P0879 - Case of Gastric Intramural Hematoma; Rare Complication of Acute Pancreatitis

INTRODUCTION
Complications of acute pancreatitis occur due to enzymatic degradation or compression by necrotic tissue, pseudocysts, or peripancreatic fluid collections on nearby structures. Of them, intramural hematoma formation is infrequently reported, but when present, is usually found in the esophagus or duodenum. Gastric intramural hematomas (GIH) have rarely been reported as a complication of pancreatitis, as they are more commonly due to trauma, specifically non-accidental trauma.
CASE DESCRIPTION
A 3-year-old African American female initially presenting with diffuse abdominal pain for two days with non-bloody, non-bilious emesis. She was found to have intussusception which was successfully reduced in the emergency department by air enema. The patient had recurrent abdominal pain and an enlarged gallbladder was incidentally found on ultrasound, thus she was admitted. She underwent magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography (ERCP). A pigmented gallstone in the common bile duct was found. She received an extensive hematology work-up, however all labs were normal. Removal via ERCP resulted in post-ERCP pancreatitis. With supportive care, she gradually improved, but on day five status post ERCP, she experienced return of diffuse abdominal pain and multiple bouts of non-bloody, non-bilious emesis, prompting further investigation. Physical exam was significant for a mildly distended and diffusely tender abdomen without rebound or guarding. A CT abdomen with contrast revealed a large 8.9 x 5.3 cm gastric wall hematoma. Patient underwent cholecystectomy and endoscopic exploration of the hematoma which revealed pancreatitis-induced vessel injury causing the GIH. The patient was started on nasojejunal feeds to bypass the hematoma and managed conservatively. Two weeks later, she was discharged upon adequate oral intake. At a three-month follow up, the patient was doing well with mild, intermittent abdominal pain. On repeat abdominal CT scan, the hematoma was drastically decreased to 3.8 x 1.7 x 1.6 cm.
DISCUSSION
High pancreatic enzyme levels led to arterial disruption and hemorrhage within the gastric wall, causing this patient’s hematoma. Diagnosis of GIH occurs via an abdominal CT scan showing a well-circumscribed, hyperdense, and homogenous mass. Treatment is mainly conservative, with vascular embolization or surgery reserved for unstable cases.
CONCLUSION
This case proved to be interesting because the development of GIH after pancreatitis is so rare with little literature available, and no previously reported cases in the pediatric population. This patient showed excellent prognosis with conservative management and has not developed any complications currently, six months after discharge. Hemorrhagic complications, though less common, should be considered in patients with acute pancreatitis, so as not to misdiagnose and perform unnecessary testing or treatment. We hope that the documentation of this case will aid in increasing cognizance of this potential complication when considering possibilities for worsening symptoms in a patient being treated for or recovering from acute pancreatitis.