Rhabdomyolysis: Difference between revisions
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==Background ==
==Background==
*Muscle necrosis and release of intracellular muscle constituents into the circulation
*Breakdown of skeletal muscle releasing intracellular contents into the circulation
*Recurrent episodes suggests inherited metabolic disorder
*Key toxins: myoglobin (nephrotoxic), creatine kinase (CK), potassium, phosphate, uric acid
*Alcohol and drugs play a role in up to 80% of cases
*Acute kidney injury (AKI) occurs in 15-40% of cases<ref name="bosch">Bosch X, et al. Rhabdomyolysis and acute kidney injury. ''N Engl J Med''. 2009;361(1):62-72. PMID 19571284.</ref>
*Overall mortality ~5%; higher with AKI, DIC, or [[Compartment syndrome|compartment syndrome]]


===Etiology===
==Etiology==
#Trauma or muscle compression
*Trauma / Crush injury (most common worldwide)
##[[Crush Syndrome]]
*'''Exertional''' (exercise, seizures, agitation, status epilepticus)
##Immobilization
*Drug/toxin-induced
##[[Compartment Syndrome]]
**Statins (especially with interacting drugs)
#Nontraumatic Exertional
**[[Cocaine toxicity|Cocaine]], [[Amphetamine toxicity|amphetamines]], MDMA, [[Ethanol toxicity|alcohol]]
##Exercise + hot weather
**[[Neuroleptic malignant syndrome|NMS]], [[Serotonin syndrome]], [[Malignant hyperthermia]]
##Exercise + sickle cell
*Prolonged immobilization (found down, intraoperative)
##Exercise + [[Hypokalemia]]
*[[Hypokalemia]], [[Hypophosphatemia]], [[Hyponatremia]]
##Hyperkinetic states
*[[Heat stroke]]
###[[Seizure]]
*Infections (influenza, COVID-19, Legionella)
###DTs
*Hypothermia, [[Electrical injury|electrical injuries]]
###Stimulant overdose
###[[Malignant Hyperthermia]]
###Neuroleptic malignant syndrome
#Nontraumatic Nonexertional
##Drugs and toxins
###Coma induced by sedatives
###Alcohol
####Coma-induced muscle compression
####Direct toxic effect
####Nutritional compromise increases risk (hypoK, hypoMg, HypoPhos)
###Statins
###Colchicine 
###[[CO Poisoning]]
##Infection
###Viral myositis - Influenza, Coxsackie, EBV, HSV, HIV, CMV
###Bacterial pyomyositis
###Septicemia
##Endocrine
###[[Hypothyroidism]]
##Inflammatory myopathies
###Moderate CK elevations only (rhabdo only described in case reports)
##Miscellaneous
###[[Status Asthmaticus]]
###TSS
###Mushroom ingestion
 
==Differential Diagnosis==
{{Red urine DDX}}


==Clinical Features==
==Clinical Features==
#Myalgia, stiffness, weakness, malaise, low-grade fever, dark urine
*Classic triad: myalgias, weakness, dark urine (tea/cola-colored)
##Musculoskeletal symptoms may be present in only half of cases
**Full triad present in <10% of cases
#N/V, abd pain, tachycardia in severe cases
*Muscle tenderness, swelling, and stiffness
#Mental status changes secondary to urea-induced encephalopathy
*May be asymptomatic with only lab abnormalities
*Complications:
**[[Hyperkalemia]] (can cause [[Cardiac dysrhythmia|cardiac dysrhythmias]]) — '''life-threatening'''
**[[Acute kidney injury]] (oliguria, anuria)
**[[Compartment syndrome]]
**[[DIC]]
**Hypocalcemia (early), hypercalcemia (recovery phase)
**Metabolic acidosis


==Work-up==
==Evaluation==
#Total CK
*Creatine kinase (CK) — diagnostic marker
#UA
**CK >5x upper limit of normal (typically >1,000 U/L) diagnostic
#CBC
**CK >5,000 U/L: significant risk of AKI
#Chemistry, including Mag, Phos
**Peak CK at 24-72 hours; monitor serial levels
#Uric acid
*Urinalysis: urine dipstick positive for "blood" but no RBCs on microscopy (myoglobinuria)
#LFTs
*BMP: potassium (may be severely elevated), creatinine, BUN, calcium, phosphate, bicarbonate
#DIC panel
*CBC, LDH, uric acid, coagulation studies
##Coags, FSP, fibrinogen
*ECG — evaluate for [[Hyperkalemia|hyperkalemia]] changes (peaked T waves, wide QRS)
*Consider compartment pressures if clinical concern


