Abdominal angina refers to an abdominal pain that develops shortly after food intake and gradually resolves after a few hours. It is related to insufficient mesenteric blood flow to meet the intestinal demand. In the majority of cases, this syndrome is caused by atherosclerotic narrowing of the mesenteric vessels. We report the case of a 61-year-old man, with a longstanding history of hypertension, diabetes mellitus, and dyslipidemia, who presented to the emergency department with acute abdominal pain that was aggravated by food intake. The patient reported similar but milder episodes of this pain for the last three years that led him to lose significant weight because of fear of eating. Despite this classic history of abdominal angina, his condition was misdiagnosed as indigestion, and was offered symptomatic treatment only. The basic laboratory findings were within the normal limits. The patient underwent a contrast-enhanced abdominal computed tomography scan in the arterial phase which demonstrated focal proximal stenosis of the celiac trunk due to thickened median arcuate ligament. Subsequently, the median arcuate ligament was resected laparoscopically to decompress the celiac artery. The surgical operation resulted in the complete resolution of the abdominal pain. Celiac artery compression syndrome is a rare etiology of abdominal angina. Computed tomography angiography is the imaging study of choice to make the diagnosis accurately. Laparoscopic resection of the median arcuate ligament is a safe and successful approach in the management.
Introduction and importance Gitelman syndrome (GS) is an autosomal recessive, salt-losing tubulopathy, also referred to as familial hypokalemia-hypomagnesemia, caused by mutation of genes encoding the sodium chloride cotransporter (NCCT) and magnesium transporters in the thiazide sensitive segments of the distal convoluted tubule (DCT) of the nephron. Patients may present with a spectrum of clinical presentations and associations. Case presentation Here, we report a case of a 39-year-old female with Gitelman syndrome and chronic pancreatitis in the absence of well-known causes of CP. Her clinical and radiographic profile constituted an indication for surgical intervention, namely pancreatic head and body coring and pancreaticojejunostomy (Frey's procedure) (FP). On follow up 3 month later, the patient is pain-free and is satisfied. To the best of our knowledge and based on literature review, this is the first reported case of GS with CP. Conclusion The purpose of this paper is to describe a case of CP in association with established GS as a first published clinical association, raising a possibility of another possible clinical manifestation of GS. Further observational studies are encouraged to support this association.
Constriction of the large and medium-sized cerebral arteries following an aneurysmal subarachnoid haemorrhage (aSAH) is a well-known condition that primarily affects the anterior circulation supplied by the internal carotid arteries. SAH is a rare but potentially fatal type of stroke. Across the literature, authors have defined vasospasm using terms such as "symptomatic vasospasm," "delayed cerebral ischemia" (DCI), "transcranial Doppler vasospasm," and "angiographic vasospasm." Because posthemorrhagic vasospasm causes significant neurologic morbidity and death, there has been a great deal of interest and research into its physiologic basis and developing effective preventative and treatment strategies. The triple-H therapy hemodynamic augmentation technique, which includes hypertension, hemodilution, and hypervolemia, has been an important part of the treatment. In this article, we'll look at cerebral vasospasm following subarachnoid haemorrhage, including its causes, epidemiology, evaluation, and, most importantly, management.
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