Sleeve gastrectomy for idiopathic acute gastric dilatation with transmural necrosis

Abstract

Acute gastric dilatation (AGD) is usually related to eating disorders, postoperative status and mechanical obstruction of the duodenum. When intragastric pressure is augmented, it can lead to alteration of blood flow and result in transmural necrosis. However, there are very few reports on idiopathic AGD and so here we describe the case of a 26-year-old woman diagnosed with AGD without any apparent cause. Conservative treatment was initially conducted, but because of the persistence of dilatation, presence of gastric ulcer and gastric pneumatosis, a surgical approach was necessary. During surgery, gastric necrosis was observed in the greater curvature. A sleeve gastrectomy was conducted from the angle of His to the antrum. No complications were present during the postoperative course. Oeso-gastro-duodenal barium study showed no signs of gastric emptying and psychiatric evaluation ruled out any eating disorder.

Introduction

Gastric necrosis is an uncommon, life-threatening complication of acute gastric dilatation (AGD). Eating disorders, postoperative status, diabetes mellitus or trauma scenario are the most common underlying conditions associated with such complications.^1,2 AGD is rarely found in patients with no predisposing factors.

Gastric perfusion is usually preserved due to the extensive vascular system in the area and the presence of multiple anastomoses within it. Nevertheless, an increase in the intragastric pressure over 20–30cm H₂O can alter intramural blood flow and may lead to transmural ischaemia.³

AGD with gastric necrosis is a severe condition that can result in gastric perforation, abdominal compartment syndrome, shock, multiorgan failure and death.

We present a case of acute gastric ischaemia and necrosis due to AGD in a young female without any previous psychiatric disorders.

Case presentation

A 26-year-old female patient presented to the Emergency Department (ED) with a 24-hour history of abdominal pain with nausea and vomiting. The patient also referred to a progressive 9-kg weight loss in the last 10 months. She had no previous history of gastrointestinal disorders. Initial examination revealed a distended abdomen, painful to palpation in the epigastrium and right upper quadrant. There were no signs of peritonism. Fever, tachycardia and hypotension were absent. Laboratory tests revealed the following abnormalities: white blood cell count (WBC) 12,300/µl, serum lactate dehydrogenase 304UI/l and C-reactive protein (CRP) 1.4mg/l.

Following fluid resuscitation and placement of a nasogastric tube, 2l of gastric content was removed. An abdominal CT scan was performed, showing a massive gastric dilatation. No clear masses were identified as obstructive aetiology, but the first and second portions of the duodenum were also distended proximal to the aortomesenteric angle.

The patient was admitted to continue with the studies. Within the first few hours, abdominal distension persisted and acute phase reactants increased. An upper endoscopy was performed, and a large necrotic ulcer was present at the greater curvature of the stomach. No apparent obstruction was found at the duodenum. The CT scan was repeated to evaluate the vascularisation of the gastric wall. Signs of gastric pneumatosis were present on the anterior and posterior walls (Figure 1). Lastly, a laparotomy was performed.

Figure 1 .

Gastric pneumatosis at the posterior wall

Gastric transmural necrosis was observed at the greater curvature of the stomach, from the angle of His to the antrum (Figure 2). No obstructive cause was found at the duodenum. The patient underwent tubular vertical gastrectomy with calibration done by placing a 32-Fr gastric tube inside the future gastric remnant. A four-load 75mm stapler was used, over-sewing with a non-absorbable 4/0 running suture (Figure 3). There were no major complications during the postoperative course. An oeso-gastro-duodenal barium study was performed with no signs of leakage and normal gastric emptying. A psychiatric evaluation was done to investigate alimentary disorders but no evidence of mental diseases was found. The patient was discharged on the seventh postoperative day with appropriate food intake. Final pathology analysis showed massive transmural necrosis.

Figure 2 .

Gastric necrosis in the greater curvature, with respect to the antrum and oesophasogastric junction

Figure 3 .

Sleeve gastrectomy with four-load 75mm stapler

Discussion

In most cases, AGD occurs related to a postoperative scenario, binge eating episodes or the vascular compression of the third duodenal portion between the superior mesenteric artery, and the aorta and the spine (superior mesenteric syndrome), among other conditions.

In extreme cases the dilated stomach can compress the majority of intra-abdominal structures and induce acute compartment syndrome, diminishing vascular splanchnic blood flow, increasing intrathoracic pressure and impairing venous return, causing a multiorgan failure if the situation persists.

Infarction not only occurs due to arterial occlusion; the increase of intragastric pressure (above 20–30cm H₂O) over the venous pressure may also lead to a massive decrease in the intramural blood flow.

Early diagnosis of AGD is essential to prevent ischaemia and necrosis, whose mortality can reach 75%. Ischaemic necrosis is more common among females (67%) and usually affects the lesser curvature of the stomach (63%).⁴

For diagnosis, thorax X-ray may be useful to detect early pneumoperitoneum, but abdominal CT scan contributes to clarifying the cause of AGD and assessing gastric wall perfusion.

The initial therapeutic approach consists of correct gastric decompression with a wide-bore nasogastric tube and fluid resuscitation. An upper endoscopy may be necessary for further and direct aspiration of gastric content, and to rule out intraluminal obstructive causes. An endoscopy is also useful to assess the mucosa status through direct visualisation.

When gastric aspiration is inefficient, or signs of persistent dilatation or presence of peritonism are found, surgery must be conducted. Delay in treatment can lead to up to a 73% mortality.⁵ Meticulous examination of the entire surface of the stomach is primordial, as an adequate resection of the necrotic zone is a key point for a successful resolution. Total or near-total gastrectomy with oesophagojejunostomy, wedge resection or partial gastrectomy have been reported based on the operative findings.

Conclusions

Although no previous eating disorder was present in this case, AGD must be considered in young women who turn up at the ED with abdominal pain, nausea or vomiting after a binge eating episode. When signs of infarction or perforation and/or instability are present, surgical intervention must not be delayed.

Sleeve gastrectomy (SG) is a feasible technique in acute gastric necrosis when enough antrum (5–6cm) and oesophagogastric junction are preserved. To the best of our knowledge, this is the first case of SG for AGD without any demonstrated aetiology.