Hypertriglyceridemia

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    Hypertriglyceridemia

    32-year-old, “otherwise healthy,” man with severe, sharp, epigastric abdominal pain. Your differential is broad enough, but you target a few questions: Drinker? (No.) Gastritis/GERD/PUD in the past? (No.) Gallstones? (No.) Smoker/Hypertensive/your-aorta-or-mesenterics-are-in-trouble? (No.) Bitten by a scorpion lately? (No.) Jokes aside, you’re thorough. He has had terrible, worsening, constant pain for the last 2-3 days. No fevers or diarrhea, but today he started vomiting (without any blood) and he’s very nauseated (even looking at the nurse’s coffee made him gag). He has no surgical history, and has never felt this way before. The exam: soft, non-distended, but tender over the epigastrium (not guarding, no rebound). He’s the slightest bit tachypneic, but no fever and his HR/BP are within-normal-limits.

    After you order some labs and see a few more patients, a bunch of “lab canceled” errors come back. You call the lab to find out why and are told his blood is grossly lipemic (i.e. filled with lipids) and the machines cannot accurately assess his electrolytes, cell counts, or much else. It will be a little while for results, she says, and asks if you want her to run a lipid profile. You do–and shockingly she already did because she was curious. The patient’s triglyceride level is >12,000mg/dl. A few minutes later the lipase pops up at 6,000 as well. Bam, diagnosis: acute pancreatitis secondary to hypertriglyceridemia.

    Pancreatitis is mostly (>80% of the time) caused by stones or alcohol, but #3 on the list: hypertriglyceridemia. This is a pearl, so read about the mechanisms elsewhere, but this (like most metabolic pathophysiology) is a derangement in manufacture and breakdown on triglycerides, most commonly occurring in patients with familial hypertriglyceride pathology (not just a buffet-style weekend). This is a simplification, so read more.

    Normal pancreatitis treatment first: IV fluids, pain control, nutritional support (later, NPO for now). In this case, you add an insulin drip (use similar doses to your DKA drips, 0.1-0.3units/kg/hr; plus a D5 added solution based on the glucose) to the treatment plan, to be discontinued at a triglyceride level <500. Insulin works by (1) up-regulating insulin-sensitive lipoprotein lipase (i.e. accelerating triglyceride metabolism) and (2) inhibiting hormone-sensitive lipase in adipocytes (preventing release of more fatty acids into circulation).

    This is a helpful flowchart from UpToDate, and includes some of the high risk features to consider when your patient is sicker–i.e. when to consider plasmapheresis.

    tl;dr — acute pancreatitis secondary to hypertriglyceridemia; treat with fluids, pain control, NPO, insulin drip, and consider plasmapheresis in the sickest patients.

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