Hypertriglyceride Induced Pancreatitis (HTGP)
Plasmapheresis: an important treatment modality option in the practice of Critical Care Medicine
A 34 year old man was admitted to Aster Hospital, Mankhool with chief complaints of severe abdominal pain, vomiting multiple episodes and general weakness since 2 days. Patient did not have any known comorbids. No personal habits contributory.
Initially evaluated in the ER at Aster Hospital, Mankhool, he was treated as Diabetic Ketoacidosis (DKA) and shifted to the ICU for further management. USG abdomen was noncontributory. Labs were suggestive of very high triglycerides levels > 17,000 mg/dl, elevated serum lipase and amylase values. The patient was treated as Hypertriglyceride induced pancreatitis (HTGP) along with DKA pathway. He was started on Fibrate, Omega3 FFA, Heparin and Insulin infusion. For analgesia, Opioids with Paracetamol IV were used. He continued to remain sick and was later transferred to another facility where Plasmapheresis was initiated with FFP as replacement fluids. After 2 sessions over 2 days, the triglycerides were down to 800 mg/dl. The patient recovered by 7th day and was discharged.
Triglycerides are an independent risk factor for adverse cardiovascular events and a potential mediator for pancreatic induced inflammation. Levels in excess of 1000 mg/dl are a risk factor for the development of pancreatitis. The sheer size of these macromolecular particles can impede pancreatic blood flow and produce local acinar ischemia. The disturbance of the acinar structure liberates pancreatic lipase.
Insulin therapy is the mainstay for the reduction of severe triglyceride levels. Insulin induces lipoprotein lipase (LPL) production.
Heparin acts similar to Insulin and promotes release of hepatic lipase and lipoprotein lipases from the endothelial surface of the capillary.
Omega-3 fatty acids reduce TGs through a variety of interactions with hepatic nuclear receptors that subsequently lead to reduced substrate for hepatic lipogenesis and enhanced beta-oxidation of fatty acids.
However, the slow action of antihyperlipidemic therapy poses a problem if patient is critically ill and needs rapid reduction. Plasmapheresis (PF) seems to be an alternative and safe therapy for these kinds of cases because it allows the rapid reduction of triglycerides (TG) within a few hours. Its use, especially in Critical Care medicine, though limited, is increasingly reported. According to the American council for Apheresis, severe hypertriglyceridemia is currently a Class III indication for plasmapheresis (specific role not determined).
Through this case presentation, a strong suggestion can be made to consider Plasmapheresis for Hypertriglyceride induced pancreatitis (HTGP) as a pragmatic therapeutic option, though not strongly supported by evidence, along with other standard therapies
Specialist Physician & HOD, Critical Care Medicine
Aster Hospital, Mankhool