchausen syndrome by proxy)
> Intravenous hypertonic saline
> Hyperaldosteronism
Causes of Hypernatremia
II. WATER DEFICIT
Nephrogenic diabetes insipidus
Acquired
X-linked (MIM 304800)
Autosomal recessive (MIM 222000)
Autosomal dominant (MIM 125800)

Central Diabetes Insipidus


Acquired
Autosomal recessive (MIM 125700)
Autosomal dominant (MIM 125700)
Wolfram syndrome (MIM 222300)

Increased insensible losses


Premature infants
Radiant warmers
Phototherapy

Inadequate intake
Ineffective breast-feeding
Child neglect or abuse
Adipsia (lack of thirst)
Causes of Hypernatremia
WATER AND SODIUM DEFICITS
Gastrointestinal losses
Diarrhea
Emesis/nasogastric suction
Osmotic cathartics (lactulose)

Cutaneous losses
Burns
Excessive sweating

Renal losses
Osmotic diuretics (mannitol)
Diabetes mellitus
Chronic kidney disease (dysplasia and obstructive uropathy)
Polyuric phase of acute tubular necrosis

Postobstructive diuresis
Causes of Hyponatremia
Causes of Hyponatremia

•PSEUDOHYPONATREMIA
•HYPEROSMOLALITY
Hyperglycemia
Mannitol
•HYPOVOLEMIC HYPONATREMIA
•EUVOLEMIC HYPONATREMIA
•HYPERVOLEMIC HYPONATREMIA
Causes of Hyponatremia

•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
• Juvenile nephronophthisis (MIM 256100/606966/602088/604387)
• Autosomal recessive polycystic kidney disease (MIM 263200)
• Tubulointerstitial nephritis
• Obstructive uropathy
• Cerebral salt wasting
• Proximal (type II) renal tubular acidosis (MIM 604278)[*]
• Lack of aldosterone effect (high serum potassium) Absent aldosterone
• (e.g.,21-hydroxylase deficiency [MIM 201910])
• Pseudohypoaldosteronism type I (MIM 264350 and 177735)
• Urinary tract obstruction and/or infection

Causes of Hyponatremia

EUVOLEMIC HYPONATREMIA

Syndrome of inappropriate antidiuretic hormone


Nephrogenic syndrome of inappropriate
antidiuresis (MIM 304800)
Desmopressin acetate
Glucocorticoid deficiency
Hypothyroidism


Causes of Hyponatremia

•EUVOLEMIC HYPONATREMIA

• Water intoxication
• Iatrogenic (excess hypotonic intravenous fluids)
• Feeding infants excessive water products
• Swimming lessons
• Tap water enema
• Child abuse
• Psychogenic polydipsia
• Diluted formula
• Marathon running with excessive water intake
• Beer potomania

Causes of Hyponatremia

•HYPERVOLEMIC HYPONATREMIA

> Congestive heart failure


> Cirrhosis
> Nephrotic syndrome
> Renal failure
> Capillary leak due to sepsis
> Hypoalbuminemia due to
gastrointestinal disease
(protein-losing enteropathy)
Disturbances in
Potassium Balance
•Serum K+ = 3.5 -5.0 mmol/L
•> principal ICF cation
•>impt in regulation of a variety of cell functions
•>effect on resting potential of nerve and muscle cells
•>dist of K+ between ICF & ECF controlled primarily by cell
membrane pump activity
•-influenced by the ffng:
• a)acid base status
• b)hormonal(insulin, mineralocorticoids)
• c) adrenergic activity(alpha & beta)
•K+ excretion
• - mainly thru the kidneys
• >distal nephron secretion
Causes of Hyperkalemia
Causes of Hyperkalemia

•I. SPURIOUS HYPERKALEMIA


> in vitro Hemolysis
> Tissue ischemia during blood drawing
> Thrombocytosis or Leukocytosis
Causes of Hyperkalemia
•INCREASED INTAKE
> Intravenous or oral supplementation
> K-containing salt substitutes
> Blood transfusions
> endogenous cell breakdown
Causes of Hyperkalemia
•DECREASED EXCRETION
- acute or chronic renal failure
- mineralocorticoid deficiency/resistance
- potassium sparing diuretics
Causes of Hyperkalemia
•SHIFTS FROM INTRACELLULAR TO
EXTRACELLULAR FLUID
•- metabolic/respiratory alkalosis
•- mineralocorticoid and insulin deficiency
•-drug-induced
•-hyperkalemic periodic paralysis
Causes of Hypokalemia

