Abstract | December 20, 2022
A Dangerous Complication of Acute Pancreatitis: Abdominal Compartment Syndrome.
Learning Objectives
- Describe a case of abdominal compartment syndrome in a patient with acute pancreatitis.
- Demonstrate that acute pancreatitis creates an ongoing inflammatory response with a high metabolic rate, which can compel physicians to initiate antibiotic therapy.
Introduction: Abdominal compartment syndrome (ACS) is defined by an increased in intra-abdominal pressure (>20 mmHg) associated with new organ dysfunction. The mortality is reported to be approximately 50%, even with surgical abdominal decompression. If not treated promptly, it can be fatal in less than 24 hours. Pancreatitis is a well-known risk factor of ACS and is associated with increased mortality and morbidity. We describe a COVID-19 positive patient, with recurrent acute pancreatitis secondary to hypertriglyceridemia, who developed ACS.
Case: A 34-year-old female with history of recurrent episodes of hypertriglyceridemia-induced acute pancreatitis, presents to the emergency department complaining of severe epigastric pain with associated intractable nausea and vomiting. Initial triglycerides level was above measurable range and lipase level was greater than 1000. Patient was admitted to intensive care unit to initiate continuous insulin infusion. On hospital day 2, patient developed an increased intra-abdominal pressure as measured by a bladder pressure greater than 37 mmHg. Patient was immediately taken to the operating room for surgical decompression via laparotomy and wound vacuum placement. While in the ICU, patient returned to the operating room 5 times for washouts. After 3 weeks in the ICU, patient was extubated, switched from TPN to parenteral feeding, and transferred to the floor. The patient continued to have persistent tachycardia, tachypnea, low-grade fevers and leukocytosis and was empirically started on broad-spectrum antibiotic and antifungal therapy. She did not have any localizing symptoms and a extensive infectious work up for infection was initiated. Blood and urine cultures did not grow any organism. Chest x-ray and bedside US confirmed a large left-sided pleural effusion. Thoracocentesis was performed and body fluid culture was negative for infection. Patient went back to the operating room 2 more times for washouts and no abscesses or signs of active intra-abdominal infection was found. At that point with a negative infectious workup, the persistent systemic inflammatory response syndrome was thought to be partially related to the underlying pancreatitis. Patient’s clinical status continued to improve through the hospital stay and she was eventually discharged home in stable condition.
Discussion: This case illustrates the complexity and difficulty of managing patients with acute pancreatitis who developed abdominal compartment syndrome. Patients with this combination have critically elevated rates of mortality and morbidity, but fortunately hers was discovered early and managed promptly. As seen in this patient, the high metabolic rate secondary to the ongoing inflammatory response of the pancreatitis can cause physiologic and systemic idiosyncrasy and does not necessitate treatment for infectious etiologies. Although pancreatitis is one of the most common diagnosis in inpatient medicine, abdominal compartment syndrome must be considered in a deteriorating patient, as the line of decompensation is extremely thin.
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