Sudden unexpected death due to rupture of the stomach

1. Introduction 

Gastrorrhexis or stomach rupture is a relatively rare condition. A search of the Japanese as well as foreign literature of the past 50 years yielded only 47 reports on gastrorrhexis of unknown etiology. In this paper, we report our experience with a case of sudden death due to gastrorrhexis suspected to be induced by excessive eating and we review previous reports on this subject as well.

2. Case report 

A 49-year-old security guard was found dead in a public lavatory. He had a history of chronic gastritis and had complained of abdominal symptoms, described as not being severe, 4 h prior to the estimated time of death. On external examination, there was no hematemesis or vomitus around the body. A pale, reddish purple livor appeared at the back of the deceased. This livor was faded by digital pressure relatively rapidly. Moderate postmortem rigor was observed in the jaw, neck, shoulder joint, and rigor in the other parts of the body was either weak or absent. The cornea was transparent, and the pupils were 5 mm in diameter bilaterally. No petechia was observed in the palpebral conjunctiva. The rectal temperature was 30 °C and the outdoor air temperature was 14 °C. From the postmortem examination findings, the time of death was estimated to be around 5 h prior to the discovery of the body. On internal examination, the abdomen was remarkably distended and there was a note of subcutaneous emphysema. There were no signs of any injury to the thoracic or abdominal walls and organs. About 3000 ml of dirty brown-black fluid containing undigested rice (stomach contents) was observed in the abdominal cavity. Gross examination of the abdominal cavity showed no fibrin formation due to inflammation, abscess formation nor adhesion between the peritoneum and intestine. The stomach was noted to be ruptured in two sites (Fig. 1A–C). There was a 14-cm rupture at the anterior wall of the corpus ventriculi on the side of greater curvature, and another, bleeding rupture, 6 cm long, was also observed in the same region. Additionally, a 5 cm slightly bleeding mucosal laceration was found at the fundus ventriculi. There were some ulcer sites in the stomach, including one in the lesser curvature measuring 0.8×0.5 cm in diameter and 0.3 cm in depth and another in the anterior portion of the corpus ventriculi measuring 1.3×0.9 cm in diameter and 0.25 cm in depth. Another ulcer 3.5×3.0 cm in diameter and 0.8 cm in depth was found near the pylorus. Although the serosal surface of this area adhered to the pancreas, no stenosis was observed at the pylorus. All the ulcers were slightly hard with a clear margin. Histologically, no ulcer or cancer was found at the ruptured region of the stomach, and no abnormal orientation of the smooth muscle layer was observed (Fig. 2). In the ulcer near the pylorus, proliferation of fibroblasts and fibers was found in the tunica muscularis. In the lungs, marked pulmonary edema and congestion were seen but no lesion was found. Strong congestion was also seen in the liver, kidneys, spleen and adrenal glands, but again no lesion was found. Toxicologically, alcohol levels were 0.193 mg/ml in left heart blood, 0.416 mg/ml in right heart blood, and 2.6 mg/ml in gastric content. n-Propanol was not detected in left and right heart blood, but a level of 0.0185 mg/ml was found in the gastric content. Based on the above findings, the cause of death was determined as ‘death from shock caused by gastric rupture’.

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Fig. 1. (A) Serosal surface of the gastric wall. The stomach was ruptured at two sites. One was 14 cm long at the anterior wall of the corpus ventriculi on the side of greater curvature, and the other was 6 cm long at the same region. (B) Mucosal surface of the gastric wall. There is an ulcer 0.8×0.5 cm in diameter and 0.3 cm in depth in the lesser curvature, and another 1.3×0.9 cm in diameter and 0.25 cm in depth in the anterior portion of the corpus ventriculi. Another ulcer 3.5×3.0 cm in diameter and 0.8 cm in depth is seen near the pylorus (white arrow), and adhesion at the serosal surface is observed. The black arrow shows the ruptured area. (C) Higher magnification of the ruptured stomach. Two ruptures measuring 14 and 6 cm in length are seen in the larger curvature of corpus ventriculi. The 6-cm rupture is accompanied by bleeding.

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Fig. 2. Histological findings of the 14-cm long rupture in the stomach. No ulcer nor tumor lesion is found in the rupture area, and no abnormality in orientation of the gastric smooth muscle layer is observed.