I. POOR DIETARY INTAKE

II. TRANSCELLULAR SHIFTS

III. EXTRARENAL LOSSES

IV. RENAL LOSSES


Causes of Hypokalemia
I. Poor dietary intake
> anorexia nervosa
Causes of Hypokalemia
II. Transcellular shifts(w/out K+ deficit)
a) insulin
b) B2 catecholamines
c) alkalosis(metabolic/respiratory)
d) hypokalemic periodic paralysis
Causes of Hypokalemia
III. TRANSCELLULAR SHIFTS
• Alkalemia
•Insulin
•β-Adrenergic agonists
•Drugs/toxins (theophylline, barium, toluene,
cesium chloride)
• Hypokalemic periodic paralysis (MIM
170400)
• Thyrotoxic period paralysis
Causes of Hypokalemia
III. Extrarenal losses
a) diarrhea
b) protracted vomiting
c) excessive sweating
d) laxative abuse
e) Na polystyrene sulfonate ingestion
f) ureterosigmoidostomy
g) obstructed long ileal loop
Causes of Hypokalemia
IV. Renal losses
a) RTA
b) DKA
c) Diuretic abuse
d) Primary/secondary hyperaldosteronism
e) Bartter’s syndrome
f) Cushing syndrome
g) Leukemias
Causes of Hypokalemia
IV. EXTRARENAL LOSSES
•Diarrhea
• Laxative abuse
• Sweating
•Sodium polystyrene sulfonate (Kayexalate)
or clay ingestion
Causes of Hypokalemia
V.RENAL LOSSES
•With metabolic acidosis
- Distal renal tubular acidosis
(MIM 179800/602722/267300)
- Proximal renal tubular acidosis
(MIM 604278)[*]
- Ureterosigmoidostomy
- Diabetic ketoacidosis
Causes of Hypokalemia
•Without specific acid-base disturbance
• Tubular toxins: amphotericin, cisplatin,
aminoglycosides
• Interstitial nephritis
• Diuretic phase of acute tubular necrosis
•Postobstructive diuresis
•Hypomagnesemia
• High urine anions (e.g., penicillin or penicillin
derivatives)
Causes of Hypokalemia
•With metabolic alkalosis
•Low urine chloride
•Emesis
•nasogastric suction
•Chloride-losing diarrhea (MIM 214700)
•Cystic fibrosis (MIM 219700)
•Low-chloride formula
•Posthypercapnia
•Previous loop or thiazide diuretic use
Causes of Hypokalemia
•High urine chloride and normal blood
pressure
- Gitelman syndrome (MIM 263800)
- Bartter syndrome (MIM
602023/607364/602522/241200/601678)
- Autosomal dominant
hypoparathyroidism (MIM 146200)
- Loop and thiazide diuretics
Causes of Hypokalemia
–High urine chloride and high blood pressure
– Adrenal adenoma or hyperplasia
– Glucocorticoid-remedial aldosteronism (MIM 103900)
–Renovascular disease
–Renin-secreting tumor
–17α-hydroxylase deficiency (MIM 202110)
–11β-hydroxylase deficiency (MIM 202010)
– Cushing syndrome
–11β-hydroxysteroid dehydrogenase deficiency (MIM
218030)
Causes of Hypokalemia
•Licorice ingestion
•Liddle syndrome (MIM 177200)
Normal Values of Arterial Blood
Gas

•pH - 7.35–7.45
•[HCO3-] - 20–28 mEq/L
•Pco2 - 35–45 mm Hg

[H+] = 24 × Pco/
[HCO3-]
Three-step process for interpreting acid-base
disturbances
step 1, determine whether the

pH is low (acidemia) < 7.35

pH high (alkalemia) >7.45

step 2, establish an explanation for


the acidemia or alkalemia.

