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Crush Injuries and Rhabdomyolysis Dr.M.Mortazavi Nephrologist
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INTRODUCTION Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. The severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening cases associated with extreme enzyme elevations, electrolyte imbalances, and acute renal failure
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“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%
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Cause of Rhabdomyolysis
Traumatic muscle injury Drugs and toxins Infections Genetic disorders Excessive muscle activity Ischemia Electrolyte and endocrine Immunologic disease
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Pathophysiology of Rhabdomyolysis
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Myocyte Injury Tolerable-no permanent histological changes
Muscle necrosis Hours of ischemia Irreversible anatomic and functional changes
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Cell Ion Physiology intracellular extracellular
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Pathogenesis of Myocyte Injury
Ca++ compression Protease activation Membrane degradation Nuclease activation Lipid peroxidation ischemia Influx of Ca++, Na+ and fluids Attraction of PMN’s Decreased ATP production cell lysis More Ca++ influx
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Pathophysiology of ARF
CONTRIBUTORS: Dehydration (hypovolemia) Aciduria Renal vasoconstriction Cast formation Heme-induced toxicity to tubule cells Not reabsorbed Binds Tamm-Horsfell proteins Myoglobin – 1-3% of wet mm weight
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Synergistic tubular damage
Rhabdomyolysis Myoglobinemia Endotoxin cascade 3,rd spacing NO scavenging Myoglobinuria Volume depletion Acidemia Proxmial tubule Fe loading Aciduria Renal hypoperfusion/ Ischemia Cast formation Luminal stasis Synergistic tubular damage ARF ATN
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Diagnosis
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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)
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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 (eg: hand) Laying on limb for long period of time –patient “found down” Long surgery Brown urine
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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 upon reperfusion
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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
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Diagnosis Serum CKMM Serum myoglobin Ca++ UA-myoglobinuria
Correlates w/severity of rhabdo Normally 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 Other measures: carbonic anhydrase III, aldolase sample UA uric acid crystals (+) for blood
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Approach to the patient with red or brown urine
Electrolyte abnormalities
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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.
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Electrolyte abnormalities
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Prevention and Treatment
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MANAGEMENT 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.
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Monitoring with serial measurements of serum potassium, calcium, phosphate, and creatinine ,CPK is recommended.
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MANAGEMENT The metabolic consequences of and renal functional impairment due to rhabdomyolysis should be anticipated, particularly potentially life-threatening hyperkalemia. Hypocalcemia? Should be treated?
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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 mannitol renal vasodilator free radical scavenger
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Late Treatment Dialysis – intermitted preferred to continuous
Reduce use of anticoagulants in trauma patients
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