bubble_chart Overview

Acute gastric dilatation refers to a syndrome caused by the rapid accumulation of a large amount of gas and fluid in the abdominal mass, leading to significant distension of the stomach and the upper segment of the duodenum. It is typically a severe complication of certain medical or surgical conditions, or anesthesia and surgery.

bubble_chart Etiology

Both organic diseases and functional factors can lead to acute gastric dilatation, with common causes summarized into three categories:

(1) Surgical Procedures Trauma, anesthesia, and surgical operations—especially those involving the abdominal or pelvic cavities, as well as vagotomy—can directly stimulate somatic or visceral nerves, disrupting the autonomic nervous function of the stomach and causing reflexive inhibition of the gastric wall. This results in relaxation of gastric smooth muscles, leading to dilatation. Anesthesia, endotracheal intubation, postoperative oxygen administration, and nasogastric tube feeding can also introduce large amounts of gas into the stomach, contributing to dilatation.

(2) Disease Conditions Gastric volvulus, incarcerated hiatal hernia, duodenal stasis due to various causes, duodenal tumors, and foreign bodies can all lead to gastric retention and acute gastric dilatation. Pathologies near the pylorus, such as spinal deformities, annular pancreas, or pancreatic cancer, may occasionally compress the gastric outlet, causing acute dilatation. The so-called "cast syndrome," occurring 1–2 days after upper body cast application, may result from excessive spinal extension and compression of the duodenum by the mesenteric artery. Emotional stress, depression, and malnutrition can disrupt autonomic nervous function, reducing gastric tone and delaying emptying. Diabetic neuropathy, the use of anticholinergic drugs, fluid and electrolyte imbalances, and severe infections (e.g., sepsis) can also impair gastric tone and emptying, leading to acute dilatation.

(3) Various External Stressors Particularly upper abdominal contusions or severe multiple traumas, the occurrence of which is related to intense stimulation of the celiac plexus.

Overeating within a short period is also an occasional cause.

When gastric dilatation reaches a certain degree, the muscle tone of the gastric wall weakens, forming acute angles at the esophagogastric and gastroduodenal junctions, obstructing gastric emptying. The distended stomach can compress the duodenum, pushing the mesentery and small intestine into the pelvis. Consequently, traction on the mesenteric artery compresses the duodenum, causing obstruction distal to the pylorus. Excessive secretion of saliva, gastroduodenal fluid, pancreatic juice, and intestinal fluid can accumulate large volumes of fluid in the stomach, worsening dilatation. The dilated stomach may also mechanically compress the portal vein, causing blood stasis in abdominal organs, or compress the inferior vena cava, reducing venous return to the heart, ultimately leading to peripheral circulatory failure. Severe vomiting, fasting, and gastrointestinal decompression drainage can result in fluid and electrolyte imbalances.

bubble_chart Clinical Manifestations

Most cases have an insidious onset, and those who undergo vagotomy often develop symptoms around the second week postoperatively after starting a liquid diet. The main symptoms include abdominal distension and fullness, dull pain in the upper abdomen or periumbilical region, nausea, and persistent vomiting. The vomitus is a turbid brownish-green or coffee bean-colored liquid, and symptoms do not improve after vomiting. As the condition worsens, the general health progressively deteriorates. In severe cases, dehydration and alkalosis may occur, accompanied by dysphoria, restlessness, rapid breathing, hand and foot spasms, hypotension, and shock. A prominent sign is upper abdominal distension, with visible gastric outlines lacking peristalsis, localized tenderness, hyperresonance on percussion, and a splashing sound. A localized mass may appear above and to the right of the umbilicus, appearing raised, smooth, elastic, and mildly tender upon palpation, with a relatively clear lower right border. This is the severely dilated gastric antrum, termed "giant gastric antrum syndrome," a distinctive and crucial sign of acute gastric dilation that serves as strong clinical evidence for diagnosis.

The disease may lead to acute gastric perforation and acute peritonitis due to gastric wall necrosis.

Laboratory tests may reveal hemoconcentration, hypokalemia, hypochloremia, and alkalosis. An upright abdominal X-ray may show a large fluid level in the left upper abdomen, an oversized gastric shadow filling the abdominal cavity, and elevation of the left diaphragm.

bubble_chart Diagnosis

Based on medical history and signs, combined with laboratory tests and abdominal X-ray findings, the diagnosis is generally not difficult. Postoperative gastric dilation is often misdiagnosed due to atypical symptoms that are confused with general postoperative gastrointestinal symptoms. Additionally, it should be differentiated from intestinal obstruction and intestinal paralysis. Intestinal obstruction and paralysis mainly affect the small intestine, with abdominal distension and fullness being most prominent in the mid-abdomen. There is no significant accumulation of fluid or gas in the stomach, and emptying the stomach contents does not provide much relief to the patient. Plain X-ray films may show multiple step-like fluid levels.

bubble_chart Treatment Measures

Temporarily fast, place a nasogastric tube for continuous gastrointestinal decompression, and correct dehydration, electrolyte imbalances, and acid-base metabolic disturbances. Hypokalemia is often masked by hemoconcentration and should be noted. If the condition improves after 24 hours, a small amount of liquid can be injected into the nasogastric tube. If there is no retention, small amounts of food can be started. If there is no improvement, surgery should be performed. For cases caused by excessive overeating, cases where the nasogastric tube cannot aspirate gastric residue, or cases with duodenal obstruction or complications, surgical treatment is also necessary. The surgical approach should generally follow the principle of simplicity and effectiveness, such as simple gastrotomy for decompression, gastric repair, or gastrostomy. Gastric wall necrosis often occurs below the cardia and near the gastric fundus. Due to inflammatory edema and thin tissue around the necrotic area, local tissue mobility is poor. For cases with large areas of necrosis, repair or gastrostomy is futile, and partial proximal gastrectomy with gastroesophageal anastomosis is more appropriate.

bubble_chart Prognosis

In modern surgery, the placement of a gastric tube after major abdominal operations, frequent postoperative position changes, and attention to water, electrolyte, and acid-base balance have significantly reduced the incidence and mortality of acute gastric dilatation.