Background: Splanchnic venous system thrombosis is a well recognized local vascular complication of acute pancreatitis (AP). It may involve thrombosis of splenic vein (SplV), portal vein (PV) and superior mesenteric vein (SMV), either separately or in combinations, and often detected incidentally, indeed some cases present with upper gastrointestinal bleed, bowel ischemia and hepatic decompensation. Incidence is variable depending on study subjects and diagnostic modalities. Pathogenesis is multifactorial centered on local and systemic inflammation. Management involves treatment of underlying AP and its complications. Universal use of anticoagulation may lead to increased risk of bleeding due to frequent need of interventions (radiologic/endoscopic/surgical). Literature on anticoagulation in setting of AP is sparse and at present there is no consensus guideline on it. Current article details our experience on splanchnic venous thrombosis (SVT) in AP in a well defined cohort of patients at a tertiary care center. Methods: Hospitalized patients with AP from January 2018 to December 2018 were included in the study. Detailed information on demographic, clinical, laboratory, radiologic features, and indication of anticoagulation use were collected prospectively during the index admission. Outcome variables were analyzed at the end of 6 months. Results: Twenty four out of 105 (22.85%) patients with AP develop SVT. Etiology of AP was alcohol use in 21/24 (87.5%) subjects. Most common vessel involved was isolated SplV in 11/24 (45.8%) patients followed by SplV along with PV and SMV 9/24 (37.50%, P < 0.001). Bowel ischemia 4/12 (33.3%), hepatic decompensation 3/12 (25%), triple vessel involvement 4/12 (33.3%) and pulmonary embolism 1/12 (8.3%) were reasons for anticoagulation. There was no statistical difference with respect to development of varices, collateral formation, recanalization, bleeding and mortality with use of anticoagulation (P > 0.05 with respect to all above variables). Conclusions: SVT is commonly seen in alcohol-induced AP. Anticoagulation does not affect outcomes of SVT. Subset of patients may benefit with anticoagulation.
Aim of the study: Autoimmune hepatitis (AIH), despite being uncommon, is on the rise in the elderly population. However, no study from India has described the natural history and treatment outcome of AIH in the elderly. The aim was to study the characteristics of AIH in the elderly population and compare them with the younger population. Material and methods: Patients with a diagnosis of AIH based on the revised International Autoimmune Hepatitis Group (IAIHG) criteria were recruited from January 2011 to June 2018. Patients were defined as elderly when ≥ 60 years and young when < 60 years of age. Clinical, serological, histological characteristics and treatment outcome with follow-up until 12 months were analyzed and compared between the two groups. Results: Out of 155 patients, 33 (21.29%) were elderly. Acute-on-chronic liver failure (ACLF) as the presentation was more common in elderly as compared to young AIH patients (39.4% vs. 13.9%, p = 0.0024). Serum alanine aminotransferases and serum creatinine levels were significantly higher in elderly patients as compared to the younger group (p < 0.05). On histology cirrhosis was significantly more common in the elderly group (75.7% vs. 56.6%, p = 0.045). Response to treatment at the end of 12 months was similar in both groups. Due to co-morbidities immunosuppressant could not be started in 18.2% of elderly and 6.5% of younger patients (p = 0.065). Conclusions: AIH is an important differential diagnosis among the elderly population presenting with ACLF and cirrhosis. When given appropriate immunosuppressants they have a similar outcome as compared to the youngest population.
Abdominal pain is a common but benign symptom after colonoscopy. We report a case of acute pancreatitis that occurred just after an elective screening colonoscopy; this is a rare event with very few reported cases. A healthy, asymptomatic male underwent screening colonoscopy at our center and developed abdominal pain and emesis after the procedure. An abdominal X-ray ruled out perforation but laboratory tests revealed elevated levels of amylase and lipase. The patient had no etiological risk factors for pancreatitis. The presumed mechanism of pancreatitis in this case is mechanical and pressure trauma from excessive insufflation, external abdominal pressure, and repeated withdrawal of the colonoscope due to tight angulation of the splenic flexure, a structure that is in close proximity to the pancreatic tail. Acute pancreatitis should be considered in the differential diagnosis of patients who present with abdominal pain after colonoscopy once more common etiologies have been excluded.
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