Pyloric stenosis is a narrowing of the pylorus that is not present at birth but develops in infants. It causes non-bilious projectile vomiting after feeding that worsens over time and starts around 3 weeks of age. Diagnosis involves palpating an olive-shaped mass above the umbilicus that is firmer after vomiting. Treatment is pyloromyotomy surgery to cut the pyloric muscle.
Pyloric stenosis is a narrowing of the pylorus that is not present at birth but develops in infants. It causes non-bilious projectile vomiting after feeding that worsens over time and starts around 3 weeks of age. Diagnosis involves palpating an olive-shaped mass above the umbilicus that is firmer after vomiting. Treatment is pyloromyotomy surgery to cut the pyloric muscle.
Pyloric stenosis is a narrowing of the pylorus that is not present at birth but develops in infants. It causes non-bilious projectile vomiting after feeding that worsens over time and starts around 3 weeks of age. Diagnosis involves palpating an olive-shaped mass above the umbilicus that is firmer after vomiting. Treatment is pyloromyotomy surgery to cut the pyloric muscle.
Associated with eosinophilic gastroenteritis, Apert syndrome, Zellweger syndrome, trisomy 18, Smith-Lemli-Opitz syndrome, Cornelia de Lange syndrome. Use of erythromycin with higher risk if given within first 2 weeks of life. Female infants of mothers treated with macrolide antibiotics during pregnancy and breastfeeding. Abnormal muscle innervation, elevated serum levels of prostaglandins, infant hypergastrinemia. Symptoms o Non-bilious vomiting – initial symptom. Progressive, occurring immediately after feeding. Emesis might follow each feeding or intermittent. Usually stars after 3 weeks of age. (1 week – 5 months). o Hyperbilirubinemia – unconjugated more than conjugated. Diagnosis o Palpating the pyloric mass. Mass is firm, movable, about 2 cm in length, olive shaped, hard, best palpated from left side and located above and right of umbilicus in mid epigastrium beneath liver’s edge. Best palpated after vomiting. o Presence of gastric peristaltic wave after eating. o Ultrasound – confirms. DDX o Gastroesophageal reflux with or without hiatal hernia. Differentiated by radiology. o Adrenal insufficiency from adrenogenital syndrome. Rule out: absence of metabolic acidosis and elevated serum potassium and urinary sodium. o Inborn errors of metabolism – includes emesis with alkalosis or acidosis and lethargy, coma, seizures. o Vomiting + diarrhea = gastroenteritis but some may have in pyloric stenosis. Treatment o Preoperative: Correcting fluid, acid-base, electrolyte losses. Correction of alkalosis to prevent postoperative apnea associated with anesthesia. Most infants need 24 hours. o Surgery: pyloromyotomy Ramstedt procedure done through short transverse skin incision. Underlying pyloric mass cut and incision closed. o Postoperative: Vomiting – half the infants. Initiate feeding within 12-24 hrs after surgery. Maintenance feeding 36-48 hours after. Atropine IV 0.01 mg/kg 6x/day 5 min before feeding. o Monitor HR by ECG. Oral feeding started at 10 mL formula 6x/day. Gradual increase until patient can tolerate 150 mL/kg/day unless vomiting occurs more than twice a day. Once patient can eat 150 mL/kg/day without vomiting, give atropine 0.02 mg/kg orally 6x/day before feeding. Persistent vomiting = incomplete pyloromyotomy, gastritis, gastroesophageal reflux disease, some other obstruction. Do endoscopic balloon dilation for incomplete pyloromyotomy. o Conservative management with nasoduodenal feedings who are not good for surgery. o Oral and intravenous atropine sulfate (pyloric muscle relaxant). Pyloric Atresia Symptoms o Nonbilious vomiting o Feeding difficulties o Abdominal distension during first day of life. o Gastric aspirate at birth is large (> 20 mL) – remove to prevent aspiration. o Rupture of stomach may occur as early as first 12 hours of life. Polyhydramnios + low birth weight. Diagnosis o Finding of large, dilated stomach on abdominal plain radiograph or in utero ultrasonography. o UGI contrast Avoid aspiration o Older children (endoscopy) Treatment o All gastric outlet obstruction in neonates start with correction of dehydration and hypochloremic alkalosis. o Persistent vomiting relieved with nasogastric decompression. o Surgical or endoscopic repair only when patient stable. Intestinal atresia, stenosis, malrotation Obstruction may be partial or complete and simple or strangulating. Intrinsic causes o Inherent abnormalities of intestinal innervation o Mucus production o Tubular anatomy (most common and manifest as obliteration or narrowing of intestinal lumen) Extrinsic o Compression of bowel by vessels, organs, cysts o Abnormalities in intestinal rotation during fetal development. Symptoms o Bowel distension – accumulation of food, gas, intestinal secretions proximal to point of obstruction. o Absorption of intestinal decreased, secretion of fluid and electrolytes increased – hypokalemia o Less blood flow – lack of mucosal integrity – bacterial proliferation (coliforms, anaerobes). Bacteria can travel – endotoxemia, bacteremia, sepsis. o High intestine obstruction: Large volume, frequent, bilious emesis with little/no abdominal distension. Intermittent pain relieved by vomiting. o Distal bowel small obstruction Moderate or marked abdominal distension with emesis that is progressively feculent. o Both have obstipation. Diagnosis o History, PE, radiology. o Polyhydramnios – high intestinal obstruction. o Radiology – contrast studies or CT because neonate colonic haustra not fully developed. Treatment o Initial for children and infants – fluid resuscitation and stabilization. o Nasogastric decompression – for pain and vomiting. o Broad spectrum antibiotics for ill looking neonates o No improvement in 12-24 hours, operation.