step 3, calculate the expected compensation and determine whether a mixed


disturbance is present. Met. alk., metabolic alkalosis; met. acid., metabolic
acidosis; resp. alk., respiratory alkalosis; resp. acid., respiratory acidosis.
.
Acid-base balance
Homeostatic responses
I. chemical buffers
II. ventilatory adjustments by the lungs
III. Alterations in acid excretions by the
kidneys
Acid-Base Balance
•bicarbonate buffer system
• -based on the relationship between
carbon dioxide(CO2) and bicarbonate
(HCO3-):
• CO2 + H2O ↔ H+ + HCO3-
Causes of metabolic acidosis
I. Loss of bicarbonate

a) GI losses
b) Renal losses

II. Increased H+ load

a) endogenous production
b) exogenous administration

III. Decreased H+ excretion

Acute and chronic kidney failure, distal RTA, carbonic anhydrase


inhibitors
METABOLIC ACIDOSIS
•3 basic mechanisms:
1) Loss of bicarbonate from the body
(gi tract or kidneys)
2) Impaired ability to excrete acid by the
kidney(depleting bicarbonate store)
3) Addition of acid to the body (exogenous
or endogenous)→ consumes bicarbonate,
depleting the buffer system
METABOLIC ACIDOSIS
•Diarrhea
• -most common cause of metabolic
acidosis in children
- loss of bicarbonate from the body.
• -kidneys attempt to balance the losses by
increasing acid secretion, but metabolic
acidosis occurs when this compensation is
inadequate
METABOLIC ACIDOSIS
•-volume depletion (losses of sodium and
water) potentially exacerbates the acidosis
by causing shock and a lactic acidosis
•-Renal failure 2ndary to dehydration also
limits acid excretion and contributes to the
acidosis.
Acid-Base dist. but w/ Normal ph

. 1)mixed disorder- the 2 processes have


opposite effects on pH (a metabolic
acidosis and a respiratory alkalosis)
changes in the hydrogen ion concentration
that are comparable in magnitude, albeit
opposite
Acid-Base dist. but w/ Normal ph

•2) simple chronic respiratory alkalosis


• -the appropriate metabolic compensation
is enough to normalize the pH.

•the presence of an acid-base disturbance is


deduced because of the abnormal carbon
dioxide and/or bicarbonate levels
DIARRHEA MGT
Epidemiology Diarrhea
•1.5B –annual incidence worldwide (CDC)
• - <5yrs old
•1.5-12.5M - annual deaths
Global trends in diarrhea incidence
Nelson 19th
Pathophysiology of Watery
Diarrhea
> Normal Intestinal Fluid Balance
> Intestinal Absorption of Water and
Electrolytes
> Intestinal Secretion of Water and
Electrolytes
ASSESS FOR DEHYDRATION
A B C
1.Look at: Well, alert *Restless, *Lethargic or
condition irritable* unconscious;
floppy*
Eyes Normal Sunken Very dry &
sunken
Tears Present Absent Absent
Mouth & Wet Dry Very Dry
Tongue
Thirst Drinks *Drinks *Drinks poorly
normally, not eagerly* or is not able to
thirsty drink*
2. Feel: Skin Goes back *Goes back *Goes back
pinch quickly slowly* very slowly*
3. Decide; NO SIGNS ≥ 2 signs inc ≥ 2 signs inc 1
OF 1 *Sign* – *Sign*-
dEHYDRA SOME SEVERE
TION DEHYRATI DEHYDRATIO
ESTIMATE THE FLUID DEFICIT
Assessment Fluid Deficit as Fluid Deficit in
% of BW ml/kg BW

No Dehydration <5 % <50 ml/kg

Some Dehydration 5-10 % 50-100 ml/kg

SevereDehydration >10 % >100 ml/kg


Objectives of Tx in Diarrhea
I. Prevent Dehydration
II. Treat Dehydration
III. Prevent Nutritional Damage
IV. Reduce the Duration of Severity of
Diarrhea & Prevent Future Episodes
4 KEY ELEMENTS- mgt of Diarrhea

•1) Fluids & Electrolytes


•2) Food
•3) Follow-up
•4) Frevention
Average composition of stool vomitus in gastroenteritis

Electrolyte Stool(mEq/L) Vomitus(mEq/L)

