Rhabdomyolysis and Hematuria
Yes, rhabdomyolysis can cause hematuria, though what appears to be blood in the urine is often myoglobinuria that mimics hematuria on visual inspection and dipstick testing. 1, 2
Pathophysiology of Rhabdomyolysis and Urinary Findings
Rhabdomyolysis involves skeletal muscle breakdown with release of intracellular contents into circulation, including:
- Myoglobin - a muscle protein that is filtered by the kidneys and can appear as reddish-brown urine
- Creatine kinase (CK) - significantly elevated in serum
- Electrolytes - particularly potassium and phosphate
Urinary Manifestations
- Myoglobinuria: Presents as tea-colored or reddish-brown urine
- False-positive hematuria: Myoglobin can cause positive dipstick reactions for blood without actual RBCs present
- True hematuria: Can occur in severe cases due to:
- Acute kidney injury with glomerular damage
- Direct renal tubular injury from myoglobin toxicity
- Coagulopathy in severe cases
Clinical Presentation and Diagnosis
Key Clinical Features
- Muscle pain, weakness, or swelling
- Tea-colored or reddish-brown urine
- Decreased urine output in severe cases
Diagnostic Tests
- Serum CK >5 times upper limit of normal (often >10,000 U/L in significant cases)
- Urinalysis showing:
- Positive dipstick for blood
- Few or no RBCs on microscopy (in pure myoglobinuria)
- Presence of granular casts
- Elevated BUN and creatinine if AKI has developed
Causes of Rhabdomyolysis
Common causes include:
- Traumatic: Crush injuries, prolonged immobilization, compartment syndrome
- Non-traumatic:
- Medications (statins, antipsychotics)
- Illicit drugs and alcohol
- Extreme physical exertion
- Infections
- Electrolyte abnormalities
- Hyperthermia/hypothermia
- Metabolic disorders
Complications
Rhabdomyolysis can lead to serious complications:
- Acute kidney injury - occurs in up to 40% of cases
- Electrolyte abnormalities - hyperkalemia, hypocalcemia, hyperphosphatemia
- Compartment syndrome - requiring surgical intervention
- Disseminated intravascular coagulation - in severe cases
Management
Early aggressive treatment is essential to prevent complications:
Fluid resuscitation:
- IV fluid therapy with isotonic saline targeting urine output of 200-300 mL/hour 3
- Daily target of at least 6L for severe cases
Monitoring:
- Serum CK levels
- Renal function (BUN, creatinine)
- Electrolytes every 4-6 hours initially
- Urine output
- Compartment pressures if indicated
Treatment of complications:
- Hyperkalemia management
- Consider renal replacement therapy for severe AKI, refractory hyperkalemia, or severe acidosis
- Surgical fasciotomy for compartment syndrome
Special Considerations
In patients with sickle cell trait, exertional rhabdomyolysis can occur under conditions that promote HbS polymerization and erythrocyte sickling, such as hyperthermia, dehydration, acidosis, and hypoxemia 1
Patients with heart failure require careful fluid management to avoid volume overload while treating rhabdomyolysis 3
Elderly patients need more careful fluid titration to prevent complications 3
Clinical Pitfalls
Misdiagnosis: Failing to distinguish between true hematuria and myoglobinuria can lead to unnecessary workup for urological conditions
Delayed treatment: Failure to recognize rhabdomyolysis early can result in preventable kidney injury
Inadequate monitoring: Not following CK levels, renal function, and electrolytes closely enough during treatment
Insufficient fluid resuscitation: Inadequate hydration is the most common preventable cause of AKI in rhabdomyolysis
Remember that what appears as hematuria in rhabdomyolysis patients is often myoglobinuria, but true hematuria can also occur as a complication of the condition, particularly when acute kidney injury develops.