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Rhabdomyolysis

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Rhabdomyolysis is potentially life-threatening syndrome due to breakdown of skeletal muscle fibers
with leakage of muscle contents into the circulation, The outcome varies depending on the extent of kidney damage, To avoid this problem Keep yourself always hydrated well supplemented with electrolytes & carbohydrates. Avoid drugs, alcohol, excessive heat & over-exercising,

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Rhabdomyolysis

  1. 1. DR. FATHI NEANA CHIEF OF ORTHOPEDICS DR. FAKHRY & ALRAJHY HOSPITAL SAUDI ARABIA NOVEBER, 30 - 2016 Rhabdomyolysis Causes, Pathophysiology & Management Rhabdo •Striated Myo •Muscle Lysis •Breakdown
  2. 2. RhabdomyolysisRhabdo • Striated Myo • Muscle Lysis • Breakdown Breakdown of skeletal muscle fibers Potentially life-threatening syndrome Leakage of muscle contents into the circulation
  3. 3. • Tea or coca cola like urine : breakdown of muscle fibers, specifically the sarcolemma resulting in release of myoglobin -> may cause acute kidney injury or renal failure • Oliguria : Shift of extracellular fluid into injured muscles -> hypovolaemia & under perfusion of the kidneys First clue 1- Tea or coca cola like urine 2- +ve urine myoglobin 3- Oliguria
  4. 4. History • First reported in 1881, in the German literature . • In 1910 Myer-Betz Syndrome, (German physician) - Triad: Muscle Pain, Weakness, Brown Urine. • World War II – First described in the victims of crush injury . Dr Bywaters described patients during London Bombings (Battle of Britain 1941). – Oliguria, pigmented casts, limb oedema, shock & death. • In 1943, in animal models, Bywaters & Stead identified myoglobin as the offending agent, & formulated the first treatment plan. • 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. – In 1995, British nephrologists introduced the Disaster Relief Task Force 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.
  5. 5. The incidence of rhabdomyolysis varies with the underlying cause Levels increase with disasters - eg, earthquakes & in war zones Rhabdomyolysis account for ~7- 8% of all new cases of acute kidney injury Epidemiology
  6. 6. Definitions • Rhabdomyolysis - destruction of striated muscle (multiple causes) • A crush injury is direct injury resulting from a crush • A crush syndrome is the systemic manifestation of muscle cell damage Resulting from 3 criteria Crushing, Prolonged pressure, Devascularization Also known as Traumatic rhabdomyolysis
  7. 7. Rhabdomyolysis Why all the worry?
  8. 8. 1- Acute Renal Failure ARF 2- Sudden Cardiac Death among young athletes SCD 3- Acute compartment syndrome ACS Sequelae of ACS -> contractures, deformities, long life disability & even amputation ex. Volkmann contracture Why all the worry? Devastating consequences is the answer (ASA)
  9. 9. Mechanisms of ARF in rhabdomyolysis • Hypovlemia -> renal vasoconstriction -> diminished renal perfusion • Cast formation leads to tubular obstruction • Direct Myoglobin nephrotoxicity • Haeme produced free radicles -Oxidants • When muscle is damaged, a protein pigment called myoglobin is released into the bloodstream and filtered out of the body by the kidneys. • The broken down myoglobin may block the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure. • Dead muscle tissue may cause a large amount of fluid to move from the blood into the muscle, leading to Hypovolemic shock. Causing reduced blood flow to the kidneys.
  10. 10. Rhabdomyolysis after an injury can be a cause of Sudden Cardiac Death among young athletes Usually in athletes, skeletal muscles are prone to injury either due to over exercises or any sports related injury Sudden Cardiac Death among young athletes
  11. 11. Sarcolemma damage release the content of sarcoplasm of muscle cells including potassium ions (K+) -> Electrolyte imbalance ->> Cardiac electrical activity changes may precipitate Sudden Cardiac Arrest Sudden efflux of potassium ions in the blood stream + High catecholamine level (exercises) Mechanisms of SCD in rhabdomyolysis
  12. 12. Acute compartment syndrome ACS = Critical increase of interstitial pressure within a confined closed fascial compartment ->> decline in the perfusion pressure to the compartment tissue Without timely diagnosis & treatment ->> microvascular compromise , ischaemia & cellular necrosis Ultimately permanent disability of the affected region.
