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ACUTE MANAGEMENT OF SEVERE HYPERTRIGLYCERIDEMIA WITH PLASMAPHERESIS IN DIABETIC KETOACIDOSIS
October 2009, Vol 136, No. 4_MeetingAbstracts Abstract: Case Reports | October 2009
ACUTE MANAGEMENT OF SEVERE HYPERTRIGLYCERIDEMIA WITH PLASMAPHERESIS IN DIABETIC KETOACIDOSIS Gilbert Seda, MD*; Dennis Amundson, DO Naval Medical Center San Diego, San Diego, CA Chest. 2009;136(4_MeetingAbstracts):6S-d-7S. doi:10.1378/chest.136.4_MeetingAbstracts.6S-d
Abstract INTRODUCTION: Abnormal elevation in serum lipids is extremely common. If severe, hyperlipidemia can have serious medical consequences. Acute pancreatitis is an acute potentially life-threatening complication of severe hypertriglyceridemia. Additionally, elevated levels of triglycerides can interfere with clinical laboratory testing. We present a case of a woman presenting with diabetic ketoacidosis and severe hypertriglyceridemia treated with plasmapheresis when conventional treatments failed to significantly reduce her triglyceridemia. CASE PRESENTATION: A 63 year old woman with chronic, untreated diabetes presented to the emergency department with a 1 week history of a tender mass at the apex of her scalp. She was hypertensive and tachycardic and required incision and drainage for a scalp abscess. Initial chemistry panel returned uninterpretable due to severe lipemia. A lipid panel revealed a cholesterol level of 1,051 mg/dL and triglyceride level of 10,132 mg/dL. Laboratory after bench ultracentrifugation at another institution revealed a glucose of 559 mg/dl, a bicarbonate of 12 mmol/L, and an anion gap metabolic acidosis consistent with diabetic ketoacidosis (DKA). The lipemia-associated interference in laboratory studies made treatment of her DKA-related electrolyte abnormalities extremely difficult. Her hypertriglyceridemia was initially managed with insulin, antilipidemic medications, and heparin but remained significantly elevated delaying labs and treatment. Plasmapheresis was initiated and serum triglycerides rapidly decreased from 7,501 mg/dL to 1,745 mg/dL in less than 24 hours. (Figure 1). DISCUSSIONS: Serum triglyceride concentrations exceeding 1000 mg/dL (11 mmol/L) are considered severely elevated and pose a high risk for development of acute pancreatitis. Severe lipemia also interferes with clinical laboratory testing by three mechanisms: (1) turbidity resulting in light scattering, (2) increase in the non-aqueous phase of the sample, or (3 partitioning between the polar and non-polar phases. Circulating lipid particles, namely VLDL and chylomicrons, cause turbidity by bending light away from its original path due to
scatter, reflectance, or absorption. Additionally RBC hemolysis is enhanced by lipemia, due to erythrocyte fragility. Because electrolytes are in the aqueous phase of blood, lipids may dilute their concentration. Lipemia can be minimized by reducing the interfering lipid, ultracentrifuging the sample (100,000g) or using polymers to precipitate the lipids out of the sample. The process of ultracentrifuging a sample may produce excess heat and cause error due to release of intracellular potassium. Plasmapheresis is one method to rapidly remove excess lipids. Case reports demonstrate successful use of plasmapheresis for hypertriglyceridemia associated with acute pancreatitis, gestational hypertriglyceridemia, induction chemotherapy associated hypertriglyceridemia, pancreatitis with ARDS due to hypertriglyceridemia, protease inhibitor-induced hypertriglyceridemia, familial hypercholesterolemia, and, like our case, poorly controlled diabetes with severe hypertriglyceridemia. CONCLUSION: Plasmapheresis is a safe, rapid and effective intervention for the emergent management of severe hypertriglyceridemia that results in significant reductions in triglycerides allowing timely measurement of serum electrolytes. Consider plasmapheresis when lipemia interferes with clinical labs and conventional treatments such as heparin, insulin, antihyperlipidemic drugs and fat-free parenteral nutrition are ineffective in acutely lowering triglyceride levels. DISCLOSURE: Gilbert Seda, No Financial Disclosure Information; No Product/Research Disclosure Information Monday, November 2, 2009 4:30 PM - 6:00 PM
