![]() In 1885, Revilloid demonstrated that the stomach had to be distended with at least 4 L of fluid before perforation occurred. Although it may be caused by traumatic or obstructive causes, it can also occur in association with gastric distention. It occurs when gas within the gastric lumen is forced into the gastric wall through a mucosal breach. Gastric emphysema is a sign of ischemia and necrosis, seen radiographically as submucosal lucent streaks. In experimental canine models, both venous and arterial occlusion were necessary to produce gastric infarction. Despite the stomach’s rich collateral blood supply, when intra-gastric pressure exceeds the gastric venous pressure (usually greater than 20–30 cm H 2O), intramural blood flow is impaired, resulting in ischemia and necrosis of the stomach wall. An NGT for decompression was never placed and an autopsy was not performed.Ĭomplications such as ischemia and perforation develop when recognition and treatment of AGD are delayed. The patient eventually suffered a cardiac arrest as a likely consequence of septic shock and was unable to be revived. He was subsequently started on vasopressors for hemodynamic instability. Hospital course was complicated by the development of pneumonia and respiratory failure requiring intubation. He was planned for an upper endoscopy, however, his conditioned deteriorated. A follow-up CT of the abdomen confirmed the finding, with no mechanical cause of obstruction identified. He underwent an AXR which showed marked distention of the stomach (Fig. He was started on IV insulin for the treatment of hyperosmolar hyperglycemic state and IV antibiotics for his foot ulcer, cultures of which grew Staphylococcus aureus. Initial labs were significant for hyperglycemia (649 mg/dL), a blood pH of 7.29, a normal anion gap, and leukocytosis (16.2 K/μL). He was a former polysubstance user and had no known drug allergies. Past surgical history was notable for a right foot debridement for osteomyelitis. His comorbidities included diabetes mellitus and chronic hepatitis C. Cardiopulmonary exam was within normal limits. On examination, his abdomen was distended with decreased bowel sounds and he was noted to have a left lower extremity infected diabetic foot ulcer. On presentation, he was hypothermic (94.5☏) but otherwise hemodynamically stable. The patient was unable to provide a history, however, accompanying family members reported periods of confusion and falls for the past 1 day. He was monitored in the intensive care unit, and over the next few days his DKA resolved, he was extubated and eventually discharged home.Ī 59-year-old male was brought to our institute by emergency services for altered mental status and a “very high” blood sugar reading. ![]() Upper endoscopy was contemplated but deferred due to the resolution of dilatation. A repeat AXR 4 hours later revealed resolution of gastric dilatation, which was confirmed by a CT scan of the abdomen. An NGT was passed which drained over 500 mL of gastric content. An AXR revealed acute gaseous distention of the stomach (Fig. He was started on intravenous (IV) insulin for the treatment of DKA and IV epinephrine for hemodynamic shock. Initial lab data revealed a blood glucose of 1,155 mg/dL and a pH of 6.97 with an elevated anion gap. On examination, his abdomen was notably distended and bowel sounds were sluggish. He denied the use of tobacco, alcohol, or illicit drugs and had no known drug allergies. His surgical history was significant for a right foot trans-metatarsal amputation. He denied any prior symptoms of delayed gastric emptying, such as nausea, postprandial fullness, or early satiety. His comorbidities included type 1 diabetes and end-stage renal disease. He was noted to be lethargic, hypotensive (76/49 mm Hg), and hypoxic (SaO 2 88%) on presentation and was emergently intubated for airway protection. A 30-year-old male presented to our institute with complaints of nausea, vomiting, decreased oral intake, and diffuse abdominal pain for the past 3 days.
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