Rhabdomyolysis: Difference between revisions

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==DDx==
==DDx==
[[Colored Urine (DDx)]]
*[[Colored Urine (DDx)]]


==Causes==
==Etiology==
===Trauma or muscle compression===
===Trauma or muscle compression===
#Crush injury
#Crush injury
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==Diagnosis==
==Diagnosis==
#Total CK
#Total CK
##Most consider if fivefold or greater increase above upper limit of normal
##Most consider if fivefold or greater increase above upper limit of normal (~2000)
##Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
##Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
##Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
##Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
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##May be normal or mildly elevated (<5% of total)
##May be normal or mildly elevated (<5% of total)
#Myoglobinuria
#Myoglobinuria
##UA = +blood, but no RBCs  
##UA = +blood, no RBCs (Sn ~80%)
###Sn = 80%  
##Myoglobin is cleared w/in 1-6hr (often see elevated CK with no myoglobinuria)
##Myoglobin is cleared w/in 1-6hr (often see elevated CK with no myoglobinuria)
#Acute renal failure
#Acute renal failure
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##Hyperuricemia
##Hyperuricemia


==Workup==
==Work-up==
#Investigate cause
#Total CK
#Total CK
#UA
#UA
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##Coags, FSP, fibrinogen
##Coags, FSP, fibrinogen


==Follow==
==Management==
#Volume status
#Urine pH
#Chemistry
#CK
#Calcium, phosphorus
 
==Treatment==
#Aggressive IVF
#Aggressive IVF
##Start with 1-2 L/hr
##Start with NS 1-2 L/hr
##Once diuresis occurs maintain urine output of 200-300 mL/hr or 235mL/kg/hr
##Once diuresis occurs maintain urine output of 200-300 mL/hr
##Frequently need ~10 L/day
##Frequently need ~10 L/day
#Trend:
##Volume status
##Urine pH
##Chemistry
##CK
##Calcium, phosphorus
#Bicarbonate
#Bicarbonate
##Controversial; no RCT to date have demonstrated benefit
##Controversial; no RCT to date have demonstrated benefit

Revision as of 15:23, 24 March 2012

Background

  • Muscle necrosis and release of intracellular muscle constituents into the circulation
  • Recurrent episodes suggests inherited metabolic disorder
  • Alcohol and drugs play a role in up to 80% of cases

DDx

Etiology

Trauma or muscle compression

  1. Crush injury
  2. Immobilization
  3. Compartment syndrome

Nontraumatic Exertional

  1. Exercise + hot weather
  2. Exercise + sickle cell
  3. Exercise + hypokalemia
  4. Hyperkinetic states
    1. Seizure
    2. DTs
    3. Stimulant overdose
    4. Malignant Hyperthermia
    5. Neuroleptic malignant syndrome

Nontraumatic Nonexertional

  1. Drugs and toxins
    1. Coma induced by sedatives
    2. Alcohol
      1. Coma-induced muscle compression
      2. Direct toxic effect
      3. Nutritional compromise increases risk (hypoK, hypoMg, HypoPhos)
    3. Statins
    4. Colchicine
    5. CO poisoning
  2. Infection
    1. Viral myositis - Influenza, Coxsackie, EBV, HSV, HIV, CMV
    2. Bacterial pyomyositis
    3. Septicemia
  3. Endocrine
    1. Hypothyroidism
  4. Inflammatory myopathies
    1. Moderate CK elevations only (rhabdo only described in case reports)
  5. Miscellaneous
    1. Status asthmaticus
    2. TSS
    3. Mushroom ingestion

Clinical Features

  1. Myalgia, stiffness, weakness, malaise, low-grade fever, dark urine
    1. Musculoskeletal symptoms may be present in only half of cases
  2. N/V, abd pain, tachycardia in severe cases
  3. Mental status changes secondary to urea-induced encephalopathy

