Diarrheal Disorders

Rebecca Abiog-Castro, M.D.

Pediatric Gastroenterology
UST Hospital
 Diarrhea
• It is passage of stool at least twice the
normal bowel movement wherein the stools
follow the shape of the container.

• It is also defined in infants and children as a

stool output of greater than 10 g/kg/day
(normal=5-10 g/kg/day) and more than the
adult limit of 200 g/24 hour.
 Definition of Terms
Acute Diarrhea
• It is the passage of loose and watery stool
of less than two weeks duration.

Chronic/Persistent Diarrhea
• It is the passage of loose and watery stool
of two weeks or longer duration.
Epidemiology:

• One of the leading cause of morbidity

and mortality in children

• One billion episodes of illness

• 3-5 million deaths annually

• Global Impact of Diarrhea:

– 1970 (late): ORT & ORS adopted by WHO & UNICEF

succeeded in managing diarrheal disorder

– 1979: 4.5 M of children under FIVE die of diarrhea

– 1990: More than 1 M deaths / year were prevented

attributable to these therapeutic management

– 2002: Deaths due to diarrhea has been reduced to 1.6 M

– At present: Knowledge on ORT in some countries have

been declining
 The Goals:

• Reduce by one half deaths due to

diarrhea among children under five by
2010 compared to 2000.

• Reduce by two thirds the mortality rate

among children under five by 2015
compared to 2000
 Pathophysiology of Diarrhea
= Diarrhea results from altered intestinal
water and electrolyte transport.

= GIT of infant handles approximately 285

ml/kg/24 hour of fluid (intake + intestinal
secretion) with a stool output of 5-10 g/kg/24
hour.
 Pathophysiologic Mechanisms of Diarrhea

• Osmotic diarrhea

• Secretory Diarrhea

• Reduction in anatomic surface area

• Alteration in Intestinal motility

 Osmotic diarrhea
• Due to presence of non-absorbable solutes in the GIT

• Classic example: Lactose Intolerance which is caused

by lactase deficiency  lactose in colon

• Colon  bacteria  lactic acids & short-chain organic

acids  osmotic load  water secreted into the lumen
Important Features of Osmotic Diarrhea

• stops with fasting

• ph <5
• positive for reducing substance
• volume of stool <200 ml/day
• stool Na+: <70 meq/L
• Na+ + K+ x 2 = < stool osmolarity
suggestive of presence of other osmols in
the stool
 Features of Secretory Diarrhea
• high volume output > 200 ml/24 hr
• diarrhea persists even with fasting
• stool Na+ >70 mEq/L
• reducing substances: (-)
• stool ph: >6
 Mechanisms of Secretory Diarrhea

1) Activation of the intracellular mediators such as cyclic AMP, cyclic

GMP, and intracellular Ca2+

A) Activation of cyclic adenosine monophosphate

B) Activation of cyclic guanosine monophosphate

C) Calcium-dependent
A) Activation of cyclic adenosine monophosphate
– Bacterial toxins:
• Enterotoxins of Cholera
• E. Coli (heat labile)
• Shigella
• Salmonella
• Campylobacter jejuni
– Hormones:
• vasoactive intestinal peptide
• Gastrin
• secretin
– Anion surfactants:
• bile acids
• ricinoleic acid
B) Activation of cyclic guanosine monophosphate
• Bacterial toxins:
– E. Coli (heat stable)
– Yersinia Enterocolitica toxin

C) Calcium-dependent
• Bacterial toxins:
– Cl. Dificile enterotoxin
• Neurotransmitters:
– acetylcholine, serotonin
• Paracrine agents:
– bradykinin
Mechanisms of Secretory Diarrhea
2) Reduction in Anatomic Surface Area
• Short bowel syndrome:
• Flattening of the proximal intestinal surface with marked
– Celiac disease, Cow milk allergy, Postenteritis
enteropathy

