A 34-year-old woman presented at our hospital with abdominal distention due to overeating. Acute gastric dilatation was diagnosed. The patient was hospitalized, and nasogastric decompression was initiated. On hospitalization day 3, she developed shock, and her respiratory state deteriorated, requiring intubation and mechanical ventilation. Nasogastric decompression contributed to the improvement in her clinical condition. She was discharged 3 mo after admission. During outpatient follow-up, her dietary intake decreased, and her body weight gradually decreased by 14 kg. An upper gastrointestinal series and endoscopy revealed pyloric stenosis; therefore, we performed gastrojejunostomy 18 mo after her initial admission. The patient was discharged from the hospital with no postoperative complications. Gastric necrosis and perforation due to overeating-induced gastric dilatation are life-threatening conditions. Surgical intervention may be required if delayed pyloric stenosis occurs after conservative treatment. We report a case of pyloric stenosis due to overeating-induced gastric dilatation treated by gastrojejunostomy 18 mo after the initial presentation.

Although gastric necrosis or perforation following gastric dilatation is unusual because of the rich blood supply to the stomach, the occurrence of these conditions may be life-threatening. We report our experience with a patient who underwent gastrojejunostomy for pyloric stenosis after presenting with acute gastric dilatation due to overeating. Furthermore, we discuss the recent literature available on the subject.

A 34-year-old woman ate an overly large meal of curry, rice, and potatoes. She gradually developed abdominal distention for which she sought medical attention. The general physician decided on an expectant approach. However, she presented at our hospital because her symptoms did not improve. This patient had a history of episodes of bulimic binging, but she had failed to self-induce vomiting this time.

Physical examination at presentation revealed a blood pressure of 117/68 mmHg, a pulse rate of 100 beats/min, and a body temperature of 36.7 °C. Her abdomen was distended, but there were no signs of peritoneal irritation. The significant laboratory test results were as follows: white blood cell count, 16700 cells/μL; C-reactive protein, 2.33 mg/dL; amylase, 1190 IU/L; serum creatinine phosphokinase, 4007 IU/L; blood urea nitrogen (BUN), 15.2 mg/dL; and creatinine, 2.33 mg/dL. Abdominal computed tomography scans revealed a massive dilation of the stomach reaching the pelvis but with no ascites or free air (Figure 1). We made a diagnosis of acute gastric dilatation due to overeating without gastric perforation or necrosis.

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Figure 1 Computed tomography on initial admission. A. Upper abdomen B. Pelvis.

A nasogastric tube was inserted, and decompression and irrigation were initiated. On post-hospitalization day 3, the patient developed shock, and her respiratory state worsened. We then performed intubation and initiated mechanical ventilation. The inferior vena cava and diaphragm were compressed by her remarkably distended stomach. Further, decreased venous return and ventilatory impairment aggravated her condition. Although we considered emergency surgery, her general condition promptly improved after fluid resuscitation and respiratory care. Therefore, we continued conservative treatment. Seven days after intubation, we performed a tracheotomy. Her respiratory state gradually improved, and she was extubated 3 wk after intubation. The abdominal distention gradually improved by decompression. Thereafter, upper gastrointestinal (UGI) endoscopy and an UGI series were performed. The UGI endoscopy showed mucosal deciduation at the pyloric antrum (Figure 2A), but the UGI series showed no leakage and good passage of the contrast medium (Figure 3A). Thus, there was no evidence of pyloric stenosis. Tube feeding was initiated on hospitalization day 30 and continued until she was able to eat rice gruel. Three months after admission, she was discharged from our hospital.

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Figure 2 Gastrointestinal endoscopy revealed pyloric stenosis. A: One month after admission, gastrointestinal endoscopy revealed mucosal deciduation at the pyloric antrum, but there were no findings of pyloric stenosis; B: One year after discharge, gastrointestinal endoscopy revealed progressive pyloric stenosis.

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Figure 3 Gastrointestinal series showed pyloric stenosis. A: Two months after admission, an upper gastrointestinal series showed no leakage and a good passage of contrast medium; B: One year after discharge, a follow-up gastrointestinal series showed advanced pyloric stenosis.

