THU365 Diabetic Ketoacidosis Unmasking Acute Pancreatitis With A Hidden Surprise

Disclosure: Y. Arya: None. A. Syal: None. S. Teja Sathi: None. J.V. Mayrin: None. Background: Development of diabetic ketoacidosis (DKA) in acute pancreatitis is rare and requires high clinical suspicion, particularly in cases such as ours where it might lead to presentation and hence, unmasking of pancreatitis. Our case was also complicated by splenic vein thrombosis, making it a therapeutic dilemma. Case Presentation: We describe the case of a female in her mid-40s who presented to the emergency department with complaints of severe epigastric abdominal pain, associated with vomiting, for the past one day. She was hemodynamically stable, and her laboratory analysis revealed a lipase greater than twenty times the upper limits of normal. Patient was also noted to have a random capillary blood glucose of 500 mg/dL with positive urine beta hydroxybutyrate and an anion gap of thirty-five. She was diagnosed with DKA and managed with intravenous (IV) insulin along with IV fluids. Her abdominal pain failed to respond which triggered us to obtain imaging. She underwent a computed tomography (CT) scan of her abdomen and pelvis which showed extensive pancreatic inflammation and necrosis along with peripancreatic fluid collection extending into the mesentery. The patient was managed with a multidisciplinary approach involving endocrinology, gastroenterology, and critical care teams. Her abdominal pain initially improved, followed by worsening around the sixth hospital day. She underwent an MRI of her abdomen which revealed a new splenic vein thrombosis. Given the risk of bleeding from the peri-pancreatic fluid collection and non-occlusive nature of the thrombosis, clinical monitoring was preferred over anticoagulation. Extensive workup did not reveal an etiology of the pancreatitis, and it was deemed idiopathic. The patient became insulin dependent from her pancreatitis. She had a prolonged hospital course and was eventually discharged after three weeks of presentation with appropriate outpatient follow-up. Discussion: The incidence of diabetes mellitus after acute pancreatitis depends on the severity of pancreatic necrosis; the degree of insulin deficiency being directly proportional to the extent of necrosis.[1] The pathophysiology of splenic vein thrombosis revolves around necrosis, venous stasis, and activation of coagulation cascade, all in the background of the inflammatory state.[2] Anticoagulation in splenic vein thrombosis secondary to pancreatitis thus remains controversial, given the increased risk of hemorrhage and formation of pseudoaneurysms. Interestingly, therapeutic anticoagulation might prevent thrombosis progression by reducing portal pressure and thereby decreasing the risk of hemorrhage. Lower rates of hemorrhage have been documented in literature in patients receiving anticoagulation in this subset of patients, versus untreated cases.[3] Thus, an individual risk-benefit analysis is needed before initiating anticoagulation. References: 1.Zhi M, Zhu X, Lugea A,et al. Incidence of New Onset Diabetes Mellitus Secondary to Acute Pancreatitis: A Systematic Review and Meta-Analysis. Front Physiol. 2019;10:637. 2.Nadkarni NA, Khanna S, Vege SS. Splanchnic venous thrombosis and pancreatitis. Pancreas. 2013;42(6):924-931. 3.E. Valeriani, M. Di Nisio, N. Riva, et al. Anticoagulant therapy for splanchnic vein thrombosis: a systematic review and meta-analysis. Blood. 2021;137(9):1233-1240 Presentation: Thursday, June 15, 2023