Rhabdomyolysis is the breakdown of skeletal muscle tissue that results in the release of intracellular contents, such as myoglobin, potassium, phosphate, creatinine phosphokinase (CPK), and urate, into the blood and extracellular space. Rhabdomyolysis has many causes, including trauma and crush injuries, drugs, overexertion, temperature extremes, infections, and prolonged immobility. The classic presenting triad of myalgia, generalized weakness, and tea-colored urine is seen in a minority of patients. The diagnosis is confirmed in patients with an elevated serum CPK, typically > 5× the upper limit of normal. Serious complications include acute kidney injury from myoglobin-induced tubular damage, cardiac arrhythmias and arrest from electrolyte derangements, and compartment syndrome. Crush syndrome is the systemic manifestation of a crush injury. It typically manifests with signs of volume depletion (hypovolemia, shock) and compartment syndrome of the affected extremity, and it is often associated with acute kidney injury. Treatment of rhabdomyolysis includes aggressive fluid resuscitation and the correction of metabolic abnormalities. In cases of renal failure, renal replacement therapy may be indicated.
- Rhabdomyolysis → release of the following substances: 
- Hypovolemia → ↓ renal perfusion → acute kidney injury (prerenal) 
- → compartment syndrome
- Generalized weakness
- Darkened urine (red to brown)
- Nonspecific symptoms: fever, nausea, vomiting
- Signs of complications: : e.g., AKI, compartment syndrome, cardiac arrhythmias (see “Complications” for details)
Many patients are asymptomatic on presentation. The classic triad of myalgia, generalized weakness, and tea-colored urine is seen in a minority of patients. 
General principles 
- Rhabdomyolysis is a biochemical diagnosis based on ↑ CPK levels.
- Clinicians should have a low threshold for checking serum CPK levels in patients with supportive clinical features and/or those who are at risk (see “Etiology”). 
- Further diagnostic studies should focus on identifying complications of rhabdomyolysis.
- The McMahon score for rhabdomyolysis helps identify patients at risk of death or requiring renal replacement therapy. 
Blood work 
- ↑ CPK > 5× the ULN or > 1000 IU/L 
- ↑ Uric acid
- ↑ Myoglobin 
- ABG: anion gap metabolic acidosis
- Coagulation studies
- Urine studies 
- ECG: may show or ECG findings of hypocalcemia
- Provide prompt .
- Consider stopping medications associated with rhabdomyolysis. 
- Identify and treat all reversible causes of rhabdomyolysis.
- Monitor and manage complications.
Consider ICU admission for patients with crush syndrome or those with increased risks for complications (e.g., CPK > 40,000 U/L, K+ > 6 mEq/L, compartment syndrome, sepsis, ECG changes, age > 65 years, comorbid cardiovascular disorders, or preexisting CKD). 
Fluid management 
- Immediate IV fluid resuscitation (e.g., ≥ 10–12 L/day)
- Urine alkalinization: not routinely recommended 
The following therapies are not routinely recommended but may be considered under specialist guidance. Their use remains controversial. 
- Loop diuretics (e.g., furosemide): may be considered to force diuresis only after the patient's volume has been expanded.
- Mannitol: may be considered under specialist guidance
Management of electrolyte derangements 
Correct hyperkalemia aggressively
- Take a based on the risk of .
- Monitor potassium levels every 4 hours until normalized.
- Consider treatment for:
Acute management checklist
- Check blood CPK, CMP, CBC, ABG, coagulation studies.
- Check urine dipstick and urine sediment.
- Obtain 12-lead ECG to assess for or .
- Start aggressive 200–300 mL/hour or 1–3 mL/kg/hour. to a target urine output of
- Assess the need for ICU level of care and (e.g., older patients or those with oliguric renal failure, comorbidities, complications).
- Monitor potassium every 4 hours; aggressively.
- Correct hypocalcemia only if symptomatic (e.g., tetany, seizures).
- Consult nephrology if the patient has .
Early complications 
- Electrolyte abnormalities
- Hepatitis 
- Cardiac arrhythmias, cardiac arrest (due to electrolyte derangements) 
Late complications 
- Acute kidney injury: can be oliguric or anuric
- Disseminated intravascular coagulation 
- Compartment syndrome: may develop as a result of direct muscle injury or after volume resuscitation
We list the most important complications. The selection is not exhaustive.