Review

First described by Duplay in 1833, acute gastric dilatation is a rare but rapidly progressive and fatal condition.^1–3 It is most commonly reported as a postoperative complication. Additional etiologies include anorexia nervosa, bulimia, trauma, volvulus, medications, electrolyte abnormalities, debilitating chronic illnesses, diabetes mellitus, acute infections, diaphragmatic herniations, psychogenic polyphagia, emotional stress, the cast syndrome, and spinal deformities. Gul and associates present a case of acute gastric dilatation in a patient with multiple vertebral fractures following a fall.⁴ Possible inciting events in this case include the vertebral factures, electrolyte abnormalities (hypokalemia, hypophosphatemia), and medications (narcotics).^1–3,5–7

There are several theories regarding the pathophysiology of acute gastric dilatation. In 1842, Karl Freiherr von Rokitansky first described superior mesenteric artery syndrome in which acute gastric dilatation followed duodenal obstruction secondary to the superior mesenteric artery as it branched from the aorta.¹ Additional theories of the pathophysiology of acute gastric dilatation include the atonic theory secondary to reflex inhibition of the gastric motor nerves; relaxation of the upper esophageal sphincter predisposed by debilitation and anesthesia; proximal gastrointestinal tract atony secondary to electrolyte disturbances; unopposed parasympathetic activity secondary to spinal cord injuries; smooth muscle degeneration of the stomach as witnessed in Duchenne muscular dystrophy; diabetic autonomic neuropathy; and gastric dysmotility following sepsis.^{1–3,6,8–14}

Clinically, the patient described by Gul and associates presented with emesis and abdominal pain.⁴ Emesis is a symptom in more than 90% of acute gastric dilatation cases.² However, the accompanying abdominal pain may be deceptively mild initially.^3,5 As the authors note, the abdominal pain is often progressive in nature, initially localized to the epigastrium and becoming more generalized as the condition progresses.¹⁵

On physical examination, percussion will result in a tympanitic note over much of the abdomen and a succession splash may be elicited.^2,3 Plain abdominal radiographs often demonstrate a markedly distended stomach, as evidenced by the patient in the case reported by Gul and coworkers.^2,4,5 A fluid level may also be appreciated. If gastric perforation has occurred, both subcutaneous emphysema and pneumoperitoneum may be found. Another diagnostic modality to consider is computed tomography. Further findings may include hypovolemia, respiratory compromise, metabolic alkalosis, and oliguria.^2,5,7

The initial therapy for acute gastric dilatation consists of nasogastric decompression and fluid resuscitation similar to that provided in the case reported by Gul and coworkers.^1,3,4,7 If these measures fail, or gastric infarction or perforation is suspected, immediate surgical intervention is required.⁷ Early recognition is essential, as there is an 80% mortality rate when operative treatment is delayed.^3,5 Critical to surgical therapy is the adequate resection of the gangrenous portion of the stomach. Surgical options include total gastrectomy with esophagojejunostomy if the patient's condition permits or gastrectomy with cervical esophagostomy in the case of peritonitis. In either case, feeding jejunostomy should be performed.⁵ Due to the early nonoperative interventions of the authors in this case, surgery was not necessary. In the direst of circumstances, damage control surgery should be considered. The surgical mortality rate is 50–65%. Without intervention, the mortality rate is 100%.

In conclusion, Gul and colleagues present a case of acute gastric dilatation 4 weeks after a fall with resultant vertebral fractures.⁴ In this case, as in those previously published, the exact etiology is uncertain and, most likely, multifactorial. The authors' expeditious management prevented any of the more grave complications of acute gastric dilatation (ie, gastric necrosis, gastric perforation). As such, this case demonstrates the need for a high index of suspicion for acute gastric dilatation.