PLT 2 LECTURE GASTRO PDF

GASTROINTESTINAL TRACT FA I T H R. B A L I S A N - D O M I N G O M D , D P P S The Digestive System  The Digestive System 12 week AOG – fetus can swallow amniotic fluid 34 weeks AOG – nutritive sucking in neonates 1 month of age – infants show preference (sweet & salty) 6 months of...

GASTROINTESTINAL TRACT FA I T H R. B A L I S A N - D O M I N G O M D , D P P S The Digestive System  The Digestive System 12 week AOG – fetus can swallow amniotic fluid 34 weeks AOG – nutritive sucking in neonates 1 month of age – infants show preference (sweet & salty) 6 months of age – start of solid foods  Normal Digestive Tract Phenomena 1. Regurgitation 3. Protuberant Abdomen - result of gastroesophageal reflux - protuberant after large feedings - common 1st year of life - Infants and children - healthy infant: 15- 30ml emesis combination of weak musculature - resolves large abdominal organs 80% at 6months lordotic stance 90% at 12months 2. Stool Frequency 4. Palpable Liver - 1st year of life - variable (none to 7x/day) - 1-2cm below the right costal margin Breastfeed infants: frequent small to Normal Liver: loose transition stools soft in consistency & percusses to normal size for age  Approach to Common GI Complaints Manifestations Definition Differential Diagnosis DYSPHAGIA Difficulty in swallowing Acute viral stomatitis Oral trauma ODYNOPHAGIA- painful swallowing Nasal obstruction GLOBUS – sensation of something stuck throat Achalasia Tracheoesophageal fistula OROPHARYNGEAL DYSPHAGIA – transfer of Strictures food from mouth to esophagus (impaired). MOST Vascular rings common complication –LIFE THREAT Mediastinal tumors ASPIRATION Vertebral anomalies Esophageal web ESOPHAGEAL DYSPHAGIA – difficulty in Gastroesophageal Reflux transport of food bolus down the esophagus Disease  Approach to Common GI complaints Manifestations Definition Differential Diagnosis REGURGITATION Effortless movement of stomach contents Gastroesophageal reflux (GER) into the esophagus and mouth Gastroesophageal reflux Disease Developmental process that improves with maturity Systemic diseases (neoplasia & inflammatory) ANOREXIA Prolonged lack of appetite Iatrogenic: drug, unpalatable diets Depression VOMITING Highly coordinated reflex process that Gastroesophageal reflux (GER) may Gastroesophageal reflux Disease Excessive loss of fluid and electrolytes in Lactose Intolerance, Malabsorption DIARRHEA the stool Acute Gastroenteritis Toxins, Tumor (Neuroblastoma) Adrenal insufficiency, Motility disorders  Approach to Common GI complaints Manifestations Definition Differential Diagnosis Depends on stool consistency and frequency Neonates: Hirschsprung disease, intestinal CONSTIPATIO and difficulty in passing stool pseudobstruction, hypothyroidism N HARD STOOL with DIFFICULTY (3days) is constipation Variation among children in their perception Functional abdominal pain and tolerance. Irritable bowel syndrome ABDOMINAL Constipation, lactose intolerance PAIN VISCERAL PAIN – dull and aching felt in Esophagitis, intestinal parasitism the dermatome from which the organ Inflammatory bowel diseases, Cholelithiasis, receives innervation Choledochal cyst, pancreatitis, Appendicitis, SOMATIC PAIN – intense and well Inguinal Abdominal Hernia, Intestinal localized (peritonitis) Obstruction, Non-GI causes (renal colic, pneumonia, sexual abuse, REFERRED PAIN – pain from other psychological causes, HSP, anaphylaxis) organs  Approach to Common GI Complaints Manifestations Definition Differential Diagnosis GASTROINTESTIN Hematemesis – originates from Erosive damage (most common cause), AL esophagus, stomach, or duodenum. Bacterial enteritis, milk protein allergy, HEMORRHAGE Intussusception, Anal fissure, Lymphonodular Hematochezia – red blood in the stools, hyperplasia, Peptic ulcer, Gastritis, Swallowed distal bleeding site or massive bleeding. epistaxis, prolapse