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    Rhabdomyolysis Medical Slides

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    Why teach Rhabdomyolysis?

    Rhabdomyolysis causes approximately 26,000 hospitalizations annually in the United States, with AKI developing in 15-33% of cases. The condition results from skeletal muscle breakdown releasing myoglobin, CK, potassium, and phosphate into the circulation. Common causes include trauma/crush injury, exertional (exercise, seizures), drugs/toxins (statins, cocaine), and immobilization. Early aggressive IV fluid resuscitation remains the cornerstone of management, targeting prevention of myoglobin-induced renal tubular obstruction and direct nephrotoxicity.

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    01Pathophysiology: Myocyte Death, Myoglobin Release, and Renal Tubular Obstruction
    02Etiology: Traumatic (Crush), Exertional, Drug/Toxin, Metabolic, and Ischemic Causes
    03Diagnosis: CK >5x Normal (>1000 U/L), Myoglobinuria, and Characteristic Lab Panel
    04IV Fluid Protocol: Normal Saline Bolus, Target UOP >200-300 mL/hr, and Duration
    05Electrolyte Management: Hyperkalemia, Hyperphosphatemia, Hypocalcemia, and Monitoring
    06Complications: AKI, Compartment Syndrome, DIC, and Cardiac Arrhythmias
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    Rhabdomyolysis Presentation FAQ

    How should the IV fluid resuscitation protocol be presented?

    Present the cornerstone therapy: early aggressive IV normal saline — initial bolus 1-2 L/hr in the first 2-6 hours, then titrate to maintain UOP 200-300 mL/hr (approximately 3-6 mL/kg/hr). Total fluid requirement often 10-20 L in first 24 hours for severe rhabdomyolysis. Fluid resuscitation should begin in the field if crush injury is suspected. NS is preferred over LR (LR contains potassium, and contains calcium which may worsen calcium-phosphate deposition). Bicarbonate-containing fluids (isotonic bicarbonate drip) are controversial — theoretical benefit of urine alkalinization (pH >6.5) to prevent myoglobin cast formation, but RCT evidence is lacking. Monitor for fluid overload, especially if oliguric AKI develops.

    What CK thresholds and monitoring frequency should be taught?

    Present the clinical thresholds: CK >5x ULN (approximately >1000 U/L) defines rhabdomyolysis. CK >5000 U/L — significant AKI risk, aggressive hydration mandatory. CK >15,000-20,000 U/L — high AKI risk (~50%), consider ICU admission. CK peaks at 24-72 hours post-injury and declines at approximately 50% per day with adequate hydration. Monitoring: check CK every 6-12 hours until peak identified and declining, then every 12-24 hours. Continue aggressive hydration until CK <5000 U/L and trending down. Also monitor: BMP every 6-8 hours (K+, Ca2+, PO4, Cr), urine output hourly, and serial ECGs if K+ >6.0.

    How should compartment syndrome surveillance be integrated into rhabdomyolysis teaching?

    Present the bidirectional relationship: compartment syndrome causes rhabdomyolysis (compression → ischemia → myocyte death), AND rhabdomyolysis treatment can worsen compartment syndrome (aggressive IV fluids increase interstitial edema in injured compartments). Surveillance: assess the 6 Ps (pain out of proportion, pain with passive stretch — earliest and most sensitive sign, paresthesia, pallor, pulselessness — late sign, paralysis — late sign). Measure compartment pressures if clinical concern: absolute pressure >30 mmHg or within 30 mmHg of diastolic pressure (delta pressure) warrants emergent fasciotomy. In crush injury patients, fasciotomy should be considered before or concurrent with fluid resuscitation if limb is compromised.

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