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Rhabdomyolysis
Rhabdomyolysis is the breakdown of skeletal muscle fibers that results in the release of muscle contents into the bloodstream. This can lead to acute kidney injury through deposition of myoglobin casts in the renal tubules. Treatment involves aggressive fluid resuscitation to prevent renal failure, treatment of hyperkalemia, and alkalinization of urine to prevent tubular obstruction. While bicarbonate and mannitol are commonly used, evidence does not clearly support their benefit over fluid resuscitation alone. Oxygen therapy and antioxidants may help reduce muscle injury. Dialysis may be needed for severe cases with refractory acidosis or hyperkalemia.
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Rhabdomyolysis
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- 2. DEFINITION Rhabdo = straited myo= muscle lysis = breakdown
- 3. DEFINITION • Rhabdomyolysis isthe breakdown of muscle fibers, specifically of the sarcolemma of skeletal muscle, resulting in the release of muscle fiber contents (myoglobin) into the bloodstream.
- 4. HISTORY • The associationbetween 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.
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- 6. pathophysiology Hypoxia leads toanaerobic metabolism Dec .ATP generation Loss of ion gradients esp Na Increase in intracellular ca Leakage of intracellular protein intoECF
- 7. pathophysiology Reperfusion injury generateso2 free radicles Vasoconstriction of pre capillary arterioles Lipid peroxidation of cell membranes,formation of peroxynitrite Self perpetuating secondary injury
- 8. Mechanism of ARF Damagedmuscle 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
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- 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. Causes cont. • TemperatureExtremes – 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. 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. Causes cont. • EndocrinologicDisorders – 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. Clinical Presentation • Manyfeatures are nonspecific • Triad :muscle pain ,weakness and dark urine • Varies depending on underlying condition • Features – Local – Systemic
- 15. Clinical Presentation • Localfeatures – Muscle pain – Tenderness – Swelling – Bruising – Weakness • Systemic features – Tea-colored urine – Fever – Malaise – Nausea – Emesis – Confusion – Agitation – Delirium – Anuria
- 16. Potential Complications • AcuteRF (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. Diagnostics • serumtotal 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. Diagnostics cont. • Laterhypercalcemia & 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. Treatment • A BC • Fluids • Treat hyperkalaemia
- 20. Fluids • The treatmentof 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. Over view ofstudies 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
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- 23. Mannitol • The diureticeffect of mannitol is controversial as it may further exacerbate hypovolumia,metabolic acidosis&pre renal AKI
- 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. Alkalization continues.. • Useof carbonic anhydrase inhibitors has been suggested when ph >7.45 after NAHCO3 therapy or if there is continued aciduria despite alkalemia.
- 26. Free radical scavengersand 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. HBO therapy • HBOtherapy 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. Dialysis • Despite optimaltreatment ,pts may still develop AKI with severe acidosis & hyperkalemia (daily haemodialysis or haemofiltration may be necessary) • Remove urea and potassium