gastropathy, colonic polyps Melena – blackened stools of tarry consistency, from mild to moderate bleeding above the distal ileum ABDOMINAL Distention results from diminished tone Ascites DISTENTION of the wall musculature or increased Solid masses (wilm’s tumor, hydronephrosis, abdominal content. neuroblastoma, hepatoblastoma, lymphoma, teratoma, mesenteric cyst). If with ascites = fluid analysis is needed Pregnancy  The ORAL CAVITY NEWBORNS do not have TEETH 5th month – start of eruption of the 1st tooth (primary eruption ) CENTRAL INCISORS 10 months – second premolars 3 y.o. - all 20 primary teeth erupted 6 y.o.-Permanent Teeth starts to erupt 13 y.o.- FULL Dentition  The ORAL CAVITY FLUOROSIS (mottled enamel) - systemic fluoride (>0.05 mg/kg/day during enamel formation) - HIGH FLOURIDE in drinking water (>2.0ppm) - swallowing excessive fluoridated toothpaste -inappropriate fluoride prescription RESULTS: inconspicuous white, lacy patches on the enamel to severe brownish discoloration and hypoplasia.  CLEFT LIP & PALATE Incidence: 1:750 white births 1:2,500 white births Male > Female Etiology: maternal drug exposure, syndrome- malformation complex, genetic factors, (400 syndromes associated with cleft lip/palate) CLINICAL MANIFESTATIONS Cleft Lip – small notch of the vermillion border – complete separation (skin, muscle, mucosa, tooth and bone), - UNILATERAL (left side), - BILATERAL (alveolar ridge)  CLEFT LIP & PALATE CLINICAL MANIFESTATIONS CLEFT PALATE – midline and may involve uvula or can extend into or through the soft/hard palate to the incisive foramen. CLEFT LIP + PALATE – midline to the soft plate extends to the hard palate on one or both sides, exposing one or both of the nasal cavities as Unilateral or Bilateral cleft palate. CLEFT LIP & PALATE TREATMENT - team approach FEEDING – Haberman bottle, - plastic obturator SURGICAL CLOSURE 3 months of age weight gain infection-free INITIAL repair – 4 to 5 years old CORRECTIVE SURGERY (nose) - adolescent MODIFICATION of the MILLARD rotation-advancement technique – MOST COMMON SURGICAL GOALS – union of the cleft segments, intelligible, pleasant speech, reduction of nasal regurgitation, avoidance of injury to the growing  DENTAL CARIES ETIOLOGY: interrelationship between tooth surface, dietary carbohydrates, and specific oral bacteria SUCROSE – most carcinogenic sugar because one of its by-product during bacterial metabolism is glucan, a polymer that enables bacteria to adhere readily to the tooth surface. CLINICAL MANIFESTATIONS – pits & fissures small lesions larger (darker) or cavitated on the surface EARLY CHILDHOOD CARIES – rampant dental caries in infants and toddlers  PREVALENCE: 3 – 9yr old COMPLICATIONS: PULPITIS – inflammation of the pulp PULP NECROSIS with bacterial invasion of the alveolar bone causing DENTAL ABSCESS. TREATMENT Dental management PENICILLIN – DRUG of CHOICE WHITE SPOT LESION – initial demineralization CLINDAMYCIN & ERYTHROMYCIN – on the enamel alternatives PAIN – oral analgesics (IBUPROFEN FLOURIDE – most preventive measure Topical fluoride and fluoridated toothpaste  COMMON Lesions of the Oral Soft Tissues CONDITION COMMENT Aphthous ulcers Painful circumscribed lesions, recurrences Traumatic ulcers Accidents, chronic cheek biter, after dental local anesthesia Hand Foot Painful lesions on the tongue, anterior oral cavity, hands and Mouth Disease feet Herpangina Painful, lesions confined to the soft palate and oropharynx Herpetic Vesicles on the mucocutaneous borders, painful, febrile gingivostomatiti s Recurrent Vesicles on the lips, painful Herpes labialis THE ESOPHAGUS EMBRYOLOGY ◦ 8-10cm length at birth ◦ Doubles in the 1st year of life POLYHYDRAMNIOS – HALLMARK of the LACK OF NORMAL SWALLOWING or of the esophageal or upper GI tract obstruction. FUNCTION of the ESOPHAGUS swallowing is initiated by the tongue, propelling the bolus into the pharynx. The larynx elevates and moves anteriorly, pulling open the relaxing UES, while the opposed aryepiglottic folds closes.  