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RHABDOMYOLISIS IN ICU CARE.pptx
- 1. SUPERVISOR: DR ZAYUAH MAT SULAIMAN BY: DR NORFARHANAH ZAKARIA RHABDOMYOLISIS IN ICU CARE
- 2. OUTLINE ⢠Introduction ⢠Epidemiology ⢠Pathophysiology ⢠Causes ⢠Presentation ⢠Complication ⢠Management ⢠Summary
- 3. INTRODUCTION ⢠Potentially life-threatening syndrome ⢠Muscle necrosis and the release of intracellular muscle constituents into the circulation. ⢠Creatine kinase (CK) levels are typically markedly elevated, and muscle pain and myoglobinuria may be present.
- 4. Myocyte necrosis Release of intracellular content into the circulation Produce life threatening complication Eg: hyperK & AKI Multiple causes that progress to:
- 5. EPIDEMIOLOGY ⢠Most common cause in ICU setting ⢠Muscular trauma due to polytrauma ⢠Vascular obstruction ⢠Occurs up to 85% in traumatic patient ⢠1/3 of all rhabdomyolysis developed AKI ⢠5-25% of all AKI resulted from rhabdomyolysis ⢠Rhabdomyolysis + AKI: mortality 20%, higher if developed multiorgan failure
- 8. CAUSES
- 11. CLINICAL MANIFESTATION ⢠Varies depending on the etiology and severity ⢠Asymptomatic rise in CK ď hypovolemic shock with life-threatening arrhythmias
- 14. â˘Serum Creatinine Kinase (CK) ⢠Sensitive indicator of muscle damage ⢠Rising within 1st 12 hours of injury ⢠Peaking at 1-3 days, declining at 3-5 days. Persistent CK level may indicate ongoing muscle injury ⢠Level over 5000u/L is related to renal failure (AKI over 50%) ⢠Level are directly proportional to the extend of muscle injury ⢠May further increase due to compartment syndrome ⢠no level to postulate rhabdomyolysis, may accept 5x > normal level
- 15. â˘Myoglobin â˘Released after muscle disintegration â˘Produce dark brown urine â˘Absence: does not exclude rhabdomyolysis â˘Why not use? ⢠Decrease rapidly compared to CK ⢠May not visible/ resolved early ⢠Use urine dipstick test to detect, may be false +ve in case of hemolysis
- 16. â˘Skeletal muscle biopsy ⢠Can be used to confirm â˘Toxicology screening ⢠caused by illicit drugs n alcohol intoxication â˘ABG, RP CaMgPo4, coagulation profile â˘ECG â˘Metabolites derangement
- 17. COMPLICATION
- 18. ⢠Hypovolemic ⢠Necrosis and inflammation result in influx of fluid into the necrotic muscle (3rd space effect) ⢠As the fluid lost from the circulation, shock developed ⢠Compartment syndrome ⢠Ischemic and edematous muscle further raises intra- compartmental pressure ď vicious cycle of continuing ischemia ⢠Rebound phenomenon: persistent elevation and rebound elevation of CK at 48-72hr after insult
- 19. ⢠Arrhythmia and cardiac arrest ⢠hyperkalemia ⢠Hypocalcaemia ⢠Disseminated intra-vascular coagulation (DIVC) ⢠Activation of the clotting cascade by component release by the damaged muscle ⢠Hepatic dysfunction ⢠Protease release from injured muscle
- 20. ⢠Acute renal failure ⢠Developed in 33% of the patient ⢠Most serious complication ⢠Factor contribute ⢠Hypovolemia ⢠Acidosis ⢠Tubular obstruction ⢠Nephrotoxic effect of myoglobulin * Within the renal tubules, myoglobin interact with protein (Tamm- Horsfall) to form brown granular cast ď obstruction * This process favoured in acidic urine, and myoglobin have no nephrotoxic effect when urine is alkaline
- 22. MANAGEMENT
- 23. ⢠There is lack of level 1 evidence of management of rhabdomyolysis ⢠Most of evidence based on case report, retrospective clinical studies and animal models ⢠Early recognition and initiation of treatment is vital
- 24. Initial resuscitation ⢠Careful history and physical examination needed to identify underlying illness and causes ⢠Intravenous line should be established ⢠IV fluid must started immediately- to promote diuresis and released toxic product ⢠Infusion of 1.5L of saline per hour is required during the initial management, followed by 300-500cc/hr once hemodynamically stable ⢠Transfusion of blood and blood product may needed in severe cases ⢠Vital sign, urine output, serial electrolyte levels and CK ⢠IV fluid should be continued until the level of CK < 1000u/L ⢠Addition of mannitol and bicarbonate recommended by many expert to prevent AKI