3) Alteration in Intestinal Motility

– Hypomotility as in malnutrition  bacterial overgrowth 
bile salt deconjugation  intracellular mediator 
secretory diarrhea
– diabetes mellitus, scleroderma and intestinal pseudo-
obstruction.
Acute Diarrhea:

1) Inflammatory diarrhea

2) Non-inflammatory Diarrhea
 Acute Diarrhea
1) Inflammatory Diarrhea:
– caused by organisms that invade the intestine
directly or produce cytotoxin

– Etiologic Agents: Shigella, Salmonella,

Enteroinvasive E.Coli, Shiga toxin-producing
E.Coli, Campylobacter jejuni, Clostridium Dificile

– Presents as bloody mucoid stool

– Stool Examination: (+) fecal leucocytes
 Acute Diarrhea

2) Non-inflammatory Diarrhea:
– Caused by organisms that:

• produce enterotoxin by some bacteria (Cholera),

• destruction of villi (viruses),

• adherence by parasites and adherence or

translocation by bacteria
 Chronic Diarrhea

• Causes of chronic Diarrhea:

– Pancreatic Disorders:
• Cystic fibrosis
• malnutrition
– Bile acid disorders:
• chronic cholestasis
• terminal ileum resection
• bacterial overgrowth
• chronic use of bile acid sequestrants
Causes of Chronic Diarrhea
– Intestinal disorders:
• Infections: bacterial, viral, fungal
• infestations: parasitic
• cow’s and soy protein intolerance
• IBD
• autoimmune enteropathy
• eosinophilic enteropathy
• carbohydrate malabsorption
• excessive carbonated fluid intake
• excessive intake of sorbitol, magnesium
hydroxide, lactulose
- Mucosal Factors:

• enterokinase deficiency
• glucoamylase deficiency
• postenteritis syndrome
• short bowel syndrome
• Hirschsprung disease
• Partial bowel obstruction
• malrotation
 Bloody Stool

1) Infectious:
Enteroinvasive organism:
Shigella, EIEC, E. Histolytica

2) Non-infectious:
a) Medical Condition: Protein Intolerance
(Cow’s milk & Soya protein)
b) Surgical Conditions: Intussusception,
Meckel’s Diverticulum
 Bloody Stool
1) Infectious:

- Shigella Dysentery:
- Acute course with high fever, vomiting,
seizure
- Laboratory Tests: Leucocytosis;
Stool analysis: numerous pus cells and rbc

- Intestinal Amebiasis:
- Chronic course at least two wks
- Clinical course: no fever & vomiting
 Bloody Stool
2) Non-infectious:

a) Food Allergy (Food Hypersensitivity):

1) Ig-E mediated :

2) Non-IG-E mediated:
 Bloody Stool
A. Ig-E mediated Food Hypersensitivity:
- Gastrointestinal Anaphylaxis:
B. Non-Ig-E Mediated Disorders:

• Allergic Proctocolitis:
 Bloody Stool
Diagnosis
• Food-induced Enterocolitis:
– Protracted vomiting & diarrhea begin between 1
week and 3 mo of age

– Stools contain occult blood, neutrophils,

eosinophils
– Diagnosis:
• Gold standard is elimination of diet and Double Blind,
placebo controlled food challenge (DBPCFC)

• Skin prick test or radioallergosorbent (RAST)

 Food-induced Enterocolitis:

Treatment:

– Elimination of diet: the only proven treatment for food

allergy 30% of infants with cow’s milk allergy is allergy to
soy protein

– Most infants improve with Protein hydrolysate ; 5% don’t

respond and maybe given amino-acid-based formulas

– 85% of infants with non-IG-E mediated food allergy are no

longer allergy by 3 years of age

– Allergy to cow’s milk and soy protein resolve by one year of

age
 Food-induced Enterocolitis:

• Prevention:
– Breastfeeding
 Bloody Stool

2) Non-infectious:

b) Surgical Causes:

