Gastrointestinal Diseases Part1

Normal Digestive Tract Phenomena GI function varies with maturity Swallowing Reflex – 12 weeks gestation Nutritive Sucking – 36 weeks gestation Coordinated oral and pharyngeal movements – within 1st few months of life in term infants Normal anatomical varies: tongue tie, scrotal tongue, bifida uvula Regurgitation – resolves in 80% of infants by 6 months old and 90% by 12 months of age Physiologic anorexia for toddlers and preschoolers Number, color, and consistency of stools vary in infants and young children Protuberant abdomen noted in infants and toddlers Common to palpate the liver 1-2 cms below right costal margin – 1st year Blood Loss from GIT is never normal Jaundice – common in neonates; physiologic vs pathologic

Different Diagnosis of Vomiting During Childhood

Major Signs and Symptoms of GI Disorder

I.

Dysphagia – due to structural defect or motility disorder – Most non-structural causes are due to motility abnormality of oropharynx or the esophagus

II.

Regurgitation – effortless movement of contents into esophagus and mouth

III.

Anorexia – appetite affected by hormones, plasma glucose, emotions

IV.

Vomiting – highly coordinated reflex process in the medulla influenced directly by afferent innervations and indirectly by the chemoreceptor trigger zone and and higher central nervous system (CNS) centers – In due to GI obstruction: mediated by intestinal visceral afferent nerves

* Cyclic vomiting – numerous episodes with well intervals – Onset: 2-5 y/o, lasts 2-3 days – Stress and Excitement: causes

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- What did you wave me down for? - Can you spare me some change for a cup of coffee? - Come with me upstairs.

When the two reached the second storey of the condominium, Jim turned to the guy and said, "Sorry, I neither have change, nor a cup of coffee."

V.

Diarrhea – excessive loss of fluid and electrolyte in the stool; basis is disturbed intestinal solute transport

a. Secretory – decrease absorption, increase secretion; watery and voluminous; persists even when no feedings are given orally. E.g. Cholera, E. coli, C. difficile (lactose or glucose)

b. Osmotic – occurs after ingestion of poorly absorbed solute; stops when feeding stops; transport defects; increase osmolality with fasting

c. Motility – decrease transmit time (E.g. Irritable bowel syndrome, thyrotoxicosis, postvagotomy

dumping syndrome) or defect in neuromuscular units or bacterial overgrowth. (E.g. Pseudoobstruction, blind loop)

d. Mucosal Inflammation – Inflammation, decreased mucosal surface area and/or colonic reabsorption, increased motility E.g. Celiac disease, Salmonella, Shigella, amebiasis, Yersinia, Campylobacter, rotavirus enteritis

VI.

VII.

Constipation – depends on stool consistency, frequency, or difficulty passing the stool; arises from defects either in filling or emptying the rectum – Common causes during infancy: Hirchsprung disease, congenital hypothyroidism, intestine pseudoobstruction – Common causes during adolescence: functional, diet

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VIII.

Abdominal pain Children differ greatly in their perception and tolerance for abdominal pain Functional vs organic cause Preschools and toddlers cannot localize 2 types of nerve fibers transmit painful stimuli: 1) A fibers – skin and muscle; sharp localized pain 2) C fibers – viscera, peritoneum and muscle; poorly localized, dull pain Pain perceived in cortex of postcentral gyrus Visceral pain: dermatome which the affected organ receives information: o Epigastrium: liver, pancreas, biliary tree, stomach or upper bowel o Umbilicus: distal small bowel, cecum, appendix, or proximal colon o Suprapubic: distal large bowel, urinary tract, or pelvic organs Parietal pain: impulses travel in C fibers of nerves corresponding to dermatomes T6–L1; such pain tends to be more localized and intense than visceral pain.

GI hemorrhage Most common: erosive damage to mucosa Hematemesis: esophagus, stomach, duodenum – Hematochezia: lower GI or massive hemorrhage above distal ileum – Melena: blackened tarry stool above distal ileum – Children may have iron deficiency anemia for chronic enteric blood loss

*3 mos: most common cause is intussusception

Risky surgery Husband Wife

IX.

