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Acute Gastroenteritis. Jie Chen , MD ,phD Children Hospital Zhe Jiang University. 教学目标. 1. 掌握小儿腹泻病的病因分类及临床表现; 2. 掌握小儿腹泻病的诊断和治疗原则. Diarrhea. Diarrhea is a clinical syndrome of diverse etiology associated with many influencing factors
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Acute Gastroenteritis Jie Chen , MD ,phD Children Hospital Zhe Jiang University
教学目标 1.掌握小儿腹泻病的病因分类及临床表现; 2.掌握小儿腹泻病的诊断和治疗原则
Diarrhea • Diarrhea is a clinical syndrome of diverse etiology associated with many influencing factors • In pediatrics, diarrhea is defined as an increase in the • Fluidity • Volume of the stool • Frequency Relative to the usual habits of each individual
Classification of Diarrhea in Infant • Acute diarrhea: • Short in duration( less than 2 weeks) • Persistent or chronic diarrhea: • 2 weeks or more Gastroenteritis or enteritis Systemic infection Overfeeding Antibiotic association Post infection Secondary dissacaridase deficiency IBS Food allergy , et al
Type of diarrhea • Acute watery diarrhea • (80% cases) • Dysentery • (10%cases) • Persistent or chronic diarrhea • (10%cases)
Etiology of Diarrhea Non infective Infective Food Allergy Symptomatic Overfeeding IntoleranceClimate Viruses Bacteria Parasites Fungi
Common Infectious Causes of Diarrhea • Viruses • Rotavirus • Astrovirus • Calicivirus (including norovirus) • Enteric adenovirus (serotypes 40 and 41)
Common Infectious Causes of Diarrhea • Bacteria • Campylobacter jejuni • Escherichia coli • EPEC; ETEC; EITC; EHEC; EAEC • Shigella • Salmonella • Yersinia enterocolitica • Staphylococcus aureus • Clostridium difficile • Vibrio cholerae • Vibrio parahemolyticus
Common Infectious Causes of Diarrhea • Parasites • Entamoeba histolytica (ambiasis) • Giardia lamblia • Cruptosporidium parvum • Fungi • Candida albicans
Epidemiology:Feces—mouthroute Infected Animal Infected Person Food Water Person
Mechanisms of diarrhea • Osmotic • Secretory • Mucosal inflammation (invasion) • Motality
Mechanisms of Diarrhea • Osmotic Defect Digestive enzyme deficiencies Ingestion of unabsorbable solute Example Viral infection Lactase deficiency Sorbitol /magnesium sulfate Comment Stop with fasting No stool WBCs
Mechanisms of Diarrhea • Secretory Defect Increased secretion Decreased absorption Example Cholera Toxinogenic E.coli Comment Persists during fasting No stool leukocytes
Mechanisms of Diarrhea • Invasion Defect Inflammation Decreased colonic reabsorption Increased motility Example Bacterial enteritis Comment Blood, mucus and WBCs in stool
Mechanisms of Diarrhea • Increased motility Defect Decreased transit time Example: Irritable bowel syndrome
Common infectious causes of diarrhea and their virulent mechanism • Viral diarrhea (osmotic) • Rotavirus • Bacterial diarrhea • Enterotoxinogenic enteritis (secretory) • ETEC • Vibrio cholerae • Entero-invasive enteritis (invasion) • Campylobacter jejuni • EIEC • Shigella species • Salmonella tymphimurium • Yersinia enterocolitica
Pathogenesis of Rotavirus enteritis Rotaviruses attach and replicate in the mature enterocytes at the tips of small intestinal villi Destroy villus tip cells, variable degrees of villus blunting mononuclear inflammatory infiltrate in the lamina propria Impairment of absorptive functions the transport of water and electrolytes via glucose and amino acid co-transporters Impairment of digestive functions discreasing hydrolysis of disaccharides Malabsorption of complex carbohydrates, particularly lactose An imbalance in intestinal fluid absorption to secretion Other than digested into monosaccharide, lactose be lysis into organic acid, hyper-osmosis Watery stool
Pathogenesis of enterotoxinogenic enteritis Ingestion small bowel mucosa and proliferate enterotoxigenic organisms Heat-labile enterotoxin Heat-stable enterotoxin binds to receptors of epithelial cells activates cellular guanylatecyclase activates cellular adenylcyclase increased intracellular concentrations of cGMP increased intracellular concentrations of cAMP promote the net secretion of water and chloride decrease absorption of sodium and chloride by villous cells Waterydiarrhea
Pathogenesis of enterotoxinogenic enteritis • The mucosa is not destroyed during this process • An imbalance in the ratio of intestinal fluid absorption to secretion, so watery stool may occur in clinical observation
Pathogenesis of invasive enteritis Ingestion Gut lumen Colon and rectum mucous membrane proper Invasive enteropathogen Extensive destruction of the epithelial layer Inflammation: Hyperemia, swelling, heavy neutrophil infiltration, inflammatory exudate The desquamation, ulceration, and formation of microabscesses in the colonic mucosa inhibit absorption of water stools that are frequent and scanty and that contain bloodinflammatory cells and mucus
Clinical manifestation • Gastrointestinal symptom • Systemic symptom • Dehydration and electrolyte disturbances • Dehydration • Hypokalemia • Metabolic Acidosis • Hypocalcemia /Hypomagnesemia
