Acute gastric dilatation raises the intragastric pressure resulting in vascular insufficiency [
6]. The pressure within the dilated stomach lumen must be greater than 20 cm H
2O, which exceeds the gastric venous pressure, before mucosal ischemia will occur [
6]. The gastric circulatory deterioration causes fragility of the gastric wall, resulting in life-threatening complications such as dehydration, metabolic alkalosis, and mucosal necrosis [
2‐
5]. In addition, acute gastric dilatation increases intra-abdominal pressure and leads to systemic circulatory failure following collapse of the inferior vena cava [
1]. The medical literature confirms gastrointestinal necrosis and intra-abdominal high pressure from marked distention of the stomach as features in lethal cases of SMA syndrome [
11]. In the present case, the significant dilatation of the stomach (shown in Figure
1) indicated a large increase in abdominal pressure, which could have induced systemic circulatory failure. Taking these findings into consideration, we surmised that acute gastric dilatation was the cause of death in the present case.
For the cause of the gastric dilation, intestinal occlusion by the SMA at the third portion of the duodenum was suspected. The SMA originates from the anterior surface of the AA behind the neck of the pancreas at the level of the first lumbar vertebra. The SMA runs into the root of the mesentery, crosses over the frontal surface of the third portion of the duodenum, and spreads over the intestines. This portion of the duodenum is located between the SMA anteriorly and the AA posteriorly. Imaging studies have shown that aortomesenteric distance between the SMA and the AA was 10 to 28 mm at the sagital plane of the third portion of the duodenum [
12]. Reduction in the aortomesenteric distance results in compression of the duodenum, and is a defining characteristic of SMA syndrome [
9,
10]. The SMA is encased in mesenteric fat and lymphatic tissue at the root of the mesentery, which is important for maintaining a wide aortomesenteric distance under normal conditions. These tissues protect the duodenum from being compressed between the SMA and the AA [
9,
10]. The most common cause of SMA syndrome is the loss of the fatty padding at the mesentery and the retroperitoneum, which reduces the aortomesenteric distance in debilitating conditions associated with marked weight loss, such as anorexia nervosa, malabsorbtion, and hypercatabolic states [
8‐
10]. In the present case, the third portion of the duodenum was compressed and narrowed severely between the SMA and the AA, but both the mesentery and the retroperitoneum were still protected by an abundance of fat tissue. Some of the factors that have been reported to precipitate SMA syndrome are as follows: external compression of the abdomen induced by wearing tight belts, body spica, or body cast; anatomic anomalies such as lumbar lordosis [
7] and high insertion of the ligament of Treitz; and surgical alterations of anatomy such as spine surgery and ileoanal pouch anastomosis [
7,
9,
10]. None of these factors were identified in the present case, whereas a dense fibrotic and thickened degenerated area arose from the posterior parietal peritoneum around the duodenum (Figure
2B) and stretched to the root of the mesentery where the SMA was involved (Figure
2A). The scarred posterior parietal peritoneum pulled the root of the mesentery together with the involved SMA, which made the SMA tense tightly (Figure
2A). These pathological degenerations could have caused a subsequent decrease in the aortomesenteric distance. Several reports have described fatal cases of acute gastric dilatation due to eating a massive volume of food [
1,
11]. In this case, the root of the mesentery was thickened and adhered to the duodenum, which reduced duodenal diameter. We concluded that this luminal narrowing caused the aggregation of an excessively large mass of food, complete obstruction of the duodenum, and acute fatal gastric dilation at last.