Diagnosis

  1. Total CK
    1. Most consider if fivefold or greater increase above upper limit of normal (~2000)
    2. Serum CK begins to rise 2-12hr after injury, peaks w/in 24-72hr
    3. Degree of CK elevation correlates w/ muscle injury, but NOT renal failure
  2. CK-MB
    1. May be normal or mildly elevated (<5% of total)
  3. Myoglobinuria
    1. UA = +blood, no RBCs (Sn ~80%)
    2. Myoglobin is cleared w/in 1-6hr (often see elevated CK with no myoglobinuria)
  4. Acute renal failure
    1. Creatinine increase
  5. Electrolyte abnormalities
    1. Hyperkalemia
    2. Hyperphosphatemia
    3. Hypocalcemia
    4. Hyperuricemia

Work-up

  1. Total CK
  2. UA
  3. CBC
  4. Chemistry
  5. Uric acid
  6. LFTs
  7. DIC panel
    1. Coags, FSP, fibrinogen

Management

  1. Aggressive IVF
    1. Start with NS 1-2 L/hr
    2. Once diuresis occurs maintain urine output of 200-300 mL/hr
    3. Frequently need ~10 L/day
  2. Trend:
    1. Volume status
    2. Urine pH
    3. Chemistry
    4. CK
    5. Calcium, phosphorus
  3. Bicarbonate
    1. Controversial; no RCT to date have demonstrated benefit
    2. Consider if CK >5000, severe muscle injury (crush injury), rising CK AND urine pH <6.5
    3. Contraindications:
      1. Severe hypocalcemia
      2. Arterial pH > 7.50
      3. Serum bicarbonate > 30 meq/L
    4. Mix 150 mL [3 amps] of 8.4% sodium bicarbonate w/ 1 L D5W
    5. Infuse at 200 mL/hour; rate is adjusted to achieve urine pH of >6.5
    6. Arterial pH and serum calcium should be monitored q2hr
    7. Discontinue if:
      1. Urine pH does not rise above 6.5 after 3-4hr
      2. Pt develops symptomatic hypocalcemia
      3. Arterial pH > 7.5
      4. Serum bicarbonate >30 meq/L
  4. Mannitol
    1. Controversial; no RCT to date has demonstrated benefit
    2. Mannitol administration can worsen dehydration and oliguria, cause hyperkalemia
    3. Consider in pts w/marked elevations in CK (>30K)
    4. Contraindicated if urinary flow is inadequate (<20 mL/hr)
    5. Add 50 mL of 20% mannitol to each liter of fluid; give at rate of 5g/hr
    6. Must check plasma osmolaity and plasma osmolal gap q4-6hr
      1. Discontinue if osmolal gap > 55 mosmol/kg

Complications

  1. Acute Renal Failure
    1. Neither presence of myoglobinuria nor degree of CK rise is predictive of ARF
    2. Rare in exertional rhabdo w/o presence of dehydration, heat stress, trauma
    3. Most commonly oliguric
  2. Hyperkalemia
    1. Renal function, not release of K+, is most important determinant
    2. Treat aggressively; insulin may be ineffective; may require dialysis
  3. Hypocalcemia (initial phase)
    1. Treat only if symptomatic or severely hyperkalemic (often have rebound hypercalcemia)
  4. Hypercalcemia (recovery phase)
  5. Hyperphosphatemia
    1. Treat cautiously (treatment may worsen calcium precipitation in muscle)
    2. Consider oral phosphate binders when level >7
  6. DIC
    1. Usually resolves spontaneously w/in several days
  7. Compartment Syndrome
  8. Peripheral nerve injury
    1. Usually resolves w/in few days-weeks

Disposition

  1. Discharge if:
    1. Exertional rhabdo
    2. Otherwise healthy
    3. No comorbidities (heat stress, dehydration, trauma)
  2. Otherwise admit to monitored bed

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

Source

  • Tintinalli
  • UpToDate