Sodium 55 60

Potassium 25 10

Bicarbonate 15 -

Chloride 55 90
ELECTROLYTE CONTENT OF STOOL
IN ACUTE WATERY DIARRHEA

Average electrolyte content, mmol/l


Na+ K+ Cl- HCO3-
•Cholera
•Adults 140 13 104 44
•Children 101 27 92 32
(<5 yrs)
•Non-cholera
•Children 56 25 55 14
(<5 yrs)
•ORS solution 75 20 65 10
COMPOSITION BY WEIGHT AND MOLAR CONC’N
OF REDUCED (LOW) OSMOLALITY ORS SOLUTION

Reduced osmolality Grams/L Reduced osmolality Mmol/L


ORS ORS
Sodium chloride 2.6 Sodium 75
Glucose anhydrous 13.5 Chloride 65
Potassium chloride 1.5 Glucose, anhydrous 75
Trisodium citrate 2.9 Potassium 20
Citrate 10

Total osmolality 245


Nutritional Supplementation
•> WHO recommendation
• -provide a comprehensive nutritional
supplement with zinc 10-20 mg/day.
•(Zinc seems to reduce the duration and
the severity of diarrhea)
FOLLOW-UP
•1. many watery stools
•2. repeated vomiting
•3. very thirsty
•4. eating or drinking poorly
•5. fever
•6. blood in stools
•7. does not get better in 3 days
PREVENTION OF DIARRHEA
(Intervention /WHO)
1. Breastfeeding
2. Improved weaning practices
3. Use of safe water
4. Handwashing
5. Food safety
6. Use of latrines and safe disposal of stools
7. Measles immunization
sholud
Fluids & Electrolytes Some dehydration
•> ~ 75ml/kg BW of ORS for 1st 4 hours
•> older children and adults- ad libitum, as
long as there are no signs of overhydration
•> feeding bottles should NOT be used
•> give fluids slowly, constantly
Food
•> introduce food after 4 hrs of hydration
• (except breastmilk)
•> after 4 hrs, give some food every 3-4 hrs
• (emphasize to mothers the importance
• of continued feeding in diarrhea)
Follow-up

•>0ngoing fluid losses

•> recompute
Failure of oral rehydration Tx
1.High rates of purging
(15-20ml/kg/hr stool loss)
2. Persistent vomiting
3. Inability to drink
4. Abdominal distention & ileus
5. glucose malabsorption
REASSESSMENT
•1. NO dehydration

•2. SOME dehydration

•3. SEVERE dehydration


IV Treatment in SEVERE dehydration
AGE First give Then give
30ml/kg in: 70ml/kg in:
Infants 1 hour 5 hours

Older 30 minutes 2 ½ hours

•> reassess every 15-30 min until a strong radial


pulse is present, then q 4 hours.
•> reassess again at end of 6th hour.
• 1. no dehydration
• 2. some dehydration
• 3. severe dehydration
IONIC COMPOSITION OF
INTRAVENOUS INFUSION SOLUTION
Solution Cations-mmol/l Anions-mmol/l
Preferred Na+ K+ Cl- Lactate Glucose
Ringer’s lactate 130 4 109 28 0

Ringer’s lactate 130 4 109 28 278


w/ 5% dextrose

Dhaka sol’n 133 13 98 48 140

Half strength 61 17 51 27 278


Darrow w/ 5%
dextrose

Acceptable
Normal Saline 154 0 154 0 0
(0.9% NaCl)

Not acceptable
Glucose(dextrose) 0 0 0 0 278
Sol’n

If IV therapy not available:
•1. send to nearest facility(within 30 min)-
give ORS to drink along the way.
•2. NGT- ORS can be given 20 ml/kg/hr for 6
hours.
•3. reassess every hour, if not improved after
3 hours, send to nearest facility.
Use of antimicrobials and
"antidiarrheal" drugs
•A. Antimicrobials should not be used routinely.
• 1) not possible to distinguish between
• episodes that are responsive or
• unresponsive to antimicrobials clinically
• 2) Sensitivity (?)
• 3) adds to the cost to Tx
• 4) risks adverse reactions
• 5) enhances the devt of resistance
Use of antimicrobials and
"antidiarrheal" drugs
•>A. Antimicrobials may benefit the ff.
▪ 1) bloody diarrhea
▪ (probable shigellosis)
▪ 2) suspected cholera
▪ w/ severe dehydration
▪ 3) serious non-intestinal infections
▪ (pneumonia)
“Anti-diarrheal” drugs
•- B. Other drugs -no practical benefits and are not
indicated for the Tx of diarrhea in children.
- do not prevent dehydration or
improve nutritional status
> have dangerous, and sometimes fatal, side-effects.

