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 / [[Sympathomimetic]]<ref> O'Connor AD et al. Prevalence of Rhabdomyolysis in Sympathomimetic Toxicity: A Comparison of Stimulants. J Med. Toxicol. 2015;11(2)195-200 </ref> 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


==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


==Differential Diagnosis==
==Evaluation==
{{Extremity trauma DDX}}
*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|hyperkalemia]] changes (peaked T waves, wide QRS)
*Consider compartment pressures if clinical concern


{{Red urine DDX}}
==Management==
 
===Aggressive IV Fluid Resuscitation===
==Diagnosis==
*Cornerstone of treatment
===Work-up===
*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>
*Obtain immediate EKG (electrolyte abnormalities)
*Target urine output 200-300 mL/hr until CK trending down and urine clears
*Total CK
*Monitor for fluid overload, especially in elderly and those with cardiac/renal disease
*UA
*Bicarbonate drip (150 mEq NaHCO3 in 1 L D5W) may be considered to alkalinize urine (target urine pH >6.5) — evidence is limited
*CBC
*Chemistry, including Mag, Phos
*Uric acid
*LFTs
*DIC panel
**Coags, FSP, fibrinogen


===Evaluation===
===Treat Hyperkalemia===
*Total CK
*See [[Hyperkalemia]] for detailed management
**Most consider rhabdo if 5x or greater increase above upper limit of normal (~2000)
*Calcium gluconate 10% 10 mL IV for cardiac membrane stabilization if ECG changes
**Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
*Insulin 10 units regular IV + D50W 50 mL IV
**Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
*[[Sodium bicarbonate]], [[Albuterol]] nebulizer, [[Kayexalate]] or patiromer
*CK-MB
*Emergent [[Hemodialysis|dialysis]] if refractory
**May be normal or mildly elevated (<5% of total)
*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==
===Other===
*Aggressive IVF
*Treat underlying cause (cool if [[Heat stroke|hyperthermic]], correct electrolytes)
**Start with NS 1-2 L/hr
*Avoid nephrotoxins (NSAIDs, contrast dye, aminoglycosides)
**Once diuresis occurs maintain urine output of 200-300 mL/hr
*[[Compartment syndrome]]: emergent fasciotomy if pressures >30 mmHg or clinical diagnosis
**Frequently need ~10 L/day
*Monitor for and treat [[DIC]] if present
*Trend:
**Volume status
**Urine pH
**Chemistry
**CK
**Calcium, phosphorus
*[[Urinary alkalinization]] (with bicarbonate)
**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==
==See Also==
*[[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]]
*[[Hyperkalemia]]
**Renal function, not release of K+, is most important determinant
*[[Acute kidney injury]]
**Treat aggressively; insulin may be ineffective; may require dialysis
*[[Compartment syndrome]]
*[[Hypocalcemia]] (initial phase)
*[[Crush injury]]
**Treat only if symptomatic or severely hyperkalemic (often have rebound hypercalcemia)
*[[Heat stroke]]
*[[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==
*[[Crush Syndrome]]
*[[Sympathomimetic Toxicity]]


==References==
==References==
<references/>
<references/>
[[Category:Renal]]
[[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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