Hyperlipidemia

Read it as a marker of vascular disease - Hyperlipidemia travels with coronary artery disease, peripheral artery disease, cerebrovascular accident, aneurysm, and type 2 diabetes. Among patients with premature coronary artery disease — men before 55 to 60, women before 65 — hyperlipidemia is present in 75% to 85%, versus roughly 40% to 48% of age-matched controls. Ask directly about family history of premature cardiovascular disease or early cardiac death: in one study 54% of patients with premature coronary artery disease had an underlying hereditary disorder.

Exam findings that change the plan - Listen for carotid and renal bruits, palpate peripheral pulses, and look at the skin for xanthomas — yellowish papules over tendons, elbows, palms, and buttocks. In familial combined hyperlipidemia, carotid ultrasound is used to detect subclinical atherosclerosis, so ask whether one has been done.

Statin muscle toxicity is not rare - Between 5% and 20% of patients on a statin report muscle-related intolerance, and myopathy and rhabdomyolysis leading to acute renal failure have been reported. Risk rises with age over 65, hypothyroidism, renal impairment, and when a statin is combined with ezetimibe. If the patient reports new myalgia or extremity pain, send a CK and a creatinine before committing them to a long case in a fixed position.

Check the liver numbers - Lipid-lowering therapy shows up in the chemistry panel: statins can raise CK, AST, ALT, alkaline phosphatase, bilirubin, and glucose, and ezetimibe hepatotoxicity presents in either a hepatocellular or a cholestatic pattern. Look at the LFTs already in the chart before you plan hepatically cleared drugs.

Hunt the secondary cause - Uncontrolled diabetes, hypothyroidism, nephrotic syndrome, and chronic renal failure all drive secondary hyperlipidemia, and each of them changes your anesthetic more than the lipid number does. A TSH, a glucose or HbA1c, and a creatinine are the three results worth having.

Triglycerides and the pancreas - Fasting triglycerides above 1000 mg/dL, often above 2000, define familial chylomicronemia syndrome and carry a real risk of acute pancreatitis. If the patient turns up with abdominal pain, serum lipase and amylase plus abdominal CT confirm it. Expect turbid, milky-looking blood in these patients.

Niacin effects you will see in the room - Niacin causes prostaglandin D2-mediated cutaneous vasodilation and flushing — don't chase it as an anaphylactic or transfusion reaction. It also decreases glucose tolerance and can cause hyperglycemia in diabetic patients, and regular-release niacin carries hepatotoxicity risk.

Hyperlipidemia covers the genetic and acquired disorders that raise circulating lipids — objectively, an LDL, total cholesterol, triglyceride, or lipoprotein level above the 90th percentile for the population, or an HDL below the 10th. Most cholesterol in circulation is made by the liver rather than eaten. Primary forms are inherited (familial combined hyperlipidemia, familial hypercholesterolemia, familial defective apolipoprotein B-100, familial hypertriglyceridemia); secondary forms follow from diet, uncontrolled diabetes, hypothyroidism, chronic renal failure, nephrotic syndrome, and drugs including thiazides, beta blockers, glucocorticoids, amiodarone, estrogen-progestin contraceptives, and antiretrovirals.

It matters at the board because of atherosclerosis: endothelial injury plus LDL deposition builds plaque that stays asymptomatic until stenosis reaches 70% to 80%, then can rupture acutely with thrombosis. Severe hypertriglyceridemia carries a separate hazard — acute pancreatitis.