Diabetes Ketoacidosis Masks the Presence of Acute Pancreatitis from Severe Hypertriglyceridemia: A Case Report

Department of Emergency Medicine, Kauvery Hospital, Trichy-Cantonment, India

Abstract

The incidence of hypertriglyceridemia-induced pancreatitis is low; however, patients with risk factors such as diabetic mellitus, alcohol, medications and pregnancy can develop severe disease. Acute pancreatitis is a potentially fatal clinical entity, and results in significant mortality and morbidity. It has multiple etiologies, and it is important to identify the exact cause and provide appropriate care. In this case report, an elderly, obese, patient’s initial presentation with Diabetic KetoAcidosis masked the presence of pancreatitis. She was efficiently managed with insulin infusion and with measures to lower serum triglycerides. Patient was advised lifestyle modification, diet, hypolipidemic drugs and discharged home.

Keywords

Acute pancreatitis, Hypertriglyceridemia (HTG), Hypertriglyceridemia induced pancreatitis (HTGP), Serum triglyceride, diabetes, Hypolipidemic drugs.

Background

Acute pancreatitis is a common condition with various possible etiologies, gallstones and alcohol being the most common. Hyperlipidemia in the form of hypertriglyceridemia, even though less frequent, is one of the well accepted underlying causes of acute pancreatitis in 7-10% of the cases – the most common after gallstones and alcohol. Primary (Genetic) and secondary disorders of lipoprotein metabolism are associated with HTGP. Primary disorders include Type 1 dyslipidemia, also known as familial chylomicronemia. Secondary disorders include poorly controlled diabetes mellitus (type 1 & 2), diabetic ketoacidosis, and medications. HTG is a disorder where a patient’s serum triglyceride level is more than 1000 mg/dl with type I, III, IV, and V.

Pathophysiology

Hypertriglyceridemia-1

Inflammation of the pancreas – intra-acinar activation of pancreatic enzymes (including trypsin, phospholipase A2, and elastase) can lead to autodigestion of the pancreas. These pancreatic enzymes damage tissue and activate the complement system and inflammatory cascade resulting in cytokine production, edema, inflammation, and sometimes necrosis. Injury occurs to the pancreatic cells with subsequent activation of the trypsinogen inside the pancreas instead of in the duodenum; trypsinogen is then activated to trypsin by enterokinase. Normally, trypsin inhibitors in the pancreas inactivate the trypsin produced, but this fails to occur in an individual with pancreatitis, as digestive enzymes are secreted improperly leading to inflammation and autodigestion of the pancreas.

Case Presentation

An elderly obese patient with risk factors of diabetes, hypertension and dyslipedemia presented to an outside hospital with multiple episodes of abdominal pain, vomiting, dehydration and tiredness for 2-3 days. She was managed as DKA, as her blood sugars were high, with plasma acetone positive. She also had severe triglyceridemia (6500 mg/dl) with normal amylase/lipase levels. CT Abdomen was initially normal (Fig. 1). The patient improved clinically.

Hypertriglyceridemia-2

Fig. 1. First CT-Abdomen showed no noteworthy changes.

On the third day of admission, she developed severe epigastric pain with biliary vomiting. And she was shifted to our ER for further management.

On initial evaluation she was found to have Systemic inflammatory response syndrome (SIRS), with pulse rate 130/min, blood pressure 110/60 mmHg, respiratory rate 28/min, and temperature 101.4°F.

On systemic examination, abdomen was distended, with epigastric tenderness, decreased bowel sounds and hepatosplenomegaly. Chest was clear, no neurological deficit.

On systemic examination, abdomen was distended, with epigastric tenderness, decreased bowel sounds and hepatosplenomegaly. Chest was clear, no neurological deficit.

Bedside USG showed a grade 1 fatty liver, hepatosplenomegaly, and bulky body and tail of pancreas.

Acute inflammatory changes around the pancreas, a non-visualized pancreatic duct, and peripancreatic fat stranding were seen in the repeated CT-abdomen (Fig. 2).

Hypertriglyceridemia-3

Fig. 2. Second CT-Abdomen showed acute inflammatory changes, with swelling not only in the pancreas but also around the spleen and ascites.

The patient has managed aggressively with intravenous fluids, insulin infusion, antibiotics, and analgesics and shifted to ICU for further care.

The patient clinically improved, shifted to a ward, and observed for a few days. She was discharged with oral hypoglycemic agents, antihypertensive, and hypolipidemic agents.

Hospital stayDay 0Day 1Day 2
Serum triglyceride level (mg/dl)65003500650
Serum lipase(U/L)3060040
Total count20000170008000
Random blood glucose(mg/dl)650450160

Discussion

Patient had a Ranson score of four points, which is associated with a 15% mortality. Patient was admitted to the intensive care unit for monitoring and management. While in the ICU, her management included treating the acute pancreatitis and reducing the serum triglyceride level with the goal of preventing necrotising pancreatitis and organ failure. Aggressive fluid resuscitation was continued. Central venous pressure and inferior vena cava diameter variability were used to manage fluid status guide along with accurate intake and output. In the first few days, a continuous nasogastric tube was inserted which helped reduce gastric distension, vomiting. Patient was started on enteral trophic feeds. In order to lower the high triglyceride level rapidly, discussions focused on the use of an insulin infusion and plasmapheresis, both of which have been used successfully in HTGP management.

The Critical Care Team decided to continue a regular insulin infusion titrated by the blood glucose level as advised by protocol. It is hypothesized that insulin works by increasing lipoprotein lipase activity, which degrades chylomicrons, thereby reducing the triglyceride level. Because HTGP often presents in patients with uncontrolled diabetes, insulin can decrease both triglyceride and glucose levels. Triglyceride level was monitored every day and I.V Insulin was stopped when triglyceride levels were <500 mg/dl. After 4 days, she showed significant improvement in her serum triglyceride level with clinical improvements such as a reduction in abdominal pain and the ability to tolerate oral feed. Pharmacotherapy to reduce serum triglyceride levels included fenofibrate. Diet modification, fat restricted diet, and tight glycemic control were advised. Plasmapheresis was not done on our patient, as she improved with insulin infusion, fluids, and oral fenofibrate.

Indication for plasmapheresis are patients with HTGP (S. Triglyceride level >1000 mg/dl and lipase >3 times the upper limit of normal) and worrisome features like hypocalcaemia, lactic acidosis, signs of worsening systemic inflammatory response or multi-organ dysfunction.

Conclusion

Hypertriglyceridemia is a common clinical problem, and if markedly elevated, can lead to pancreatitis. General and specific therapies are available to reduce triglycerides during the acute phases of pancreatitis. Pharmacological therapy, Lifestyle modification and avoiding aggravating factors are essential for preventing further attacks.

References

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