•1. Adsorbents- bind and inactivate toxins or


other substances.
•(kaolin, attapulgite, smectite, activated
charcoal, cholestyramine)
“Anti-diarrheal” drugs
•2. Anti-motility drugs- opiate or opiate like drugs
inhibits intestinal motility and reduce frequency of
stool passage.
• a) may cause severe paralytic ileus, which
could be fatal.
• b) delay elimination of causative organisms.
• c) may cause sedation; could lead to fatal CNS
toxicity.
•(loperamide, diphenoxylate with atropine, tincture
of opium, camphorated tincture of opium,
paregoric, codeine)
“Anti-diarrheal” drugs
3. Other Drugs
a) anti-emetics- may cause sedation. Vomiting
usually stops when pt has been hydrated.
(prochlorperazine, chlorpromazine)
b) cardiac stimulants- never indicated.
Correct Tx of Hypovolemia and subsequent shock
is IV fluids of balanced electrolyte soln
( adrenaline, nicotinamide)
“Anti-diarrheal” drugs
•c. Purgatives (Cathartics)- makes diarrhea
and dehydration worse.
• -never used.
•d. Steroids- no benefit, never used.
Types of Shock
•HYPOVOLEMIC •CARDIOGENIC
•Decreased preload •Cardiac pump failure
secondary to internal or secondary to poor
external losses myocardial function
- Loss of components of - Congenital heart
intravascular volume disease
- Blood:hemorrhage - Cardiomyopathies:
- Plasma:burns, infectious or acquired,
- nephrotic syndrome dilated or
restrictive Ischemia
- Water and electrolytes:
diarrhea, vomiting, - Dysrhythmias
diabetes
Types of Shock
•DISTRIBUTIVE •SEPTIC
Abnormalities of vasomotor •Includes multiple forms of
tone shock Hypovolemic:third
• Loss of venous spacing Distributive:early
capcitance decreases shock with decreased
preload afterload Cardiogenic:depre
•Loss of arterial capcitance ssion of myocardial function
decreases afterload or by endotoxinsC
systemic blood pressure - Bacterial
- Anaphylaxis - Viral
- Neurologic:loss of - Fungal
sympathetic vascular (immunocompromised
tone secondary to spinal patients are at increased
cord or brainstem injury risk)
- Drugs
Signs of Decreased Perfusion
ORGAN ↓PERFUS’ ↓↓PERFUSIO ↓↓↓PERFUSION
SYSTE N N
M
Central — Restless, Agitated/confused,
nervous apathetic, stuporous, coma
system anxious
Respiration — ↑Ventilation ↑↑Ventilation
Metabolism — Compensated Uncompensated metabolic
metabolic acidemia
acidemia
Gut — ↓Motility Ileus
Kidney ↓Urine Oliguria (<0.5 Oliguria/anuria
volume mL/kg/hr)
↑Urinary
specific
gravity
Skin Delayed Cool extremities Mottled, cyanotic, cold
capillary extremities
CLINICAL TYPES OF DIARRHEAL DISEASES

I. Acute Watery diarrhea – last several hours or day. Main danger is


dehydration, (including cholera)
II.Acute Bloody Diarrhea (dysentery) – main dangers are damage
of the intestinal mucosa, sepsis and malnutrition and
dehydration
III. Persistent Diarrhea – last 14 days or longer; main danger is
malnutrition and serious non-intestinal infection. Dehydration
may also occur.
IV. Diarrhea with Severe Malnutrition – (Marasmus or Kwashiorkor):
Main dangers are severe systemic infection, dehydration, heart
failur and vitamin and mineral deficiency.

