acute gastric dilatation is a rare condition with several possible etiologies , including eating disorders ( e.g. , anorexia nervosa and bulimia ) , postoperative complications following abdominal surgery , electrolyte disturbances , and mechanical obstruction due to a foreign body , tumor , or pyloric stenosis [ 1 - 8 ] . although complications of acute gastric dilatation , such as gastric necrosis or perforation , shock , sepsis , and abdominal compartment syndrome , are very rare , death may result if complications do occur . therefore , early diagnosis and prompt treatment are very important in the management of acute gastric dilatation , particularly since delayed treatment can result in respiratory failure , shock , sepsis , gastric necrosis , or perforation . in rare cases , acute gastric dilatation is caused by decreased gastric motility resulting from bacterial toxins in patients with diabetes mellitus or parkinson s disease who suffer from respiratory infections such as pulmonary tuberculosis or pneumonia . here , we report a case of delayed pneumoperitoneum and acute pulmonary edema caused by acute gastric dilatation in a patient with parkinson s disease . a 78-year - old woman with parkinson s disease , cerebral lacunar infarction , and hyperlipidemia presented to the emergency department of our hospital with a chief complaint of fever and general weakness . the eastern cooperative oncology group performance status for this patient was grade 3 . she had developed a cough with fever 2 days before admission , followed by anorexia , altered mental status , and general weakness . she visited the local medical clinic for treatment , at which time her blood pressure was 70/40 mm hg , and her body temperature was 38.5c . she was immediately transferred to our emergency department for advanced care . in the emergency room , her blood pressure was 90/48 mm hg , pulse rate was 88 beats per minute , respiratory rate was 20 breaths per minute , body temperature was 38.0c , and oxygen saturation was 91% in room air . the initial laboratory evaluation provided the following results : white blood cell count , 8,850 cells / mm ( neutrophils , 90.3% ) ; hemoglobin , 10.2 g / dl ; hematocrit , 30.6% ; platelet count , 18210 cells / mm ; erythrocyte sedimentation rate , 42 mm / hr ; c - reactive protein , 19.41 mg / dl ; blood urea nitrogen , 78.9 mg / dl ; procalcitonin , 3.75 mg / ml ; and creatinine , 2.46 mg / dl . arterial blood gas analysis showed a ph of 7.502 , pco2 of 22 mm hg , po2 of 63.5 mm hg , hco3 of 17.4 mmol / l , and sao2 of 94.5% with oxygen at a rate of 2 l / min via a nasal cannula . a thorax computed tomography ( ct ) scan without contrast revealed pneumonic infiltration in the lower lobe of the left lung ( fig . 1a ) and severe distension of the stomach from the upper abdomen to the pelvis without the presence of free air ( fig . intravenous fluid replacement , intravenous infusion of empirical antibiotics ( 400 mg moxifloxacin and 2 g cefotaxime sodium ) once every 24 hours , vasopressor administration , and oxygen supply via a nasal cannula were initiated . a nasogastric tube was inserted , and 4 l of a dark brown liquid was drained through the tube . after the initial treatment , her vital signs became relatively stable and her mental status improved . an esophagogastroduodenoscopy ( egd ) was performed 24 hours after admission , and the remnant food and liquid material in the stomach ( 1,500 ml ) was drained . egd revealed acute gastric mucosal erosion , multiple gastric superficial ulcers , and the absence of gastric outlet obstruction , duodenal ulcers , or necrosis ( fig . 2 ) . approximately 36 hours after admission , the patient suddenly complained of severe dyspnea , chest pain , and aggravated abdominal pain . her blood pressure was 90/50 mm hg ; pulse rate , 106 beats per minute ; oxygen saturation , 86% ; and breathing oxygen , 10 l / min through a non - rebreather mask . we immediately performed a follow - up plain chest radiography , which revealed free air in both subphrenic spaces and pulmonary edema in both lung fields ( fig . her general condition worsened rapidly with a dramatic decrease in her mental condition and blood pressure along with aggravated dyspnea , which resulted in the death of the patient . acute gastric dilatation can be caused by conditions such as eating disorders , trauma , gastric hypomotility related to diabetic autonomic neuropathy , and mechanical obstruction [ 1 - 8 ] . however , the pathogenesis of this condition remains largely unknown and several theories have been suggested . the atony theory states that the stomach in a patient with an eating disorder becomes atonic and atrophic during fasting , and sudden ingestion of a large amount of food in this state may result in acute gastric dilatation because of the aggravation of an already weakened stomach . according to the mechanical theory , acute gastric dilatation is caused by gastric outlet obstruction related to superior mesenteric artery syndrome , pyloric stenosis , presence of a foreign body , or gastric cancer , among other causes . acute gastric dilatation may also be caused by regional alterations that occur with biliary tract disease , pancreatitis , or appendicitis . it can also be the result of aerophagia , which is caused by the relaxation of the upper esophageal sphincter , usually during anesthesia or due to debilitation after surgery . with gastric hypomotility , as is present with diabetes mellitus or parkinson s disease owing to gastric autonomic neuropathy [ 1 - 8 ] , bacterial toxins produced in patients with respiratory infections ( e.g. , pneumonia or pulmonary tuberculosis ) may lead to acute gastric dilatation . our patient had