  13. 13. Acute compartment syndrome • Immediate fasciotomy & decompression of all tissues within the affected compartment • Normal resting ICP is around 0 - 8 mmHg in adults & slightly higher (13 to 16 mmHg) in children • DBP – ICP = >30mmhg –> surgical assessment -> conservative -> normal muscle function at follow up - (McQueen and Court-Brown) • DBP – ICP = < 30 -> (fasciotomy) NB: Differential pressure = ( DBP) diastolic BP – (ICP) Intra compartment Pressure
  14. 14. Acute compartment syndrome • DBP - ICP = >30mmhg –> Non- operative techniques to delay the onset of ischemia & preserve soft tissues. • All restrictive dressings , tight pop cast should be loosened and removed. • Extremity elevation to maximize venous return and minimize edema. • Fracture reduction to limit ongoing soft tissue damage. • AVI System
  15. 15. Severe deformity, chronic pain, paralysis & even amputation. The best treatment is immediate Decompression Fasciotomies & prevention of late contractures Deformities depend on the most fibrotic & ischemic muscles Complications of A. compartment syndrome late sequelae of A. compartment syndrome
  16. 16. Skeletal Muscle
  17. 17. Skeletal Muscle Cell The sarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli and surround The sarcoplasm
  18. 18. Skeletal Muscle Cell function
  19. 19. Pathogenesis of Rhabdomyolysis 1 • Compressive forces  cellular hypoperfusion  hypoxia • Decrease in ATPase  failure of ATPase pump & sacrolemma leakage • Lysed cell release inflammatory mediators • platelet aggregation • Vasoconstriction • increase vascular permeability
  20. 20. Electrolyte disturbances Hyperkalaemia Hypocalcaemia Hyperphosphatemia Hyperuricaemia Metabolic acidosis Pathogenesis of Rhabdomyolysis 2 Revascularization • Fluids trapped in damaged tissue • Oedema of affected limb • Haemoconcentration and shock (hypovolaemia) • Myoglobin, potassium, phosphate enter venous circulation Lysed cell release Potassium Phospate Creatine kinase Myoglobin Lysed cell retain Ca water
  21. 21. Causes of Rhabdomyolysis (Muscle Breakdown) Traumatic Nontraumatic -Multiple Trauma -Crush Injury -Surgery -Coma -Immobilization Exertional Non exertional -Exertion -Heat illness -Seizures -Metabolic myopathies -Malignant hyperthermia -Neuroleptic Malignant Syndrome -ETOH (ethyl alcohol Abuse) -Drugs ( statins, OTC, illicit) -Infection -Electrolytes
  22. 22. Causes • Trauma • Exertion • Infection – viral myositis • Body temperature change: heat stroke, hypothermia • Connective tissue diseases • Genetic defects: metabolic disorders • Drugs and toxins: statins, OTC, illicit drugs
  23. 23. TABLE 1 Medications and Toxic Substances That Increase the Risk of Rhabdomyolysis HMG-CoA = 3-hydroxy-3-methylglutaryl coenzyme A; LSD = lysergic acid diethylamide; MDMA = 3,4-methylene dioxymethamphetamine. Direct myotoxicity HMG-CoA reductase inhibitors, especially in combination with fibrate-derived lipid-lowering agents such as niacin (nicotinic acid; Nicolar) Cyclosporine (Sandimmune) Itraconazole (Sporanox) Erythromycin Colchicine Zidovudine (Retrovir) Corticosteroids Indirect muscle damage Alcohol Central nervous system depressants Cocaine Amphetamine Ecstasy (MDMA) LSD Neuromuscular blocking agents
  24. 24. Statins act by inhibiting HMG-CoA reductase (3-hydroxy-3-methyl-glutaryl-CoA Reductase) All metabolic functions further down the pathway are affected (isoprenoids) HMG-CoA reductase inhibitors
  25. 25. Clinical Mmanifestations of Rhabdomyolysis ? Range from asymptomatic to acute renal failure and DIC Triad : muscle pain , weakness , dark urine Systemic features • Coca-cola coloured urine – Results from Myoglobinuria • General weakness • Confusion, unconsciousness • Fever, nausea/vomiting, Tachycardia • Less frequent urination • In severe cases: AKI (acute kidney injury) renal failure • Disseminated intravascular coagulation Additional symptoms Overall Malaise - Fatigue - Joint pain – Seizures - Weight gain Local features • Muscle pain, swelling, stiffness & tenderness • Bruising & compartment syndrome • Muscle & Limb weakness
  26. 26. Complications of Rhabdomyolysis Early complications (< 12- 72 hrs) • Hypovolaemia • Hyperkalaemia • Hypocalcaemia • Cardiac arrhythmias • Cardiac arrest Late complications (< 12- 72 hrs) • Kidney damage • Acute tubular necrosis • Acute renal failure 15% • DIC • ARDS • sepsis Early or late complications Acute compartment syndrome
  27. 27. Laboratory Findings • Creatine kinase: >5x ULN (1500-100,000) (heart, brain, skeletal muscle) Rises within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hours. A decline is usually seen within three to five days of cessation of muscle injury1,2. • Myoglobinuria • Hyperkalemia • Hyperphosphatemia • Hypocalcemia • Hyperuricemia
