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A5170 - Acute Pancreatitis: Not Always Alcohol-Induced, Even in an Alcoholic
Author Block: T. Su1, G. Barmaimon2, A. Rothman3, E. Bang4; 1Mount Sinai Beth Israel, New York, NY, United States, 2Mount Sinai Beth Israel, New york, NY, United States, 3Pulmonary, Critical Care, and Sleep Medicine, Mount Sinai Beth Israel/West/St. Luke's, New York, NY, United States, 4Critical Care, Mount Sinai Beth Israel, New York, NY, United States.
Acute pancreatitis is most commonly caused by alcohol and gallstones, but the third leading cause, albeit rare, is hypertriglyceridemia (HTG). HTG is responsible for up to 9% of cases and is considered more severe than other types, as it has been associated with higher rates of complications, including pancreatic necrosis, renal failure, sepsis and longer hospitalizations. Early recognition of HTG-induced pancreatitis is essential to initiate life-saving targeted therapy. This case report describes a patient who was initially diagnosed with alcoholic pancreatitis and found to have severe HTG, leading to prompt initiation of insulin drip and apheresis, enabling earlier recovery and improved prognosis.
A 29-year-old obese man with a history of alcohol abuse who presented with epigastric pain for one day was found to have a lipase of 1,974 U/L and radiographic findings of acute pancreatitis on CT abdomen. He had developed acute kidney injury and his hemoglobin A1c of 12.6% revealed a new diagnosis of diabetes. His presentation was initially attributed to alcohol; he received IV fluids and analgesics until lipid panel showed triglycerides of 3,893 mg/dl. He was persistently tachycardic despite aggressive fluid resuscitation and had 22% bands, so he was started empirically on piperacillin-tazobactam due to concerns for intra-abdominal sepsis. He was transferred to the ICU to initiate an insulin drip and apheresis for life-threatening levels of triglycerides and hemodynamic instability. His course was further complicated by fluid overload, intra-abdominal hypertension with bladder pressures ranging 12 to 24 mmHg, and pulmonary edema requiring BIPAP. After combined therapy with insulin and two apheresis sessions, triglycerides down-trended to 346 mg/dl, with improvement in patient’s abdominal pain, respiratory status and acute kidney injury. He was transferred to medical floors and started on fenofibrate and pravastatin.
This patient’s presentation reflects the potential severity of HTG-induced pancreatitis. Delay in apheresis and insulin drip may be associated with high mortality and morbidity. If done in a timely manner, both interventions can rapidly lower triglycerides and improve outcomes. Triglyceride levels should be routinely checked in patients with acute pancreatitis, particularly those with risk factors for HTG, even in the presence of other likely etiologies. This case provides further evidence of the efficacy of early initiation of insulin and apheresis in HTG-induced pancreatitis. Early workup and high clinical suspicion with prompt intervention of life-saving modalities is key for the intensivist in HTG-induced pancreatitis and crucial for preventing recurrences of pancreatitis.