parkinson s disease and she presented with symptoms of pneumonia and was diagnosed with acute gastric dilatation on the abdominal ct . the patient showed no gastric necrosis or pyloric stenosis during the egd , but later developed pneumoperitoneum and acute pulmonary edema resulting in rapid deterioration of her medical condition and eventual death . although we did not observe a gastric perforation during laparotomy or autopsy , we suspect that the pneumoperitoneum resulted from the aggravation of previous multiple superficial gastric ulcers and erosions induced by ischemia . the other possibility is that gastric micro - perforation was masked by the large amount of remnant food and liquid material in the stomach . these perforations might have clearly been observed if air insufflation during the egd was performed . our patient did not undergo any imaging study to evaluate complications after egd because she did not develop any symptoms . however , if initial endoscopic evaluation is limited by food residue in the stomach or is performed in patients who are less expressive about changes of their symptoms , follow - up endoscopy or abdominal imaging studies should be performed to recognize complications of acute gastric dilatation , such as gastric ischemia or necrosis , even if patients do not have any signs or symptoms . we think that the acute pulmonary edema , which was considered to be noncardiogenic pulmonary edema , was caused by septic shock . the first step in the development of gastric perforation is necrosis of the gastric mucosa ; when the necrosis advances to all layers of the stomach , perforation can occur . the stomach receives sufficient blood supply , and hence , gastric ischemia and necrosis very rarely occur . however , ischemia of the stomach wall due to venous insufficiency may develop when the intragastric pressure exceeds 20 mm h2o [ 10 - 12 ] . spontaneous perforation and necrosis of the stomach is more common in women ( 67% ) and frequently occurs along the lesser curvature of the stomach ( 63% ) . leukocytosis or azotemia on laboratory analysis may suggest complications of acute gastric dilatation , such as ischemia or necrosis . the common presenting symptoms of acute gastric dilatation are emesis and diffuse abdominal distension with mild tenderness ; however , severe pain is uncommon . it is occasionally accompanied by hypotension or tachycardia as signs of shock , which may be caused by decreased venous return owing to the compression of the inferior vena cava by increased intra - abdominal pressure . plain radiography of the abdomen may indicate a distended stomach or free air in the right subphrenic spaces without any evidence of a small bowel gas shadow . abdominal ct is the most useful diagnostic tool for visualizing gastric distension and observing small amounts of free intraperitoneal gas and associated abdominal organic lesions . egd is used to evaluate pyloric stenosis and the general condition of the gastric mucosa ( i.e. , the presence of ischemia and necrosis ) . the initial treatment consists of prompt nasogastric decompression , fluid resuscitation , and correction of electrolyte imbalance . intragastric pressure can be decreased with only partial decompression in most patients , which is usually followed by an improvement in the symptoms of acute gastric dilatation . prompt emergency exploration must be performed if nasogastric decompression fails or in the presence of suspected peritonitis or abdominal compartment syndrome . the surgical methods may include surgical decompression , duodenojejunostomy , or partial or total gastrectomy . in most cases , severe sepsis is already present at the time of diagnosis in patients with gastric perforations . in these cases , surgical interventions result in poor outcomes , including a mortality rate as high as 33% to 65% in patients who receive aggressive surgical treatment , such as laparotomy . however , the mortality rate is nearly 100% in patients with complications , including gastric perforation or necrosis , who not receive a surgical intervention . in conclusion , early recognition and nasogastric decompression prompt surgical intervention should be considered when gastric perforation or necrosis is suspected , as it can significantly reduce the patient mortality rate . immunocompromised patients with chronic illness require close observation even when they do not show any symptoms suggestive of complications . in particular , if initial endoscopic or abdominal radiologic findings show no gastric ischemia or necrosis , follow - up egd or abdominal imaging studies are essential to recognize complications of acute gastric dilatation at an early stage .
pneumoperitoneum caused by acute gastric dilatation ( agd ) is a very rare complication . 
 we report a case of pneumoperitoneum and acute pulmonary edema caused by agd in a patient with parkinson s disease . a 78-year - old woman presented with pneumonia and agd 
 . we inserted a nasogastric tube and administered empirical antibiotics . 
 we performed an endoscopy , and perforation or necrosis of the stomach and pyloric stenosis were not observed . 
 thirty - six hours after admission , the patient suddenly developed dyspnea and shock , and eventually died . 
 we suspected the cause of death was pneumoperitoneum and acute pulmonary edema caused by agd during the conservative treatment period . 
 immunocompromised patients with chronic illness require close observation even if they do not show any symptoms suggestive of complications . 
 even if the initial endoscopic or abdominal radiologic findings do not show gastric necrosis or perforation , follow - up with endoscopy is essential to recognize complications of agd early .