Topic 1: Acute gastroenteritis Causes of acute gastroenteritis in children: Viruses (70%) -> rotavirus, norovirus, enteric adenovirus, calicivirus, astrovirus, enterovirus Bacteria (20%) -> Campylobacter jejuni, non-typhoid salmonella, EPEC, shigella, Yersinia enterocolitica, shiga toxin producing E.coli, salmonella typhi, vibrio cholera. Protozoa (10%) -> Cryptosporidium, giardia lamblia, entamoeba histolytica Helminths -> strongyloides stercoralis Villus -> absorption Crypts -> secretion Acute gastroenteritis -> decrease in the consistency of stools ± an increase in the frequency of evacuations (typically ≥ 3 in 24 hours) ± fever or vomiting in the first months of life, a change in stool consistency is generally more indicative of diarrhea than simply an increase in the number of stools because: 🍼 Normal Infant Stool Patterns Vary Widely Breastfed infants may pass multiple loose stools per day — sometimes with every feeding — and that's normal. Formula-fed infants tend to have fewer stools, often more formed. Some healthy infants may go several days without stooling. So, frequency alone isn't diagnostic. ✅ What Indicates Diarrhea in Infants: A sudden change from a baby’s usual stool pattern toward looser, more watery stools. Increased fluidity (more than just being soft — truly watery or mucousy). Explosive stools, or stools that soak through the diaper more than usual. Sometimes accompanied by other signs: fever, vomiting, poor feeding, dehydration signs. Acute diarrhea typically lasts less than 7 days (chronic > 14 days) Key facts: Second leading cause of death in children under five (525,000) each year. Globally 1.7 billion episodes diarrheal every year leading cause of malnutrition in children under five years old It is both preventable and treatable Peak incidence is between 6-11 months: Age of complementary feeding Related to developmental age (mouthing) Declining maternal antibodies Complications of diarrhea: Dehydration leading to shock Electrolytes imbalance Metabolic acidosis Convulsions (brain edema) Malnutrition if chronic or recurrent Sepsis and DIC Assessment of dehydration: ORS osmolarity: Na+1 Cl-1 Glucose K+1 Citrate or (HCO3-1 -> 30 mM) Total 90 mM 80 mM 110 mM 20 mM 10 mM 310 mM Give: 75ml/kg in 3-4 hours Regular food 100 ml after each loose stool Nutritional management Who needs workup for diarrhea? Most children with acute gastroenteritis do not require diagnostic workup except: very young children underlying chronic conditions (e.g. cancer, inflammatory bowel diseases, immune deficiency disorders, diabetes mellitus) very sick febrile invasive diarrhea or bloody diarrhea with or without fever known travel to high-risk areas or during disease outbreak. Indications for hospital admissions: Shock Moderate-to-severe dehydration in young children Neurological abnormalities (lethargy, seizures, etc.) Intractable vomiting Failure of oral rehydration Suspected surgical conditions Electrolyte and/or acid/base imbalance Unmet conditions for safe follow-up and home management. Diarrhea management: Oral rehydration solution (first line for mild/moderate) Feeding Additional therapies -> Probiotics – Antibiotics – Antidiarrheal drugs – Antispasmodics Prevention of acute gastroenteritis: Wash hands thoroughly before and after eating or when preparing the meals Make sure that the tools used for eating and preparing the meals are clean Cover our food or put them in the fridge to prevent any contamination Rotavirus vaccines Topic 2: Chronic diarrhea Chronic diarrhea is a decrease of the consistency ± 🔹 Abdominal distension ->Possible causes: increase of frequency ± volume of stools lasting longer than two weeks, where the change in stool consistency is more important than stool frequency Pathogenesis of diarrhea: Osmotic Secretory Inflammatory Dysmotility Factitial Malabsorption syndromes (e.g., celiac disease, lactose intolerance) Protein-energy malnutrition Ascites in liver disease or protein-losing enteropathy A distended abdomen in a child with diarrhea could suggest intestinal dysfunction or low protein levels. 