Gastric ischaemia

Clinical History

The patient presented with severe acute allergic reaction/anaphylactic shock 10 hours after treatment with NSAIDs for epigastric pain. He had pruritus, generalized erythema, hypotension(TA-63/35mmHg) and metabolic acidosis with elevated lactate concentrations.

He received treatment and had adequate clinical evolution. Epigastric pain persisted and nasogastric drainage revealed the presence of blood.

Imaging Findings

Un-enhanced abdominal and pelvic CT scan demonstrated marked gastric wall thickening in the fundus and greater gastric curvature, with gastric pneumatosis.

Small quantity of gas was noted in periphery of the hepatic parenchyma, consistent with hepatic portal venous gas. Peri-hepatic fluid was also noted.

Follow-up abdominal and pelvic CT scan with iodine intravenous contrast administration was performed after gastric emptying, which revealed complete resolution of the hepatic portal venous gas and reduction of extent of gastric wall thickening and pneumatosis. A small quantity of peri-hepatic ascites persisted.

Endoscopic evaluation showed mildly erythematous mucosa in the gastric body and superficial ulcerative lesion in the greater gastric curvature, suggestive of ischemic origin. Mucosal biopsy analysis confirmed the ischemic changes.

Discussion

The occurrence of gastric ischaemia is rare, as the stomach has a rich vascular supply from the celiac trunk and its branches, being a infrequently reported pathology in the medical literature, and likely under-recognized both clinically and histopathologically[1, 2].

Gastric ischaemia usually occurs due to decrease in gastric blood flow either by vascular insufficiency factors or following reperfusion injury, with the present case exemplifying the marked reduction of gastric blood flow due to systemic hypotension/shock as the cause for ischaemia[1].

The etiologies of gastric ischaemia can be stratified in three main causal groups [2]:

I - Local vascular causes: Arterial stenosis[2,3]; Vasculitis[1]; Thrombosis[4]; Post-operative[5, 6]; Following therapeutic interventions–Sclerotheraphy[7], Endoscopic submucosal dissection[8], Transarterial chemoembolization(TACE) for hepatocellular cancer[9].

II - Systemic hypoperfusion: Shock[1]; Disseminated intravascular coagulation[10].

III - Mechanical obstruction: Para-esophageal hernia[11]; Gastric volvulus[12]; Gastric dilatation[13].

The typical clinical presentation consists on abdominal pain and GI bleeding, with most patients having predisposing factors to ischaemia, such as advancing age, atherosclerosis, diabetes, smoking and hypertension[2].

Endoscopic findings can range from mucosal congestion to large surface ulcerations and frank necrosis, usually occurring near the anastomoses between the 2 arterial arches (lesser and greater curvature)[1, 2].

CT imaging plays an important role in the assessment of gastric ischaemia, being able to detect intramural gastric air and portal venous gas, and helping rule out other intra-abdominal causes for the clinical presentation[2]. Gastric pneumatosis can be caused by gastric ischaemia, increased intragastric pressure, or bacterial infection[1,14].

Presence of hepatic portal venous gas is also an unusual and serious finding, commonly associated with intestinal ischaemic changes. Characteristically, portal venous gas has a peripheral distribution in the liver (within 2 cm beneath the liver capsule), and should be distinguished from pneumobilia, which presents with a more centrally distributed gaseous component[15].

Depending on the etiology, gastric ischaemia prognosis can vary in severity, ranging from life-threatening causes to self-limited afflictions as in the reported case.

Medical treatment includes fluid resuscitation, placement of NG tube for prevention/reduction of gastric distention and acid reduction therapy with proton pump inhibitors. The use of antibiotics is recommended in patients with sepsis or gastric pneumatosis and portal venous gas. In patients with severe gastric ischaemia or mechanical obstruction, multidisciplinary management and surgical evaluation are needed[1].

Early diagnosis is critical to allow the use of potential interventions and guide the therapeutic management and a delay in the diagnosis can lead to severe complications and increase in the mortality rates[2].

Written informed patient consent for publication has been obtained.

Differential Diagnosis List

Final Diagnosis

Gastric ischaemia following acute allergic reaction and hypoperfusion

URL:	https://eurorad.org/case/16344
DOI:	10.1594/EURORAD/CASE.16344
ISSN:	1563-4086