Abdominal Distention and Masses Enlargement of the abdomen from decreased tone of wall muscle or increased content: fluid, gas, solid/tumor – Ascites: accumulation of fluid in peritoneal cavity – Masses may occur in lumen, wall, or mesentery – Constipated child: mobile, nontender fecal masses found or palpated – Diffuse enlargement of the liver – Anomalies, cysts, or inflammatory disease can affect the wall of the gut

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Different Diagnosis of GI bleeding in Chidhood

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Ang taong walang bisyo Pauper Student Pauper Student Pauper Student Pauper Student Pauper Student

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Esophagus

*Frothing and bubbling at mouth and nose, cough, cyanosis, respiratory distress (Normal RR of neonates: 40-60 bpm) *Feeding exacerbates symptoms, causes regurgitation and precipitate aspiration *Diagnosis: inability to pass NGT or OGT in the newborn is suggestive

Manifestations of Esophageal Disease Abnormal retrograde movement of gastric contents (reflux, regurgitation, vomiting) Pain in chest unrelated to swallowing (“heartburn”) Pain during swallowing (odynophagia) Difficulty swallowing (dysphagia) Most common in children: GERD Causes of dysphagia: 1. Incomplete occlusive esophageal obstruction (by extrinsic compression, intrinsic narrowing, foreign bodies) 2. Dysmotility of the esophagus (Primary/Idiopathic or secondary to systemic disease) 3. Inflammatory lesions of the esophagus without obstruction or dysmotility; eosinophilic esophagitis, most often afflicting older male children, is a relatively common cause. Diagnostic Aids 1. Radiography – most common 2. Endoscopy 3. Histology 4. Scintography 5. Manometry 6. pH-metry 7. Intraluminal impedance Endoscopy – allows direct visualization of esophageal mucosa and helps therapeutically in the removal of foreign bodies and treatment of esophageal varices – also allows biopsy samples to be taken, thus improving the diagnosis of “endoscopy-negative” GERD, differentiating GERD from eosinophilic esophagitis, and identifying viral or fungal causes of esophagitis Radionuclide Scintography Scans –helpful in evaluating the efficiency of peristalsis and demonstrating reflux episodes. They can be specific, although not very sensitive, for aspiration and can quantify gastric emptying, thus hinting at a cause for GERD. Intraluminal electric impedance – method for pHindependent detection of bolus movements in the esophagus and can distinguish between acid and nonacid liquid and gaseous reflux Esophageal Atresia and TEF 1 in 4000 neonates; >90% have TEF Type A – 87% most common 50% of infants have associated anomalies (VATER/VACTERL – vertebral, anorectal, trachea, esophagus, cardiac, renal, radial, limb syndrome)

Management: Maintain a patent airway Prone position, esophageal suctioning Treatment: surgical (ligation of tissue) GERD Most common in children of all ages LES, supported by the crura of the diaphragm at the GE junction, with valvelike functions of esophagogastric junction anatomy, form the antireflux barrier Retrograde movement across LES into esophagus Physiologic vs pathologic (frequent or persistent episodes with respiratory complications) Factors: Duration, causticity, susceptibility to damage Transient LES relaxation: major mechanism allowing efflux to happen Gastric distention: major stimulus Peaks at 4 months, resolves at 1 y/o Genetic: AD

Diagnosis: Barium study of esophagus and upper GIT Clinical Manifestation: o Infants: post prandial regurgitation, signs of esophagitis (irritability, arching, choking, gagging, feeding aversion), and resulting failure to thrive; symptoms resolve spontaneously in the majority by 12 to 24 months o Older children, in contrast, may have regurgitation during the preschool years; complaints of abdominal and chest pain supervene during later childhood and adolescence. o Older children: regurgitation, abdominal and chest pains; respiratory manifestations related to primary airway disease such as laryngomalacia or bronchopulmonary dysplasia Management o Conservative therapy and lifestyle modification o Dietary measures:  normalization of feeding techniques, volumes, and frequency if abnormal  thicken formula  avoid to avoid acidic foods (tomatoes, chocolate, mint) and beverages (juices, carbonated and caffeinated drinks, alcohol)  hypoallergenic diet  weight reduction for obese patients  elimination of smoke exposure at all ages o Awake: prone or upright + carried position o Antacids, H2RAs, PPIs, prokinetic agents o Fundoplication – for intractable GERD, refractory esophagitis and strictures, with morbidities from chronic pulmonary disease

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*90% foreign bodies pass out of stool within 48 hrs *diameter of foreign body <25 mm – easily pass out rectum Asymptomatic blunt objects and coins lodged in the esophagus may be observed for up to 24 hr in anticipation of passage into the stomach. If there are no problems in handling secretions, meat impactions can be observed for up to 12 hr. An alternative technique for removing esophageal coins impacted for under 24 hr, performed most safely by experienced radiology personnel, consists of passage of a Foley catheter beyond the coin at fluoroscopy, inflating the balloon, and then pulling the catheter and coin back simultaneously with the patient in a prone oblique position. Caustic Ingestions Results in esophagitis, necrosis, perforation, and stricture formation Liquid alkali – severe, deep liquefaction necrosis Acidic agents – coagulation necrosis (bitter so less ingested) Vomiting, drooling, refusal to drink, oral burns, dysphagia, abdominal pain Circumferential ulcers, white plaques, sloughing of mucosa Absence of oropharyngeal lesions does not exclude the possibility if significant esophagogastric injury Endoscopy: rapidly identifies tissue damage Dilution by water / milk is recommended Neutralization, induced emesis and gastric lavage are contraindicated (DO NOT induce vomiting!!!) Surgical resection: small intestine or colon interposition (for Grade VI lesion)

