Rhabdomyolysis: Difference between revisions

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==Background ==
==Background ==
# Muscle necrosis and the release of intracellular muscle constituents into the circulation
#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==
==DDx==
[[Colored Urine (DDx)]]
[[Colored Urine (DDx)]]


===Causes===
==Causes==
# Trauma or muscle compression
===Trauma or muscle compression===
## Crush injury
#Crush injury
## Immobilization
#Immobilization
## Compartment syndrome
#Compartment syndrome
# Nontraumatic exertional
===Nontraumatic Exertional===
## Exercise + hot weather
#Exercise + hot weather
## Exercise + sickle cell
#Exercise + sickle cell
## Exercise + hypokalemia
#Exercise + hypokalemia
## Hyperkinetic states
#Hyperkinetic states
### Seizure
##Seizure
### DTs
##DTs
### Stimulant overdose
##Stimulant overdose
### Malignant hyperthermia
##Malignant hyperthermia
### NMS
##Neuroleptic malignant syndrome
# Nontraumatic nonexertional
===Nontraumatic Nonexertional===
## Drugs and toxins
#Drugs and toxins
### Coma induced by sedatives
##Coma induced by sedatives
### Statins
##Alcohol
### Colchicine   
###Coma-induced muscle compression
### CO poisoning
###Direct toxic effect
## Infection
###Nutritional compromise increases risk (hypoK, hypoMg, HypoPhos)
### Viral myositis - Influenza, Coxsackie, EBV, HSV, HIV, CMV
##Statins
### Bacterial pyomyositis
##Colchicine   
### Septicemia
##CO poisoning
## Endocrine
#Infection
### Hypothyroidism
##Viral myositis - Influenza, Coxsackie, EBV, HSV, HIV, CMV
## Inflammatory myopathies
##Bacterial pyomyositis
### Moderate CK elevations only (rhabdo only described in case reports)
##Septicemia
## Miscellaneous
#Endocrine
### Status asthmaticus
##Hypothyroidism
### TSS
#Inflammatory myopathies
### Mushroom ingestion
##Moderate CK elevations only (rhabdo only described in case reports)
#Miscellaneous
##Status asthmaticus
##TSS
##Mushroom ingestion
 
==Clinical Features==
#Myalgia, stiffness, weakness, malaise, low-grade fever, dark urine
##Musculoskeletal symptoms may be present in only half of cases
#N/V, abd pain, tachycardia in severe cases
#Mental status changes secondary to urea-induced encephalopathy
 
==Diagnosis==
#Total CK
##Most consider if fivefold or greater increase above upper limit of normal
##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
#CK-MB
##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)
##Is pathognomonic
 
 
 
#Transaminitis
#Creatinine increase (if renal failure)
#Electrolyte Abnormalities
##Hyperkalemia
##Hyperphosphatemia
##Hypocalcemia
## Hyperuricemia
## Metabolic acidosis


==Workup==
==Workup==
#Investigate cause
#Investigate cause
#Total CK
#Total CK
#UA
#CBC
#CBC
#Chem 10
#Chemistry
#UA
#Uric acid
#LFTs
#LFTs
#PT/PTT
#DIC panel
#Urine pH
##Coags, FSP, fibrinogen
#Ionized Ca
 
#Consider ABG
 
 


===Follow===  
===Follow===  
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##Potassium
##Potassium


==Diagnosis==
===Clinical===
# Instigating cause
# Myalgias
## May progress to weakness
# Red/brown "tea colored" urine
# Renal failure


===Laboratory===
# Elevated Total CK (no defined threshold)
## >5-10K (injury possible)
###Normally associated with co-existing conditions (e.g. sepsis + chronic myopathies)
## >15-20K (injury more likely) 
## CK-MB may be entirely normal or may be mildly elevated (reflects small amount found in skeletal tissue)
# Myoglobinuria
## UA = +blood, but no RBCs
### Sensitivity = 80% (for rhabdo)
## Is cleared much faster than CK (may see elevated CK with no myoglobinuria)
## Is pathognomonic
# Transaminitis
# Creatinine increase (if renal failure)
# Electrolyte Abnormalities
## Hyperkalemia
## Hyperphosphatemia
## Hypocalcemia
## Hyperuricemia
## Metabolic acidosis


==Treatment==
==Treatment==
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##Treat aggressively
##Treat aggressively
#[[Hypocalcemia]] (initial phase)
#[[Hypocalcemia]] (initial phase)
## Treat only if symptomatic or severely hyperkalemic (pts often have rebound hypercalcemia)
##Treat only if symptomatic or severely hyperkalemic (often have rebound hypercalcemia)
#[[Hypercalcemia]] (recovery phase)
#[[Hypercalcemia]] (recovery phase)
#[[Hyperphosphatemia]]
#[[Hyperphosphatemia]]
##Treat cautiously (treatment may worsen calcium precipitation in muscle)
##Treat cautiously (treatment may worsen calcium precipitation in muscle)
#[Diss


==Evidence Based Questions==
==Evidence Based Questions==

Revision as of 00:11, 4 August 2011

Background

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

DDx

Colored Urine (DDx)

Causes

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
    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, but no RBCs
      1. Sn = 80%
    2. Myoglobin is cleared w/in 1-6hr (often see elevated CK with no myoglobinuria)
    3. Is pathognomonic


  1. Transaminitis
  2. Creatinine increase (if renal failure)
  3. Electrolyte Abnormalities
    1. Hyperkalemia
    2. Hyperphosphatemia
    3. Hypocalcemia
    4. Hyperuricemia
    5. Metabolic acidosis

Workup

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



Follow

    1. Urine pH
    2. Potassium


Treatment

  1. Aggressive IVF
    1. Start with 1-2 L/hr
    2. Once diuresis occurs maintain urine output of 200-300 mL/hr (3mL/kg)
    3. Frequently need ~10 L/day
  2. Bicarb^
    1. Indication = Urine pH is <6.5
    2. After initial IVF, give 75mmol NaHCO3 in 1L 1/2NS
      1. Alternative regimen = 100mmol NaHCO3 in 1L 1/2NS, alternated with 1L NS (no NaHCO3), repeat
      2. Goal urine pH is >6.5
      3. Monitor for hypocalcemia closely!
      4. If urine pH is not > 6.5 after 3-4 hrs or symptomatic hypocalcemia results d/c
  3. Mannitol^^
    1. Consider if unable to establish diuresis after significant volume repletion
      1. Must check plasma osmolaity and plasma osmolal gap q4-6hr
      2. D/c if osmolal gap > 55 mosmol/kg
      3. If mannitol establishes diuresis, continue until urine discoloration clears and CK decreases to <10K

^Degrees of controversy

Complications

  1. Acute Renal Failure
  2. Hyperkalemia
    1. Treat aggressively
  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)
  6. [Diss

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

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