Dehydration • Excessive loss of water, • especially loss of extracellular fluid
Metabolic Acidosis • Pathogeny • lose of large amount of basic substances from gastrointestinal tract • too much acid metabolite • Blood gas analysis pH nomarl HCO3- CO2 pH HCO3- CO2 • Degree • MildHCO3-18~13 mmol / L • Moderate HCO3-13~9 mmol / L • SevereHCO3-<9 mmol / L
hypokelemia • Pathogeny • Lake of intake • Loss of potassium from gastrointestinal tract • Blood electrolytes analysis • K+ < 3.5 mmol/L
Hypokelema • Clinical manifestation • Nervous system • depressed • Muscle • inertia of limbs,muscular tension down,severely retardant paralysis,respiratory muscle paralysis • Heart • heart rate increasing, arrhythmia, Adams-Stokes syndrome,heart rate decreasing,atrioventricular block, heart sound lowering, • Cardiogram • U wave appearing,U≥T,flattened T wave,
Laboratory and Imaging Studies • Initial laboratory evaluation • CBC • Stool examination: mucus, blood, and leukocytes • Gas and electrolytes analysis • BUN, Cr, and urinalysis for specific gravity • Rapid test for Rotavirus • Stool cluture • for patients with fever, profuse diarrhea, and dehydration or if HUS is suspected • Stool evaluation for parasitic agents • identification of the organism in the stool • Blood culture • uncommom
Diarrhea? Infective Antibiotic associate diarrhea Persisting or chronic diarrhea Acute stage Watery, loose stools without or only a minute amount ofWBC WBC and RBC, mucus instools Persisting infection? Stool culture Serous assay Epidemic data Stool culture Serous assay Shigella EIEC CJ Salmonella Yersinia Entamoeba histolytic Giardia lamblia Cryptosporidium Staphylo CD Candida Virus ETEC EPEC Non-infective Allergic state? Symptomatic diarrhea? Inappropriate feeding? food intolerance Lack of disaccharidase? Immunodeficience? Malnutrition? Malabsorption ? etc.
Treatment • Primarily supportive • Fluid therapy • Rehydration • Correcting acidosis • Potassium supplement • Correcting ongoing loss • Managing secondary complication resulting from mucosa injury • Antibiotic treatment • for only some bacterial and parasitic causes of diarrhea • Start food as soon as possilble
Fluid Management of Dehydration • Calculate 24-hr water needs • Calculate maintenance water • Calculate deficit water • Calculate 24-hr electrolyte needs • Calculate maintenance sodium and potassium • Calculate deficit sodium and potassium • Select an appropriate fluid (based on total water and electrolyte needs) • Administer half the calculated fluid during the first 8 hr, first subtracting any boluses from this amount • Administer the remainder over the next 16 hr • Replace ongoing losses as they occur
Fluid Therapy • Deficit of water and electrolytes • Water Deficit: Percent dehydration × weight • Sodium Deficit:Water deficit × 80 mEq/L • Potassium Deficit:Water deficit × 30 mEq/L • Ongoing loss • After they occur • Sodium: 55 mEq/L • Potassium: 25 mEq/L • Bicarbonate: 15 mEq/L • Maintenance • 0-10kg 100 mL/kg • 11-20kg 1000 mL + 50 mL/kg for each 1 kg >10 kg • >20kg 1500 mL + 20 mL/kg for each 1 kg >20 kg*(max 2400mL) • Sodium:2 - 3 mEq/kg/day • potassium:1-2mEq/kg/day
Fluid Therapy • ORT • Mild to moderate dehydration from diarrhea • Intravenous • With severe dehydration • with uncontrollable vomiting • unable to drink because of extreme fatigue, stupor, or coma • with gastric or intestinal distention
ORS composition • Sodium Chloride • Tri-Sodium Citrate (bicarbonate) • Potassium Chloride • Glucose
ORT • Mild: ORS 50 mL/kg within 4 hours • Moderate: ORS 100 mL/kg over 4 hours to • Supplementary ORS is given to replace ongoing losses • An additional 10 mL/kg of ORS is given for each stool • Breastfeeding should be allowed after rehydration in infants who are breastfed • usual formula, milk, or feeding for other patients should be offered after rehydration
Intravenous treatment • Restore intravascular volume • Normal saline: 20 mL/kg over 20 min (repeat until intravascular volume restored) • Deficit of water and electrolytes • Solution: 5% dextrose in half NS + 20 mEq/L of potassium chloride • Ongoing loss • Solution: 5% dextrose in ¼ normal saline + 15 mEq/L bicarbonate + 25 mEq/L potassium chloride • Maintenance • Solution: 5% dextrose in ¼ normal saline + 20 mEq/L of potassium chloride Given over the first 8 hrs Given over the next 16 hrs
Complication _watery diarrhea • Hypovolemic shock • Tetany & Convulsions • Hypoglycemia • Renal failure
Complication _dysentery • Toxic encephalopathy • Hemolytic uremic syndrome (HUS) • Intestinal abcess • Protein losing enteropathy • Arthritis • Perforation
Prognosis Mortality Dehydration Malnutrition
Global Impact of Enteric Disease Deaths in young children Average of 2.2 million deaths per year worldwide ETEC 380 000 Cholera 120 000 Typhoid 600 000 Rotavirus 450 000 Shigella 670 000 WHO, 2000
Prevention • Safe drinking water and food • “Boil it, cook it, peel it, or forget it. " • Hand washing • Proper sanitation • Vaccines