ABSTRACT
Gastric volvulus is a surgical emergency that requires prompt recognition and management. The acromegalic patient has a number of pathophysiological factors that predispose to gastric volvulus and slow gastrointestinal (GI) transit. Authors aimed to present a case of hiatus hernia and gastric volvulus in a patient with acromegaly and review the current literature on GI anomalies in this population. A 70-year-old female presented to our institute with epigastric pain and coffee-ground vomiting on the background of acromegaly secondary to pituitary adenoma (resected in 1997). She was found to have a gastric volvulus and hiatus hernia which was repaired laparoscopically. She was discharged home but re-presented six days later with abdominal distension and vomiting. Computed tomography (CT) scan of abdomen showed recurrent gastric volvulus with involvement of the transverse colon. She underwent a laparotomy but no evidence of gastric or colonic volvulus was seen intra-operatively. The CT findings were attributed to a large stomach and coiled redundant transverse colon which could be misinterpreted as volvulus on imaging. Gastroparesis and slow bowel transit were the likely aetiology of this second presentation. This is consistent with literature reporting slow bowel transit and dolichocolon in acromegalic patients. Gastric volvulus is a rare finding associated with acromegaly. Structural anomalies in the anatomy of the acromegalic patient can make CT diagnosis challenging. This case demonstrates the need for caution when interpreting imaging in this cohort, as well as the need for further research on GI pathology associated with acromegaly.
ABSTRACT
Acute pancreatitis is a common surgical presentation with a multitude of causative factors. While the pathogenesis is not completely understood, new potential triggers have been described in recent literature. Contrast-induced pancreatitis is one of these rare phenomena. We present a case of acute pancreatitis in a patient who underwent coronary angiography and discuss the suspected pathogenesis behind contrast-induced pancreatitis. A 65-year-old man with background of cholecystectomy and UroLift procedure underwent two-stage elective coronary angiography following an episode of angina. He had been started on perindopril, rosuvastatin, aspirin and clopidogrel the week prior following first-stage percutaneous transluminal angioplasty of the right coronary artery. The patient underwent uncomplicated angiography, receiving 120 ml of Omnipaque 350. After transfer to the ward, he complained of progressive epigastric pain and nausea. On examination, the patient was afebrile, haemodynamically stable and tender in the epigastrium. His lipase was 888 U/l. Liver ultrasound showed an absent gallbladder but no other abnormalities. Total cholesterol was 2.7 mmol/l and IgG subclasses within normal range. There was no indication to perform an EUS. His symptoms resolved and his lipase normalised within three days. Although contrast-induced pancreatitis is rare, it should be considered in patients exposed to intravenous contrast who manifest symptoms. It occurs due to reduced capillary flow resulting from increased viscosity of radiographic contrast. The rate of invasive coronary investigations continues to rise with cardiovascular disease affecting one in five Australians. Therefore contrast-induced pancreatitis will likely become more common in this population hence it is important to be recognised.