A chest x-ray should be obtained to rule out aspiration and toinspect for mediastinal air. The child should be admitted to the hospital and given intravenous (IV) fluids until endoscopy. Thetrue extent of burns may not be endoscopically apparent immediately, but delayed endoscopy can increase the risk of perforation. Most endoscopists perform the initial endoscopy soonafter injury, when the patient has been stabilized. The extent ofinjury and severity of the burn should be carefully determined.Risk of subsequent esophageal strictures is related to the degreeof burn and whether the injury is circumferential.
A nasogastric tube can be placed over a guidewire at the timeof the initial endoscopy to provide a route for feeding and to stent the esophagus. Systemic steroid use has not beenfound to be beneficial in reducing stricture formation. Broad-spectrum antibiotics should be prescribed if infection is suspected.
Esophageal strictures, if they occur, usually develop within 1 to 2 months and can be treated with endoscopic dilation. There is a risk of perforation during dilation. Whenesophageal destruction is severe, surgical reconstructionof the esophagus using stomach or intestine may be necessary.
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Pyloric stenosis is an acquired condition caused by hypertrophy and spasm of the pyloric muscle, resulting in gastric outlet obstruction. It occurs in 6 to 8 per 1000 live births, has a 5-to-1 male predominance, and is more common in first-born children. Its cause is unknown.
Infants with pyloric stenosis typically begin vomitingduring the first weeks of life, but onset may be delayed.The emesis becomes increasingly frequent and forceful astime passes. Vomiting differs from spitting up because ofits extremely forceful and often projectile nature. The vomited material never contains bile, because the gastric outlet obstruction is proximal to the duodenum. This featuredifferentiates pyloric stenosis from most other obstructivelesions of early childhood. Affected infants are ravenouslyhungry early in the course of the illness, but become morelethargic with increasing malnutrition and dehydration.The stomach becomes massively enlarged with retainedfood and secretions, and gastric peristaltic waves are often visible in the left upper quadrant. A hypertrophied pylorus (the “olive”) may be palpated. As the illness progresses,very little of each feeding is able to pass through the pylorus, and the child becomes progressively thinner and moredehydrated.
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Repetitive vomiting of purely gastric contents results inloss of hydrochloric acid; the classic laboratory finding is a hypochloremic, hypokalemic metabolic alkalosis with elevated blood urea nitrogen (BUN) secondary to dehydration. Jaundice with unconjugated hyperbilirubinemia may also occur. Plain abdominal x-rays typically show a huge stomach and diminished or absent gas in the intestine(Fig. 128-4). Ultrasound examination shows marked elongation and thickening of the pylorus (Fig. 128-5). A bariumupper GI series also may be obtained whenever doubt aboutthe diagnosis exists; this shows a “string sign” caused bybarium moving through an elongated, constricted pyloricchannel.
Figure 128-4 Pyloric stenosis. Note the huge, gas-filled stomach extending across the midline, with minimal air in the intestine down-stream. (Courtesy Warren Bishop, MD.)
Figure 128-5 Ultrasound image of infant with pyloric steno-sis. Large, fluid-filled stomach (S) is seen at right, with an elongated, thickened pylorus. The length of the pylorus is marked by the red arrows; the wall thickness is marked by the yellow arrows.
Drugs NSAIDs, including aspirin Tobacco use Bisphosphonates Potassium supplements