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Traumatic rhabdomyolysis: causes, pathophysiology and management strategies PowerPoint Presentation
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Traumatic rhabdomyolysis: causes, pathophysiology and management strategies

Traumatic rhabdomyolysis: causes, pathophysiology and management strategies

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Traumatic rhabdomyolysis: causes, pathophysiology and management strategies

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  1. Traumatic rhabdomyolysis: causes, pathophysiology and management strategies By Sharon Fish

  2. Overview • Definitions • Historically • Causes • Pathophysiology • Clinical • Management

  3. 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

  4. Based on 3 criteria: Involvement of a muscle mass Prolonged compression Compromised local circular

  5. 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.

  6. 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.

  7. 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

  8. 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

  9. 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

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

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

  12. Mechanisms of ARF in rhabdomyolysis Renal vasoconstriction with diminished renal perfusion Cast formation leads to tubular obstruction Direct Myoglobin nephrotoxicity- Haeme produced free radicles

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

  14. Musculoskeletal signs Pain Weakness Swelling

  15. General manifestation Malaise Fever Tachycardia Nausea vomiting

  16. Complications Early Hypovolaemia Hyperkalaemia Hypocalcaemia Cardiac arrhythmias Cardiac arrest Compartment syndrome Late(12-72hrs) Acute renal failure DIC ARDS sepsis

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

  18. CK-peak Huerta-Alardin et al :CK>5000U/L serious muscle injury, related to renal failure Gonzales et al:>10000U/L related to ARF Brown et al :2083 trauma ICUadmission,85%abn CK (>520) 74 of 382 <5000U/L developed RF(8%) 143 of 1701 >5000U/L developed RF(19%) Renal failure defined peak creatinine >2mg/dl

  19. CK-peak Oda et al: 372 crush injury pts at Hanshin earthquake CK < 75000 45 of 115 (39%) developed RF requiring dialysis CK > 75000 43 of 51 (84.3%) developed renal failure requiring dialysis Note different definitions of renal failure

  20. 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 >100mg/dl Myoglobin has short T1/2 (2-3hours) Serum level return to normal after 6-8hours

  21. Carbonic anhydrase 3 Aldolase Trop T I

  22. Lab tests Raised U&E Hyperkalaemia hypocalcaemia hyperphosphataemia uric acid

  23. Treatment A B C Fluids Treat hyperkalaemia

  24. 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 al:adult • 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 (>3mmhg after 15 min ) • Stop fluids if patient oliguric, fluid overloaded, consider dialysis

  25. 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 8.5%sodium bicarbonate to each litre HOWEVER little clinical evidence to support use Brown and colleagues CK >5000U/L 154(40%) received mannitol and bicarbonate 228 (60%) didn’t No significant difference in renal failure ,dialysis,or mortality between the groups.

  26. Mannitol

  27. 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

  28. Dialysis Despite optimal treatment ,daily haemodialysis or haemofiltration may be necessary Remove urea and potassium

  29. 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

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

  31. Compartment syndrome Increased interstitial pressure in a close fascial compartment leading to microvascular compromise and cellular death Pressures measuring >30mmhg –surgical assessment DBP-compartment =< 30 –fasciotomy

  32. References Oda, Jun MD; Tanaka, Hiroshi MD; Analysis of 372 Patients with Crush Syndrome Caused by the Hanshin-Awaji Earthquake,J of trauma:Volume 42(3), March 1997, pp 470-476 Gonzalez, Dario MD ,Crush syndrome,J of critical care:Volume 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, 9:158-169Crush Injury and Crush Syndrome: A Review Smith, Jason MD; Greaves, Ian Crush Injury and Crush Syndrome: A Review .J of trauma:Volume 54(5) Supplement, May 2003, pp S226-S230 Brown,carlos V MD:Rhee,Peter MD ;Preventing Renal Failure in Patients with Rhabdomyolysis: Do Bicarbonate and Mannitol Make a difference . J of Trauma :Vol 56 ,June2004,pp1191-1196

  33. Also Check… San Fran crush protocol