Crush injury-rhabdomyolysis
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Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. It can range from asymptomatic to life-threatening acute renal failure. It was first documented in victims of bombings in London during World War II who developed crush injuries, swollen extremities, and dark urine before dying of renal failure. Early and aggressive intravenous fluid therapy is the primary treatment to prevent acute kidney injury by maintaining adequate renal perfusion and dilution of myoglobin in the kidneys.
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Crush injury-rhabdomyolysis
- 1. Crush Injuries and Rhabdomyolysis Dr.Marwa Elwasif Nephrologist
- 3. “Crush syndrome” first recorded in bombing of London during WWII: 5 people who were crushed presented in shock with swollen extremities, dark urine. Later died from renal failure. 5-35% of patients with rhabdomyolysis develop ARF mortality is 3-50%
- 4. Cause of Rhabdomyolysis • Traumatic muscle injury • Drugs and toxins • Infections • Genetic disorders • Excessive muscle activity • Ischemia • Electrolyte and endocrine • Immunologic disease
- 5. RHABDOMYOLYSIS Traumatic / Compression Nontraumatic Exertional Nonxertional -Multiple Trauma -Crush Injury -Surgery -Coma -Immobilization -untrained Exertion, marathon running -Heat illness -Seizures -Metabolic myopathies -Malignant hyperthermia -Neuroleptic Malignant Syndrome -ETOH alcohol -Drugs statins -Infection -Electrolytes hypokalemia, hypophosphatemia -Endocrine hypothyrodism, DKA
- 7. Myocyte Injury 0 2 4 6 Hours of ischemia 0 2 4 6 Tolerable-no permanent histological changes Irreversible anatomic and functional changes Muscle necrosis
- 9. Pathogenesis of Myocyte Injury compression Influx of Ca++, Na+ and fluids Ca++ Protease activation Membrane degradation Nuclease activation Lipid peroxidation ischemia Decreased ATP production More Ca++ influx Attraction of PMN’s cell lysis
- 10. Pathophysiology of ARF Not reabsorbed Binds Tamm- Horsfell proteins CONTRIBUTORS: •Dehydration (hypovolemia) •Aciduria •Renal vasoconstriction •Cast formation •Heme-induced toxicity to tubule cells Myoglobin – 1-3% of wet mm weight
- 12. Rhabdomyolysis Endotoxin cascade Renal hypoperfusion/ Ischemia 3,rd spacing Volume depletion Acidemia Aciduria Myoglobinemia NO scavenging Myoglobinuria Proxmial tubule Fe loading Cast formation Luminal stasis Synergistic tubular damage ATNARF
- 13. Diagnosis • “Triad”: Muscle pain, weakness, dark urine • Fatigue • Joint pain • Seizures • AKI • Compartment syndrome • Disseminated intravascular coagulation
- 14. CLINICAL MANIFESTATIONS AND DIAGNOSIS • The classic presentation of rhabdomyolysis includes myalgias, red to brown urine due to myoglobinuria, and elevated serum muscle enzymes (including creatine kinase)
- 15. When to Suspect Rhabdo • Occurs in up to 85% of patients with traumatic injuries. Those with severe injury who develop rhabdomyolysis- induced renal failure have a 20% mortality rate • Multiple orthopedic injuries • Crush injury to any part of the body • Laying on limb for long period of time, patient “found down” • Long surgery • Red to Brown urine
- 16. What to Watch for if you suspect Rhabdo: • Clinical: Mm pain, weakness, dark urine • Hypovolemia, shock • Electrolyte abnormalities : ↑K+, ↓ Ca++ (sequestered in injured tissues), acidemia
- 17. Clinical and laboratory features of rhabdomyolysis • History and physical examination • Urinalysis • Serum potassium concentration • Creatine kinase • Acid –Base balance • Uric acid • BUN/Cr • Ca/Ph methabolism • DIC
- 18. Diagnosis • Serum CKMM Correlates w/severity of rhabdo Normally 145-260 U/L Levels peak w/in 24h >3000 high correlation with renal failure #’s in 100,000’s not uncommon high t(1/2): 1.5 days • Serum myoglobin t(1/2) 2-3 h Excreted in bile • Ca++ • UA-myoglobinuria dipstick will be (+) for hemoglobin, RBC’s and myoglobin Microscopy: no RBC’s, brown casts, uric acid crystals sample UA (+) for blood uric acid crystals
- 19. Muscle enzymes • The hallmark of rhabdomyolysis is an elevation in serum muscle enzymes. Serum CK levels may be massively elevated to above 100,000 IU/L. • Elevations in serum aminotransferases are common and can cause confusion if attributed to liver disease.
- 21. Managment • Plasma volume expansion with intravenous isotonic saline should be given as soon as possible, even while trying to establish the cause of the rhabdomyolysis. • Treatment of the underlying cause of the rhabdomyolysis.
- 22. • Monitoring with serial measurements of serum potassium, calcium, phosphate, and creatinine, CPK is recommended.
- 23. • The metabolic consequences and renal functional impairment due to rhabdomyolysis should be anticipated, particularly potentially life-threatening hyperkalemia. • Hypocalcemia usually self-limited and rarely requires therapy.
- 24. Early Treatment FLUIDS Begin early, even on the field • Damaged muscles attract a lot of fluid Up to 10L/day • Ideally NS with bicarb prevents tubular precipitation reduces risk of hyperkalemia from damaged mm corrects academia
- 25. Late Treatment Dialysis intermitted preferred to continuous (Reduce use of anticoagulants in trauma)
- 26. Treatment Summary Do Isotonic fluids 1-2 L/h UOP 200-300 ml/h Consider Sodium bicarbonate to cause forced alkaline diuresis Ph < 7.5 HCO3 < 30 mEq/L Don’t Loop diuretics Mannitol Ca supplementation
- 27. Conclusion • Rhabdomyolysis is The result of muscle breakdown secondary to traumatic & nontraumatic causes • CK 5 normal & history to make diagnosis • Myoglobin is fleeting • AKI if CK > 5000 IU/L • Early IV fluids to perfuse the kidneys & prevent tubular obstruction simply save the kidneys.
- 28. Thank you