We present the case of a 57-year-old gentleman referred to the acute medical take with abdominal pain and weight loss. The learning point is the differential diagnosis for continued gastric ulceration in the face of optimal treatment. In our discussion, we consider the uncommon condition of chronic mesenteric ischemia – our patient’s eventual diagnosis.
A 57-year-old Caucasian gentleman presented to his GP with a 2 month history of weight loss and epigastric pain, which was exacerbated by eating. There were no other GI symptoms of note. Past medical history and family history were both unremarkable. He took no medication. Alcohol intake was minimal, but he did have a 30 pack per year smoking history. Physical examination, routine blood tests and ECG were normal, but an OGD revealed striking superficial gastric ulceration (see Fig. 1). He was started on full dose lansoprazole and sucralfate.
His symptoms failed to improve and further outpatient investigations were organized. A barium meal noted mild reflux, but no mucosal abnormality of the upper GI tract. Subsequent CT abdomen showed normal appearances to the abdominal viscera, including pancreas, with no biliary dilatation. Biopsies from the initial OGD had indicated mild atypia but no dysplasia. A repeat endoscopy after 2 months on medication revealed continuing ulceration and gastritis. He was referred to the acute medical take shortly afterwards with worsening pain, by which point he had lost 3 stones (19 kg) in weight.
The patient was cachectic, but cardiovascular, respiratory and neurological examinations were all normal. The abdomen was soft with only mild tenderness over the epigastrium and no masses or organomegaly.
Routine bloods, abdominal and chest radiographs and ECG were all unremarkable. The patient’s previous investigations were reviewed, confirming no abnormalities in his solid organs or the mucosal lining of his upper GI tract. Serum gastrin levels were normal.
With the common causes of non-healing gastric ulceration and weight loss excluded, we sought to examine the patient’s GI blood supply with Doppler studies of the coeliac axis and superior mesenteric artery. This indicated turbulence at the origins of both arteries and distal high velocity jets, suggesting stenosis of the arteries. A CT angiogram was performed to confirm these findings, which revealed occlusion of the coeliac axis and tight stenosis of the superior mesenteric artery (see Fig. 2). The diagnosis was of chronic mesenteric ischemia.
Our patient was treated with endoluminal stenting of the superior mesenteric artery with splendid results. Postprandial pain disappeared overnight and he felt, in his own words, “like a new man”.
Within 3 weeks, our patient had gained 7kg (15.5 pounds) and he remains asymptomatic to this day.
The question facing us, when this gentleman presented to the medical take, was what could cause non-healing gastric ulceration in the face of full-dose PPI?
Non-compliance with medication and inadvertent use of NSAIDs are the most common culprits, yet both of these could be excluded from the history.
Zollinger-Ellison syndrome was a possibility, but ulcer distribution is more typically duodenal and serum gastrin levels were normal.
Linitis plastica merited consideration, as its submucosal nature frequently precludes endoscopic diagnosis. Nevertheless, there are usually suggestive features on barium swallow (classically a “leather bottle” stomach), which was normal.
Rare causes would include gastric lymphoma, Crohn’s disease and chronic mesenteric ischemia, our eventual diagnosis.
Chronic mesenteric ischemia is an uncommon condition, usually affecting the small bowel and typically a result of atherosclerotic disease. It classically presents with a triad of postprandial pain, fear of eating (sitophobia) and consequent weight loss .
Examination findings are often nonspecific, but there are almost invariably signs of atherosclerotic disease in other vascular beds. The infrequency of presentation is largely a result of redundancy within the visceral circulation – indeed radiologists will often embolize entire gastric arteries as a treatment for bleeding ulcers .
Endoluminal stenting is now the treatment of choice, with a much lower rate of complications compared to open revascularization .
Even for a rare diagnosis, this case was particularly unusual. Firstly, stomach as opposed to small bowel was primarily affected. Secondly, our patient’s sole hard risk factor for atherosclerotic disease was smoking. Finally, there were no other symptoms to suggest atherosclerotic disease in other circulatory beds. With this in mind, we have referred the patient for exercise stress testing to exclude silent coronary artery disease.
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