Case 4: Gastric pneumatosis in an eight-month-old girl

An eight-month-old girl with Down syndrome presented to the emergency department with a two-month history of twice-daily ‘spit-ups’ with recent progression. Following the ingestion of an egg yolk on the day before admission, the infant experienced six postprandial ‘spit-up’ episodes involving nonbilious, nonprojectile regurgitation of formula or breast milk after most feeds. On the morning of admission, the child experienced three additional episodes. Medical attention was sought due to the increased frequency of these episodes. The patient's stool was described as small and somewhat hard; there was no history of diarrhea. Urine output was adequate, the patient was afebrile and there were no respiratory symptoms. On examination, vital signs were stable, and there was an appropriate interval weight increase compared with the infant's most recent primary care appointment. Abdominal examination was unremarkable and the infant was not in distress. She was found to be dehydrated, and was treated with intravenous fluids and ondansetron. Nasogastric decompression yielded approximately 135 mL of fluid from her stomach. Initial blood work was concerning, showing evidence of metabolic alkalosis, hyponatremia and hypokalemia (Na+ level 122 mmol/L, K+ level 2.6 mmol/L, Cl− level 67 mmol/L). The infant required significant fluid resuscitation for hydration and correction of the metabolic alkalosis. An abdominal x-ray was abnormal, showing gastric intramural air (Figure 1). Anteroposterior (AP) supine abdominal x-ray was abnormal, showing gastric distention with significant gastric pneumatosis circumscribing both the lesser and greater curvature, and the pylorus. Arrows indicate locations of most prominent pneumatosis Following initial resuscitation, a computed tomography scan of the abdomen with contrast confirmed gastric intramural air and showed evidence of partial distal duodenal obstruction (Figure 2). Referral from the community to a tertiary-level surgical facility resulted in operative intervention for partial duodenal obstruction secondary to duodenal stenosis. Follow-up x-ray demonstrated resolution of gastric pneumatosis. Abdominal computed tomography scan showing marked gastric and duodenal distension associated with significant gastric intramural air, and notable pneumatosis of the duodenal wall. In contrast, the jejunum is of normal diameter Isolated gastric pneumatosis – or air in the wall of the stomach – is an exceedingly rare finding that was first described by Brouardel in 1895 (1). This condition has been described in both adult and paediatric populations. It can be divided into two categories: emphysematous gastritis and gastric pneumatosis. In infants, the term ‘emphysematous gastritis’ is typically used to describe conditions caused by inflammation, infection or ischemia, such as necrotizing enterocolitis, whereas the term ‘gastric pneumatosis’ describes conditions involving gastroduodenal obstruction such as pyloric stenosis, malrotation and duodenal atresia (2,3). The terms ‘gastric pneumatosis’, ‘gastric emphysema’ and ‘nongangrenous gastric pneumatosis’ are used synonymously (4). Only 35 cases of gastric pneumatosis have been described in the literature in infants, and only five of these involved duodenal obstruction (2,4–7). Several theories attempt to describe the pathogenesis of gastric pneumatosis – the bacterial theory, mucosal integrity theory, mechanical damage theory, and cardiopulmonary disease theory (1,8). The mechanical damage theory is the most common theory regarding the pathophysiology of gastric pneumatosis in infancy. It involves proximal gastrointestinal obstruction, typically at the pylorus or duodenum, leading to gastric dilation and elevated gastric pressure. Chronically elevated gastric pressure accompanied by emesis causing transient pressure peaks leads to gastric mucosal tears, allowing air to dissect into the submucosal space (1,4,7). Patients with gastric pneumatosis secondary to proximal gastroduodenal obstructions, such as pyloric stenosis, present classically with projectile, nonbilious emesis and metabolic alkalosis. However, there is no pathognomonic constellation of symptoms among patients with more distal gastroduodenal obstructions (duodenal stenosis, atresia or web) (5). As was the case in our clinical scenario, the presentation of duodenal obstruction is often nonspecific but may mimic pyloric stenosis in some respects (2,4,7). Gastric pneumatosis and emphysematous gastritis are often indistinguishable on plain film x-ray. Radiographically, gastric pneumatosis may appear linear, cystic or as small, clustered bubbles (3,9). While the cystic distribution is often associated with proximal gastrointestinal obstruction, the present case involved a linear air distribution, emphasizing that intramural air patterns cannot be considered to be specific to any particular pathology (3). Given the prognostic consequences of misdiagnosis, it is imperative that the clinician navigate the differential diagnosis using the clinical picture in combination with radiographic evidence (10). Following a diagnosis of gastric pneumatosis secondary to distal duodenal stenosis, successful management in this case involved correction of electrolyte disturbances and fluid imbalance, gastric decompression, and subsequent surgical correction of the duodenal obstruction. A recurring theme among similar cases in the literature suggests that gastric decompression with correction of the underlying pathology comprises a reasonable management strategy for gastric pneumatosis (2,4–7). This is consistent with the mechanical damage theory. Gastric pneumatosis in infants is a rare sign of several pathologies including proximal gastrointestinal obstruction and necrotizing enterocolitis. Clinicians must use the clinical picture, in combination with radiographic evidence, to distinguish between gastric emphysema and emphysematous gastritis because there are significant prognostic differences among these pathologies. Chronic emesis in trisomy 21 (bilious or not) may indicate partial duodenal obstruction. The authors thank the patient's family for their permission to share this case, Dr D'Arcy Little for providing the x-ray image and its interpretation, and Dr John Atkins for providing the computed tomography image and its interpretation.

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