Presentation

Classic presentation

• Triad of myalgias, weakness, and dark urine (classically reddish brown, or “tea-colored”).
  
• Myalgias occur most commonly in the proximal muscle groups.
  
• Physical examination may reveal muscle swelling and tenderness, with occasional skin changes including discoloration, induration, and blistering.
  
• It is possible for rhabdomyolysis to present without any of these signs or symptoms, making serum markers essential to the diagnosis.

Critical presentation

• Severe cases may present with hypovolemic shock, AKI, metabolic acidosis, disseminated intravascular coagulation (DIC), compartment syndrome, hyperkalemia, and cardiac arrhythmias.
  
• Compartment syndrome occurs due to swelling and edema of the injured muscle: classic physical examination findings include pain, paresthesias, paralysis, pallor, and pulselessness.

Diagnosis and evaluation

• History and physical examination
  
  
  
  • Take a history to elicit traumatic and nontraumatic causes of rhabdomyolysis. Always inquire about drug and alcohol use.
    
  • Physical examination may reveal muscle swelling and tenderness with overlying skin changes including discoloration, induration, or blistering.
    
  • Affected muscle should be evaluated for signs of compartment syndrome.
  
  
• Diagnostic tests
  
  
  
  • Serum creatine kinase (CK):
    
    
    
    • CK elevated >5 times normal value is the hallmark of rhabdomyolysis.
      
    • CK rises in 2–12 hours and peaks in 24–72 hours.
      
    • The CK-MM fraction (found in skeletal and cardiac muscle) predominates.
      
    • If serum CK levels fail to stabilize with appropriate therapy, or continue to rise for longer than 72 hours, consider ongoing muscle injury or compartment syndrome.
    
    
  • Urine myoglobin:
    
    
    
    • Myoglobin released from damaged muscle produces the classic reddish-brown urine color.
      
    • Results as (+) “blood” on urine dipstick without RBCs on the microscopic urine analysis.
    
    
  • Urine studies:
    
    
    
    • Urine electrolytes are typically consistent with a prerenal picture as a result of volume depletion.
      
    • Granular casts may also be seen and suggest acute tubular necrosis.
    
    
  • Serum AST, ALT, LDH, and aldolase:
    
    
    
    • Elevated levels of these intramyocyte enzymes may appear following release from damaged muscle cells.
    
    
  • Serum electrolytes with calcium, phosphate, and uric acid:
    
    
    
    • Hyperkalemia, hyperphosphatemia, and hyperuricemia: serum levels will be elevated due to release from damaged muscle cells.
      
    • Hypocalcemia: serum levels will be low due to calcium influx into damaged muscle cells, precipitation with excess serum phosphate, and decreased bone responsiveness to parathyroid hormone in the setting of AKI.
      
    • Creatinine, blood urea nitrogen (BUN), and glomerular filtration rate (GFR) may demonstrate renal dysfunction.
    
    
  • DIC panel: platelets, fibrinogen, PTT, D-dimer, blood smear:
    
    
    
    • DIC is a pathological activation of clotting seen during severe illness, inflammation, or infection, and is a known complication of rhabdomyolysis.
    
    
  • ECG:
    
    
    
    • If electrolyte disturbances are present, an ECG is needed to screen for arrhythmias and conduction abnormalities.
  
  
• The following specialized tests may be utilized when the diagnosis is unclear:
  
  
  
  • Electromyography (EMG), muscle biopsy, and magnetic resonance imaging (MRI).

Critical management

• The cornerstone of management includes discontinuation of inciting factors and aggressive management of fluid and electrolyte abnormalities.
  
• Volume repletion
  
  
  
  • Intravenous fluids enhance renal perfusion and increase urinary flow in order to prevent AKI and increase potassium excretion.
    
  • Early and aggressive resuscitation (studies have not determined the ideal rate or total amount) using isotonic fluids (normal saline or lactate ringer) with the following clinical markers as guides of adequate resuscitation:
    
    
    
    • Serum CK nadirs or decreases to <5000 U/L and
      
    • Urine output 200–300 mL/hour and
      
    • Initial (+) urine dipstick for “blood” (myoglobin) becomes (−), or
      
    • The patient is unable to tolerate volume of fluid given.
  
  
• Electrolyte management
  
  
  
  • Hyperkalemia: anticipate and treat aggressively as indicated.
    
  • Hypocalcemia: supplement calcium if symptomatic (weakness, tetany, seizures, prolonged QTc interval, cardiac arrhythmias), but otherwise use with caution as rebound hypercalcemia may occur as rhabdomyolysis resolves.
    
  • Hyperuricemia: treat with allopurinol 300 mg every 8–12 hours if uric acid >8 mg/dL.
  
  
• Sodium bicarbonate
  
  
  
  • No definitive evidence of benefit over isotonic volume repletion.
    
  • Potential benefit: urine alkalinization (maintaining a urine pH >6.5) may help prevent AKI.
    
  • Risk: may induce calcium-phosphate precipitation resulting in hypocalcemia.
    
  • Recommendation: use in severe cases, if calcium levels are normal, arterial pH <7.50, and serum bicarbonate is <30 mEq/L.
    
  • A bicarbonate infusion consists of 3 ampules of sodium bicarbonate (150 mEq) in 1 liter of D5W. Infuse at 200 mL/hour to maintain urinary pH >6.5.
  
  
• Loop diuretics
  
  
  
  • No definitive evidence of benefit.
    
  • Potential benefit: may be helpful in patients with volume overload and evidence of ongoing rhabdomyolysis.
    
  • Risk: may worsen hypocalcemia.
  
  
• Mannitol
  
  
  
  • No definitive evidence of benefit. A trend toward improved success has been observed in patients with CK levels >30 000 U/L.
    
  • Potential benefit: may be protective in encouraging diuresis, and in its role as a free radical scavenger.
    
  • Risk: volume depletion, hypernatremia, and acute kidney injury if >200 g/day is given.
    
  • Contraindicated in patients with low urine output (<0.5 mL/kg/hour for more than 24 hours).
  
  
• Dialysis
  
  
  
  • Indicated in cases of severe rhabdomyolysis complicated by
    
    
    
    • Persistent metabolic acidosis
      
    • Volume overload
      
    • Uremia
      
    • Severe electrolyte disorders.
    
    
  • Dose or type of dialysis is dependent on the hemodynamic stability of the patient and the desired speed of solute (potassium, urea, myoglobin) clearance. If the patient is hemodynamically stable and rapid solute clearance is preferred (i.e., critical hyperkalemia), then intermittent hemodialysis (iHD) is the method of choice. If the patient is hemodynamically unstable or there is concern for too rapid solute clearance, then continuous veno-venous hemodiafiltration (CVVHD) is chosen.

Sudden deterioration

• Sudden deterioration suggests worsening metabolic acidosis secondary to renal failure, compartment syndrome, or arrhythmias due to severe electrolyte disturbance.
  
• Metabolic acidosis: consider bicarbonate infusion while waiting to initiate renal replacement therapy in consultation with nephrology. Intubation may be needed if significant pulmonary edema has occurred in the setting of aggressive fluid repletion and worsening kidney function.
  
• Compartment syndrome: elevate the affected limb and request surgical consultation for fasciotomy.
  
• Arrhythmias: recheck serum electrolytes, ECG, and treat accordingly using ACLS protocols.

Vasopressor of choice: none.

References

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