The management of each type should prevent or treat the main


danger(s) that each presents
DIAGNOSIS OF MODERATE OR SEVERE
MALNUTRITION
Assessment Weight-for- Height-for- Mid-arm** Other
Age* Age* Circumferenc
e

Moderate 60-75 % 70-80 % Yellow band


Malnutrition 11.0-12.5 cm

Severe <60 % <70 % Red band Obvious


Malnutrition <11.0 cm marasmus/
Edema with
Muscle
wasting
Important microbial causes of Acute Diarrhea in
Infants & Children

• I. Viruses
• II. Bacteria
•III. Protozoa
Important microbial causes of Acute Diarrhea in
Infants & Children

. Viruses
A. Rotavirus
>worldwide; cold, dry season
>15-25%
> 5 serotypes epidemiologically impt
> patchy damage -> blunting of the vili
> absorptive capacity return in 2-3 weeks
Important microbial causes of Acute Diarrhea in
Infants & Children

II. Bacteria
•A. Escherichia coli
•B. Shigella
•C. Campylobacter jejuni
•D. Vibrio cholera 01 & 0139
•E. Salmonella (non-typhoidal)
Important microbial causes of Acute Diarrhea in
Infants & Children

•II. Bacteria
• A. Escherichia coli
• a. ETEC (Enterotoxigenic E. coli)
• b. LA-EC (Localized- Adherent E.coli )
• c. DA-EC (Diffuse- Adherent E. coli)
• d. EIEC (Enteroinvasive E.coli)
• e. EHEC(Enterohemorrhagic E. coli)
Important microbial causes of Acute Diarrhea in
Infants & Children
•II. Bacteria
• A. Escherichia coli
a. ETEC (Enterotoxigenic E. coli)
• > traveller’s diarrhea, self-limiting
• >2 impt virulent factors
• 1. colonization factors
• 2. enterotxins
Important microbial causes of Acute Diarrhea in
Infants & Children
B. Shigella
>10-15% for <5yrs old group
> 4 serogroups
> most common cause of bloody diarrhea
> warm seasons
> colonic epithelium-> cell death and
mucosal ulcers
> Shiga toxin- cytotoxic, neurotoxic.
> has smooth lipopolysaccharide cell wall
antigen, and antigens that promote cell invasion
Important microbial causes of Acute Diarrhea in
Infants & Children
B. Shigella
4 serogroups:
1. S . Flexneri
> developing countries
2. S. sonnei
> developed countries
3. S. dysenteriae type 1
> epidemics with high mortality
4. S. boydii
>less common
Important microbial causes of Acute Diarrhea in
Infants & Children
B. Shigella
>fever, watery diarrhea
>dysentery with fever, abdominal
cramps, tenesmus
> frequent small, bloody, mucoid stools
with many leucocytes
> severe in malnourished and non-breastfed
infants
Important microbial causes of Acute Diarrhea in
Infants & Children

B. Shigella
•C. Campylobacter jejuni
•D. Vibrio cholera 01 & 0139
•E. Salmonella (non-typhoidal)
Important microbial causes of Acute Diarrhea in
Infants & Children

D. Vibrio cholera 01 & 0139


> cause epidemics
> contaminated food and water
> hot, humid seasons
> small intestines -> endotoxin
> definite serotyping & biotyping-
not impt for Tx and control

Important microbial causes of Acute Diarrhea in
Infants & Children

•III. Protozoa
• A. Giardia duodenalis
• B. Entamoeba histolytica
• C. Cryptosporidium
Important microbial causes of Acute Diarrhea in
Infants & Children

A. Giardia duodenalis
• >worldwide distribution
• > 1-5 yrs old: prevalence could be100%
• > food or waterborne;
• fecal oral transmission common
• > small bowel-flattening of intestinal epith.
Important microbial causes of Acute Diarrhea in
Infants & Children

A.Giardia duodenalis
B. > majority asymptomatic
• > acute, persistent diarrhea
• > malabsorption with fatty stools,
• abdominal pain, and bloating
Important microbial causes of Acute Diarrhea in
Infants & Children

B. Entamoeba histolytica
• > worldwide; incidence increases with age
• -highest in adult males
• >mucosa of colon
• -> neurohumoral substances
• -> inflammatory type of diarrhea
Important microbial causes of Acute Diarrhea in
Infants & Children

B. Entamoeba histolytica
• > 90% asymptomatic
• > Dx- requires
• (+)haematophageous trophozoites
• in feces or in colonic ulcers
• > persistent mild diarrhea
• -> fulminant dysentery
• -> liver abscess
When to suspect Cholera:
1)Acute diarrhea with vomiting rapidly
develops severe dehydration
2) Cholera is known to be occurring in the
area
MGT of suspected Cholera
•Why cholera is diff compared to Acute
Diarrhea:
• 1) occurs usually in large epidemics
• 2) voluminous watery diarrhea
• -> severe dehydration
• -> hypovolemic shock
• 3) appropriate antibiotics may shorten
course
Treatment of Dehydration in Cholera

