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==Background ==
==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<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]]


* Muscle necrosis and the release of intracellular muscle constituents into the circulation
==Etiology==
* Causes
*Trauma / Crush injury (most common worldwide)
** 1. Traumatic or muscle compression
*'''Exertional''' (exercise, seizures, agitation, status epilepticus)
*** a. Crush injury
*Drug/toxin-induced
*** b. Immobilization
**Statins (especially with interacting drugs)
*** c. Compartment syndrome
**[[Cocaine toxicity|Cocaine]], [[Amphetamine toxicity|amphetamines]], MDMA, [[Ethanol toxicity|alcohol]]
** 2. Nontraumatic exertional
**[[Neuroleptic malignant syndrome|NMS]], [[Serotonin syndrome]], [[Malignant hyperthermia]]
*** a. Exercise + hot weather
*Prolonged immobilization (found down, intraoperative)
*** b. Exercise + sickle cell
*[[Hypokalemia]], [[Hypophosphatemia]], [[Hyponatremia]]
*** c. Exercise + hypokalemia
*[[Heat stroke]]
*** d. Hyperkinetic states
*Infections (influenza, COVID-19, Legionella)
**** Seizure
*Hypothermia, [[Electrical injury|electrical injuries]]
**** DTs
**** Stimulant overdose
**** Malignant hyperthermia
**** NMS
** 3. Nontraumatic nonexertional
*** a. Drugs and toxins
**** Coma induced by sedatives
**** Statins
**** Colchicine 
**** CO poisoning
*** b. Infection
**** Viral myositis - Influenza, Coxsackie, EBV, HSV, HIV, CMV
**** Bacterial pyomyositis
**** Septicemia
*** c. Endocrine
**** Hypothyroidism
*** d. Inflammatory myopathies
**** Moderate CK elevations only (rhabdo only described in case reports)
*** e. Miscellaneous
**** Status asthmaticus
**** TSS
**** Mushroom ingestion


==Diagnosis==
==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:
**[[Hyperkalemia]] (can cause [[Cardiac dysrhythmia|cardiac dysrhythmias]]) — '''life-threatening'''
**[[Acute kidney injury]] (oliguria, anuria)
**[[Compartment syndrome]]
**[[DIC]]
**Hypocalcemia (early), hypercalcemia (recovery phase)
**Metabolic acidosis


Clinical
==Evaluation==
* Myalgias
*Creatine kinase (CK) — diagnostic marker
** May progress to weakness
**CK >5x upper limit of normal (typically >1,000 U/L) diagnostic
* Red/brown urine
**CK >5,000 U/L: significant risk of AKI
* Renal failure
**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


==Management==
===Aggressive IV Fluid Resuscitation===
*Cornerstone of treatment
*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>
*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


Laboratory
===Treat Hyperkalemia===
* Elevated total CK (typically > 10K)
*See [[Hyperkalemia]] for detailed management
** CK-MB may be entirely normal or may be mildly elevated (reflects small amount found in skeletal tissue)
*Calcium gluconate 10% 10 mL IV for cardiac membrane stabilization if ECG changes
* Transaminitis
*Insulin 10 units regular IV + D50W 50 mL IV
* Creatinine increase (if renal failure)
*[[Sodium bicarbonate]], [[Albuterol]] nebulizer, [[Kayexalate]] or patiromer
* Myoglobinuria
*Emergent [[Hemodialysis|dialysis]] if refractory
** Is cleared much faster than CK (may see elevated CK with no myoglobinuria)
* Electrolyte Abnormalities
** Hyperkalemia
** Hyperphosphatemia
** Hypocalcemia
** Hyperuricemia
** Metabolic acidosis


==Treatment==
===Other===
1. Aggressive IVF
*Treat underlying cause (cool if [[Heat stroke|hyperthermic]], correct electrolytes)
* Often up to 10L per day)
*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==
    -type of fluid = controversial    -NaBicarb (to alkalize urine)          -may exacerbate the symptoms of the initial hypocalcemic phase of rhabdomyolysis.          -urine pH and serum bicarbonate, calcium, and potassium levels should be monitored          -if urine pH does not rise after 4 to 6 hours of treatment or if symptomatic hypocalcemia develops, alkalinization should be discontinued and hydration continued with NS2) Monitor electrolytes    -correct hyperkalemia    -early hypocalcemia should NOT be treated unless symptomatic or severe hyperkalemia present    -Calcium-containing chelators should be used with caution to treat hyperphosphatemia, since the calcium load could increase the precipitation of calcium phosphate in injured muscle.==Disposition==
*Admit patients with:
 
**CK >5,000 U/L
 
**AKI (elevated creatinine)
Insert
**[[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
 
==Evidence Based Questions==
 
 
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.
 
A. Bozch X et al. Rhabdomyolysis and Acute Kidney Injury. NEJM 2009; 361: 62-72
 


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


==References==
<references/>


Insert
[[Category:Renal]]
 
[[Category:Orthopedics]]
 
==Source==
 
 
KajQuestions
 
 
 
 
[[Category:GU]]

Revisión actual - 09:31 22 mar 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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