Arterio-venous malformation (AVM) of the head of the pancreas is a rare condition that may cause upper gastro-intestinal tract (GIT) bleeding. A 45-year-old man with a large AVM at the pancreato-biliary region is described. The patient had recurrent episodes of hematemesis and melena. Enlargement of the AVM was documented by serial abdominal CT scans performed after each bleed. Whipple procedure was successfully performed in this patient.
Celiac trunk is the first ventral branch of the abdominal aorta. It usually terminates by giving three branches; the common hepatic artery, the left gastric artery and the splenic artery. We report a rare variation of the branching pattern of the celiac trunk. The Celiac trunk divided into two branches; left gastric artery and splenicogastroduodenal trunk. The splenico-gastroduodenal trunk divided into splenic and gastroduodenal arteries. The superior mesenteric artery and hepatic artery took origin from a common hepato-mesenteric trunk. The hepatic artery had a winding course around the portal vein and hepatic duct. The knowledge of these variations is important while doing radiological investigations and liver transplant and pancreatic surgeries.
Superior Mesenteric Artery Syndrome (SMAS) is a rare clinical entity presenting as acute or chronic upper gastrointestinal obstruction. It occurs due to compression of third part of duodenum between abdominal aorta and overlying superior mesenteric artery caused by a decrease in angle between the two vessels. Rapid loss of retroperitoneal fat, in conditions leading to severe weight loss is the main factor responsible for this disorder. Superior mesenteric artery syndrome in association with abdominal tuberculosis has not been reported earlier to the best of our knowledge. Therefore, an unknown cause (SMAS) of upper gastrointestinal obstruction in a patient of abdominal tuberculosis is being presented for the first time through this case report. An imaging diagnosis of SMAS was made on contrast enhanced CT abdomen which also confirmed the clinical suspicion of abdominal tuberculosis in the patient. The patient was managed conservatively and recovered without requiring any surgical intervention for the obstructive symptoms.
True and pseudoaneurysms of the visceral arteries are uncommon. They represent 0.1-0.2 percent of all vascular aneurysms. Visceral artery aneurysms (VAAs) should be treated due to their propensity to rupture and associated high mortality. We describe a 58-year-old man with pseudoaneurysm of the inferior pancreaticoduodenal artery and who presented with post-motor vehicle accident abdominal pain and a pulsatile epigastic mass. Computed tomography (CT) showed a pseudoaneurysm of the visceral artery, and selective mesenteric angiography showed the aneurysm to be arising from the inferior pancreaticoduodenal artery. The aneurysm was successfully treated with endovascular coil embolisation. CT angiogram at one month post-procedure revealed persistent occlusion of the aneurysm. To the best of our knowledge, this is the first reported pseudoaneurysm of inferior pancreaticoduodenal artery secondary to blunt abdominal trauma from a motor vehicle accident and also the first reported VAA from Malaysia.
An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I in isolated perfused kidneys and mesenteric beds of WKY and SHR. In the renal vasculature, angiotensin III induced a dose-dependent pressor response, which was more marked in the SHR than WKY in terms of significant greater magnitude of response and lower threshold. DAA-I attenuated the pressor action of angiotensin III in both the WKY and SHR. The attenuation in SHR was much more marked, occurring at doses as low as 10(-15) M DAA-I, while effective attenuation was only seen with 10(-9) M in WKY. The effects of DAA-I was not inhibited by PD123319 and indomethacin, indicating that its action was not mediated by angiotensin AT2 receptors and prostaglandins. However, the direct pressor action of angiotensin III in the SHR but not the WKY was attenuated by indomethacin suggesting that this notable difference could be due to known decreased response of renal vasculature to vasodilator prostaglandins in the SHR. Pressor responses to angiotensin III in the mesenteric vascular bed was also dose dependent, but smaller in magnitude compared to the renal response. The responses in the SHR, though generally smaller, were not significantly different from those of the WKY. This trend is in line with the similar observations with angiotensin III and II by other investigators. In terms of the effect of DAA-I, indomethacin and PD123319 on angiotensin III action, similar patterns to those of the renal vasculature were observed. This reaffirms that in the perfused kidney and mesenteric bed, where the majority of the vessels are contractile, femtomolar concentrations of DAA-I attenuates the pressor action of angiotensin III. The attenuation is not indomethacin sensitive and does not involve the angiotensin AT2 receptor. The findings suggest that DAA-I possesses protective vascular actions and is involved in the pathophysiology of hypertension.