Traumatic rhabdomyolysis: causes, pathophysiology an

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Traumatic rhabdomyolysis causes, pathophysiology
and management strategies

• By Sharon Fish

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Overview

• Definitions
• Historically
• Causes
• Pathophysiology
• Clinical
• Management

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Definitions

• Rhabdomyolysis - destruction of striated muscle
• A crush injury is direct injury resulting from a
  crush
• A crush syndrome is the systemic manifestation of
  muscle cell damage, resulting from pressure or
  crushing.
• Also known as traumatic rhabdomyolysis

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• Based on 3 criteria
• Involvement of a muscle mass
• Prolonged compression
• Compromised local circular

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History

• In 1910 Myer-Betz Syndrome, German physician.
• Triad Muscle Pain, Weakness, Brown Urine.
• World War II
• Dr Bywaters described patients during London
  Bombings (Battle of Britain 1941).
• Oliguria, pigmented casts, limb oedema, shock and
  death.
• In 1943, in animal models, Bywaters Stead
  identified myoglobin as the offending agent, and
  formulated the first treatment plan.

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History

• In 1950 Korean War, dialysis reduces mortality
  rate from 84 to 53.
• Natural Disasters Earthquakes
• 1976 Tangshan (near Beijing) 20 of 242,000
  deaths due to crush syndrome.
• 1988 Spitak (Armenia)
• In 1995, British nephrologists introduced the
  Disaster Relief Task Force with the goal to
  prevent acute renal failure.
• 1999 Marmara (Turkey) 7.2 Richter scale
  earthquake. 12 hospitalised patients had renal
  failure, 76 received dialysis, 19 fatality rate.

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Causes - Traumatic

• Trauma and compression
• Crush injuries
• MVA
• Long-term confinement without changing position
• Physical torture and abuse
• Prolonged hours of surgery without changing
  position

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Causes Non-traumatic

• Strainful muscle exercise
• Electrical current
• Lightning
• Cardioversion
• Electric shock
• Hyperthermia
• Neuromuscular malignant syndrome
• Heat stroke
• Metabolic disorders
• Mcardles disease
• Palmitoyotransferase def
• Drugs
• Cocaine
• statins
• Sepsis

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pathogenesis

• Compressive forces leads to cellular
  hypoperfusion and hypoxia
• Decrease in ATPase?failure of ATPase pump and
  sacrolemma leakage
• Lysed cell release inflammatory mediators
• platelet aggregation
• vasoconstriction
• inc vasc permeability

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• Lysed cell release
• Potassium
• Phospate
• Creatine kinase
• Myoglobin
• Electrolyte disturbances
• Hyperkalaemia
• Hypocalcaemia
• Hyperphosphatemia
• Hyperuricaemia
• Metabolic acidosis

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• Revascularization
• Fluids trapped in damaged tissue
• Oedema of affected limb
• Haemoconcentration and shock
• Myoglobin, potassium, phosphate enter venous
  circulation

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Mechanisms of ARF in rhabdomyolysis

• Renal vasoconstriction with diminished renal
  perfusion
• Cast formation leads to tubular obstruction
• Direct Myoglobin nephrotoxicity- Haeme produced
  free radicles

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Clinical manifestations

• Range from asymptomatic to acute renal failure
  and DIC
• Triad muscle pain weakness ,dark urine
• Musculoskeletal signs
• General manifestations
• Complications
• early
• late

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Musculoskeletal signs

• Pain
• Weakness
• Swelling

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General manifestation

• Malaise
• Fever
• Tachycardia
• Nausea
• vomiting

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Complications

• Early
• Hypovolaemia
• Hyperkalaemia
• Hypocalcaemia
• Cardiac arrhythmias
• Cardiac arrest
• Compartment syndrome

• Late(12-72hrs)
• Acute renal failure
• DIC
• ARDS
• sepsis

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Lab findings

• CK n 45-260U/L
• Rises within 12hours
• Peaks 1-3 days
• Declines 3-5days after cessation of muscle injury

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CK-peak

• Huerta-Alardin et al CKgt5000U/L serious muscle
  injury, related to renal failure
• Gonzales et algt10000U/L related to ARF
• Brown et al 2083 trauma ICUadmission,85abn CK
  (gt520)
• 74 of 382 lt5000U/L developed RF(8)
• 143 of 1701 gt5000U/L developed RF(19)
• Renal failure defined peak creatinine gt2mg/dl

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CK-peak

• Oda et al 372 crush injury pts at Hanshin
  earthquake
• CK lt 75000 45 of 115 (39) developed RF
  requiring dialysis
• CK gt 75000 43 of 51 (84.3) developed renal
  failure requiring dialysis
• Note different definitions of renal failure

