Rhabdomyolysis

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Rhabdomyolysis

• by Ri ???

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Outline

• Introduction
• Cause
• Pathophysiology
• Laboratory findings
• Treatment

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• Bench-to-bedside review Rhabdomyolysis an
  overview for clinicians
• Ana L Huerta-Alardín1, Joseph Varon2 and Paul E
  Marik3
• Critical Care 2005, 9158-169
• Chapter 114 Rhabdomyolysis
• Goldman Cecil Medicine 23rd ed

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Introduction

• Destruction or disintegration of striated muscle
• Resulting in the leakage of the intracellular
  muscle constituents into the circulation and
  extracellular fluid
• Weakness, myalgia and tea-colored urine are the
  main clinical manifestations

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Cause
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Cause
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Drugs that may induce rhabdomyolysis
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Statin related rhabdomyolysis

• Directly or indirectly impairs the production or
  use of ATP by skeletal muscle
• Increases energy requirements that exceed the
  rate of ATP production
• Interfere with ATP production by reducing levels
  of coenzyme Q, chronic myositis syndrome
• Risk factors high dosages, increasing age,
  female, renal and hepatic insufficiency, DM and
  concomitant therapy with drugs such as fibrates

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Pathophysiology
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Pathophysiology

• Goldman Cecil Medicine 23rd ed

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Pathophysiology

• Goldman Cecil Medicine 23rd ed

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(No Transcript)
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Pathophysiology of ARF

• Two crucial factors hypovolemia/ dehydration and
  aciduria
• Heme protein toxicity
• 1. Renal vasoconstriction with diminished
• 2. Renal circulation, intraluminal cast
  formation and direct
• 3. Heme Protein-induced cytotoxicity
• Synergistic effect on renal vasoconstriction
• Pigmented casts TammHorsfall protein with
  myoglobin
• Heme-produced free radicals

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Laboratory findings

• CK levels most sensitive
• Rises within 12 hours of the onset
• Peaks in 13 days, and declines 35 days
• 5000 U/l or greater is related to renal
  failure
• Myoglobin in serum or urine
• The early phases
• Filtered by the kidney, plasma gt 1.5 mg/dl?
  appear in urine
• Redbrown color to urine, gt100 mg/dl
• short half-life (23 hours)
• Metabolized by liver

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Laboratory finding

• Other muscle markers carbonic anhydrase III,
  Aldolase
• Creatinine is elevated greater than the blood
  urea nitrogen?normal 101 ratio to 61
• Hyperkalemia, hyperphosphatemia, hypocalcemia,
  and hyperuricemia

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Management

• Hydration with isotonic fluid, saline
  1-2L/hr(Grade IB)
• keep 200-300ml/hr urine output till CK begin
  to decrease.
• Forced diuresis Mannitol minimizes intratubular
  heme pigment deposition, free-radical scavenger,
  reduces blood viscosity, renal vasodilator
• Evaluate plasma osm Q4-6H, osmolal gap?
  gt55mosm/kg gt stop Mannitol
• Other diuretics

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Management

• Alkalinization of the urinegt pH 6.5(Grade 2B)
  bicarbonate(75mmol in 1-1.5L saline), may worsen
  the degree of hypocalcemia
• Volume expansion with saline alone prevented
  progression to renal failure and that the
  addition of mannitol and bicarbonate had no
  additional benefit Homsi E, Barreiro M, Orlando
  J, Higa E

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Management

• Role of free-radical scavengers and antioxidants
  
• Experimental models reduced ischemia
  reperfusion injury
• Pentoxyphylline improve microvascular blood
  flow, neutrophil adhesion? cytokine release?
• Vitamin E, C

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Management

• Dialysis
• ARF developed, Daily hemodialysis or continuous
  hemofiltration?remove urea and potassium
• Peritoneal dialysis is inadequate
• The removal of myoglobin by plasma exchange has
  not demonstrated any benefit

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Management

• Administration of calcium should be avoided
  during the renal failure phase, unless the
  patient has symptomatic hypocalcemia or severe
  hyperkalemia(Grade IB)

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Management of Crush syndrome

• Mannitol and a forced alkaline diuresis are
  recommended when CK levelsgt 20,000 U/L
• Urine output of 200 mL/hr
• Urine pH between 6 7, serum pH lt 7.50
• A bolus of 1 L of 5 dextrose plus 0.22 NaCl and
  100 mEq NaHCO3 ?infusion at 2 to 5 mL/kg/hr
• 20 mannitol infusion 0.5 g/kg in 15min? 0.1
  g/kg/hr.

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Take home message

• Impairment of the production or use of ATP is the
  basic cause
• Most useful laboratory findings are elevated CK(gt
  5000U/L related to ARF), initial detection of
  myglobulin
• Management Aggressive hydration, diuresis, urine
  alkalinzation, free-radical scavengers, dialysis
• Do not treat hypocalcemia unless symptom
  developed

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Reference

• Bench-to-bedside review Rhabdomyolysis an
  overview for clinicians
• Ana L Huerta-Alardín1, Joseph Varon2 and Paul E
  Marik3
• Critical Care 2005, 9158-169
• Chapter 114 Rhabdomyolysis
• Goldman Cecil Medicine 23rd ed
• Clinical features and prevention of heme
  pigment-induced acute tubular necrosis, UpToDate