1)Follow guidelines for fluid mgt of some & severe


dehydration
2) For severe dehydration & shock, initial IV
infusion should be given rapidly to restore
adequate blood volume- guided by N BP and
strong radial pulse.
3) Unusually large ORS may be needed to replace
large continuing fluid losses after dehydration
is corrected.
Treatment of Dehydration in Cholera

•4.Additional K may be provided by ORS as


soon as the patient can drink
•5. constantly observe & reassess pt until
diarrhea stops or is infrequent and of small
volume.
MGT of Acute Bloody Diarrhea
(Dysentery)
1.If with severe malnutrition
-> refer to hospital
2. All others
-> give appropriate fluids to prevent
dehydration
-> give food
-> treat infection- oral antimicrobials
(eg Shigella for 3-5 days)
3. If (+) trophozoites -> tx for amoebiasis
4. Follow up after 2 days
MGT of persistent diarrhea

> Last for at least 14 days


> (+) weight loss
> (+) serious non-intestinal infections
> rare in breastfed babies
> If with severe malnutrition
-> refer to hospital
MGT of persistent diarrhea

1.Appropriate fluids for hydration


2. Nutritious diet (110 calories/kg/day)
3. Supplementary vit & minerals, including
zinc for 10-14 days
4. Antimicrobials to treat diagnosed
infections
Antimicrobials Used to Treat
Specific Causes of Diarrhea
CAUSES Antibiotic(s) of Alterative(s)
choice
Cholera Doxycycline Erythromycin
Adults: 300 mg once Children: 12.5mg/kg
Tetracycline 4x/day x 3days
Children: 12.5 mg/kg Adults: 250mg
4x /dayx3 days 4x/day x 3 days
Adults: 500mg
4x/day x 3 days

Shigella Ciprofloxacin Pivmecillinam


dysentery Children: 15mg/kg Children: 20 mg/kg
2x/day x 3 days 4x/day x 5 days
Adults: 500mg/day Adults: 400mg
2x/day x 3 days 4x/day x 5 days
Cefriaxone:
Children : 50-100mg/kg
once a day IM x 2-5 days

Amoebiasis
Giardiasis
Antimicrobials Used to Treat
Specific Causes of Diarrhea
CAUSES Antibiotic(s) of choice Alternative(s)

Amoebiasis Metronidazole
Children: 10 mg/kg 3x/day for
5-10 days
Adults: 750 mg 3x /day for 5-
10 days
Giardiasis Metronidazole
Children: 5 mg/kg 3x day x 5
days
Adults: 250 mg 3x / day x 5
days
PREVENTION OF DIARRHEA

1. Breastfeeding
2. Improved weaning practices
3. Use of safe water
4. Handwashing
5. Food safety
6. Use of latrines and safe disposal of stools
7. Measles immunization
1) Breastfeeding
•>complete food
•>composition always IDEAL for the infant
•>has immunological properties
•>is clean
•>encourages the “bonding”
•>milk intolerance rare
•>helps with birth spacing
2) Improved weaning practices
•>select nutritious foods
•>use hygienic practices
Global trends in diarrhea incidence
Nelson 19th
3) Use of Plenty, Safe water
•>collect water from cleanest source;
• store in clean containers.
•>Latrines should be located more than 10
m away and downhill
•>Keep animals away from protected water
sources
•>if fuel is available, boil water used for food
and drink of young children
4)Handwashing
•> fecal–oral route of transmission
•>advise family members to wash hands
thoroughly after defecation, after cleaning
child after defecation, after disposing of a
child’s stool, before preparing food, and
before eating.
5)Food safety
•>Do not eat raw foods, except undamaged
fruits and veggies that are peeled and eaten
immediately
•>cook food until it is hot throughout
•>Protect food from flies
•> Eat food while it is still hot or reheat it
thoroughly before eating
6) Use of latrines
•>fecal – oral route of transmission
•>proper disposal of feces including infant
stools
7) Measles immunization
THANK YOU!

Good luck!!!

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