- 25. TREATMENT OF REVERSIBLE CAUSE OF MUSCLE DAMAGE ⢠Underlying cause should be treated immediately ⢠Hyperthermia ⢠External cooling ⢠Control muscular activity using benzodiazepine ⢠Malignant hyperthermia ⢠Anaesthesia should be discontinued ⢠Dantrolene 2.5-4mg/kg, then 1mg/kg/4hr up to 48hr ⢠Electrolyte abnormalities ⢠Correct accordingly ⢠Drugs/ toxins ⢠Gastric lavage/ antidotes/ hemodialysis ⢠Correct hypoxia
- 26. PREVENTION OF COMPLICATION ⢠Aggressive rehydration to prevent ARF ⢠May need dialysis ⢠Hyperkalemia ⢠Treatment to prevent cardiac complication ⢠Lytic cocktail ⢠If fail, dialysis maybe required ⢠Hypocalcaemia ⢠Usually required no treatment ⢠Only given to treat hyperkalemia/ profound sign and symptoms
- 27. ⢠Hyperphosphatemia ⢠Rarely clinically significant ⢠Treated when serum level > 7mg/dl ⢠Give oral phosphate binders ⢠Hypophosphatemia ⢠If serum level < 1 mg/dL ⢠Compartment syndrome ⢠Need orthopedic consultation for fasciotomy ⢠DIVC ⢠Usually resolved spontaneously after several days if u/l causes treated ⢠If haemorrhagic occur: plt, vit k, FFP ⢠Metabolic acidosis ⢠Aggressive intravenous fluid hydration ⢠Sodium bicarbonate administration
- 28. Mannitol ⢠Increase in renal blood flow and glomerular filtration rate â prevent obstruction by myoglobin cast ⢠How? Osmotic diuretic draw fluid from interstitial compartment to intravascular compartment ⢠Counteract hypovolemia ⢠Reduce muscle swelling and nerve compression ⢠Scavenging free radical ⢠20% mannitol infusion 0.5g/kg over 15min, then 0.1g/kg/hr, aim urine output > 200mls/hr
- 29. Sodium bicarbonate ⢠To alkalinisation of urine ⢠Decreasing cast formation ⢠Minimising the toxic effects of myoglobin on renal tubules ⢠Inhibiting lipid peroxidation ⢠Decreasing the risk of hyperkalemia ⢠1 amp nahco3 (44mEq) added to 1L HS, run at rate 100mls/hr recommended to prevent ARF
- 30. Journal review of NaHCO3 and Mannitol ⢠Ron et al 1984 ⢠7 patient treated for crush injuries after the collapse of building ⢠Mannitol and nahco3 used over 1st 5 days ⢠Visible myoglobinuria cleared at average 48hrs ⢠None required HD ⢠Zager RA 1992 ⢠Mannitol maybe protective due to associate diuresis that minimize intratubular heam pigment deposition ⢠Knottenbelt 1994 ⢠200 patient with extensive STI from severe beating ⢠Received fluid without nahco3 and mannitol ⢠Increase rate of ARF and death < 12hr of admission ⢠Shows severe metabolic acidosis, low hemoglobin, heavy pigmenturia, high CK ⢠Large volume of crystalloid infusion sufficient to alkalinise the urine
- 31. ⢠Homsi et al 1997 ⢠Retrospective analysis of rhabdomyolysis patient at risk of ARF ⢠Saline vs saline + nahco3 + mannitol ⢠Conclude progression of renal failure can be totally avoided with prophylactic treatment ⢠If adequate saline given, use of nahco3 and mannitol is unnecessary ⢠Brown et al 2004 ⢠Used of nahco3 and mannitol does not prevent ARF, dialysis or mortality in patient with CK > 5000
- 33. SUMMARY ⢠Initial fluid resuscitation immediately ⢠Treat acute hyperkalemia ⢠Monitor for complication ⢠Serial CK measurement ⢠RRT maybe required
- 34. THANK YOU
Editor's Notes
- summarises hereditary and acquired causes of rhabdomyolysis. Of acquired causes, ischaemia causes dysfunction of the energy-dependent pumps resulting in increased intracellular sodium (Na), activation of the 2Na/Ca2+Â exchange pump and increased cytoplasmatic calcium (Ca2+). Elevated concentrations of cytoplasmatic Ca2+Â cause osmotic oedema and activate the enzymatic cascade that leads to cell death with the consequent release of skeletal muscle components into the bloodstream (ATP: adenosin-triphosphate; CO: carbon monoxide).