  28. 28. Laboratory Findings High CPK levels may be seen in people who have: Brain injury or stroke Convulsions Delirium tremens Dermatomyositis or polymyositis Electric shock Heart attack Inflammation of the heart muscle (myocarditis) Lung tissue death (pulmonary infarction) Creatine phosphokinase Creatine phosphokinase (CPK) an enzyme found mainly in heart, brain, skeletal muscle Muscular dystrophies Myopathy Rhabdomyolysis Other conditions that may give positive test results include: Hypothyroidism Hyperthyroidism Pericarditis following a heart attack
  29. 29. Prevention • Balanced diet & exercise • Risk: Antipsychotics, statin & fibrate medications for high cholesterol , Selective serotonin reuptake inhibitors, Zidovudine, Colchicine, lithium, Antihistamines, and several others • Don’t: Over exercising in extreme heat conditions, take drugs & alcohol • Keep: hydrated – electrolytes
  30. 30. How can I prevent Rhabdomyolysis • Drink plenty of fluids after strenuous exercise to dilute the urine and flush the myoglobin out of the kidney • Proper hydration is also necessary after any condition or event that may involve damage to skeletal muscle
  31. 31. Treatment • A B C • Fluids Early aggressive fluid resuscitation. • Electrolyte replacement. • Alkalinization of urine? • Treat hyperkalaemia • Treat underlying cause. • Fasciotomy. • Free radical scavengers and antioxidants
  32. 32. EMS Treatment 1. Immediately obtain intravenous access with a large-bore catheter. 2. Administer isotonic crystalloid 500 mL/h and then titrate to maintain a urine output of 200- 300 mL/h.
  33. 33. Fluid Resuscitation • Give as much fluid as you would give a severely burned patient. • Optimal fluid and rate of repletion are unclear. • No studies comparing efficacy/safety of different types and rate of fluid administration. • Early and aggressive fluids (hydration) may prevent complications by rapidly remove myoglobin out of the kidneys. Administer isotonic crystalloid fluids (Normal Saline or Lactated Ringer’s). • Studies of patients with severe crush injuries resulting in Rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide FLUID RESUCITATION!
  34. 34. Algorithm Isotonic Saline -Initial Resuscitation: 1-2 L/hr -100-200 ml/hr (if hemolysis induced injury) -Correct electrolyte abnormalities Titrate IVF UOP goal: 200-300ml/hr Serial CK measurements CK>5000 CK<5000 Stop Treatment
  35. 35. Bicarbonate, Mannitol, Dialysis Bicarbonate: Forced alkaline diuresis • May reduce renal heme toxicity • May also decrease the release of free iron from myoglobin, the formation of vasoconstricting F2-isoprostanes, and the risk for tubular precipitation of uric acid3,4 • No clear clinical evidence that an alkaline diuresis is more effective than a saline diuresis in preventing AKI. Mannitol: Forced diuresis • May minimize intratubular heme pigment deposition and cast formation, and/or by acting as a free radical scavenger, thereby minimizing cell injury6,7. • Net clinical benefit remains uncertain, therefore, not routinely administered. Dialysis • Use of dialysis to remove myoglobin, hemoglobin, or uric acid in order to prevent the development of renal injury has not been demonstrated.
  36. 36. 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
  37. 37. Prognosis of Rhabdomyolysis • The outcome varies depending on the extent of kidney damage. Source: Silberber, 2007 Automatic Positive Airway Pressure
  38. 38. Rhabdomyolysis is the breakdown of skeletal muscles ATP depletion ->> increase in intracellular Ca2+ ->> triggering a series of proteolytic enzymes =>> myocyte destruction ->> leakage of cell components in blood stream (myoglobin, creatine kinase, K, P, electrolytes, etc.) Summary and Conclusions
  39. 39. Summary and Conclusions • Excess myoglobin —>> precipitate in glomerular filtrate —>> acute renal failure • Rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure • The overall mortality rate for patients with Rhabdomyolysis is approximately 5% • Rhabdomyolysis is more common in Males than in Females • May occur in infants, toddlers, and adolescents
  40. 40. Summary and Conclusions • High index of suspicion (coca- cola coloured urine, muscle pain, nausea, confusion) • On scene treatment Aggressive fluid treatment Adequate monitoring • Recognition & early treatment of complications Laboratory tests: Plasma creatine kinase levels Plasma potassium levels urine myoglobin assay
  41. 41. Summary and Conclusions • When rhabdomyolysis is suspected aggressive fluid resuscitation should started to prevent pigment nephropathy. • Titrate to UOP 200-300cc/hr. • The use of bicarbonate, mannitol, and dialysis: net clinical benefit has not been shown.
  42. 42. Keep always hydrated Well supplemented with electrolytes & carbohydrates Avoid drugs, alcohol, excessive heat & over-exercising Summary and Conclusions Prevention strategies

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