Rhabdomyolysis: Difference between revisions

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==Background ==
==Background==
# Muscle necrosis and the release of intracellular muscle constituents into the circulation
*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<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==
# Trauma or muscle compression
*Trauma / Crush injury (most common worldwide)
## Crush injury
*'''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
### NMS
# Nontraumatic nonexertional
## Drugs and toxins
### Coma induced by sedatives
### 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


==Diagnosis==
==Clinical Features==
===Clinical===
*Classic triad: myalgias, weakness, dark urine (tea/cola-colored)
# Myalgias
**Full triad present in <10% of cases
## May progress to weakness
*Muscle tenderness, swelling, and stiffness
# Red/brown "tea colored" urine
*May be asymptomatic with only lab abnormalities
# Renal failure
*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


==Workup==
==Evaluation==
#Total CK
*Creatine kinase (CK) — diagnostic marker
#CBC
**CK >5x upper limit of normal (typically >1,000 U/L) diagnostic
#Chem 10
**CK >5,000 U/L: significant risk of AKI
#UA
**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


===Laboratory===
==Management==
# Elevated Total CK (typically > 10K)
===Aggressive IV Fluid Resuscitation===
## CK-MB may be entirely normal or may be mildly elevated (reflects small amount found in skeletal tissue)
*Cornerstone of treatment
# Myoglobinuria
*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>
## UA = +blood, but no RBCs
*Target urine output 200-300 mL/hr until CK trending down and urine clears
### Sensitivity = 80% (for rhabdo)
*Monitor for fluid overload, especially in elderly and those with cardiac/renal disease
## Is cleared much faster than CK (may see elevated CK with no myoglobinuria)
*Bicarbonate drip (150 mEq NaHCO3 in 1 L D5W) may be considered to alkalinize urine (target urine pH >6.5) — evidence is limited
## Is pathognomonic
# Transaminitis
# Creatinine increase (if renal failure)
# Electrolyte Abnormalities
## Hyperkalemia
## Hyperphosphatemia
## Hypocalcemia
## Hyperuricemia
## Metabolic acidosis


==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
*Insulin 10 units regular IV + D50W 50 mL IV
## Frequently need ~10 L/day
*[[Sodium bicarbonate]], [[Albuterol]] nebulizer, [[Kayexalate]] or patiromer
# Bicarb?
*Emergent [[Hemodialysis|dialysis]] if refractory
## If IVF establishes diuresis consider adding 75 mmol of NaHCO3 to 1L of 1/2NS
### Goal urine pH is > 6.5
### Monitor for hypocalcemia closely!
### If urine pH is not > 6.5 after 3-4 hrs or symptomatic hypocalcemia results d/c
# Mannitol?
## Consider if unable to establish diuresis with volume repletion
### Must check plasma osmolaity and plasma osmolal gap q4-6hr
### D/c if osmolal gap > 55 mosmol/kg
# If mannitol establishes diuresis continue until urine discoloration clears and CK decreases to <10K


==Complications==
===Other===
#[[Acute Renal Failure]]
*Treat underlying cause (cool if [[Heat stroke|hyperthermic]], correct electrolytes)
#[[Hyperkalemia]]
*Avoid nephrotoxins (NSAIDs, contrast dye, aminoglycosides)
##Treat aggressively
*[[Compartment syndrome]]: emergent fasciotomy if pressures >30 mmHg or clinical diagnosis
#[[Hypocalcemia]] (initial phase)
*Monitor for and treat [[DIC]] if present
## Treat only if symptomatic or severely hyperkalemic (pts often have rebound hypercalcemia)
#[[Hypercalcemia]] (recovery phase)
#[[Hyperphosphatemia]]
##Treat cautiously (treatment may worsen calcium precipitation in muscle)


==Evidence Based Questions==
==Disposition==
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.
*Admit patients with:
 
**CK >5,000 U/L
A. Bozch X et al. Rhabdomyolysis and Acute Kidney Injury. NEJM 2009; 361: 62-72
**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==
==See Also==
Insert
*[[Hyperkalemia]]
*[[Acute kidney injury]]
*[[Compartment syndrome]]
*[[Crush injury]]
*[[Heat stroke]]


==Source==
==References==
KajQuestions
<references/>


[[Category:GU]]
[[Category:Renal]]
[[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.