Rhabdomyolysis is a condition characterized by massive muscle cell breakdown with the release of the cellular contents on the bloodstream and adjacent tissue. The substances released further increase the inflammation in the affected area, which can cause local complications (e.g. compartmental syndrome, ischemia). The substances released on the bloodstream, on the other hand, may cause systemic issues (e.g. hyperkalemia, acute kidney injury).
Every year around 26.000 new cases of rhabdomyolysis occur in USA.
It may be caused by a myriad of different mechanisms. The causes, clinical features, diagnosis and treatment are discussed below.
Muscle necrosis can be caused by many different mechanisms, including:
Direct Trauma (crush injury, accidents, electrocution, surgery)
Indirect Trauma (exercise, seizures, coma, immobilization, neuroleptic malignant syndrome)
Drug intoxication (e.g. MDMA, opiates, mushrooms, alcohol, cocaine)
Medications (e.g. neuromuscular blockers, statins)
Infections (e.g. tetanus)
Electrolyte abnormalities (e.g. hypokalemia, hypophosphatemia)
Toxins from poisonous animals (e.g. spiders)
Genetic/Hereditary myopathies (e.g. PPK deficiency, Carnitine palmitoyltransferase deficiency)
Inflammatory muscle diseases (e.g. polymyositis)
SIGNS & SYMPTOMS:
The signs of muscle necrosis can range from mild discomfort and pain to severe weakness. Tenderness on the affected muscle groups may be observed.
Patients with acute kidney injury (AKI) may manifest with dark brown or red urine. Oliguria can also be present.
Every patient with a suggestive clinical history should be tested. Complete metabolic panel (which includes kidney function), CK and urinalysis should be obtained. Other tests may be useful as well (drug tests, CBC, among others).
Creatine Kinase (CK) begins to rise after 2 hours and reach its peak after 24-72h. After that the levels are supposed to decline by ~50% every 24-48 hours. There is no clear-cut value for CK elevation to establish diagnosis of rhabdomyolysis, but at least 5000 U/L is usually the minimum (the peak for most patients is around 10-25.000 U/L)
To diagnose pigment-induced AKI, a suggestive clinical scenario (e.g. rhabdomyolysis) and decreased kidney function must be present.
Urinalysis in patients with heme pigment-induced AKI may be positive for micro hematuria without visible erythrocytes. Pigmented granular casts may also be present (consisting of Tamm-Horsfall protein precipitation). Proteinuria may also be present.
Hyperkalemia may develop regardless of the presence or absence of AKI.
Hypocalcemia due to the release of phosphate is very common (>60%). Hypercalcemia, on the other hand, may occur during the recovery stage.
When AKI is present, FENa can be <1% even without tubular injury, since these patients are often hypovolemic as well (so they have a pre-renal component on top of the renal component).
The treatment of rhabdomyolysis focuses on preventing complications (e.g. kidney function deterioration, electrolyte abnormalities). Underlying causes (e.g. drug intoxication, poisons) should be managed accordingly when present.
Fluids (normal saline ideally) are a vital part of the management because they reduce the hypovolemia due to sequestration and prevent acute kidney injury. Victims of crush trauma may receive volume expansion even before extraction to prevent AKI. Normal saline should be administered (1L/h for 1-2 hours). After that, fluid administration may be decreased to 500-250mL/h to obtain a desired rate of diuresis of 200-300mL/h. Since the patients will be receiving large volumes of fluids, the urine output should be measured to guarantee a good input-output balance and avoid fluid overload (if the urine output is adequate = > 20mL/h but lower than 200-300mL/h, mannitol (1-2g/kg/day) may be added to the normal saline to increase the diuresis to the 200-300mL/hour levels.
If the patient gets fluid overloaded, loop diuretics may be used. In those with inappropriate urine output, dialysis is an option.
Urine alkalinization may be beneficial (although the evidence is not strong). Only patients with proper urine output, arterial pH <7.5, serum bicarbonate <30mEq/L, and absence of severe hypocalcemia may be candidates for urine alkalinization. The goal is to maintain an urinary pH > 6.5. That is done by giving 150mL of sodium bicarbonate 8.4% mixed with 1L or D5% at 200mL/h (adjusting the rate to reach an urinary pH >6.5). If arterial pH gets > 7.5, serum BIC > 30mEq/L or symptomatic hypocalcemia develops, bicarbonate infusion should be discontinued.
SOURCES & FURTHER READING:
- Torres PA et al. Rhabdomyolysis: Pathogenesis, Diagnosis, and Treatment. Ochsner J. 2015 Spring; 15(1): 58–69.
- Hunter JD et al. Rhabdomyolysis. Contin Educ Anaesth Crit Care Pain (2006) 6 (4): 141-143.
- Sauret JM et al. Rhabdomyolysis. Am Fam Physician. 2002 Mar 1;65(5):907-913.
- Efstratiadis G et al. Rhabdomyolysis updated. Hippokratia. 2007 Jul-Sep; 11(3): 129–137.
- Khan FY. Rhabdomyolysis: a review of the literature. Neth J Med. 2009 Oct;67(9):272-83.