Recurrent acute pancreatitis secondary to hypertriglyceridemia (HTG) with levels below 1000 mg/dL has been rarely reported in the literature. HTG is the third most common cause of acute pancreatitis and has been established in the literature as a risk factor when levels are greater than 1000 mg/dL. A 43-year-old patient presented to the hospital with severe epigastric abdominal pain. Initial laboratory investigations were significant for a lipase level of 4143 U/L and a triglyceride level of 600 mg/dL. Computed tomography (CT) of the abdomen showed diffuse enlargement of the pancreas consistent with pancreatitis. A diagnosis of severe acute pancreatitis secondary to high triglycerides was made based on the revised Atlanta classification 2012. The patient was initially managed with intravenous boluses of normal saline followed by continuous insulin infusion. Diabetic Ketoacidosis (DKA) was ruled out due to a past medical history of diabetes. Her clinical course was complicated by acute respiratory distress syndrome requiring intubation and mechanical ventilation. During the course, she improved symptomatically and was extubated. She was started on nasogastric feeding initially and subsequently switched to oral diet as tolerated. After initial management of HTG with insulin infusion, oral gemfibrozil was started for long-term treatment of HTG. Emerging literature implicates HTG as an independent indicator of poor prognosis in acute pancreatitis (AP). Despite the paucity of data, the risk of developing AP must be considered even at triglyceride levels lower than 1000 mg/dL.
Acute pancreatitis is the leading gastrointestinal cause of hospitalization in the United States [
Hypertriglyceridemia is the third most common cause of acute pancreatitis and accounts for 1 to 4 percent of total cases [
A morbidly obese 43-year-old female with a history of hypertension, dyslipidemia, and diabetes mellitus presented with severe abdominal pain. She had an episode of acute pancreatitis one year ago. She complained of right upper quadrant pain radiating to the back over 6-hour duration alongside six episodes of vomitus. A review of systems was only notable for a headache and dizziness. She reported no family history of dyslipidemia or acute pancreatitis. She denied tobacco, alcohol, or illicit substance use. There was no history of gallstones, appendectomy, new medications, procedures (including ERCP), or any complications related to her diabetes.
Admission vitals revealed afebrile patient with a heart rate of 103/min, respiratory rate of 20/min, BP 116/62 mmHg, and oxygen saturation of 96% on a nasal cannula at 5 liter/min. The patient was alert and orientated but was in moderate distress. The abdomen was obese and soft and with tenderness in the epigastric region. There was no guarding, rigidity, or Murphy’s sign. Her body mass index (BMI) was 47.1. Other systemic signs of elevated triglycerides including xanthelasma, corneal arcus, and tendon xanthoma were absent.
Initial laboratory investigations showed an elevated white cell count of 16.9
The patient had an elevated lipase of 4143 U/L (reference 22-51 U/L), total cholesterol of 694 mg/dL (100-199 mg/dL), and a triglyceride level of 600 mg/dL (reference 0-149 mg/dL). Computed tomography (CT) of the abdomen showed diffuse enlargement of the pancreas consistent with pancreatitis (Figure
CT scan of the abdomen showing acute pancreatitis (arrow).
The patient was treated with boluses of intravenous (IV) normal saline and supportive care. On the second day of admission, the patient developed hypotension and had persistent tachycardia. She likely developed acute respiratory distress syndrome (ARDS) from complications of acute pancreatitis. Fluid overload was ruled out with a sonogram of the inferior vena cava (diameter of 1.5 cm), a central venous pressure of 6 cm of H2O, and echocardiography indicating left ventricular ejection fraction of 55% with no left ventricular diastolic dysfunction. The patient was subsequently transferred to the intensive care unit for hypovolemic shock and respiratory distress requiring intubation and mechanical ventilation. As per revised Atlanta classification, she was categorized as severe acute pancreatitis based on Marshall scoring system for organ failure with a score of 3, with a score of 1 from respiratory failure (PaO2/FiO2 of 240) and two from cardiovascular (systolic BP <90, not fluid responsive). Patient’s fasting blood glucose was 288 mg/dL (74-117 mg/dl), and diabetic ketoacidosis (DKA) was ruled out with the absence of serum or urine ketones, no elevated anion gap, and no acidosis. ABG analysis showed pH of 7.5, bicarbonate of 23, and an anion gap of 2.
Following the patients decline into shock, an ABG indicated an acidic pH of 6.99, PCO2 9.4, PO2 134, and HCO3 of 5.4. The serum bicarbonate level was low at 15
Repeat abdominal contrast-enhanced CT on the third day showed marked pancreatic and peripancreatic infiltration consistent with AP and no signs of necrosis. Continuous insulin infusion was started for HTG from day 1, lowering her triglyceride levels down to 247 mg/dL over five days as shown in Table
Showing trend of Triglycerides level during the hospital stay.
Lab parameters | Day 1 | Day 3 | Day 5 | Day 11 |
---|---|---|---|---|
Triglyceride level | 600 mg/dL | 393 mg/dL | 247 mg/dL | 165 mg/dL |
Acute pancreatitis has several etiologies, but alcohol and gallstones make up the majority of the cases [
There is emerging literature implicating HTG as an independent indicator of poor prognosis in AP [
A prior meta-analysis concluded that HTG AP is associated with worse outcomes including higher mortality and the higher rates of systemic inflammatory response syndrome (SIRS) as compared to non-HTG AP [
Management is important in HTG AP due to a high risk of complications. Insulin infusion has been used in literature successfully [
Informed consent was obtained from the patient.
The authors declare that they have no conflicts of interest.