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Rhabdomyolysis managment

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  1. 1. Rhabdomyolysis SHEEBA HAKAK AMNCH
  2. 2. DEFINITION Rhabdo = straited myo = muscle lysis = breakdown
  3. 3. DEFINITION • Rhabdomyolysis is the breakdown of muscle fibers, specifically of the sarcolemma of skeletal muscle, resulting in the release of muscle fiber contents (myoglobin) into the bloodstream.
  4. 4. HISTORY • The association between rhabdomyolysis and ARF was first established during world war II.After the bombing of London,crush victims developed AKI with pigmented casts in renal tubules at autopsy.
  5. 5. PATHOPHYSIOLOGY hypoxia reperfusion Direct injury to membrane integrity
  6. 6. pathophysiology Hypoxia leads to anaerobic metabolism Dec .ATP generation Loss of ion gradients esp Na Increase in intracellular ca Leakage of intracellular protein intoECF
  7. 7. pathophysiology Reperfusion injury generates o2 free radicles Vasoconstriction of pre capillary arterioles Lipid peroxidation of cell membranes,formation of peroxynitrite Self perpetuating secondary injury
  8. 8. Mechanism of ARF Damaged muscle cells myoglobin Precipitation of casts,occlude renal tubules O2 free radicles,peroxidation of mem lipids Release of PAF,andothelin,PGF2 Constriction of renal arterioles ,dec GFR
  9. 9. causes rhabdomyolysis Muscle injury Medications & illicit drugs Increased muscle activity
  10. 10. What causes rhabdomyolysis? • Direct Muscle Injury – Crush injuries, deep burns, electrical injuries, acute necrotizing myopothy of certain cancers, assaults with prolonged and vicious beating/repetitive blows • Excessive Physical Exertion – Results in state in which ATP production can’t keep up with demand  exhaustion of cellular energy supplies & disruption of muscle cell membrane – Protracted tonic-clonic seizures, psychotic hyperactivity (mania or drug-induced psychosis) • Muscle Ischemia – Interference with O2 delivery to cells and therefore limiting production of ATP – Generalized ischemia from shock & hypotension, carbon monoxide poisoning, profound systemic hypoxemia, localized compression leading to skeletal muscle ischemia, tissue compression d/t immobilization of muscle, intoxicated/comatose down for long periods, immobilization from acute SCI, compartment syndrome, arterial/venous occlusions
  11. 11. Causes cont. • Temperature Extremes – Excessive Cold   muscle perfusion, ischemia; freezing causes cellular destruction – Excessive Heat  destroys cells &  metabolic demands (every degree  temp =  metabolic demand by ~ 10%) & if body can’t keep up with  requirement, cellular hypoxia  anaerobic environment – Malignant hyperthermia, neuroleptic malignant syndrome (d/t psychotropic medications) • Electrolyte & Serum Osmolality Abnormalities – Chronic hypokalemia  significant total body loss of K+ disrupts Na+ K+ pump  cell membrane failure, leak of toxic intracellular contents from muscle cells – Overuse of diuretics , hyperemesis gravidarum, some drugs (amphotericin B), hyperglycemic hyperosmolar nonketotic coma
  12. 12. Causes cont. • Infections – Pneumococcal & Staphylococcus aureus sepsis, salmonella & listeria infections, gas gangrene, NF – Can destroy large quantities of muscle tissue through generation of toxins or direct bacterial invasion • Drugs, Toxins, Venoms – Ethanol  depresses CNS and leads to  periods of immobility; alcohol also has toxic effects on myocytes with binge drinking – -statins – Drugs that mimic or stimulate SNS (cocaine, methamphetamines, ecstasy, pseudoephedrine, excessive caffeine) – Chemicals & toxic plants – Snake venoms, multiple stings by wasps, bees, hornets – Pharmaceutical agents – benzodiazepines, corticosteroids, narcotics, immunosuppressants, antibiotics, antidepressants, antipsychotics
  13. 13. Causes cont. • Endocrinologic Disorders – Either wasting or hypermetabolic conditions – K+ wasting  diabetic ketoacidosis, hyperosmolar nonketotic coma, hyperaldosteronism – Na+ depletion  Addison disease –  sympathetic stimulation & metabolic demands beyond sustainability  thyroid storm & pheochromocyoma • Genetic & Autoimmune Disorders – Carbohydrate & lipid metabolism; muscular dystrophies, autoimmune disorders such as polymyositis & dermatomyositis
