Rhabdomyolysis

Hyperkalemia kills first - Potassium pours out of dying muscle and the ECG shows it before the lab does: peaked T waves, prolonged PR, widening QRS, then ventricular tachycardia or asystole. Treat the potassium before you chase the CK.

Isotonic saline, not lactated Ringer's - Potassium-containing fluids are avoided in rhabdomyolysis. Guidance from the International Society of Nephrology renal disaster relief task force favors isotonic saline over alkaline fluids in the field, and adding dextrose helps limit the hyperkalemia.

Volume early and generously - In crush injury, start fluid before the compression is relieved if you can, and keep it running during transport. A well-built adult gets roughly 1 L/h for 2 hours then 500 mL/h, targeting 200 to 300 mL/h of urine output. Continue until myoglobinuria clears and the CK is downtrending.

Confirm the pigment, then size the injury - A urine dipstick positive for blood with no red cells on microscopy is myoglobinuria, but its sensitivity is under 25%, so a clean dipstick rules nothing out. CK is the sensitive test: above 5,000 IU/L means significant muscle injury, and AKI risk climbs sharply above 40,000 IU/L. CK rises 2 to 12 hours after injury and peaks at 1 to 5 days, so a CK that keeps climbing means muscle is still dying - think compartment syndrome.

Calcium goes the other way - Calcium floods into damaged myocytes, so expect hypocalcemia with QTc prolongation alongside the hyperkalemia, plus a metabolic acidosis from released organic acids. Send an ionized calcium, phosphate, and a blood gas, not just a potassium.

Positioning is a cause, not a footnote - Lower-extremity compartment syndrome is a recognized complication of prolonged lithotomy from inadequate limb perfusion, and long procedures plus extremes of body weight raise the risk. Lower the legs periodically during long lithotomy cases and pad every bony prominence.

Succinylcholine in an undiagnosed myopathy - The FDA label carries a boxed warning for acute rhabdomyolysis with hyperkalemia, followed by ventricular dysrhythmias, cardiac arrest, and death, after succinylcholine given to apparently healthy pediatric patients later found to have an undiagnosed skeletal muscle myopathy, most often Duchenne muscular dystrophy. The label contraindicates it in skeletal muscle myopathies, in known or suspected malignant hyperthermia susceptibility, and after the acute phase of major burns, multiple trauma, extensive denervation, or upper motor neuron injury. In a child with unexplained weakness, delayed motor milestones, or a raised baseline CK, reach for a nondepolarizer.

Malignant hyperthermia is one of the causes - Sustained contracture depletes ATP, membrane integrity fails, and potassium, CK, and myoglobin spill into the blood. Dantrolene 2.5 mg/kg IV push immediately, repeat boluses of 1 to 2.5 mg/kg to a cumulative maximum of 10 mg/kg, then 1 mg/kg every 6 hours for 24 hours after the last sign. See the Malignant Hyperthermia (MH) entry for the full crisis drill.

Urine alkalinization is optional, not reflexive - Consider it only after urine output is established and alkalosis is excluded. Fifty mEq of sodium bicarbonate in half-normal saline is the traditional recipe, targeting a urine pH just above 6.5 and a serum pH no higher than 7.5. Stop the bicarbonate once serum pH reaches 7.5. It can precipitate hypocalcemia with tetany and seizures.

Mannitol only after urine flows - Give it only once urine output is at least 20 mL/h. Trial 60 mL of 20% mannitol over 5 minutes and continue only if output rises 30 to 50 mL/h above baseline. Avoid it in established AKI, oliguria, or anuria, and current evidence does not support pairing it with bicarbonate.

Know when it becomes a dialysis problem - Anuric acute kidney injury, hyperkalemia, or volume overload that conservative measures failed to control. Peritoneal dialysis is not preferred after trauma.

A second episode changes the next anesthetic - Recurrent rhabdomyolysis should prompt a workup for an underlying metabolic myopathy, and muscle biopsy is generally deferred until after full recovery. Until that comes back, plan future anesthetics trigger-free and without succinylcholine.

Rhabdomyolysis is the dissolution of skeletal muscle, with myoglobin, creatine kinase, potassium, phosphate, and organic acids leaking out of dying myocytes into the circulation. The common pathway is ATP depletion or direct sarcolemmal injury: without ATP the cell cannot pump calcium out, sarcoplasmic calcium stays high, the muscle stays contracted, and calcium-dependent proteases and phospholipases digest the fiber.

Three consequences drive the perioperative plan. Potassium and phosphate flood the blood while calcium is trapped inside damaged muscle, so hyperkalemia arrives alongside hypocalcemia. Heme pigment reaching the distal tubule obstructs it and causes acute kidney injury, which complicates 5% to 30% of cases and accounts for about 15% of all AKI. Third-spacing into injured muscle drops intravascular volume. Trauma and crush, immobilization, sepsis, cardiovascular surgery, statins, malignant hyperthermia, and prolonged pressure under anesthesia are all recognized causes.