INTRODUCTION: Dunbar Syndrome, also known as median arcuate ligament syndrome (MALS), is a rare condition with a reported incidence of 2 per 100,000. It is characterized by an extrinsic compression of the celiac trunk, and should be considered when evaluating patients with abdominal pain of unknown etiology. CASE DESCRIPTION/METHODS: A 78 year old female presented with a complaint of epigastric discomfort that was post-prandial in nature, with associated weakness and early satiety. Her symptoms had been persistent for one year. Workup prior to her presentation included a normal nuclear medicine (NM) gastric emptying scan and normal NM hepatobiliary scan with CCK. A detailed history revealed that her pain was particularly worse after eating and was associated with early satiety. Laboratory results on admission were unremarkable. Contrast-enhanced CT scan of the abdomen and pelvis showed external compression and indentation of the superior aspect of the proximal celiac axis with post-stenotic dilation. Further diagnostic evaluation utilized end-inspiratory phase CT angiography of the abdomen, which showed an approximately 1 cm length segment of proximal celiac arterial narrowing, measuring 70% maximally at its origin. She was diagnosed with MALS after review of the CTA reconstructive images which showed moderate external compression of the celiac artery. DISCUSSION: MALS predominantly affects women between the ages of 30 and 50 and is marked by the hallmark feature of postprandial abdominal pain. Other signs and symptoms may include nausea, vomiting, and consequent weight loss from an inability to tolerate oral intake. Symptoms are thought to have both a vascular (mesenteric ischemia) as well as neurogenic component (somatic pain thought to originate from the splanchnic plexus). CT angiography and conventional angiography are considered to be gold standard imaging modalities for Dunbar syndrome. They demonstrate focal stenosis that has a characteristic hooked appearance due to the indentation of the celiac trunk on its superior surface. Imaging for an accurate diagnosis should ideally be performed during the end-inspiratory phase, as indentation of the celiac trunk may be seen normally during expiration. Additional imaging features may include post-stenotic dilation, prominent collateral vessels, and thickening of the median arcuate ligament. Treatment includes endovascular transluminal angioplasty and stent placement, as well as laparoscopic division of the arcuate ligament and resection of the celiac plexus.

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INTRODUCTION: Gastric pneumatosis is a term used to describe gas within the wall of the stomach. It is due to either one of two causes: emphysematous gastritis or gastric emphysema. The latter carries a better prognosis and is generally characterized by hemodynamic stability and spontaneous resolution with conservative management8. CASE DESCRIPTION/METHODS: A 58 year old female presented to the hospital with dyspnea and vomiting. Past medical history included coronary artery disease and diabetes mellitus type II. She was found to have a non-ST elevation myocardial infarction which was treated medically. Because of persistent vomiting, a gastroenterology consultation was requested. Physical examination at the time of consultation revealed an obese female with stable vital signs and a moderately distended abdomen. Laboratory tests revealed white blood cell count: 13.7 10 × 3/uL, hemoglobin 12.4 g/dL, lactic acid 1.0 mmol/L, lipase 30 U/L, and amylase 52 U/L. Computed tomography (CT) scan of the abdomen/pelvis was performed and revealed diffuse wall thickening of the stomach and a large amount of intramural air, particularly involving the fundus. Based on her symptoms and radiological findings, the diagnosis of gastric emphysema was made and she was treated with conservative measures. Her symptoms improved and a repeat CT scan of the abdomen ten days later failed to reveal any gastric pneumatosis. DISCUSSION: Gastric emphysema is benign and managed with observation and conservative treatment. Patients are hemodynamically stable without any associated infection3,8 The cause of either gastric emphysema or emphysematous gastritis can be due to an increase in intraluminal pressure or a mucosal injury that leads to intramural gas formation. Mucosa may be compromised in patients who are on immunosuppressive/cytotoxic therapy or in those patients who suffer from autoimmune and inflammatory diseases7. Diagnosis of gastric pneumatosis is made using CT imaging6 which can detect small amounts of gas in the stomach wall.3,5 Treatment for gastric pneumatosis includes supportive care. This includes adequate bowel rest and fluid support as needed. Surgical intervention or antibiotic therapy may be needed in certain cases of emphysematous gastritis5. In our patient, we suspect her development of gastric emphysema was due to her intractable nausea and vomiting. As in the majority of cases, her symptoms improved with conservative treatment and follow-up radiological imaging revealed resolution of her findings.

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