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Acute Diarrhea
- 1. Acute Diarrhea By: Dr.Noshirwan P. Gazder
- 2. Defenition • Passage ofthree or more stools in a day, of consistency softer than usual for the child, or one watery stool is defined as “Diarrhea”.
- 3. • Diarrhea isone of the leading causes of morbidity and mortality in children. • There are 3-4 episodes of diarrhea per child per year. • Maximum incidence is in the 1st year of life. • Major transmission is fecal/oral or by ingestion of contaminated food or water.
- 4. Factors Increasing SusceptibilityTo Diarrhea • Exposure to unsanitary conditions. • Ingestion of contaminated food or water. • Lack of breastfeeding. • Malnutrition. • Measles. • Level of Maternal Education.
- 5. Common Causes ofAcute Diarrhea
- 6. Enterotoxigenic E. Coli •Diarrhea results from action of toxins released by the bacteria on intestinal mucosa. • Toxins are heat labile (LT) and heat stable (ST). • The LT toxins bind to the epithelial surface of enterocytes, causing accumulation of cyclic AMP causing massive secretion of sodium and chloride in the gut lumen. • The ST toxin activates guanylate cyclase, which increases secretory activity of the gut.
- 8. Entero-Inasive (Shigella &Salmonella) • These cause invasion of enterocytes and results in necrosis and ulcer formation leading to diarrhea with blood and mucus in the stool. • It presents as fever, abdominal cramps and tenesmus and small volume of bloody mucoid stools with many pus cells.
- 9. Rota Virus • Itinvades intestinal cells and alters their functioning and reproduction. • The exact mechanism in Rota virus is not known. But towards the end of the illness it causes shedding of mucosal cells with loss of disaccharides. • It manifests as osmotic diarrhea due to failure of digestion of lactose and other disacharrides. • Recovery occurs when the mucosal surface regenerates.
- 10. Vibrio Cholerae • Theyadhere to and multiply on the mucosa of small intestine and produce heat labile enterotoxin, which attaches to a receptor (GM1 ganglioside) on gut epithelium. • It activates adenylate cyclase to produce increased amount of cyclic AMP, which causes decreased absorption of sodium and chloride resulting in water and electrolyte loss.
- 11. Giardia Lamlia • Pearshaped, flagellated trophozoite with ventral sucking discs. • Spread via the oro-fecal route. • Humans ingest cysts which form trophozoites in the duodenum. • Trophozoites attach to the duodenal wall but do not invade and interferes with absorption of fat and protein.
- 13. Effects of Diarrhea 1.Loss of Water: • Loss of skin turgor. • Weak or absent pulse. • Sunken eyes. • Sunken fontanelles. • Dry Mucous membranes. • Anuria. 2. Loss of Nutrients: • Hypoglycemia, convulsions or coma. • Weight loss or marasmus.
- 15. 3. Loss ofbicarbonate: • Vomitting and retching. • Deep and sighing respiration. • Irritability (Increased O2 demand of brain) 4. Loss of Potassium: • Abdominal distention. • Paralytic ileus. • Sustained Shock.
- 16. Clinical Features • Onsetis sudden with diarrhea and vomitting. • Stools are large in volume, watery in consistency. • Dehydration develops rapidly due to loss of body water and electrolytes in stools and vomitting. • Acute diarrhea is usually a self-limited disease. Vomitting and fever usually resolve quickly but diarrhea persists for 3-4 days then gradually diminishes over another 4-5 days.
- 17. Grading of Stools Grade Grade1 Normal formed stools. Grade 2 Soft stools. Grade 3 Liquid stools taking shape of the container. Grade 4 Watery stools with flakes, appearing opaque in glass container. Grade 5 Watery stools with few flakes, appearing translucent in color.
- 18. Complications • Dehydation andShock. • Metabolic acidosis. • Convulsions or Coma. • Malnutrition. (long standing diarrhea) • Acute Renal shutdown. • Super-added infections. • Death.
- 19. Evaluation of thePatient -History: • Loose motions.(duration, frequency, grade, color of stool, blood in stool) • If the child has vomitting.(duration, frequency, relation with food, quantity, color of vomitus, blood in vomitus) • If the child has a fever.( duration, low or high grade) • Abdominal pain or distention. • Any history of seizures. • Urine passed or not within 6 hours, and in how much quantity. • Any associated symptoms such as cough, rash or urinary complains. • BIND.
- 20. Examination • General behaviour( drowsy, irritable) • Anthroprometry and General physical examination. • Mucous membranes (normal, dry or parched) • Skin turgor (normal, goes back slowly, goes back very slowly) • Eyes (Shiny with tears, not sunken, sunken) • Anterior fontanelle ( open, closed, depressed) • Abdomen (normal, distended, any mass palpable,bowel sounds) • CNS and respiratory system examination to find any associated abnormality.
- 21. Investigations • CBC. • Stoolexamination for pH, Giardia cysts or entamoeba, Bioassay for E.coli, Culture and Sensitivity. • Serum electrolytes. • Blood culture. (salmonellosis or shigellosis) • X-ray chest. (pneumonia)
- 22. Management • Before startingtherapy, we assess degree and type of dehydration. • If the child has diarrhea we Ask, For how long and if there is blood in the stool • We will then Look at the child's general condition. Is the child: Lethargic or unconscious or restless and irritable • Look for sunken eyes. • Offer the child fluid, Is the child not able to drink or drinking poorly or is the child drinking eagerly. • Pinch the skin of the abdomen, does it go back slowly or very slowly (longer than 2 seconds).
- 27. Treatment of Choice •Cholera: Tetracycline 50mg/kg/day PO for 2 days. Furazolidine 5mg/kg/day PO for 3 days. • Shigella: Ampicllin 100mg/kg/day for 5 days. Nalidixic acid 55mg/kg/day for 5 days. • Giardiasis: Metronidazole 15mg/kg/day for 5 days. • Amebiasis: Metronidazole 30mg/kg/day for 5 days.
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