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Other muscle markers

• Measuring myoglobin level in serum or urine
• Appears in urine when plasma concentration
  exceeds 1.5mg/dl
• Urine becomes dark red brown colour gt100mg/dl
• Myoglobin has short T1/2 (2-3hours)
• Serum level return to normal after 6-8hours

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• Carbonic anhydrase 3
• Aldolase
• Trop T I

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Lab tests

• Raised UE
• Hyperkalaemia
• hypocalcaemia
• hyperphosphataemia
• uric acid

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Treatment

• A B C
• Fluids
• Treat hyperkalaemia

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Fluids

• When
• if possible before the crush is relieved
• What
• isotonic crystalloids are favoured normal saline
  preferred (consensus meeting crush syndrome
  2001-Edinburgh) (R/L have 4 mEq K )
• How much
• Gonzalez et aladult
• extrication 1.5l/hr
• postextrication .5l/hr alternating with D5W
• Children 10-20ml/kg/hr
• Urine output -.50ml/hr -200mls/hr
• Children 2mls/kg/hr
• CVP Smith et al suggest fluid bolus until a
  sustained increase in CVP (gt3mmhg after 15 min )
• Stop fluids if patient oliguric, fluid
  overloaded, consider dialysis

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Alkalinisation of urine

• Alkalinisation increases the solubility of
  myoglobin and promotes its excretion .
• Bicarbonate is used to raise the urine pH to 6.5
  thereby increasing solubility of Haeme pigments
• Add 50 ml 8.5sodium bicarbonate to each litre
• HOWEVER little clinical evidence to support use
• Brown and colleagues CK gt5000U/L
• 154(40) received mannitol and bicarbonate
• 228 (60) didnt
• No significant difference in renal failure
  ,dialysis,or mortality between the groups.

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Mannitol
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• It was postulated that treatment with mannitol
  was more efficacious than isotonic volume
  expansion alone.
• It is argued that it forces an osmotic diuresis,
  thereby diluting nephrotoxic agents and
  encouraging their excretion.
• little evidence to prove mannitol alone
• Brown et al Failed to show benefit of bic/man

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Dialysis

• Despite optimal treatment ,daily haemodialysis or
  haemofiltration may be necessary
• Remove urea and potassium

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Free radical scavengers and antioxidants

• The magnitude of muscle necrosis caused by
  ischemia-reperfusion injury has been reduced in
  experimental models by the administration of
  free-radical scavengers .
• Many of these agents have been used in the early
  treatment of crush syndrome to minimize the
  amount of nephrotoxic material released from the
  muscle
• Pentoxyphylline is a xanthine derivative used to
  improve microvascular blood flow. In addition,
  pentoxyphylline acts to decrease neutrophil
  adhesion and cytokine release
• Vitamin E , vitamin C , lazaroids
  (21-aminosteroids) and minerals such as zinc,
  manganese and selenium all have antioxidant
  activity and may have a role in the treatment of
  the patient with rhabdomyolysis

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Summary

• High index of suspicion
• On scene treatment important
• Aggressive fluid treatment
• Adequate monitoring
• Recognition and early treatment of complications

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Compartment syndrome

• Increased interstitial pressure in a close
  fascial compartment leading to microvascular
  compromise and cellular death
• Pressures measuring gt30mmhg surgical assessment
• DBP-compartment lt 30 fasciotomy

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References

• Oda, Jun MD Tanaka, Hiroshi MD Analysis of 372
  Patients with Crush Syndrome Caused by the
  Hanshin-Awaji Earthquake,J of traumaVolume
  42(3), March 1997, pp 470-476
• Gonzalez, Dario MD ,Crush syndrome,J of critical
  careVolume 33(1) Supplement, January 2005, pp
  S34-S41
• Ana L Huerta-Alardín1, Joseph Varon2 and Paul E
  Marik .Bench-to-bedside review Rhabdomyolysis
  an overview for clinicians Critical Care 2005,
  9158-169Crush Injury and Crush Syndrome A
  Review
• Smith, Jason MD Greaves, Ian Crush Injury and
  Crush Syndrome A Review .J of traumaVolume
  54(5) Supplement, May 2003, pp S226-S230
• Brown,carlos V MDRhee,Peter MD Preventing Renal
  Failure in Patients with Rhabdomyolysis Do
  Bicarbonate and Mannitol Make a difference . J of
  Trauma Vol 56 ,June2004,pp1191-1196

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Also Check

• San Fran crush protocol