Rhabdomyolysis
Rhabdomyolysis is necrosis of skeletal muscle with release of myoglobin, creatine kinase, and intracellular electrolytes into the circulation, diagnosed by a serum creatine kinase at least five times the upper limit of normal (typically over 1500 U/L) with a urine dipstick positive for blood but no red cells on microscopy; treatment is aggressive isotonic intravenous fluid to a urine output of 200 to 300 mL/h and correction of hyperkalemia, with acute kidney injury from pigment nephropathy the dominant complication.
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What this article covers
- Overview
Definition: rhabdomyolysis is necrosis of skeletal muscle fibers releasing intracellular contents, myoglobin, creatine kinase (CK), potassium, phosphate, and urate, into the circulation.
- Epidemiology
Common final pathway from many triggers: trauma/compression, extreme exertion, toxins/drugs, and myopathic syndromes converge on the same picture, so rhabdomyolysis is frequently seen rather than rare in any single bucket.
- Risk factors
Direct muscle injury: crush trauma, prolonged immobilization ("found down"), compartment syndrome, and extensive burns, especially deep muscle injury from electrical current.
- Pathophysiology
Sarcolemmal injury is the common final step: disruption of the muscle membrane or failure of the calcium pump lets extracellular calcium flood into the myocyte, whatever the trigger.
- Clinical features
Myalgia and muscle weakness are the most common symptoms, but many patients, especially with a toxic or metabolic trigger, are asymptomatic despite a CK over 5x the upper limit of normal.
- Differential diagnosis
Acute coronary syndrome: troponin is the cardiac-specific biomarker; a normal troponin with high total CK and a CK-MB fraction under 3% of total CK excludes cardiac muscle as the source.
- Diagnosis
The diagnosis is confirmed by a serum CK at least five times the upper limit of normal, usually greater than 1500 U/L, in the appropriate clinical setting; there is no separate formal diagnostic…
- Management
First, start aggressive isotonic intravenous fluid resuscitation (0.9% saline) to expand intravascular volume, reverse renal vasoconstriction, and flush myoglobin through the tubules, titrated to a…
- Complications
Acute kidney injury from pigment nephropathy: the dominant complication, in 15% to 50% of cases, from volume depletion, renal vasoconstriction, direct tubular toxicity, and myoglobin cast…
- Prognosis
Most patients recover renal function fully, even those who develop AKI, once the pigment load clears and volume status is corrected.
- Prevention
Hydrate before and during unaccustomed intense exertion: athletes and recruits doing heavy exertion in heat should use generous fluid intake and graded conditioning, not abrupt intensity jumps.
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Related articles
- Acute kidney injury
Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.
- Hyperkalemia
Hyperkalemia is a serum potassium level above 5.0 mEq/L, most often from decreased kidney excretion, transcellular shifts, or excess intake, with levels above 6.0-6.5 mEq/L or any ECG change constituting a medical emergency from the risk of fatal arrhythmia. Treatment sequences cardiac membrane stabilization with calcium, transcellular potassium shifting with insulin/dextrose and albuterol, then definitive potassium removal with binders, diuretics, or dialysis.
- Hypocalcemia
Hypocalcemia is a low serum calcium concentration, most often from insufficient parathyroid hormone action (postsurgical or autoimmune hypoparathyroidism, hypomagnesemia, or PTH resistance) or from vitamin D deficiency and chronic kidney disease. Severe or symptomatic disease requires urgent intravenous calcium, while chronic disease is managed with oral calcium, vitamin D repletion, and calcitriol when PTH is absent or the kidney cannot activate vitamin D.