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]]


==DDx==
==Etiology==
[[Colored Urine (DDx)]]
*Trauma / Crush injury (most common worldwide)
 
*'''Exertional''' (exercise, seizures, agitation, status epilepticus)
==Causes==
*Drug/toxin-induced
===Trauma or muscle compression===
**Statins (especially with interacting drugs)
#Crush injury
**[[Cocaine toxicity|Cocaine]], [[Amphetamine toxicity|amphetamines]], MDMA, [[Ethanol toxicity|alcohol]]
#Immobilization
**[[Neuroleptic malignant syndrome|NMS]], [[Serotonin syndrome]], [[Malignant hyperthermia]]
#Compartment syndrome
*Prolonged immobilization (found down, intraoperative)
===Nontraumatic Exertional===
*[[Hypokalemia]], [[Hypophosphatemia]], [[Hyponatremia]]
#Exercise + hot weather
*[[Heat stroke]]
#Exercise + sickle cell
*Infections (influenza, COVID-19, Legionella)
#Exercise + hypokalemia
*Hypothermia, [[Electrical injury|electrical injuries]]
#Hyperkinetic states
##Seizure
##DTs
##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


==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:
==Diagnosis==
**[[Hyperkalemia]] (can cause [[Cardiac dysrhythmia|cardiac dysrhythmias]]) — '''life-threatening'''
#Total CK
**[[Acute kidney injury]] (oliguria, anuria)
##Most consider if fivefold or greater increase above upper limit of normal
**[[Compartment syndrome]]
##Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
**[[DIC]]
##Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
**Hypocalcemia (early), hypercalcemia (recovery phase)
#CK-MB
**Metabolic acidosis
##May be normal or mildly elevated (<5% of total)
#Myoglobinuria
##UA = +blood, but 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


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


==Follow==
==Management==
#Volume status
===Aggressive IV Fluid Resuscitation===
#Urine pH
*Cornerstone of treatment
#Chemistry
*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>
#CK
*Target urine output 200-300 mL/hr until CK trending down and urine clears
#Calcium, phosphorus
*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


==Treatment==
===Treat Hyperkalemia===
#Aggressive IVF
*See [[Hyperkalemia]] for detailed management
##Start with 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 or 235mL/kg/hr
*Insulin 10 units regular IV + D50W 50 mL IV
##Frequently need ~10 L/day
*[[Sodium bicarbonate]], [[Albuterol]] nebulizer, [[Kayexalate]] or patiromer
#Bicarbonate
*Emergent [[Hemodialysis|dialysis]] if refractory
##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


==Complications==
===Other===
#[[Acute Renal Failure]]
*Treat underlying cause (cool if [[Heat stroke|hyperthermic]], correct electrolytes)
##Neither presence of myoglobinuria nor degree of CK rise is predictive of ARF
*Avoid nephrotoxins (NSAIDs, contrast dye, aminoglycosides)
##Rare in exertional rhabdo w/o presence of dehydration, heat stress, trauma
*[[Compartment syndrome]]: emergent fasciotomy if pressures >30 mmHg or clinical diagnosis
##Most commonly oliguric
*Monitor for and treat [[DIC]] if present
#[[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


==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
#Otherwise admit to monitored bed
**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


==Evidence Based Questions==
==See Also==
No randomized, controlled trial has supported the evidence-based use of mannitol, and some clinical studies suggest no beneficial effects. In addition, high accumulated doses of mannitol (>200 g per day or accumulated doses of >800 g) have been associated with acute kidney injury due to renal vasoconstriction and tubular toxicity, a condition known as osmotic nephrosis. However, many experts continue to suggest that mannitol should be used to prevent and treat rhabdomyolysis-induced acute kidney injury and relieve compartmental pressure. During the time mannitol is being administered, plasma osmolality and the osmolal gap (i.e., the difference between the measured and calculated serum osmolality) should be monitored frequently and therapy discontinued if adequate diuresis is not achieved or if the osmolal gap rises above 55 mOsm per kilogram.
*[[Hyperkalemia]]
*A. Bozch X et al. Rhabdomyolysis and Acute Kidney Injury. NEJM 2009; 361: 62-72
*[[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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