1) Intussusception
- Barium Enema, Ultrasound

2) Meckel’s Diverticulum:
- Pertechnetate technetium
Scan
 Diagnostic Work-ups for Diarrhea

1. Acute Diarrhea:
• Stool examination: look for mucus, blood,
leucocytes
• fecal leucocytes indicates the presence of an invasive
or cyto-toxin-producing organism such as Shigella,
salmonella, C. Jejuni, invasive E. Coli, C. Dificile
• Stool culture:
• Chronic Diarrhea: Pls refer to page
1280 Fig 322-3
 Complications of Diarrhea
• Fluid & electrolyte losses:
sodium, potassium, bicarbonate
• Malabsorption and malnutrition
• Lactose Intolerance
Fluid & Electrolyte Losses

Assessment of Hydration Status

• Look:
• Feel:
• Ask
 Classification of Dehydration
• Group A : No Signs of Dehydration
(<5% of body weight fluid loss)

• Group B: Some Signs of Dehydration

= Mild Dehydration
(5-6% of Body weight fluid loss)

= Moderate Dehydration
(7-10% of BW fluid loss)

• Group C: Severe Signs of Dehydration

(>10% BW fluid loss)
• Group A:
– No evidences of dehydration
Additional Clinical Parameters of Dehydration

Some signs of Dehydration: (Group B)

• Mild dehydration (5-6%):

– Volume loss: 50-60 ml / kg
• Average: 50 ml / kg

• Clinical Manifestations:
– Normal pulse
– decreased urine output
– thirsty
– normal physical examination
 Additional Clinical Parameters of Dehydration

Some signs of Dehydration: (Group B)

• Moderate dehydration (7-10%):

– Volume Loss: 70-100 ml / kg
• Average: 80 ml / kg

– Clinical Manifestations:
• Tachycardia
• irritable / lethargic
• sunken eyes and fontanel
• decreased tears
• Mottled skin
- dry mucous membranes
- little or no urine output
- mild tenting of the skin
- delayed capillary refill
 Laboratory Tests

• Serum sodium: determines the type of dehydration

• Serum potassium
• Blood gases: determines the presence of metabolic acidosis
• Blood urea nitrogen and serum creatinine concentration
• Urinalysis
• Complete blood count
 Types of dehydration based on the serum
sodium concentration

Isotonic Dehydration:
• Proportional loss of water and sodium
• Serum sodium= 135 - 155 meq/l
 Types of dehydration based on the serum
sodium concentration

Hyponatremic Dehydration:

• Serum sodium: <135 meq/l

• Excessive sodium loss or decrease sodium intake

• ↓ ECF osmolality  ICF higher osmolality  water

from ECF space  ICF space  maintain osmotic
equilibrium  cellular swelling  cerebral edema
 Types of dehydration based on the serum
sodium concentration

• Hyponatremic Dehydration

– Cerebral edema  increased intracranial pressure

 herniation, seizures

– Increased risk of Central Pontine Myelinolysis CPM)

– More manifestations of intravascular volume

depletion

– ICF movement of sodium  depletes the ECF

space with Na & plasma volume
 Fluid Management of Specific Fluid &
Electrolytes Disturbance
Hyponatremia:

• Initial goal: Correction of intravascular volume

depletion with isotonic fluid (NSS or Ringer lactate)

• Increase sodium level to 135 meq / L

• Avoid ‘overly rapid correction’ i.e. >12 meq / L/day 

central pontine myelinosis (CPM).

