Eduardo P. Manrique M.D.

DIARRHEA -EXCESSIVE LOSS OF FLUID AND ELECTROLYTE IN THE STOOL

NORMAL AMOUNT YOUNG INFANT = 5 -10 G/KG/24 HOUR ADULT = 200 G/24 HOUR

NORMAL STOOL OUTPUT PER LITER

SODIUM = 20 – 25 MEQ

POTASSIUM = 50 – 70 MEQ

CHLORIDE= 20 – 25 MEQ

ACUTE DIARRHEA   INCREASE TOTAL DAILY STOOL OUTPUT INFANTS AND CHILDREN

= MORE THAN 10 G/KG/24HR ADULT

=MORE THAN 200G/24HR

CHRONIC DIARRHEA  

WHEN DIARRHEA LAST FOR MORE THAN 2 WEEKS

ANATOMY

GASTROENTERITIS

INFECTION OF THE GASTROINTESTINAL TRACT CAUSED BY BACTERIAL, VIRAL, OR PARASITIC PATHOGENS DIARRHEAL DISORDERS   INFECTIOUS DIARRHEA IN PUBLIC HEALTH SETTINGS

BASIS FOR ALL DIARRHEA DISTURBED INTESTINAL SOLUTE TRANSPORT (WATER MOVEMENT ACROSS INTESTINAL MEMBRANES IS PASSIVE AND IS DETERMINED BY BOTH ACTIVE AND PASSIVE FLUXES OF SOLUTES – SODIUM, CHLORIDE, GLUCOSE )

DIARRHEA PATHOGENESIS 

1) SECRETORY2) OSMOTIC3) MUTATIONAL DEFECTS IN ION TRANSPORT PROTEINS 4) REDUCTION IN ANATOMIC SURFACE AREA5) ALTERATION IN INTESTINAL MOTILITY

SECRETORY DIARRHEA  MECHANISM : 

ACTIVATION OF THE INTRACELLULAR MEDIATORS (CAMP,CGMP,CALCIUM)

 1) STIMULATE ACTIVE CHLORIDE SECRETION FROM THE CRYPT CELLS AND INHIBIT THE NEUTRAL COUPLED NACL ABSORTION

2) ALTER THE PARACELLULAR ION FLUX BECAUSE OF TOXIN MEDIATED INJURY TO THE TIGHT JUNCTION

SECRETORY DIARRHEA  

-HIGH VOLUME; EXTREMELY WATERY-HIGH SODIUM AND CHLORIDE CONTENT.-CONTINUES WITH FASTING

CLASSIC EXAMPLES

-CHOLERA-ESCHERICHIA COLI ENTEROTOXINS

CAUSE OF SECRETORY DIARRHEA ACTIVATION OF CYCLIC ADENOSINE MONOPHOSPHATE BACTERIAL TOXINS: ENTEROTOXINS OF CHOLERA, ESCHERICHIA COLI (HEAT-LABILE),SHIGELLA ,SALMONELLA, CAMPYLOBACTER JEJUNI,PSEUDOMONAS AERUGINOSA

HORMONES: VASOACTIVE INTESTINAL PEPTIDE, GASTRIN, SECRETINANION SURFACTANTS: BILE ACIDS, RICINOLEIC ACID ACTIVATION OF CYCLIC GUANOSINE MONOPHOSPHATE

BACTERIAL TOXINS: E.COLI (HEAT-STABLE)ENTEROTOXIN, YERSINIA ENTEROCOLITICA TOXIN CALCIUM-DEPENDENT BACTERIAL TOXINS: CLOSTRIDIUM DIFFICILE ENTEROTOXINENEUROTRANSMITTERS: ACETYLCHOLINE, SEROTONINPARACRINE AGENTS :BRADYKININ

OSMOTIC DIARRHEA

MECHANISM 

-OCCURS AFTER INGESTION OF A POORLY ABSORBED SOLUTE(MAGNESIUM, PHOSPHATE, LACTULOSE, SORBITOL).  -STOPS WITH FASTING -HAS LOW PH -POSITIVE FOR REDUCING SUBSTANCES

CAUSES OF OSMOTIC DIARRHEA MALABSORPTION OF WATER-SOLUBLE NUTRIENTS

GLUCOSE – GALACTOSE MALABSORPTION

CONGENITAL

ACQUIRED

DISACCHARIDASE DEFICIENCIES (LACTASE AND SUCROSE-ISOMALTASE)