3. Discussion 

According to our literature review, a total of 62 cases of ‘spontaneous rupture of the stomach’ were reported in 47 articles in the past 50 years. In those cases, there was a female predominance with a male to female ratio of 1:4. The age of onset ranged from 16 to 86 years, with the highest prevalence in the sixties. Ruptures were located in the lesser curvature of stomach in 73% of the cases, were solitary in 87%, and were larger than 6 cm in only 22% of the cases. Several features such as relative rarity in males, characteristics of the rupture, i.e. the site (the greater curvature), number (2) and size (14 and 6 cm) make our case remarkable. Rupture due to increased internal pressure commonly results in rupture at one site. However, the present case had ruptures at multiple sites and in a longitudinal direction, which may suggest gastric wall damage due to Mallory–Weiss syndrome or as a result of postmortem autolysis. In the present case, however, there was no hematemesis or vomitus at the site of death, and only trace levels of alcohol were detected (0.193 mg/ml in left heart blood and 0.416 mg/ml in right heart blood). Furthermore, the fold of the gastric mucosa was clear, and no longitudinal rupture was found at the esophagogastric junction. The rupture was located in the anterior wall of the corpus ventriculi, and gross and histological examinations detected only mild bleeding at the margin of the rupture. These findings ruled out Mallory–Weiss syndrome. The morphology of the rupture wound and the features of the gastric wall surrounding them were also completely different from those of damage due to postmortem autolysis. According to the reports of Albo et al. [1] and Corrado et al. [2], damage in two or more sites may also occur as a result of increased intragastric pressure. Even in cases of rupture due to increase internal pressure, the gastric wall may rupture in multiple sites, although rarely. Furthermore, review of the literature for the past 50 years showed that the duration from onset of clinical symptoms to hospital visit was less than one day in over half of the patients in previously reported cases. However, the mortality of gastrorrhexis even with surgical intervention was reported to be 65% [3], indicating difficulties in life-saving even with prompt management. Our case is the first reported case of gastrorrhexis discovered after death. Supposing the deceased had been transported to a hospital 4 h before he was discovered dead, saving his life would have been difficult. The reason is that autopsy revealed marked findings of sudden death but no fibrin formation, abscess formation nor peritoneal adhesion, indicating that the shock due to gastrorrhexis had resulted in death within an extremely short period of time.

Kikuchi [4] and Cassebaum et al. [5] stated that gastrectasis invariably precedes gastrorrhexis. Albo et al. [1], in a review of the literature, found that gastrectasis was observed in 27 of 43 cases. Various factors such as excessive eating or drinking [6], [7], [8], [9], sodium bicarbonate administration [10], [11], oxygen inhalation through a nasal cannula [12], [13], [14], mouth-to-mouth resuscitation [5], and pyloric constriction [11] may induce gastrectasis. Pregnancy [15] and parturition [16] have also been reported as factors contributing to development of gastrectasis. In our case, approximately 3000 ml of dark brown fluid, mainly gastric contents, was found in the abdominal cavity. Gastrectasis was present and passage of food into the duodenum was not observed. These findings indicate that the stomach was full at the time of rupture, and suggest that excessive eating may have been the cause of gastrectasis.

Two mechanisms have been reported that may lead to rupture of a distended stomach. In the first, the esophagogastric junction, a valve-like structure, prevents the extrusion of the gastric content into the esophagus while spasm or organic stenosis at the pylorus prevents passage into the duodenum. Vomiting, cough or grand mal seizures may then cause an acute increase in intragastric pressure resulting in rupture [1], [17], [18]. In the second, it has been suggested that necrosis of the gastric wall causes gastrorrhexis. Prolonged, severe gastric distension impairs venous drainage of the gastric wall, leading to ischemia and necrosis and eventually, perforation [8], [18], [19].

In the present case, no organic stenosis was found in either the cardia or the pylorus, no necrosis of the gastric wall was detected at the rupture site, and there were no lesions such as ulcer or carcinoma at the site. Therefore, rupture cannot be explained by either of the two mechanisms described above. One cannot completely rule out the possibility that a slow external force in an anteroposterior direction may rupture a distended stomach, although there is no evidence (such as hemorrhage) in the thoracoabdominal wall and parenchymatous organs that suggests an external force.

In this case, histological examination of the ruptured tissue revealed no lesions such as ulcer and cancer or abnormal orientation of gastric smooth muscle layer, and the presence of an ulcer in the lesser curvature undoubtedly resulted in impaired dilation of the lesser curvature due to hypertrophy and scarring. Under these conditions, excessive over-eating would have increased the internal pressure, and the resulting over-extension of the stomach wall at the greater curvature was speculated to have caused stomach rupture.