• D5 ½ NS + 20 meq / L KCl is effective

half of the fluid can be administered over the first 8
hours.
 Types of dehydration based on the
serum sodium concentration
Hypernatremic Dehydration:
• Serum sodium: >145 meq/l

• Excessive intake of sodium or excessive water loss 

ECF osm  ICF fluid depletion  brain cell shrinkage
 brain movement away from skull  tearing of the
Intracerebral & bridging blood vessels subdural,
subarachnoid, parenchymal hemorrhage  seizure.
 Types of dehydration based on the serum
sodium concentration
Hypernatremic Dehydration:

• Most dangerous type of dehydration due to

complications of hypernatremia and during
therapy

• Thrombotic complications (stroke) due to

hemoconcentration  hypercoagulability /
stasis

• CPM & extrapontine myelinolysis

 Hypernatremic Dehydration:

• Patients are lethargic but irritable when touched; it

may cause fever, hypertonicity, hyperreflexia

• Patients appear less ill / dehydrated

• Because of the ICF loss, the skin has “doughy” feel

• Intravascular volume is protected

Blood pressure is maintained, less tachycardia and
urine output preserved longer
 Management of Specific Fluid & Electrolytes
Disturbance
Hypernatremia:

• Sodium concentration decrease: not > 12 meq / L/24

hour at the rate of 0.5 mEq/l / hour

• Severe hypernatremia should be corrected over 2-4 days

• Guide in the fluid treatment:

– Determine the time for correction based on the initial sodium
concentration
• Na+: 145-157 meq / L = 24 hours
• Na+: 158-170 meq / L = 48 hours
• Na+: 171-183 meq / L = 72 hours
• Na+: 184-196 meq / L = 84 hours
 New Developments on ORT
(Oral Rehydration Treatment):

– Based on recent scientific advances:

• Improved ORS formulation

• Zinc supplementation

• Protective effects of zinc supplementation

Composition of Standard & New Improved ORS

Standard WHO-ORS New Improved ORS

(meq or mmol/l (meq /l or mmol/l

Glucose 111 75
Sodium 90 75
Chloride 80 65
Potassium 20 20
Citrate 10 10
Osmolarity 311 245
 Composition of Intravenous solutions

Fluid Na+ Cl+ K+ Ca++ Lactate

-
Normal saline 154 154
(0.09%NaCl)
½ Normal Saline 77 77
(0.45% NaCl)
¼ Normal Saline 38.5 3
(0.225% NaCl) 8.5
Ringer lactate 130 109 4 3 28
 Maintenance fluid
• Replaces the obligatory fluid losses both measurable
(urine and stool) and not measurable (insensible losses
from the skin and lungs)

• Goals:
– Prevent dehydration
– Prevent electrolyte disorders
– Prevent ketoacidosis
– Prevent protein degradation

• It is composed in general of a solution consisting of water,

glucose, sodium and potassium;
 Maintenance fluid
• It provides approximately 20% of the normal caloric
needs of the patient enough to prevent ketoacidosis
from starvation and protein degradation

• It does not provide adequate calories, protein, fat,

minerals ( calcium, phosphorus, magnesium or
bicarbonate) and vitamins.

• Calculation of maintenance fluid

 Components of Maintenance water

Urine 60%

Insensible (skin and lungs) 35%

Stool 05%
 Computation of Maintenance Fluid

10 kg: 100 ml/kg/day

11-20 kg 1000 ml + 50 ml/kg > 10 kg
>20 kg 1500 ml + 20 ml/kg > 20 kg
 Adjustments in maintenance Water
Source Causes of Increased Causes of
Water needs Decreased water
needs
Skin •radiant warmer mist tent
•Fever
•Sweat
•Burns
Lungs Tachypnea Humidified ventilator

Gastrointestinal •Diarrhea
Tract •Emesis
•Nasogastric suction
Renal Polyuria Oliguria / anuria

Miscellaneous •Surgical drain Hypothyroidism

•Third spacing
 Replacement Fluid
• Losses should then be replaced as they
occur using a solution with the same
approximate electrolyte concentration as the
GI fluid;

• the losses are replaced every 1-6 hour

depending on the rate of loss
 Replacement Fluid
• GI tract is potentially a source of considerable water
loss;

• GI losses are often associated with loss of

potassium, leading to hypokalemia and bicarbonate,
causing metabolic acidosis which maybe aggravated
when there is hypoperfusion causing a concurrent
lactic acidosis;