==Diagnosis==
==Management==
#Total CK
===Aggressive IV Fluid Resuscitation===
##Most consider rhabdo if 5x or greater increase above upper limit of normal (~2000)
*Cornerstone of treatment
##Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
*Normal saline at 200-300 mL/hr (or 1-2 L/hr initially if severely hypovolemic)<ref name="scharman">Scharman EJ, et al. Prevention of kidney injury following rhabdomyolysis: a systematic review. ''Ann Pharmacother''. 2013;47(1):90-105. PMID 23324509.</ref>
##Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
*Target urine output 200-300 mL/hr until CK trending down and urine clears
#CK-MB
*Monitor for fluid overload, especially in elderly and those with cardiac/renal disease
##May be normal or mildly elevated (<5% of total)
*Bicarbonate drip (150 mEq NaHCO3 in 1 L D5W) may be considered to alkalinize urine (target urine pH >6.5) — evidence is limited
#Uric Acid - elevates before CK
#Myoglobinuria
##UA = +blood, no RBCs (Sn ~80%)
##Myoglobin is cleared w/in 1-6hr (often see elevated CK with no myoglobinuria)
#Acute renal failure
##Creatinine increase
#Electrolyte abnormalities
##[[Hyperkalemia]]
##Hyperphosphatemia
##[[Hypocalcemia]]
##Hyperuricemia


==Management==
===Treat Hyperkalemia===
#Aggressive IVF
*See [[Hyperkalemia]] for detailed management
##Start with NS 1-2 L/hr
*Calcium gluconate 10% 10 mL IV for cardiac membrane stabilization if ECG changes
##Once diuresis occurs maintain urine output of 200-300 mL/hr
*Insulin 10 units regular IV + D50W 50 mL IV
##Frequently need ~10 L/day
*[[Sodium bicarbonate]], [[Albuterol]] nebulizer, [[Kayexalate]] or patiromer
#Trend:
*Emergent [[Hemodialysis|dialysis]] if refractory
##Volume status
 
##Urine pH
===Other===
##Chemistry
*Treat underlying cause (cool if [[Heat stroke|hyperthermic]], correct electrolytes)
##CK
*Avoid nephrotoxins (NSAIDs, contrast dye, aminoglycosides)
##Calcium, phosphorus
*[[Compartment syndrome]]: emergent fasciotomy if pressures >30 mmHg or clinical diagnosis
#[[Urinary alkalinization]] (with bicarbonate)
*Monitor for and treat [[DIC]] if present
##Controversial; no RCT to date have demonstrated benefit
##Consider if CK >5000, severe muscle injury (crush injury), rising CK AND urine pH <6.5
##Contraindications:
###Severe hypocalcemia
###Arterial pH > 7.50
###Serum bicarbonate > 30 meq/L
##Mix 150 mL [3 amps] of 8.4% sodium bicarbonate w/ 1 L D5W
##Infuse at 200 mL/hour; rate is adjusted to achieve urine pH of >6.5
##Arterial pH and serum calcium should be monitored q2hr
##Discontinue if:
###Urine pH does not rise above 6.5 after 3-4hr
###Pt develops symptomatic hypocalcemia
###Arterial pH > 7.5
###Serum bicarbonate >30 meq/L
#[[Mannitol]]
##Controversial; no RCT to date has demonstrated benefit
##Mannitol administration can worsen dehydration and oliguria, cause hyperkalemia
##Consider in pts w/marked elevations in CK (>30K)
##Contraindicated if urinary flow is inadequate (<20 mL/hr)
##Add 50 mL of 20% mannitol to each liter of fluid; give at rate of 5g/hr
##Must check plasma osmolaity and plasma osmolal gap q4-6hr
###Discontinue if osmolal gap > 55 mosmol/kg
#Intubation/RSI
##Use Rocuronium


==Disposition==
==Disposition==
#Discharge if:
*Admit patients with:
##Exertional rhabdo
**CK >5,000 U/L
##Otherwise healthy
**AKI (elevated creatinine)
##No comorbidities (heat stress, dehydration, trauma)
**[[Hyperkalemia]] or other electrolyte derangements
##Downtrending total CK
**Ongoing symptoms or rising CK
###Consider admission for CK >30,000
*Discharge may be considered for mild rhabdomyolysis (CK <5,000, normal renal function, normal K) with close follow-up and oral hydration
#Otherwise admit to monitored bed
 
