Acute Gastric Necrosis: Assessing the Risk Factors

John B. Ammori, MD Senior Resident

Department of Surgery

Jonathan McHugh, MD Senior Resident

Department of Pathology

Vincent M. Cimmino, MD Professor of Surgery

Department of Surgery

University of Michigan

Ann Arbor, MI

Gastric necrosis is a rare condition with many etiologies that can be attributed to a patient’s lifestyle or underlying morbidities or result from a postoperative complication. The authors report the case of a patient who had many risk factors for developing this life-threatening condition. Her medical history included congestive heart failure and atrial fibrillation, for which she underwent various treatments, yet she continued to smoke and consume multiple alcoholic beverages on a daily basis. Diagnosis of gastric ischemia is often delayed because of its rarity, but it may be considered in any patient presenting with abdominal symptoms who has risk factors for compromised gastric perfusion. Once gastric necrosis is suspected, treatment needs to be undertaken immediately.

Acute gastric ischemic necrosis with perforation is rare because of the stomach’s rich vascular supply. The cases reported in the literature note various causes, including arterial thrombosis of mesenteric vessels; acute gastric dilatation related to excessive food intake due to psychogenic polyphagia, bulimia, and Prader-Willi syndrome; intrathoracic herniation; volvulus; acute necrotizing gastritis; ingestion of caustic substances; therapeutic embolizations; and postoperative complications.^1-22 Our patient had a history of vascular disease and atrial fibrillation. She presented with an acute abdomen and was found to have acute, near-total gastric ischemic necrosis with posterior wall perforation.

Case report

A 66-year-old woman presented to the emergency department reporting a 24- to 48-hour history of diffuse abdominal pain that had progressively worsened, along with distention, anorexia, chills, and night sweats. She reported no nausea, vomiting, or objective fevers. Her medical history was significant for congestive heart failure requiring digitalis; atrial fibrillation without systemic anticoagulation; and upper gastrointestinal bleeding while on anticoagulation therapy, which required two endoscopic interventions. Her only surgical history was a left femoral to the distal artery bypass for peripheral arterial occlusive disease. She had an 80-pack-year history of smoking and smoked half a pack of cigarettes daily. She also consumed four alcoholic beverages daily.

On physical examination, the patient appeared ill and elderly. She was hypothermic at 34.6°C with a pulse of 97 beats per minute, blood pressure of 150/80 mm Hg, and a respiratory rate of 30 breaths per minute. Her heart rhythm indicated atrial fibrillation. An abdominal examination found diffuse rebound tenderness with involuntary guarding on palpation.

Laboratory findings included a white blood cell count of 9,300 mm³ with 93% polymorphonuclears and normal hemoglobin and platelet counts. The patient was in acute renal failure; her blood urea nitrogen was 62 mg/dL (normal, 8—23 mg/dL) and creatinine was 3.3 mg/dL (normal, 0.6—1.2 mg/dL). She was coagulopathic, with an international normalized ratio (INR) of 1.8 and partial thromboplastin time (PTT) of 40 seconds (normal, 30—45 seconds). Arterial blood gas showed a pH of 7.23 (normal, 7.35—7.45), bicarbonate of 13 mEq/L (normal, 21—28 mEq/L), and Pco₂ compensated at 22 mm Hg (normal, 35—45 mm Hg). Lactic acid was elevated to 4.0 mEq/L (normal, 0.7—2.1 mEq/L).

The patient underwent imaging studies prior to surgical evaluation. An abdominal radiograph did not show any evidence of free air, bowel dilatation, or pneumatosis intestinalis (Figure 1). A subsequent computed tomography (CT) scan showed free intraperitoneal air and fluid, with a small amount of right-side retroperitoneal fluid (Figure 2). The presumptive diagnosis was bowel necrosis secondary to mesenteric ischemia.

After initial resuscitation with fresh frozen plasma and crystalloids, the patient was taken to the operating room for an emergency exploratory laparotomy. She was found to have peritoneal contamination with succus entericus, particularly in the lesser sac. Two posterior gastric wall perforations were discovered: one in the prepyloric channel and the other in the body. The entire posterior gastric wall appeared necrotic and paper-thin. A posterior gastrotomy was performed without any bleeding from the wall. The anterior gastric mucosa was congested and inflamed. The esophagus, small bowel, colon, and rectum were pink and viable. A total gastrectomy with Roux-en-Y esophagojejunostomy and feeding jejunostomy was performed.

Pathologic examination of the surgical specimen revealed a total gastrectomy with a large, full-thickness, posterior-wall defect involving the antrum and distal body (Figure 3). The posterior gastric mucosa proximal to this was hemorrhagic, with numerous erosions, and resembled acute hemorrhagic gastritis. The anterior wall was also hemorrhagic, with scattered punctate erosions. Histological examination observed multifocal acute necrosis, which was predominantly superficial (acute mucosal necrosis); however, some areas of necrosis were deeper, resulting in perforation with serositis (Figure 4). The pattern of involvement was consistent with ischemia. There was no reactive gastropathy, such as would occur with nonsteroidal anti-inflammatory drug use, and there were no vascular lesions.