Esophageal Atresia & Tracheoesophageal Fistula ESOPHAGEAL FISTULA – THE MOST COMMON CONGENITAL ANOMALY of the ESOPHAGUS ◦ Prevalence: 1.7: 10,000 live births ◦ >90% + TEF MANIFESTATIONS: Neonate has frothing and bubbling at the mouth and nose after birth, episodes of coughing, cyanosis, respiratory distress. Feeding exacerbates symptoms regurgitation ASPIRATION DIAGNOSIS ◦ INABILITY to PASS an NGT or OGT in the NEWBORN is suggestive especially in the setting of early onset respiratory distress. ◦ PLAIN RADIOGRAPH: coiled NGT/OGT in the ESOPHAGEAL POUCH ◦ 50% associated with VACTERRL (Vertebral, Anorectal, Cardiac, Trachea, Esophagus, Renal, Rectal, Limb syndrome) MANAGEMENT SUPPORTI Maintain a Patent airway VE Pre-operative proximal pouch decompression to prevent aspiration of secretions. Anti-biotic therapy for consecutive pneumonia Prone positioning to reduce regurgitation & esophageal suctioning SURGER SURGICAL LIGATION of the TEF & primary end-to-end Y anastomosis of the esophagus via right –sided thoracotomy.  GASTROESOPHAGEAL REFLUX DISEASE GERD – the most common esophageal disorder in children of all ages. GER – retrograde movement of gastric contents across the lower esophageal sphincter (LES) into the esophagus. Physiologic process PATHOLOGIC GERD - frequent & persistent & with complications (esophagitis, respiratory symptoms, failure to thrive, feeding refusal A. Pathophysiology – LES is supported by the crura at the gastroesophageal (GE) junction which has a valve like function and acts as an anti-reflux barrier. TRANSIENT LES RELAXATION – the major mechanism allowing the reflux to occur. GASTRIC DISTENTION – the main stimulus for the TLESR (straining & coughing, large volume or hyperosmolar meals. EPIDEMIOLOGY Infant Reflux evident at 1st few months of life, peaks at 4 months, resolves mostly at 12 months & 24months GENETICS: Autosomal dominant (locus GERD1 in chromosome 13q14) MANIFESTATIONS AGE GROUP MANIFESTATIONS INFANTS Regurgitation, excessive crying/irritability, vomiting, food refusal Persistent hiccups, abnormal posturing, impaired quality of life CHILDREN Impaired quality of life, vomiting, esophagitis Persistent/chronic cough, aspiration pneumonia, wheezing Ear infections, stridor, heartburn ADOLESCENTS & Impaired quality of life, esophagitis, dysphagia ADULTS Heartburn, epigastric pain, chest pain  DIAGNOSTICS BARIUM STUDY of the To rule out anatomic causes of vomiting UPPER GIT ESOPHAGEAL PH GOLD STANDARD Monitoring Document acidic reflux episodes (normal value of distal esophageal acid exposure 48hours History of chronic constipation ‘ Tympanitic and distended abdomen SIGNS Large fecal mass palpable in the left lower quadrant Pellet-like or ribbon like stool with fluid consistency Rectal Rectum usually empty of feces on exam with normal anal tone Examination May have an explosive discharge “gush of air” once finger is removed HIRSCHSPRUNG DISEASE RECTAL SUCTION BIOPSY GOLD STANDARD (easy and reliable) Abdominal xray with contrast Transition zone between normal and dilated proximal colon and the enema smaller-calibre obstructed distal colon due to nonrelaxation of the aganglionic bowel. A rectal diameter that is the same as or smaller than the sigmoid colon is SUGGESTIVE MANAGEMENT OPERATIVE REPAIR with surgical options/techniques: Swenson, Duhamel, Soave PRIMARY pull through procedures unless there is associated enterocolitis or other complications Acute Gastroenteritis ETIOPATHOGENESIS ACUTE DIARRHEA < 14days and CHRONIC DIARRHEA > 14days Majority – foodborne illnesses Viruses are one of the most common cause of acute diarrhea in children ETIOLOGY of ACUTE DIARRHEA Inflammatory C. jejuni, c.difficile, EIEC (enteroinvasive e. coli), Salmonella, Shigella, Yersinia