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
- 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)