rhabdomyolysis
DESCRIPTION
Rhabdomyolysis managmentTRANSCRIPT
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Rhabdomyolysis
SHEEBA HAKAKAMNCH
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DEFINITION
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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.
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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.
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PATHOPHYSIOLOGY
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pathophysiology
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pathophysiology
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Mechanism of ARF
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causes
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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
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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
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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
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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
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Clinical Presentation
• Many features are nonspecific• Triad :muscle pain ,weakness and dark urine• Varies depending on underlying condition• Features– Local– Systemic
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Clinical Presentation
• Local features– Muscle pain– Tenderness– Swelling– Bruising– Weakness
• Systemic features– Tea-colored urine– Fever– Malaise– Nausea– Emesis– Confusion– Agitation – Delirium– Anuria
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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
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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
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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
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Treatment
• A B C• Fluids• Treat hyperkalaemia
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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.
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Over view of studies for fluid management of Rhabdomyolysis
Study design No.of patients treatment conclusion
Brown et al2004
Retrospective 1771 Bicarbonate,mannitol&saline VS. saline
No improvement over saline alone
Homsi et al1997
Retrospective 24 Bicarbonate,mannitol & saline vs.saline
No improvement over saline alone
Cho et al2007
prospective 200 Lactated ringer vs.saline
Decreased amount of NAHCO3 & diuretics given with LR solution
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Mannitol
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Mannitol
• The diuretic effect of mannitol is controversial as it may further exacerbate hypovolumia,metabolic acidosis&pre renal AKI
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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.
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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.
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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
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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.
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Dialysis• Despite optimal treatment ,pts may still
develop AKI with severe acidosis & hyperkalemia (daily haemodialysis or haemofiltration may be necessary)
• Remove urea and potassium