While our patient was followed-up as an outpatient, her dietary intake gradually decreased. Although we recommended surgical treatment for her several times during the course of an outpatient, she rejected surgical treatment. Ultimately, she lost 14 kg from her original weight on admission. At present, her height and weight are 160 cm and 40 kg, respectively. However, because the UGI series and endoscopy revealed pyloric stenosis (Figures 2B and 3B), we performed Roux-en-Y gastrojejunostomy 18 mo after the first admission, with her consent. The postoperative course was uneventful, and she was discharged from our hospital 3 wk after surgery. The passage of contrast medium during the postoperative UGI series indicated that the anastomosis was accurate (Figure 4). At two years after surgery, the patient had gained 20 kg.

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Figure 4 A postoperative gastrointestinal series showed improvement in the contrast medium passage through the stomach and intestine.

Acute gastric dilatation is a medical condition in which the stomach becomes progressively hypotonic and overstretched despite the absence of mechanical obstruction[1]. This condition can be caused by overeating, postoperative ileus, child birth, chronic debilitating affection, central nervous system damage, severe infection, and trauma[2]. Among these causes, acute gastric dilatation due to overeating is more common in females with underlying eating disorders, such as anorexia nervosa[3]. The rich collateral blood flow of the stomach generally protects the gastric wall from ischemia; gastric necrosis or perforation following gastric dilatation is unusual. However, a remarkable increase in the intragastric pressure by massive gastric dilatation can decrease the intramural blood flow, resulting in possible gastric necrosis or perforation[4]. Immediate nasogastric decompression and sufficient fluid resuscitation are necessary for the treatment of acute gastric dilatation[5]. These procedures can decrease the intragastric pressure and reduce the risk of necrosis and perforation; therefore, they should be implemented as early as possible. If gastric necrosis or perforation is suspected or if draining the gastric contents is difficult, immediate surgical intervention is required. Resection of the necrotic portion of the stomach is required in some cases, and total gastrectomy is required in others.

In our case, the pyloric stenosis progressed more than a year after initial treatment. The partial necrosis of the gastric wall may have been caused by acute gastric dilatation because the serum creatinine-phosphokinase level increased at onset. We promptly performed nasogastric decompression, which may have prevented complete gastric necrosis and perforation. Because of the increase in the intragastric pressure caused by massive gastric dilatation, the intramural blood flow decreased, resulting in partial necrosis of the gastric mucosa and muscle scarring due to fibrosis. Together, these regenerative processes can lead to pyloric stenosis. In this case, acute gastric dilatation occurred only once. However, the dilatation of the stomach was severe, and it took approximately one month to drain the gastric contents completely. Therefore, delayed pyloric stenosis might have occurred.

From a literature search of the PubMed database between l966 and 2013, in addition to our patient, we retrieved 25 cases of acute gastric dilatation due to overeating (Table 1). The mean age of these patients was 22.7 (range, 4-48) years, indicating a greater frequency among young patients. There were more female patients than males (n = 20 and 5 patients, respectively, with the gender of one patient being unknown). Eighteen patients had underlying eating disorders, such as anorexia or bulimia nervosa. Sixteen patients underwent laparotomy, three of whom underwent total gastrectomy. In contrast, eight patients were treated by nasogastric decompression alone. Eleven patients underwent emergency surgery: three within several hours and one within several days. In most cases, emergency or semi-emergency surgery was performed. To the best of our knowledge, our patient was the first to undergo surgery more than a year after initial treatment. According to our literature search, six patients died despite immediate treatment, including surgical intervention. Despite the many reports of young patients, some patients died shortly after surgery or the onset of symptoms. Therefore, gastric perforation following acute gastric dilatation may be more severe than usually considered.

In conclusion, although acute gastric dilatation due to overeating is rare, physicians should be aware of its potential complications, such as gastric necrosis or perforation. Moreover, if conservative treatment is preferred over surgery, physicians should be aware of the possibility of delayed pyloric stenosis.