• emesis or losses from NG tube cause a metabolic

alkalosis.
 Other Metabolic complications
Hypokalemia:

• It is common among children, with most cases

related to gastroenteritis

• Clinical manifestations:
– Heart and skeletal muscles are vulnerable to hypokalemia

– ECG changes include a flattened wave, depressed ST

segment and appearance of a U wave and a P wave

– Ventricular fibrillation and torsades de pointes (ventricular

arrhythmia / tachycardia) may occur
 Other Metabolic complications
Hypokalemia:

• Effects on skeletal muscles: muscle weakness and cramps; possible

paralysis with levels < than 2.5 meq / L

• It slows gastrointestinal motility: manifests as constipation, or with

levels <2.5 meq / l  ileus.

• It may also slow bladder function  urinary retention

• Diagnosis: History: child’s diet, gastrointestinal losses and

medications

• Treatment: Oral potassium is the choice because of the risk of

hyperkalemia when given by IV (Dose 0.5-1 meq / L give
over an hour.
 Metabolic Acidosis

• Most common etiology is diarrhea due excessive

losses of bicarbonate from the body;

• Clinical manifestations:
– Hyperventilation
– At ph < 7.2, there is impaired cardiac contractility
and an increased arrythmias

• Treatment:
– Most effective therapeutic approach: repair of the
underlying disorder
 Lactose Intolerance
• It’s a condition wherein lactases are reduced
as a result of gut injury as in diarrheal
infection;

• Reasons why Lactose Intolerance is

common:

– infant diet is high in lactose; lactose hydrolysis is

the rate-limiting step in its absorption

– Lactase has the lowest activity among the brush

borders disaccharidases
 Lactose Intolerance
Reasons why lactose intolerance is common:

• Lactases are superficially located and preferentially degraded

by proteolytic enzymes

• IF lactose is not digested and absorbed in the intestine

 degradation  lactic acids and short chain fatty acids
( butyrate, acetate and propionate) and production of methane,
carbon dioxide and hydrogen gases.
 Lactose Intolerance
Clinical manifestations:

• Acidic stools  perineal chemical burn

• Flatulence  abdominal distention, discomfort

• Intake of lactose containing food  aggravates

diarrhea; while fasting  resolves diarrhea.
 Lactose Intolerance

Diagnosis:

• Stool ph of <5 is suggestive of carbohydrate /

lactose malabsorption

• Stool clinitest for the determination of reducing

sugars (all carbohydrates are reducing sugars
except sucrose); 2+ or higher (blue-green to brick-
red) indicative of the presence of reducing sugars
such as lactose.
 Lactose Intolerance
• Hydrogen Breath Test:

– Mechanics:

The gas produced by bacterial degradation of lactose is

absorbed in the colon , enters the portal and systemic
venous return, goes to the lungs, and is then released in
the breath.

• A release of > 20 ppm from baseline is consistent with

lactose intolerance.
 Lactose Intolerance

Treatment:

• Small frequent feeding to decrease lactose

load

• If ineffective: Partial removal of milk from

diet or use of yoghurt
 Protein Intolerance
(Cow’s Milk Allergy)

• Food allergy is a group of disorders in which

symptoms result from immunologic responses
to specific food antigens

• Food allergy occurs in as many as 6% of

children during the first year of life, including
the 2-3% of infants and toddlers with cow’s
milk allergy
 Protein Intolerance
(Cow’s Milk Allergy)

Clinical Manifestations:
A. Ig-E mediated Food hypersensitivity:
Gastrointestinal Anaphylaxis:

• Rapid onset of nausea, cramping abdominal

pain, vomiting or diarrhea or a combination of
these conditions

• Occurs after ingestion of peanuts, nuts, fish

and shellfish.
 Protein Intolerance
(Cow’s Milk Allergy)

B. Non-Ig-E Mediated Disorders:

– Allergic Proctocolitis:
• Infants may present between 1 day to 3 mo of age with spots
or
streaks of blood and mucus in stool and occasional mild
diarrhea

