Epidemiology
Etiology
Toxin
- Barium Ingestion (see xxxx, [[Barium]]): accidental or intentional ingestion
- Widow Spider Bite (see Widow Spider Bite, [[Widow Spider Bite]])
Muscle Trauma
- Crush Injury
- Prolonged Pressure: typically in patient who has been unconscious
Physiology
Clinical Manifestations
Renal Manifestations
Acute Kidney Injury (AKI) (see Acute Kidney Injury, [[Acute Kidney Injury]])
- Epidemiology
- Rhabdomyolysis accounts for 28% of trauma-associated AKI requiring HD
- AKI develops in 30-40% of rhabdomyolysis cases
- Mechanisms of AKI
- Decreased Glomerular Perfusion
- Nephrotoxic Effects of Ferrihemate
- Ferrihemate and globin are breakdown products of myoglobin (occurs when pH is <5.6)
- Ferrihemate contains iron, which accepts and donates electrons -> generation of free radicals, which cause direct renal cell injury
- Effects of Heme-Proteins On Nitrous Oxide (NO), Endothelin Receptors, and Various Cytokines
- Precipitation of Myoglobin and Uric Acid Crystals within Renal Tubules
- Risk Factors for AKI [MEDLINE]
- Peak CK >6000 IU/L: AKI may occasionally occur in severely dehydrated patients with peak CK levels as low as 2000 IU/L
- Dehydration (hematocrit >50, serum sodium level >150 mEq/L, orthostasis, pulmonary wedge pressure < 5 mm Hg, urinary fractional excretion of sodium < 1%)
- Hyperkalemia/Hyperphosphatemia: present on admission
- Hypoalbuminemia
- Sepsis
Electrolyte Abnormlaities
- Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]])
- Hyperphosphatemia (see Hyperphosphatemia, [[Hyperphosphatemia]])
- Hypocalcemia or Hypercalcemia (see Hypocalcemia, [[Hypocalcemia]] and Hypercalcemia, [[Hypercalcemia]])
- Patients are typically hypocalcemic during the oliguric phase of AKI (ATN): probably due to calcium deposition in the injured muscle tissues
- Approximately 30% of patients are hypercalcemic during the recovery/diuretic phase of AKI (ATN): due to increased 1,25-Dihydroxyvitamin D3, which occurs during this phase
Abnormal Findings on Urinalysis
- Large Blood Detected on Urinary Dipstick with Minimal RBC’s on Microscopy: as urinary dipstick detects myoglobin
- Coca Cola-Colored Urine (see Urine Discoloration, [[Urine Discoloration]])
Orthopedic Manifestations
- Elevated CK: may be in the hundreds of thousands
Other Manifestations
- Sites of Muscle Injury: may be notable on exam
Treatment
Management of Electrolyte/Metabolic Abnormalities
- Hyperkalemia: standard treatment
- Hypocalcemia (During Early Oliguric Phase of ATN): should not be treated unless patient has arrhythmias, hemodynamic instablity, hyperkalemia, or seizures
- Administered calcium may complex with phosphate and produce metastatic calciification (especially intramuscularly)
- Hypercalcemia (During Recovery/Diuretic Phase of ATN): no treatment necessary (as this occurs due to increased 1,25-Dihydroxyvitamin D3, which occurs during this phase)
- hyperphosphatemia : usually not clinically significant (but will respond to urinary alkalinization with diuresis
- Hyperuricemia: usually not clinically significant and does not require treatment
IVF Hydration + Urinary Alkalinization
- IVF Hydration (Normal Saline) + Bicarbonate Drip (3 Amps Sodium Bicarb/1L D5W): titrate bicarbonate drip + normal saline IVF (and diuretics PRN) to maintain urine outpt of >200 ml/hr + urine pH >6.5-7.0
- Role of Hydration
- Expansion of extracellular volume is critical: injured myocytes sequester fluids
- Expansion of intravascular volume increases the glomerular filtration rate, oxygen delivery, and dilutes myoglobin and other renal tubular toxins
- Although there are no randomized trials of hydration in rhabdomyolysis, retrospective studies in crush injury patients indicate that early (pre-hospital) IVF hydration improves prognosis
- Patients with CK >15,000 IU/L may require IVF resuscitation in excess of 6L
- Role of Urinary Alkalinization
- Urinary alkalinization decreases ferrihemate and myoglobin cast formation (at urine pH >6.5-7.0)
- Recommended for patients with CK >6000 IU/L
- Urinary alkalization should be considered earlier in patients with acidemia, dehydration, or pre-existing renal disease
- Although randomized trials are lacking, retrospective and animal studies support this practice
- Bicarbonate infusion may precipitate hypocalcemia: must follow serial calcium during bicarbonate infusion
- Invasive Monitoring (Central Venous Pressure, Swan-Ganz Catheterization, Arterial Line): may be required to assure adequate fluid resuscitation (especially in patients with cardiac or renal disease)
- Role of Diuretics: lasix or mannitol may be considered in cases with oliguria despite adequate intravascular volume (however, these should be avoided in cases with inadequate intravascular volume)
Monitor Serial CK Levels + Myoglobinuria
- Follow serial CK levels at least q6hrs
- Aggressive IVF resuscitation should be continued until myoglobinuria is cleared
Hemodialysis
- May be required in cases with AKI + refractory hyperkalemia/acidosis or pulmonary edema/congestive heart failure
Free-Radical Scavengers/Antioxidants
- Examples: pentoxifylline, vitamin E, and vitamin C
- Despite animal studies, these have an unclear role in management of rhabdomyolysis
Treatment of Fractures/Sites of Muscle Injury
- Orthopedic treatment, as required
- Management of Compartment Syndrome (see Compartment Syndrome, [[Compartment Syndrome]]): if present
- Intracompartment pressure >30 mm Hg: requires fasciotomy
- Prolonged elevated intracompartmental pressure may lead to further muscle injury and/or irreversible peripheral nerve injury
References
- Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med. Jul 1988;148(7):1553-7 [MEDLINE]
- Rhabdomyolysis and secondary renal failure in critically ill surgical patients. Am J Surg 2004; 188:801– 806 [MEDLINE]
- Hypocalcemia and hypercalcemia in patients with rhabdomyolysis with and without acute renal failure. J Clin Endocrinol Metab. 1986 Jul;63(1):137-42 [MEDLINE]