🔹 Tenderess -> Palpating the abdomen for tenderness or guarding helps rule out: Chronic diarrhea evaluation: Chronic diarrhea usually starts gradually (insidiously) and is often not associated with fever, unlike acute infectious diarrhea. This suggests non-infectious causes like malabsorption, food intolerance, or inflammatory conditions If the small intestine is involved -> Stool tends to be large volume, watery, and foul-smelling (offensive). Usually no blood present. Causes may include celiac disease, lactose intolerance, giardiasis, or other malabsorptive disorders If the colon is affected: o Diarrhea tends to be smaller in volume but may be more frequent. o Blood or mucus is often present → suggests dysentery or colonic inflammation. o Possible causes: inflammatory bowel disease, infections, or allergic colitis. Dietetic history (formula, gluten, soy, eggs etc..) Drugs (antibiotics, laxatives, colchicine, propranolol etc..) Inflammatory conditions (e.g., IBD, infections) Complications like mesenteric adenitis, enterocolitis, etc. 🔹 Perianal area -> Examining the perianal region helps detect: Perianal dermatitis, often due to stool acidity or infection Fissures, fistulas, tags, which are seen in Crohn's disease Signs of abuse or trauma, if suspected 🔹 Oral lesion -> Seen in some chronic GI and systemic diseases: Aphthous ulcers → can be a sign of Crohn’s disease or celiac disease Glossitis, angular cheilitis → due to vitamin deficiencies (e.g., B12, iron) 🔹 Other organs affected (e.g., skin, respiratory…) History Age Family history Growth Associated symptoms Dietary history Stool characteristics -> undigested food, blood, steatorrhea, offensive smell Physical examination Weight and height for age Abdominal distention Tenderness Perianal area Oral lesions Other organs affected (respiratory, skin) Dermatitis herpetiformis (small clusters of itchy bumps) 🔹 Weight and height for age -> Why important? Chronic diarrhea often leads to malnutrition, which can show as: Weight loss Growth faltering or stunting Tracking growth over time helps assess severity and chronicity of illness. Chronic diarrhea may be part of a systemic condition: Skin: Rashes, dermatitis herpetiformis (in celiac), acrodermatitis enteropathica, eczema (in food allergies) Respiratory: Suggests cystic fibrosis, which affects both lungs and pancreas Eyes, joints, etc.: May point toward autoimmune or inflammatory conditions (like IBD) Acrodermatitis (Enteropathica) The pictures show symmetrical erythematous, scaly plaques around the mouth, buttocks, and limbs. This is classic for Acrodermatitis Enteropathica, a condition due to zinc deficiency, often seen in: o o o Malabsorption Chronic diarrhea Genetic defects in zinc transport Causes of chronic diarrhea for children: Birth – 1 month: DH (Dermatitis Herpetiformis) Seen in celiac disease, particularly in older children and adults. Skin lesions are symmetrical, itchy, and typically located on elbows, knees, and buttocks Older children: Gluten ingestion → production of IgA antibodies against tissue transglutaminase (tTG). These antibodies cross-react with epidermal transglutaminase (eTG) in the skin. IgA gets deposited in the dermal papillae → inflammation → blistering and itching Chronic diarrhea investigations: 1. Red flags: Poor weight gain, weight loss or FTT Night stool Acid stools with burning sensation and redness Presence of blood and mucus Associated symptoms of systemic disease, rash, fever, arthritis etc.. Feces 2. Blood tests Celiac disease: Age of onset Usually manifests in infants or young children after the introduction of gluten-containing foods. Can appear at any age, but often between 6 months to 2 years when cereals are introduced. 3. Implicated food Gluten-containing grains: Wheat, barley, rye. Oats are controversial; some patients tolerate oats, others do not. Pathology Characteristic changes in the small intestinal mucosa: Imaging o o o 4. An immune-mediated reaction (IgE or non-IgE) to proteins found in cow’s milk. Most common food allergy in infants and young children. Different from lactose intolerance (which is non-immune and enzyme deficiency) Presentation o o o o Endoscopy & Pathology Cow’s milk protein allergy: Villus atrophy (flattening of the villi → decreased absorption surface). Crypt hyperplasia (increased depth of intestinal crypts). Increased intraepithelial lymphocytes (IELs) (immune cells infiltrate mucosa). Abdominal distension (bloating). Chronic diarrhea. Failure to thrive (FTT) or poor growth. Other symptoms may include abdominal pain, anemia, fatigue. Screening: Tissue transglutaminase IgA antibody (tTG-IgA). Total serum IgA to rule out IgA deficiency. GFD (Gluten-Free Diet) The cornerstone of treatment is a lifelong gluten-free diet. Complete avoidance of wheat, barley, and rye gluten-containing foods. Associations: Type 1 diabetes, thyroid disorders, and dermatitis herpetiformis. Cystsic fibrosis: 1. Neonatal Period: Meconium Ileus Many CF infants present early with intestinal obstruction called meconium ileus, caused by thick, sticky meconium blocking the intestines. 2. Respiratory Symptoms Recurrent or persistent cough, often accompanied by wheeze due to chronic lung infections and mucus plugging. 3. Malabsorption Pancreatic enzyme insufficiency leads to malabsorption of nutrients. Results in large, pale, bulky, and foul-smelling stools. Toddlers diarrhea (chronic non specific diarrhea): 4. Failure to Thrive (FTT) Due to malabsorption and increased energy needs from chronic illness. 5. Rectal Prolapse Most common cause between two and four years of age Intermittent and self limited No pain, no distension, no vomiting No effect on weight and on nutrition Large consumption of juices Undigested food particles Occurs due to frequent coughing and malnutrition. 6. Heat Stroke (Rare) CF patients can develop heat stroke because of abnormal salt loss in sweat. 7. Sweat Chloride Concentration Elevated sweat chloride (>60 mmol/L) is a diagnostic hallmark of CF. 8. Common Pathogens Treatment of chronic diarrhea: Chronic lung infections with Staphylococcus aureus and Pseudomonas aeruginosa are typical. 9. Management Physiotherapy: Chest physiotherapy to clear mucus from lungs. Enzyme Replacement: Pancreatic enzyme supplements to aid digestion. Increased Fluid and Salt Intake: Especially important in hot weather to prevent dehydration and heat stroke. Supportive : Dehydration, Electrolyte imbalance, Nutrients Empirical: Antidiarrheal drugs Curative: Antibiotics, pancreatic enzymes, dietary Topic 3: Neonatal jaundice Jaundice is yellowish discoloration of the skin ± conjunctiva caused by bilirubin deposition. Hyperbilirubinemia is a state of excessive amount of bile pigment bilirubin in the body visibly manifested as jaundice (TSB > 1 mg/dL [17.1 µmol/L]) Significant neonatal hyperbilirubinemia in infants ≥35 weeks gestational age is defined as: TSB >95 percentile on the hourspecific Bhutani nomogram Severe neonatal hyperbilirubinemia: TSB > 25 mg/dL [428 µmol/L] -> Associated with BIND (Bilirubin - Induced Neurologic Dysfunction) BIND -> spectrum of neurologic problems caused by elevated levels of unconjugated bilirubin in the brain. This condition occurs when bilirubin crosses the blood-brain barrier and accumulates in brain tissues, particularly the basal ganglia, leading to neurotoxicity. Clinical Spectrum of BIND: Acute Bilirubin Encephalopathy (ABE) – early, potentially reversible phase: Kernicterus – chronic, irreversible neurologic damage. Longterm effects: Cerebral palsy (especially athetoid type) Hearing loss (sensorineural) Gaze abnormalities Intellectual disability Dental enamel hypoplasia 85 % of infants > 35 weeks have visible jaundice due to hyperbilirubinemia in the first week after birth. Nearly all preterm have hyperbilirubiemia 10% of term. require intervention 25% of late preterm require intervention Bilirubin source: 80 – 90 % = Hb degradation 10 – 20 % = Hemoproteins (Catalases +cytochrome oxidase) degradation in liver Bilirubin metabolism -> retriculoendothelial system (monocytes and macrophages) in the spleen, liver and bone marrow. 🚫 Unconjugated bilirubin, even when elevated, still doesn’t show up in urine Bilirubin is transported to the liver through carrier proteins organic anion transporter protein OATP-2 Breast milk jaundice: prolonged unconjugated hyperbilirubinemia that occurs in healthy, breastfed infants, usually after the first week of life. It’s benign, self-limited. Unconjugated bilirubin in plasma is bound reversible to albumin. Can be displaced by free fatty acids and drugs (valium, ceftriaxone, sulfa drugs) Unconjugated bilirubin is: 1. Not soluble in water because it's lipid-soluble, UB cannot be excreted directly by the kidneys or into bile. 2. Potentially toxic especially in newborns, high levels of unconjugated bilirubin can cross the immature bloodbrain barrier, leading to BIND or kernicterus. 