• Increased white blood cells in stool and peripheral eosinophilia

• Patchy mild colitis is present; (+) nodular hyperplasia in 25%

• Often results from hypersensitivity to cow’s milk; soy

sensitivity is less common
 Protein Intolerance
(Cow’s Milk Allergy)

B. Non-Ig-E Mediated Disorders:

– Allergic Proctocolitis:

– Breast-fed infants may suffer this disorder but usually

abates with maternal diet modification and elimination of
milk products

– Non-breastfed infants can be treated with protein

hydrolysate formulas
Protein Intolerance (Cow’s Milk Allergy)

Food-induced Enterocolitis:
• Protracted vomiting & diarrhea begin between 1 week and 3 mo
of age
• Stools contain occult blood, neutrophils, eosinophils,

• Jejunal biopsy shows flattened villi, edema and inflammatory

cells
• Symptons resolve within 72 hour of removal of the offending
food and recur within 1-6 hour of reintroduction
 Protein Intolerance
(Cow’s Milk Allergy)

Food-induced Enteropathy:

• Malabsorption, protracted diarrhea, vomiting

and failure to thrive occur most often during
the first month of life

•
Protein Intolerance (Cow’s Milk Allergy)

Food-induced Enterocolitis:

• Older infants may develop poorly characterized

syndrome of anemia, hypoproteinemia or
failure to thrive.
• Eosinophilia is common
 Protein Intolerance
(Cow’s Milk Allergy)
Diagnosis:
• Gold standard:
– Elimination of diet
– Double Blind, placebo controlled food challenge (DBPCFC)

• Open food challenge: less reliable

• Skin prick test

• Radioallergosorbent (RAST):
determines whether an Ig-E allergic reaction is the cause of a
food allergy

• Small bowel biopsy: Patchy villus atrophy with mononuclear

cell inflammatory response
Treatment:
• Elimination of diet: the only proven treatment for
food allergy
• 30% of infants with cow’s milk allergy is allergy to
soy protein
• Most infants improve with Protein hydrolysate ;
5% don’t respond and maybe given amino-acid-
based formulas
 Prognosis

– 85% of infants with non-IG-E mediated food allergy

are no longer allergy by 3 years of age

– Allergy to cow’s milk and soy protein resolve by one

year of age

– Symptons to Ig-E mediated allergy to peanut, nuts,

fish, or shellfish DO NOT resolve
 Malabsorption

• May present as watery diarrhea, acidic

diarrhea, or steatorrhea
Generalized Malabsorptive States in Childhood

Site More Common

Exocrine pancreas Protein – Energy
Malnutrition
Liver, Biliary Tree Biliary Atresia
Intestine
– Anatomic Defects Massive resection
Stagnant Loop Syndrome
– Chronic Infection Giardiasis
Chronic Diarrhea
– Others Protein Intolerance
(Cow’s milk or Soya Protein
Hypersensitivity)
 Malabsorption
Clinical manifestations:

• Abdominal distention, pale foul smelling, bulky

stools

• Muscle wasting

• Poor weight gain or weight loss

• Growth retardation
 Malabsorption
Diagnosis:

• Stool examination for fat globulesfollowed by Sudan

staining III
• 72-hour quantitative fecal fat test: gold standard for
assessing steatorrhea
– Premature Infant: absorbs about 65-75% of ingested fats
– Term infants: absorbs about 90%
– Older children and adults: absorbs 95% of ingested fats; with
vegetable fats absorbed better.

Treatment: Treat the main problem

 Drug Therapy
For dysentery:
• Cotrimoxazole ( Trimethoprim + sulfamethoxazole):
Trimethoprim: 7 mg/kg/day
Sulfamethoxazole: 50 mg/kg/day
Given 2x a day for 5 days
• Nalidixic Acid
For cholera:
• Tetracycline (only for 6 years old and >)
• Co-Trimoxazole
• Erythromycin
• Furazolidone