Foreign Bodies Coins – most common Most lodge at level of oncopharyngeus (UES), the aortic arch or superior to the diaphragm at LES Choking, gagging, or coughing followed by excessive salivation, dysphagia, food refusal, emesis, or pain in the throat or sterna notch Diagnosis: X-ray of neck, chest, abdomen (AP & lateral views) o Flat (coronal) surface of coin seen on AP view and edge on lateral view; the reverse is true for coins lodged in the trachea o Sharp object, disc button batteries, or FBS with respiratory symptoms mandate urgent removal

Intestinal Obstruction Partial vs complete Simple (failure of progression of low of luminal contents) vs Strangulation (impaired blood flow

to the intestines in addition to obstruction of the flow of the luminal contents) Accumulation of food, gas, intestinal secretions proximal to the point of obstruction → Bowel distention →  Intestinal absorption →  Fluid and electrolyte secretion → Isotonic intravascular depletion →  Contractions then hypoactive bowel sounds → Nausea, vomiting Intrinsic (atresia, stenosis, meconium ileus, aganglionis, megacolon) vs Extrinsic (malrotation, constricting bands, intrabdominal hernias, duplication) ATRESIA – Complete obstruction of the bowel lumen STENOSIS – Partial block of luminal contents Classic Symptoms: o Nausea & vomiting o Abdominal distention o Obstipation High obstruction o Large volume frequent billous emesis o Intermittent epigastrial/periumbilical pain relieved by vomiting Low obstruction o Moderate/marked distension with progressively feculent emesis o Diffuse pain over the entire abdomen Plain supine/ upright/ decubitus x-rays Upright/ cross table lateral view: distended bowel ABOVE the obstruction with fluid level and gas in the distended loops Pneumoperitoneum may be seen in perforation with free air in the subphrenic area or over the liver in the left lateral decubitus position

Water-soluble enemas, useful in: o Malrotation o Meconium ileus/plug o Intussusception (diagnostic and therapeutic) Management: o Fluid resuscitation o Nasogstric decompression o Cultures o Antibiotics o Surgery for strangulation o Conservative measures for adhesions or strictures (if clinical signs of improvement are not evident within 12-24 hrs, surgery is indicated) o *Metronidazole – for anaerobic GI infection Pyloric Stenosis Most common cause of nonbilious vomiting (White>Asians; M>F) Unknown cause; abdominal muscle innervation is implicated (3wks – 5months) Post prandial vomiting, hypochloremic metabolic alkalosis Diagnosis: o Firm, moveable, olive-shaped mass o Visible gastric peristaltic wave after feeding Ultrasound is confirmatory: Pyloric thickness >4mm or length >14mm Barium: Elongated pyloric channel, a bulge of the pyloric muscle into the antrum (shoulder sign) and streaks of barium in the narrowed channel (double tract sign) Surgery: Ramstedt pyloromyotomy

Ground glass appearance in the RLQ with trapped air bubbles seen in meconium ileus Ultrasound: Stenosis, Malrotation, Volvulus, Intussusception Contrast studies used when plain films or sonograms fail to identify the source of obstruction

Gastric Volvulus TRIAD (1) Sudden onset of epigastric pain (2) Intractable retching with emesis (3) Inability to put a tube into the stomach Stomach rotates itself when the ligaments are absent or stretched

May advance to strangulations and perforations Diagnosis: o Plain abdominal x-ray: Dilated stomach o Double fluid level with a “beak” near the lower esophageal junction Treatment: Emergent surgery

Majority present within the 1st year of life with symptoms of acute/chronic obstruction Diagnosis o Ultrasound or contrast x-ray studies: usually nonspecific but may demonstrate evidence of duodenal obstruction with a doublebubble sign o Upper gastrointestinal series show malposition of the ligament of Treitz o Ultrasonography demonstrates inversion of the superior mesenteric artery and vein: suggestive of malrotation o Malrotation with volvulus is suggested by duodenal obstruction, thickened bowel loops to the right of the spine, and free peritoneal fluid Treatment: surgery to any patient with signifant rotational abnormality regardless of age Merckel Diverticulum