CONGENITAL

ACQUIRED

EXCESSIVE INTAKE OF CARBONATE FLUIDSEXCESSIVE INTAKE OF NONABSORBABLE SOLUTESORBITOLLACTULOSEMAGNESIUM HYDROXIDE

MUTATIONAL DEFECTS IN ION TRANSPORT PROTEINS.  MECHANISM  

-CONGENITAL DEFECTS OF SODIUM HYDROGEN EXCHANGE, CHLORIDE – BILE ACID TRANSPORT

PROTEINS 

-RESULT IN SECRETORY DIARRHEA PRESENTING AT BIRTH-FAILURE TO THRIVE DURING THE NEONATAL

PERIOD

REDUCTION IN ANATOMIC SURFACE AREA  -SHORT BOWEL SYNDROME =RESECTION OF THE BOWEL SECONDARY TO SURGICAL INDICATIONS (NECROTIZING ENTEROCOLITIS, MIDGUT VOLVULUS, INTESTINAL ATRESIA)

-CELIAC DISEASE =FLATTENING OF THE PROXIMAL INTESTINAL SURFACE AREA WITH MARKED DECREASE IN THE DIGESTIVE AND ABSORPTIVE FUNCTION OF THE VILLUS EPITHELIUM

=LOSS OF FLUIDS, ELECTROLYTES, MACRONUTRIENTS AND MICRONUTRIENTS.

ALTERATION IN INESTINAL MOTILITY.

-CAUSES: MALNUTRITION, SCLERODERMA, INTESTINAL PSEUDO-OBSTRUCTION SYNDROMES, DIABETES MELLITUS

= RESULTS IN HYPOMOTILITY,ALLOWING BACTERIAL OVERGROWTH THAT LEADS TO DECONJUNCTION OF BILE SALTS, RESULTING IN AN INCREASE INTRACELLULAR MEDIATOR CAMP AND LEADING TO SECRETORY DIARRHEA.

ETIOLOGY

-FECO-ORAL ROUTE-INGESTION OF CONTAMINATED FOOD OR WATER-ANTIBIOTIC ASSOCIATED

=ASSOCIATED WITH POVERTY, POOR ENVIRONMENTAL HYGIENE, AND

DEVELOPMENT INDICES

CLINICAL MANIFESTATION  -RELATED TO THE INFECTING PATHOGENS -DEGREE OF DEHYDRATION AND ELECTROLYTES IMBALANCE

Dehydration

There is a delicate balance in the body between water and dissolved substances. Dehydration occurs when the body is deprived of its normal supply of water or excessive water is lost. This condition is most life-threatening in newborns, infants and persons over 60. Dehydration occurs when the body loses more fluids then it takes in. The loss of fluid can come from vomiting, diarrhea, sweating, or urination. Severe dehydration can lead to renal failure, and cardiovascular collapse

CLINICAL EVALUATION OF DEHYDRATION MILD DEHYDRATION (<5% IN AN INFANT; <3% IN OLDER CHILD OR ADULT): NORMAL OR INCREASE PULSE;DECREASE URINE OUTPUT; NORMAL PHYSICAL FINDINGS MODERATE DEHYDRATION (5-10% IN AN INFANT; 3-6% IN OLDER CHILD OR ADULT):TACHYCARDIA; LITTLE OR NO URINE OUTPUT; IRRITABLE/LETHARGIC; SUNKEN EYES AND FONTANEL; DECREASED TEARS; DRY MUCOUS MEMBRANES; MILD DELAY IN ELASTICITY (SKIN TURGOR); DELAYED CAPILLARY REFILL(>1.5SEC);COOL AND PALE SEVERE DEHYDRATION (>5% IN AN INFANT; >3% IN OLDER CHILD OR ADULT): RAPID AND WEAK OR ABSENT PERIPHERAL PULSES; DECREASE BLOOD PRESSURE; NO URINE OUTPUT; VERY SUNKEN EYES AND FONTANEL; NO TEARS; PARCHED MUCOUS MEMBRANES; DELAYED ELASTICITY (POOR SKIN TURGOR);VERY DELAYED CAPILLARY REFILL(>3SEC);COLD AND MOTTLED; LIMP, DEPRESSED CONSCIOUSNESS

ISOTONIC DEHYDRATION=70-80%-LOSSES OF WATER AND SODIUM ARE

PROPORTIONATE HYPONATREMIC DEHYDRATION

= 10-15%- LARGE AMOUNT OF ELECTROLYTES ARE LOST IN STOOL OUT OF PROPORTION TO FLUID LOSSES- BACILLARY DYSENTERY OR CHOLERA

 HYPER NATREMIC DEHYDRATION

=10-20%- LARGE NET LOSSES OF WATER COMPARED WITH LOSSES OF ELECTROLYTES.

DIARRHEAL DISORDERS IN CHILDHOOD ACCOUNT FOR A LARGE PORTION OF CHILDHOOD DEATH (18%) WITH AN ESTIMATED 1.8 MILLION DEATHS PER YEAR GLOBALLY.

THE DECLINE OF DIARRHEAL MORTALITY, DESPITE THE LACK OF SIGNIFICANT CHANGES IN INCIDENCE, IS THE RESULT OF IMPROVED CASE MANAGEMENT OF DIARRHEA, AS WELL AS IMPROVED NUTRITION OF INFANTS AND CHILDREN.

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