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Rhabdomyolysis managment

Rhabdomyolysis managment



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    Rhabdomyolysis Rhabdomyolysis Presentation Transcript

    • Rhabdomyolysis SHEEBA HAKAK AMNCH
    • DEFINITION Rhabdo = straited myo = muscle lysis = breakdown
    • 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.
    • 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.
    • PATHOPHYSIOLOGY hypoxia reperfusion Direct injury to membrane integrity
    • pathophysiology Hypoxia leads to anaerobic metabolism Dec .ATP generation Loss of ion gradients esp Na Increase in intracellular ca Leakage of intracellular protein intoECF
    • pathophysiology Reperfusion injury generates o2 free radicles Vasoconstriction of pre capillary arterioles Lipid peroxidation of cell membranes,formation of peroxynitrite Self perpetuating secondary injury
    • 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
    • causes rhabdomyolysis Muscle injury Medications & illicit drugs Increased muscle activity
    • 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
    • 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
    • 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
    • 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
    • Clinical Presentation • Many features are nonspecific • Triad :muscle pain ,weakness and dark urine • Varies depending on underlying condition • Features – Local – Systemic
    • Clinical Presentation • Local features – Muscle pain – Tenderness – Swelling – Bruising – Weakness • Systemic features – Tea-colored urine – Fever – Malaise – Nausea – Emesis – Confusion – Agitation – Delirium – Anuria
    • 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
    • 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
    • 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
    • Treatment • A B C • Fluids • Treat hyperkalaemia
    • 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.
    • 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
    • Mannitol
    • Mannitol • The diuretic effect of mannitol is controversial as it may further exacerbate hypovolumia,metabolic acidosis&pre renal AKI
    • 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.
    • 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.
    • 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
    • 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.
    • Dialysis • Despite optimal treatment ,pts may still develop AKI with severe acidosis & hyperkalemia (daily haemodialysis or haemofiltration may be necessary) • Remove urea and potassium