Duodenal Atresia Due to failure to recanalize the lumen during the 4th-5th week of gestation 25-40% of all intestinal atresias; 50% are premature; Obstruction usually distal to the ampulla of Vater; May have other congenital anomalies Hallmark: o Billous vomiting without abdominal distension usually noted on the 1st day of life o Polyhydramnios in 50% due to failure of absorption of amniotic fluid in the distal intestine o Jaundice in 1/3 of the patients Diagnosis: Double bubble sign in plain abdominal x-ray due to distended gas-filled stomach and proximal duodenum

Treatment: o NGT/OGT decompression with IV fluid replacement o Surgery: Duodenostomy with gastrostomy tube Malrotation Incomplete rotation of intestine during fetal development which is completed 3 months gestation Most common type: failure of cecum to move into RLQ

Remnant of the omphalomesenteric duct which connects the yolk sac to the gut in the embryo and provides nutrition. This duct separated from the intestines between 5th-7th week of gestation Partial or complete involution results in residual structures Most frequent congenital GI anomaly With clinical signs of anemia Typical diverticulum is a 3-6 cm outpouching of the ileum along the animesenteric border 50-75 cm from the ileocecal valve Symptoms usually rise within the 1st-2nd years of life Diverticula is lined by an acid secreting ectopic mucosa causing intermittent painless rectal bleeding and brick colored stool Diagnosis: Meckel radionuclide scan (sensitivity of 85% & specificity of 95%) Treatment: Surgical excision if symptomatic

Hirschsprung Disease Lack of innervation Aka Congenital aganglionic megacolon Most common cause of lower intestinal obstruction in neonates; M>F Arrest of neuroblast migration from the proximal to distal bowel  absence of ganglion cells in the bowel wall beginning in the internal anal sphincter Dominant and recessive patterns seen RET genes on chr10q11 & the EDNRB gene on chr13q22 Aganglionic segment limited to the rectosigmoid in 75%

Absence of Meissner & Auerbach plexus & hypertrophied bundles with high concentrations of acetylcholinesterase between the muscular and submucosa layers Symptoms usually begin at birth with the delayed passage of meconium Some present with a history of chronic constipation Failure to pass stool leading to enterocolitis: Failure to pass stool → Dilatation of the proximal bowel and abdominal distension →  intraluminal pressure →  blood flow and deterioration of mucosal barrier → Bacteria proliferates → Enterocolitis Rectum usually empty of feces on examination with a normal anal tone Pellet-like or ribbon-like stool Currarino triad in older patients: o Anorectal malformation o Sacral bone anomalies o Presacral masses Diagnosis: o Rectal manometry o Rectal suction biopsy (easy and reliable) o X-ray transition zone between normal dilated proximal colon and a smaller caliber obstructed distal colon due to nonrelaxation of the aganglionic bowel Treatment: o Definitive procedure:

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(Swenson, Duhamel, Boley, endorectal pull-through via laparoscopy) Temporary colostomy and wait until the infant is 6-12 months old to perform definitive repair

Intussusception Occurs when a portion of the alimentary tract is telescoped into an adjacent segment Most common cause of intestinal obstruction between 3months-6y/o; M>F Unknown cause in most cases Correlation with adenovirus Most often ileocolic and ileoileocolic How? o Upper portion of bowel intussusception invaginates into the lower part (intussuscipiens) dragging its mesentery along with it into the enveloping loop o Mesentery constricts and obstructs venous return o Intussusceptum engorges o Edema and bleeding from the mucosa leads to bloody stool Severe paroxysmal colicky pain that recurs at frequent intervals with straining efforts; legs and knees are flexed with loud cryings If not reduced  shock-like state 60% of infants pass currant jelly stools Palpation of abdomen: Slightly tender sausageshaped mass in the RUQ which may increase in size and firmness during the paroxysm of pain Plain abdominal x-ray: (+) density

Barium enema: Filling defect or cupping in the head of barium coiled-spring sign (thin rim of barium trapped around the invaginating part within the intussuscepiens) Ultrasound: Tubular mass and a doughnut or target appearance Treatment: Reduction of an acute intussusception in an emergency procedure Success for x-ray reduction is 50% if symptoms are present > 48 hours and 70-9-% if reduction is done within the 1st 48hours Resection with end-to-end anastomosis is done if manual operative reduction fails Hydrostatic reduction vs air enema

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In God we trust

Babae - Baka magbunga ang pagkakasala natin, Padre. Natatakot ako... Padre - Ipaubaya natin ang lahat sa nasa itaas. Di nya tayo pababayaan. Sakristan - Hoy, huwag nyo akong idamay dyan at naglilinis lang ako ng kampana dito sa itaas!