Epidemiology

Etiology

Crush injury/trauma: Building collapse, motor vehicle accidents, prolonged entrapment.
Prolonged immobilization: Elderly patient fallen and unable to get up, obtundation from alcohol/drug overdose.
Exertional: Marathon runners, military recruits, heat stroke, status epilepticus.
Non-exertional/toxins: Statins (especially combined with CYP3A4 inhibitors like fibrates, macrolides), cocaine (alpha-1 adrenergic vasoconstriction), amphetamines, alcohol (prolonged Immobilization and compression on muscle).
Malignant hyperthermia/Neuroleptic malignant syndrome (NMS): Drug-induced extreme muscle rigidity.

Rhabdomyolysis → release of the following substances:
- Creatine phosphokinase (CPK) and serum myoglobin → pigment nephropathy → acute tubular necrosis → acute kidney injury (intrinsic)
- Potassium → cardiac arrhythmia
- Lactic acid → metabolic acidosis
Hypovolemia → ↓ renal perfusion → acute kidney injury (prerenal)
- Hypovolemia is predominantly due to third spacing of extracellular fluid into damaged muscle tissue.
Reperfusion syndrome → compartment syndrome

Classic Triad: Myalgias (muscle pain/tenderness), transient muscle weakness, and dark/tea-colored urine.
Local signs: Swollen, firm, or tense muscle groups; loss of pulses/sensation if compartment syndrome develops.
Systemic features (Crush Syndrome): Hypotension, hypovolemic shock (due to third-spacing of fluid into damaged muscle), oliguria/anuria.

Initial/Screening: Urine dipstick positive for blood but no RBCs on microscopic urinalysis (dipstick detects orthotolidine reaction of heme, cross-reacting with myoglobin). c
Confirmatory/Gold Standard: Serum Creatine Kinase (CK) > 5 times the upper limit of normal (typically > 5,000 U/L; levels rise within 12 hours of injury and peak in 24–72 hours).
Key Labs:
- Hyperkalemia & hyperphosphatemia: Released from damaged intracellular compartments.
- Hypocalcemia: Calcium deposits into damaged muscle tissue early; can lead to rebound hypercalcemia during the recovery phase as calcium is released back into circulation.
- Hyperuricemia: Nucleoside release from damaged muscle cells.
- Elevated BUN and Creatinine: Indicates pigment-induced AKI.
ECG: Crucial to screen for hyperkalemic cardiotoxicity (peaked T waves, PR prolongation, QRS widening).

tags	—
aliases	Rhabdomyolysis, Crush syndrome