  14. 14. Clinical Presentation • Many features are nonspecific • Triad :muscle pain ,weakness and dark urine • Varies depending on underlying condition • Features – Local – Systemic
  15. 15. Clinical Presentation • Local features – Muscle pain – Tenderness – Swelling – Bruising – Weakness • Systemic features – Tea-colored urine – Fever – Malaise – Nausea – Emesis – Confusion – Agitation – Delirium – Anuria
  16. 16. Potential Complications • Acute RF (myoglobinuric RF) • Compartment syndrome (with crush injuries)  decompression fasciotomy • DIC  give FFP • Disturbances in serum & urine electrolyte levels/balance  cardiac arrhythmias • Hypovolemia • Metabolic Acidosis • Respiratory failure • Acute muscle wasting
  17. 17. Diagnostics •  serum total CK & CK-MM (CK isoenzyme in skeletal muscle) – Begins  2-12h post-injury, peak 1-3 days, declines 3-5 days •  serum myoglobin – Until filters into urine causing characteristic coke-colored urine •  serum K+ – Major cause of morbidity/mortality d/t muscle breakdown & release K+ which  further by acidosis & RF • Give calcium gluconate/chloride cautiously so as to prevent hypodynamic instability •  serum BUN & Cr – d/t escape of massive amounts Cr from damaged muscle • Early hypocalcemia – Deposit of Ca in necrotic muscle, soft tissues calcify in necrosis
  18. 18. Diagnostics cont. • Later hypercalcemia & hyperphosphatemia – Phosphate and calcium leakage from damaged muscle cells  give PO calcium carbonate/hydroxide & calcium will follow being fixed when phosphate distribution fixed (inverse relationship) •  uric acid (hyperuricemia) • ABC – To detect hypoxia and acidosis & when giving sodium bicarb therapy • Clotting Studies – Useful in detecting DIC • Urinalysis – Will reveal presence of protein, brown casts, uric acid crystals • Urine Dipstick – Quick initial test – Myoglobin will react to hemoglobin reagent on stick  if positive, need to determine if Hgb or myoglobin
  19. 19. Treatment • A B C • Fluids • Treat hyperkalaemia
  20. 20. Fluids • The treatment of rhabdomyolysis includes initial stabilization and resusitation of the pt. • Saline has been used as the fluid of choice for resusitation. • A recent prospective randomized single-blind study compared saline or RL solution for initial resusitation.In addition, all pts were treated with bicarbonate & diuretics.The study found less bicarbonate & diuretics were needed for pts receiving RL.
  21. 21. Over view of studies for fluid management of Rhabdomyolysis Study design No.of patients treatment conclusion Brown et al 2004 Retrospective 1771 Bicarbonate,m annitol&saline VS. saline No improvement over saline alone Homsi et al 1997 Retrospective 24 Bicarbonate,m annitol & saline vs.saline No improvement over saline alone Cho et al 2007 prospective 200 Lactated ringer vs.saline Decreased amount of NAHCO3 & diuretics given with LR solution
  22. 22. Mannitol
  23. 23. Mannitol • The diuretic effect of mannitol is controversial as it may further exacerbate hypovolumia,metabolic acidosis&pre renal AKI
  24. 24. Alkalinisation of urine • Alkalinization of the urine with sod bicarb has been suggested to minimize renal damage after rhabdomyolysis. • Although mannitol and NAHCO3 are frequently considered the standard of care in preventing AKI,little evidence exists to support the use of these agents. • In a retrospective study of 24pts,vol expansion with saline alone prevented progression to renal failure,& the addition of mannitol&NAHCO3 had no additional benefit • 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.
  25. 25. Alkalization continues.. • Use of carbonic anhydrase inhibitors has been suggested when ph >7.45 after NAHCO3 therapy or if there is continued aciduria despite alkalemia.
  26. 26. 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
  27. 27. HBO therapy • HBO therapy also has been advocated for treatment of crush injuries because of its effects to increase perepheral o2transport. • A RDBS examined the effect of HBO on wound healing.36 pts were divided into 2 groups ,one received HBO therapy & other conventional therapy.complete healing was achieved for 17 pts in HBO grp v/s 10 pts in placebo grp.
  28. 28. Dialysis • Despite optimal treatment ,pts may still develop AKI with severe acidosis & hyperkalemia (daily haemodialysis or haemofiltration may be necessary) • Remove urea and potassium