ACUTE MANAGEMENT OF SEVERE HYPERTRIGLYCERIDEMIA WITH PLASMAPHERESIS IN DIABETIC KETOACIDOSIS Gilbert Seda, MD*; Dennis Amundson, DO Naval Medical Center San Diego, San Diego, CA Chest. 2009;136(4_MeetingAbstracts):6S-d-7S. doi:10.1378/chest.136.4_MeetingAbstracts.6S-d
Abstract INTRODUCTION: Abnormal elevation in serum lipids is extremely common. If severe, hyperlipidemia can have serious medical consequences. Acute pancreatitis is an acute potentially life-threatening complication of severe hypertriglyceridemia. Additionally, elevated levels of triglycerides can interfere with clinical laboratory testing. We present a case of a woman presenting with diabetic ketoacidosis and severe hypertriglyceridemia treated with plasmapheresis when conventional treatments failed to significantly reduce her triglyceridemia. CASE PRESENTATION: A 63 year old woman with chronic, untreated diabetes presented to the emergency department with a 1 week history of a tender mass at the apex of her scalp. She was hypertensive and tachycardic and required incision and drainage for a scalp abscess. Initial chemistry panel returned uninterpretable due to severe lipemia. A lipid panel revealed a cholesterol level of 1,051 mg/dL and triglyceride level of 10,132 mg/dL. Laboratory after bench ultracentrifugation at another institution revealed a glucose of 559 mg/dl, a bicarbonate of 12 mmol/L, and an anion gap metabolic acidosis consistent with diabetic ketoacidosis (DKA). The lipemia-associated interference in laboratory studies made treatment of her DKA-related electrolyte abnormalities extremely difficult. Her hypertriglyceridemia was initially managed with insulin, antilipidemic medications, and heparin but remained significantly elevated delaying labs and treatment. Plasmapheresis was initiated and serum triglycerides rapidly decreased from 7,501 mg/dL to 1,745 mg/dL in less than 24 hours. (Figure 1). DISCUSSIONS: Serum triglyceride concentrations exceeding 1000 mg/dL (11 mmol/L) are considered severely elevated and pose a high risk for development of acute pancreatitis. Severe lipemia also interferes with clinical laboratory testing by three mechanisms: (1) turbidity resulting in light scattering, (2) increase in the non-aqueous phase of the sample, or (3 partitioning between the polar and non-polar phases. Circulating lipid particles, namely VLDL and chylomicrons, cause turbidity by bending light away from its original path due to
scatter, reflectance, or absorption. Additionally RBC hemolysis is enhanced by lipemia, due to erythrocyte fragility. Because electrolytes are in the aqueous phase of blood, lipids may dilute their concentration. Lipemia can be minimized by reducing the interfering lipid, ultracentrifuging the sample (100,000g) or using polymers to precipitate the lipids out of the sample. The process of ultracentrifuging a sample may produce excess heat and cause error due to release of intracellular potassium. Plasmapheresis is one method to rapidly remove excess lipids. Case reports demonstrate successful use of plasmapheresis for hypertriglyceridemia associated with acute pancreatitis, gestational hypertriglyceridemia, induction chemotherapy associated hypertriglyceridemia, pancreatitis with ARDS due to hypertriglyceridemia, protease inhibitor-induced hypertriglyceridemia, familial hypercholesterolemia, and, like our case, poorly controlled diabetes with severe hypertriglyceridemia. CONCLUSION: Plasmapheresis is a safe, rapid and effective intervention for the emergent management of severe hypertriglyceridemia that results in significant reductions in triglycerides allowing timely measurement of serum electrolytes. Consider plasmapheresis when lipemia interferes with clinical labs and conventional treatments such as heparin, insulin, antihyperlipidemic drugs and fat-free parenteral nutrition are ineffective in acutely lowering triglyceride levels. DISCLOSURE: Gilbert Seda, No Financial Disclosure Information; No Product/Research Disclosure Information Monday, November 2, 2009 4:30 PM - 6:00 PM