Differential Diagnosis

The approach to evaluation of persistent emesis in an infant begins with classification of the emesis as bilious or nonbilious. Causes of nonbilious emesis with or without failure to thrive include pyloric stenosis, duodenal atresia, gastroesophageal reflux, formula intolerance, intestinal malrotation, gastric or intestinal bezoar, gastroenteritis, and obstructing abdominal (intraintestinal or extraintestinal) mass or malignancy. We consider causes of bilious emesis especially in cases where the history obtained may be unreliable, as these can have fatal consequences. Intestinal malrotation with bowel obstruction was also considered in our patient because this can cause nonbilious emesis if the obstruction is proximal to the bile duct. Bloody emesis may point to esophagitis, gastritis, or trauma to the upper gastrointestinal mucosa, and projectile vomiting is classic for pyloric stenosis.

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Actual Diagnosis

The patient underwent fluoroscopic barium esophagography, which showed a large filling defect in the gastric antrum from which thick fluid was aspirated, suggestive of a gastric lacto-bezoar (GLB). Notably, this was not visualized on initial pyloric ultrasonography. Pyloric narrowing was not seen on the esophagogram because the gastric outlet was completely obstructed by the bezoar, and no contrast passed beyond the bezoar. Repeated pyloric ultrasonography 2 days later, however, performed due to persistent vomiting, demonstrated pyloric stenosis.

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The Condition

A bezoar represents an agglomeration of material in the gastrointestinal tract and can be classified by the makeup of its contents.  Lacto-bezoars are made of undigested milk products and mucus and are the most common type of bezoar found in infants.  First described in 1959 by Wolf and Bruce, lacto-bezoars occur almost exclusively in infants, with most cases documented in the first month after birth.  They are most often found in the stomach, with rare reports in the small bowel found in the literature. Originally thought to be limited to premature infants taking calorically dense formula, GLBs have been described in term infants and toddlers as well, although most reported cases (76%) occur in premature infants. Overwhelmingly, abdominal distention and vomiting are the most common reported and presenting symptoms. Dehydration (i.e., from vomiting) is a presenting symptom in up to 25% of patients and is thought to lead to more water absorption from the gastrointestinal tract, which can facilitate consolidation of gastric contents and bezoar formation. Vomiting and dehydration can lead to electrolyte derangements, which must be considered in any patient presenting with GLBs. Other pathogenic factors for GLB formation that were not seen in our patient include prematurity and/or low birthweight (due to reduced production of gastric acid and pepsin), use of casein-predominant or medium-chain triglyceride-rich formulas, and certain medications that antagonize gastric secretion or motility, such as atropine, sucralfate, and aluminum hydroxide.  Diagnosis requires a high degree of clinical suspicion but is confirmed with a thorough dietary history and is supported by imaging. Abdominal radiography, ultrasonography, or upper gastrointestinal contrast study might show a round gastric mass surrounded by air or fluid, evidence of intra-bezoar air trapping, or a gastric filling defect with minimal forward flow, respectively.  The prognosis of GLBs is generally very good if the diagnosis is made in a timely manner; if delayed, progressive distention can lead to gastric perforation and mortality.

 

Treatment and Management

In a large analysis of 96 patients with GLBs, conservative management with intravenous fluids, holding enteral feeds, and in some cases gastric lavage led to resolution of GLBs in 85%. Gastric decompression with a nasogastric tube can lessen discomfort if there is pronounced distention. If enteral feeds are continued, calorie reduction can be beneficial to avoid overconcentration of formula. Parenteral feeds can also be used for nutritional support. In cases in which conservative management fails to produce improvement or more aggressive therapy is preferred as first-line, N-acetylcysteine has been used successfully for the disintegration of GLBs in toddlers and newborns in a few reports. N-acetylcysteine is a mucolytic that functions to break disulfide bonds in mucus, lessening its viscosity. This permits dissolution of the GLB and aspiration of contents through an nasogastric tube.

Surgical intervention may be indicated when pneumoperitoneum is identified, a GLB fails to resolve within 72 hours given conservative management and/or mucolytic treatment is not available (or the patient cannot tolerate it), or an acute abdomen develops.

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Patient Course

Our patient received additional normal saline boluses and was started on dextrose-containing intravenous fluids. Her hypokalemia and hypochloremia were corrected with potassium chloride via IV bolus and maintenance fluid. Electrocardiography showed no abnormalities.

On hospital day 2, N-acetylcysteine infusions of 10 mg/kg via nasogastric tube every 6 hours for eight total doses was given. On hospital day 3 gastric aspirate was negative for milk products and N-acetylcysteine was discontinued. Pyloric ultrasound the same day revealed pyloric stenosis and the patient underwent converted open pyloromyotomy on the fourth day of admission without complication. Of note, outpatient pyloric ultrasonography as well as pyloric ultrasonography on hospital day 1 had not shown pyloric stenosis; it is difficult to say whether the GLB contributed to the formation of the pyloric stenosis or vice versa because both could be plausible. She received 4 days of TPN until oral feeding was optimized; on hospital day 7 she was tolerating oral feeds of 30 to 60 mL of a 22-kcal formula every 3 hours without emesis. During her stay she achieved an average weight gain of 42 g per day. She was discharged in good condition after 9 days.

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