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Published on: August 23, 2022
[Gastric perforation caused by a lactobezoar in an infant: a case report]
Insights
Lactobezoars, undigested milk masses, cause gastric outlet obstruction in infants. This rare case involved perforation and necrosis, requiring surgery, but conservative management is often successful with early diagnosis.
Area of Science:
- Pediatric Surgery
- Neonatology
- Gastroenterology
Background:
- Lactobezoar, a mass of undigested milk, commonly causes gastric outlet obstruction in infants.
- Risk factors include prematurity, low birth weight, altered gastric function, and specific infant formulas.
Observation:
- A premature female infant presented with shock, food intolerance, abdominal distension, and sepsis.
- Imaging revealed a distended stomach with a heterogeneous mass consistent with a lactobezoar and pneumoperitoneum.
Findings:
- Emergency laparotomy showed gastric perforation and necrosis secondary to a large lactobezoar.
- Surgical treatment involved lactobezoar extraction, partial gastrectomy, and gastrostomy, followed by prolonged sepsis and NPO status.
Implications:
- Early diagnosis of lactobezoar in infants with gastrointestinal obstruction is crucial.
- While surgery is sometimes necessary for complications like perforation, conservative management often leads to good outcomes.
- Understanding etiopathogenic factors can help prevent lactobezoar formation in high-risk infants.
Abstract:
Lactobezoar is a compact mass of undigested milk concretions and mucous secretions in the gastrointestinal tract. It is usually located in the stomach, resulting in various degrees of gastric outlet obstruction. Lactobezoar is the most common type of bezoar in infancy. We report the case of rare and complicated gastric outlet obstruction secondary to lactobezoar. A female infant, 35weeks and 4days' gestation, one of dichorionic, diamniotic twins (birth weight, 1.890kg), was referred to our center at 5days of life for shock and food intolerance. She was on discontinuous oral feedings with a maltodextrin-enriched infant formula. On examination on day 4, there was a tender mass palpable in the left hypochondrium and on day 5, there was abdominal distension with signs of hemodynamic instability and sepsis. Plain abdominal X-ray showed a pneumoperitoneum associated with a heterogeneous mass in a distended stomach, consistent with a bezoar. An emergency laparotomy revealed a gastric perforation secondary to a large lactobezoar, with necrosis of the greater curvature and anterior wall of the stomach. Surgical treatment consisted of extraction of the lactobezoar, partial gastrectomy (resection of necrotic areas), and gastrostomy. Pathological examination confirmed the necrosis of the gastric mucosa. The postoperative course was complicated by prolonged sepsis. The child was kept NPO for 21days. On day 21 postsurgery, an upper gastrointestinal contrast study showed a well-dimensioned stomach, with a good pyloric passage. Gastrostomy and oral feedings were then initiated with good outcome at 6months. Etiopathogenic factors of lactobezoar are prematurity, low birth weight, altered gastric secretions and disturbed gastric emptying, hypercaloric and predominantly casein-based formulas, and inadequate milk composition. Lactobezoar should be considered in infants with symptoms of gastrointestinal obstruction with evocative images. Conservative management with nil per os, parenteral nutrition, and regular saline gastric washes has a good prognosis with rapid resolution of symptoms. Surgical indications are rare, and early and appropriate diagnosis should help limit and reduce the morbidity of lactobezoar.
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