Rhabdomyolysis

Rhabdomyolysis

David Ray Velez, MD

Table of Contents

Definition and Pathophysiology

Definition: Muscle Necrosis Causing Release of Intracellular Contents

Pathophysiology

  • The Ultimate Exact Pathways are Often Unclear
  • Final Common Pathway: Release of Intracellular Calcium
    • From Either Direct Myocyte Injury or Energy (ATP) Depletion
    • Cell Death from Protease Activation, Mitochondria Dysfunction, and Reactive Oxygen Species
  • Cell Death Causes Release of CK, Electrolytes, Myoglobin, and Other Enzymes

Causes

  • Trauma
  • Crush Injury
  • Intense Exertion
  • Ischemia (Arterial Thrombosis, Embolism, or Vessel Clamping During Surgery)
  • Malignant Hyperthermia
  • Neuroleptic Malignant Syndrome (NMS)
  • Infection
  • Electrolyte Disturbances
  • Autoimmune Disorders (Dermatomyositis or Polymyotitis)
  • Drugs (Alcohol, Cocaine, Amphetamines, etc.)
  • Medications (Statis, Psychiatric Medications, Antihistamines, etc.)

Presentation and Complications

Classic Triad

  • Myalgia/Muscle Pain
  • Muscle Weakness
  • Dark Red-Brown Urine
  • *The Classic Triad is Rare and Only Seen in < 10% of Patients

Additional Symptoms

  • Lethargy
  • Tachycardia
  • Fever
  • Nausea/Vomiting
  • Abdominal Pain
  • Altered Mental Status

Complications

  • Acute Kidney Injury (AKI)
    • The Most Significant Complication
    • From Hypovolemia and Nephrotoxic Myoglobin
    • Risk: 10-40%
  • Compartment Syndrome
  • Hypovolemia – From Fluid Accumulation within the Damaged Muscle
  • Hyperkalemia
  • Hyperphosphatemia
    • From Hyperphosphatemia and Calcium Deposition in Damaged Muscle
  • Disseminated Intravascular Coagulation (DIC)

Tea-Colored Urine of Rhabdomyolysis 1

Diagnosis

Labs

  • Elevated Creatinine Kinase (CK)
  • Myoglobinuria
  • Electrolyte Disturbances:
    • Hyperkalemia – Released from Damaged Cells
    • Hyperphosphatemia – Released from Damaged Cells
    • Hypocalcemia (Early) – Calcium Initially Enters into the Damaged Myocytes
    • Hypercalcemia (Late) – Calcium within the Damaged Cells Eventually Efflux Out
  • Anion Gap Metabolic Acidosis
  • High Uric Acid

Clinical Diagnosis

  • Diagnosis: Acute CK Elevation with Either Clinical Signs (Weakness/Dark Urine) or Myoglobinuria on UA
  • CK > 5,000 U/L is Often Used but No Absolute Cutoff is Defined

Treatment

Correct Any Underlying Pathology (Fasciotomy, etc.)

Primary Treatment: Aggressive IV Fluid Resuscitation (LR or NS) 

  • Goal Urine Output: 1-3 mL/kg/hr
  • The Primary Goal of Fluid Resuscitation is to Prevent AKI
  • May Require Dialysis for Volume Overload, Acidemia, Hyperkalemia, or Uremia
  • Generally Avoid Mannitol or Diuretics

Sodium Bicarbonate

  • Goal: Urinary Alkalinization to Prevent Cast Formation
  • Use is Poorly Defined and Controversial
  • Does Not Reduce the Risk of AKI or Mortality
  • Contraindications:
    • Hypocalcemia – May Worsen
    • pH ≥ 7.5
    • HCO3 ≥ 30

References

  1. Ganeshram P, Goundan PN, Jeyachandran V, Arthur P. Five factors contributing to severe rhabdomyolysis in a 21 yr old IV drug abuser: a case report. Cases J. 2009 Jul 7;2:6479. (License: CC BY-3.0)