3. Made soluble and less toxic by albumin binding. In the bloodstream, UB is tightly but reversibly bound to albumin, which prevents it from entering tissues and keeps it less toxic and transportable to the liver for conjugation Breastfeeding jaundice: Why Unconjugated Bilirubin Is Not Found in Urine? UB is bound to albumin in the blood Albumin is a large protein that is not filtered by the glomerulus in the kidney This is why no bilirubin in urine is a hallmark of unconjugated hyperbilirubinemia. High UGB -> can exaggerate physiologic jaundice. Weight loss more than 8 % of birth weight (day 3-4). Associated with increased Na+ serum and dehydration and fever. 🔹 Normal Serum UB Levels: < 1.5 mg/dL is the typical upper limit At this level, most bilirubin in blood is: o Unconjugated o Bound to albumin o Not dangerous under normal conditions 🔹 Exception – When You Might See Bilirubin in Urine: Conjugated bilirubin is water-soluble and can appear in urine if: o Liver disease (e.g., hepatitis impairs excretion) o Biliary obstruction (e.g., gallstones block bile flow) May need phototherapy. No water or dextrose supplementation. Bilirubin is excreted actively into bile canaliculus by MRP – 2 (multi resistant associated protein 2) enhanced by phenobarbital. Dubin – Johnson syndrome -> Abnormal MRP2 -> Conjugated bilirubin increases in blood. Pattern: o o 3-4 days term, 5- 7 days preterm Disappears by 4-5 days term, 7-9 preterm The baby is well Bilirubin rise trend: o o Increase < 0.2 mg/dL/h and < 5 mg/dL/day Mean peak according to race (<15) Maybe exaggerated when: Obstruction of GI (delayed meconium, or fasting) -> more time for conjugated bilirubin to be deconjugated by beta glucuronidase in the intestinal mucosa. The UCB gets reabsorbed and enters the entero – hepatic circulation. Bilirubin measurement: Transcutaneous bilirubinometer TSB o o o o o o o o o o Breast feeding Male sex Cephal hematoma Cutaneous bruising Polycythemia Weight loss/ caloric deprivation Dehydration Maternal DM Trisomy Drug (K3, novobiocin, oxytocin) Types of neonatal jaundice: 1. Physiologic Mechanism: o o o o Increased RBC + ineffective erythropoiesis Shortened RBC lifespan Immature hepatic uptake and conjugation Increased EHC (increased intestinal glucoronidase) Prolonged jaundice (persists after 2 weeks (term) , 3 weeks (preterm) -> evaluate): 2. Breast feeding jaundice After birth: 3. Breast – milk jaundice 4. Pathologic Medical emergency Causes of high UGB causing jaundice: Increased production: o Hemolysis (ABO or RH incompatibility, Inherited spherocytosis, G6PD) o Sepsis o RBC breakdown (polycythemia, cephalohematoma) o Ineffective erythropoiesis o Galactosemia Post-discharge follow – up: ABO incompatibility: o Early onset (within 24 h after birth) o Baby blood A/B, mother bood is O o Direct combs test positive o Blood smear shows increased spherocytes o Can be controlled with phototherapy Decreased clearance / excretion: o Inherited (galactosemia, crigler najjar, gilbert, OATP polymorphism) o Congenital hypothyroidism Increased EHC o NPO o Obstruction Infants discharged before 72 hours of life should be seen within 2 days of discharge Infants with significant risk factors for development of severe hyperbilirubinemia should be seen within 1 day Therapeutic options: Phototherapy for neonates with mild jaundice Exchange transfusion for severe cases Iv immune globulin How to recognize pathologic jaundice? 1. Jaundice appearing in the first 24 hours of life is always pathologic until proven otherwise. early bilirubin values have high sensitivity and specificity for predicting severe hyperbilirubinemia later on: 2. 3. 4. Rapidly rising TSB (> 5 mg/dL per day > 0.2 mg/dl/hour TSB high risk zone (> 75th) Persists after two weeks High conjugated bilirubin (physiologic is UGB) 5. Assess risk factors Topic 4: Liver disease
0
You can add this document to your study collection(s)
Sign in Available only to authorized usersYou can add this document to your saved list
Sign in Available only to authorized users(For complaints, use another form )