Non-inflammatory EPEC, ETC, V. cholera Viral Rotavisu, Adenovirus, Astrovirus, Norwalk, Calicivirus Parasitic G. lambdia, E. histolytica, Strongyloides, spore-forming protozoa Other causes Malabsorption, endocrinopathies, food poisoning, neoplasms, etc like milk allergy, laxative abuse Acute Gastroenteritis 2 types of Acute Infectious Diarrhea Inflammatory Due to bacteria that invade intestine directly or produce cytotoxins Non- Enterotoxin produced by bacteria inflammatory Destruction of villus by viruses Adherence by parasites  MECHANISMS of DIARRHEA OSMOTIC DIARRHEA SECRETORY DIARRHEA Pathogenesis Presence of nonabsorbable solutes in Activation of intracellular the GIT: mediators (eg CAMP cGMP) that Intestinal damage stimulate active chloride secretions Reduced absorptive surface & inhibit the neutral coupled NaCl Defective digestive enzymes absorption Decreased intestinal transit time Toxin mediated injury to the Nutrient overload tight junctions (sorbitol in fruit juice, Results in extremely watery overfeeding) stool Causes Lactose Intolerance due to Cholera, E.coli enterotoxins lactase enzyme deficiency Clostridium difficile Vasoactive peptides Volume of Stool Moderately increased Very large volume diarrhea Responding to Diarrhea stops Diarrhea continues fasting  MECHANISMS of DIARRHEA OSMOTIC DIARRHEA SECRETORY DIARRHEA Stool Na+ 70mEq/L Stool pH 5.6 Ion Gap > 100mOsm/kg 10 years = as much as tolerated Feeding: continue breastfeeding/regular feeding to prevent malnutrition Give supplemental zinc: ◦ 10mg/day (6months) WHO CDC PROTOCOL on REHYDRATION PLAN B INTUSSUSCEPTION Occurs when a portion of the alimentary tract is telescoped into an adjacent segment MOST COMMON: ILEOCOLIC Upper portion of the bowel (intussusceptum) invaginates into the lower part (intussuscipiens) dragging its mesentery along with into the enveloping loop. Mesentery constricts and obstructs venous return. Intussusceptum engorges leading to edema & bleeding from the mucosa. INTUSSUSCEPTION ETIOPATHOGENESIS MOST COMMON CAUSE of intestinal obstruction: 5months – 3y.o. MOST COMMON Cause of emergency in children < 2years IDIOPATHIC 90% of cases with some degree of correction with Adenovirus CLASSIC TRIAD: PAIN PALPABLE SAUSAGE SHAPED ABDOMINAL MASS CURRANT JELLY STOOL MANIFESTATIONS SYMPTO Severe paroxysmal colicky pain that recurs at frequent intervals. MS Straining effort with legs and knees flexed & loud crying Infant comfortable to play normally between paroxysms, becoming progressively lethargic. IF NOT REDUCED shock like state, with fever and peritonitis, can develop. VOMITING: present in early phase and later on becomes bile- stained. SIGNS 60% infants pass currant jelly stool DIGITAL RECTAL EXAM- presence of blood is supportive of diagnosis DIAGNOSIS ULTRASOUND 98-100% screening sensitive, 98% specific TUBULAR MASS in longitudinal view DOUGHNUT MASS sign in transverse view Xray vague and non-specific findings Pain abdominal BARIUM ENEMA COILED SPRING SIGN (thin rim of barium trapped around the invaginating part within the INTUSSUSCEPIENS TREATME REDUCTION SURGICAL NT MECKEL DIVERTICULUM a remnant of the omphalomesenteric duct which connects the yolk sac to the gut in the embryo & provides nutrition. MOST COMMON CONGENITAL GI tract ANOMALY ETIOPATHOGENESIS: Rule of “2’s” ◦ - present in -2% of the population ◦ - usually located 2 feet proximal to the ileocecal valve ◦ - approximately 2 inches in length ◦ - can contain 2 types of ectopic tissue (gastric or pancreatic) ◦ -generally present before 2 years old ◦ - female to male ratio= 2:1 MANIFESTATIONS, DIAGNOSIS & MANAGEMENT MANIFESTATIO Symptoms usually arise within the 1st year of life NS Diverticula is lined by an acid-secreting ectopic mucosa causing intermittent PAINLESS rectal bleeding and brick- colored or currant jelly colored stool. Accounts for 50% of all lower GI bleeds in children