Case Presentation: A thirty-four year-old man with a past medical history of hyperlipidemia initially presented with sharp, ten-out-of-ten in intensity, epigastric pain associated with nausea and non-bloody emesis. He had never experienced this pain before which prompted his decision to come to the emergency department. He was not able to tolerate oral intake since the start of his symptoms. The rest of the review of systems was negative and he denied any alcohol, drug use, or recent sick contacts. He reported compliance with his pravastatin, which was his only medication. On presentation, his physical exam was significant for tachycardia of 110, with epigastric tenderness on palpation, with no abdominal distention and normal bowel sounds. Upon lab draw, the nurse noted the blood to be “milky white”. The lab results were inaccurate due to abnormal lipid levels, but serum sodium was 116, with serum glucose of 108 and a serum lipase of 108. A MICU evaluation was requested because of an elevated beta-hydroxybutyrate of 50, with a venous blood gas that showed a pH of 7.33, pCO2 of 32 and HCO3 of 18. The MICU team, deemed that patient was stable for the general medical floor given clinical stability and because the bloodwork was inaccurate due to hyperlipidemia. A CT Abdomen/Pelvis was also obtained which showed acute uncomplicated pancreatitis. At that time, the suspicion for euglycemic diabetic ketoacidosis (DKA) was also raised, and patient was transferred to the MICU for an insulin drip and aggressive intravenous fluids. Additional lab work showed that he had a triglyceride level of 6,389 mg/dl. An endocrinology consultation resulted in recommendations to discontinue pravastatin and to start high-dose atorvastatin, fenofibrate, and omega 3 fatty acids, with supportive care for his abdominal pain. Within one day of starting him on this therapy plus an insulin drip for his DKA, his triglyceride levels drop to below 3,000 mg/dl with improvement of his symptoms. Eventually, once the insulin drip was discontinued, the patient was transferred to the medical floor to continue his fenofibrate, atorvastatin, and omega 3 fatty acids, in addition to starting him on a subcutaneous insulin regimen for his diabetes mellitus.
Discussion: Acute pancreatitis is commonly seen by the hospitalist. Hypertriglyceridemia is a well-established cause of acute pancreatitis, but because of the associated bloodwork abnormalities, diagnosing and triaging of the patient to an appropriate level of care can be difficult. Pseudo-hyponatremia is a very well-known abnormality of hyperlipidemia, but bicarbonate and beta-hydroxy butyrate values should not be affected. Typically the treatment involves apheresis, but given that the patient responded well to an insulin drip and medical management, the decision was to forgo this. In our hospital, insulin drips can only be started in the medical ICU, therefore, appropriate triage should not be delayed due to suspicion of inaccurate lab tests.
Conclusions: Although hypertriglyceridemia-induced acute pancreatitis is associated with pseudohyponatremia, suspicion of inaccurate laboratory values should not delay appropriate triaging of patients.