==Complications==
#[[Acute Renal Failure]]
##Neither presence of myoglobinuria nor degree of CK rise is predictive of ARF
##Rare in exertional rhabdo w/o presence of dehydration, heat stress, trauma
##Most commonly oliguric
#[[Hyperkalemia]]
##Renal function, not release of K+, is most important determinant
##Treat aggressively; insulin may be ineffective; may require dialysis
#[[Hypocalcemia]] (initial phase)
##Treat only if symptomatic or severely hyperkalemic (often have rebound hypercalcemia)
#[[Hypercalcemia]] (recovery phase)
#Hyperphosphatemia
##Treat cautiously (treatment may worsen calcium precipitation in muscle)
##Consider oral phosphate binders when level >7
#[[DIC]]
##Usually resolves spontaneously w/in several days
#[[Compartment Syndrome]]
#Peripheral nerve injury
##Usually resolves w/in few days-weeks


==See Also==
==See Also==
*[[Crush Syndrome]]
*[[Hyperkalemia]]
*[[Sympathomimetic Toxicity]]
*[[Acute kidney injury]]
*[[Compartment syndrome]]
*[[Crush injury]]
*[[Heat stroke]]


==Source==
==References==
*Tintinalli
<references/>
*UpToDate


[[Category:Nephro]]
[[Category:Renal]]
[[Category:Trauma]]
[[Category:Orthopedics]]

Latest revision as of 09:31, 22 March 2026

Background

  • Breakdown of skeletal muscle releasing intracellular contents into the circulation
  • Key toxins: myoglobin (nephrotoxic), creatine kinase (CK), potassium, phosphate, uric acid
  • Acute kidney injury (AKI) occurs in 15-40% of cases[1]
  • Overall mortality ~5%; higher with AKI, DIC, or compartment syndrome

Etiology

Clinical Features

  • Classic triad: myalgias, weakness, dark urine (tea/cola-colored)
    • Full triad present in <10% of cases
  • Muscle tenderness, swelling, and stiffness
  • May be asymptomatic with only lab abnormalities
  • Complications:

Evaluation

  • Creatine kinase (CK) — diagnostic marker
    • CK >5x upper limit of normal (typically >1,000 U/L) diagnostic
    • CK >5,000 U/L: significant risk of AKI
    • Peak CK at 24-72 hours; monitor serial levels
  • Urinalysis: urine dipstick positive for "blood" but no RBCs on microscopy (myoglobinuria)
  • BMP: potassium (may be severely elevated), creatinine, BUN, calcium, phosphate, bicarbonate
  • CBC, LDH, uric acid, coagulation studies
  • ECG — evaluate for hyperkalemia changes (peaked T waves, wide QRS)
  • Consider compartment pressures if clinical concern

Management

Aggressive IV Fluid Resuscitation

  • Cornerstone of treatment
  • Normal saline at 200-300 mL/hr (or 1-2 L/hr initially if severely hypovolemic)[2]
  • Target urine output 200-300 mL/hr until CK trending down and urine clears
  • Monitor for fluid overload, especially in elderly and those with cardiac/renal disease
  • Bicarbonate drip (150 mEq NaHCO3 in 1 L D5W) may be considered to alkalinize urine (target urine pH >6.5) — evidence is limited

Treat Hyperkalemia

Other

  • Treat underlying cause (cool if hyperthermic, correct electrolytes)
  • Avoid nephrotoxins (NSAIDs, contrast dye, aminoglycosides)
  • Compartment syndrome: emergent fasciotomy if pressures >30 mmHg or clinical diagnosis
  • Monitor for and treat DIC if present

Disposition

  • Admit patients with:
    • CK >5,000 U/L
    • AKI (elevated creatinine)
    • Hyperkalemia or other electrolyte derangements
    • Ongoing symptoms or rising CK
  • Discharge may be considered for mild rhabdomyolysis (CK <5,000, normal renal function, normal K) with close follow-up and oral hydration

See Also

References

  1. ↑ Bosch X, et al. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. PMID 19571284.
  2. ↑ Scharman EJ, et al. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother. 2013;47(1):90-105. PMID 23324509.
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