The patient’s postoperative course was complicated by acute renal failure, which required hemodialysis. She also experienced respiratory failure, necessitating mechanical ventilation. The patient had skin sloughing off her upper and lower extremities secondary to sepsis, which affected approximately 15% to 20% of her total body surface. Her family decided to withdraw care on postoperative day 5, and she died soon thereafter. The family declined the offer of an autopsy.

Discussion

Acute gastric necrosis is thought to be rare because of the stomach’s abundant blood supply, which includes five major direct arterial sources (right and left gastric, right and left gastroepiploic, and short gastric) and numerous minor and collateral sources.²³ Schein and Saadia showed that complete gastric wall vascular filling can be achieved in cadavers with only one patent major artery.²⁴ Somervell found he could achieve gastric necrosis in animal models only after ligation of the right and left gastric arteries, right and left gastroepiploic arteries, and 80% of collaterals.²⁵ Babkin and colleagues noted that ligating most of the arterial supply to dogs’ stomachs did not result in ischemia; however, both venous and arterial occlusion produced infarction in every case.²⁶ Cohen reported three cases of complete gastric necrosis and one case of partial gastric necrosis from a series of 23,836 autopsies in Los Angeles County General Hospital over a 12-year period. Cohen determined that all four patients not only had mesenteric arterial occlusions but also profound venous congestion secondary to right-sided heart failure.¹

Our patient had many risk factors for compromised gastric perfusion. She had vasculopathy and underwent a peripheral vascular bypass but continued to smoke cigarettes. She had atrial fibrillation and was unable to receive chronic anticoagulation therapy, which may have led to embolic phenomena. However, a lack of hepatic or small bowel ischemia excludes celiac artery thrombosis. She had undergone two previous endoscopic interventions to control massive gastric bleeding, and this may have played a role in reduced gastric blood flow. The role of digitalis in mesenteric vasospasm has been reported and may have been a contributing factor.²⁷ Furthermore, the patient had venous congestion due to her congestive heart failure. The cause of our patient’s compromised gastric perfusion was most likely multifactorial, with all of these conditions contributing. Notably, her esophagus and duodenum were healthy and viable despite near-complete gastric ischemia.

Diagnosis of gastric ischemia is often delayed because of its rarity. Initially, patients may have symptoms of mild epigastric tenderness, vomiting, or diarrhea that rapidly progress to acute peritonitis, septic shock, and death. The preliminary diagnosis may be supported by CT scan findings of pneumoperitoneum, gastric pneumatosis, and portal venous gas. Actual diagnosis is often made at laparotomy or autopsy.

If a diagnosis of gastric ischemia is being considered, resuscitation and intravenous antibiotics should be initiated immediately, followed by an emergency exploratory laparotomy. Resection of a necrotic stomach is required, with total gastrectomy if necessary. One-stage resection with esophagojejunostomy has been reported and was performed in this case. Alternatives include resection with cervical esophagostomy for proximal diversion or resection and placement of an esophageal drain. A jejunal feeding tube should always be placed. Revascularization of acute thromboses or embolism is necessary if either is found to be the etiology. Diagnosis and treatment must be expeditious, because mortality rates for gastrectomy due to acute ischemia are high, ranging from 50% to 80%.^6,28-30

Conclusion

Although gastric ischemia is rare, it is important to recognize the risk factors. Disease or insult to both the arterial inflow and venous outflow is necessary for the condition to occur. Progression to necrosis leads to peritonitis and sepsis. Urgent laparotomy is warranted, and the diagnosis is made at operation. Treatment should consist of resection and feeding tube placement. Increased awareness of this rare entity and its risk factors may lead to more prompt diagnosis and an increased chance for patient survival.

References

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Self-assessment questions

Choose the best answer for each of the following questions.

1. Occlusion of which vessels results in ischemic gastric necrosis?

a) Right and left gastric arteries

b) Right and left gastroepiploic arteries

c) Both gastric and both gastroepiploic arteries

d) Both gastric arteries, both gastroepiploic arteries, 80% of collateral arteries, and venous congestion

2. Risk factors for acute gastric ischemia include all of the following, except:

a) atrial fibrillation.

b) chronic obstructive pulmonary disease.

c) digitalis use.

d) previous endoscopic interventions.

3. When a diagnosis of acute gastric necrosis is made, surgical options include:

a) resection of necrotic stomach and gastrointestinal reconstruction.

b) resection of necrotic stomach and cervical esophagostomy.

c) resection of necrotic stomach and placement of an esophageal drain.

d) all of the above.

4. The mortality rate following gastrectomy due to acute ischemia is:

a) ≥50%.

b) 30% to 50%.

c) 10% to 30%.

d) <10%.

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