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Crush injuries and rhabdomyolysis

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Crush injuries and rhabdomyolysis

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Crush injuries and rhabdomyolysis

  1. 1. Rhabdomyolysis …a big word for big problEMS Reappropriated from the internet… SORT OF
  2. 2. Causes of Rhabdomyolysis • In US: alcohol abuse and subsequent immobility and coma, direct myotoxic effects of alcohol • Crush injuries, long surgeries in lithotomy or lateral decub, surgery on morbidly obese patients (gluteal), contact sports, burns, lifting heavy weights • Vascular compromise – compartment syndrome, embolus and subsequent reperfusion • DT’s, NMS, hyperthermia, long-term vecuronium • Electrolyte disturbances • Drugs (HMGCoA red. inh., psychedelic) • Infections-Legionella, strep, influenza, HIV
  3. 3. Hemlock (Conium maculatum ) •Old Testament Book of Numbers 11 (31-35): Israelites suffered a “mass plague” during their exodus following ingestion of quail. • In the Mediterranean, quails eat hemlock during spring migration, and rhabdo from eating the birds is a recognized phenomenon. Rhabdomyolysis • Release of intracellular components from injured myocytes into the circulation Poison hemlock was used to execute Socrates.
  4. 4. Pathophysiology of ARF • “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%
  5. 5. Myocyte Injury Hours of ischemia 0 2 4 6 Tolerable-no permanent histological changes Irreversible anatomic and functional changes Muscle necrosis
  6. 6. Cell Ion Physiology intracellular extracellular
  7. 7. 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
  8. 8. Patient Will Develop: • Hypovolemia • Hyperkalemia (too much Potassium) • Hyperphosphatemia • Hypocalcemia
  9. 9. 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
  10. 10. What to Watch for if you suspect Rhabdo: • Clinical: Pain, weakness, dark urine • Hypovolemia, shock • Electrolyte abnormalities : ↑K+, ↓ Ca++ (sequestered in injured tissues), acidemia upon reperfusion
  11. 11. Pathophysiology of ARF Not reabsorbed Binds Tamm- Horsfell proteins Kidneys just cannot handle it ! Myoglobin – 1-3% of wet mm weight
  12. 12. Diagnosis: (above my pay grade, but still interesting) • Serum CKMM – Correlates w/severity of rhabdo – Normally 145-260 U/L – Levels peak w/in 24h – >5000 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 (+) for blood uric acid crystals
  13. 13. Malinoski, et al. (2004) Treatment Algorithm for preventing renal failure WAY ABOVE MY PAY GRADE
  14. 14. EMS TREATMENT • Rapid Transport • Airway Mgmt / ECG • Normal Saline (not LR) • Sodium Bicarb? • Calcium Chloride? • D50/Insulin? • Albuterol neb treatment? • Diuretics?
  15. 15. Hyperkalemia = peaked T-waves
  16. 16. LCEMS CRUSH INJURY PROTOCOL ALS LEVEL 1: PARAMEDIC ONLY PRE-EXTRICATION 1. Establish two large bore IVs of NS (or LR). 2 liters NS bolus, followed by 500 ml/hr (limit fluid bolus for pediatric (20 ml/kg) and patients with history of cardiac or renal dysfuction 2. Pain control per Pain Protocol 2.1.5. Fentanyl is preferred to Morphine. a. Fentanyl 50 – 100 mcg IV or IM b. Morphine 4 mg initial then 2 mg increments prn up to 10 mg 3. IMMEDIATELY PRIOR TO EXTRICATION: Give Sodium Bicarbonate 1 mEq/kg up to 100 mEq IVP 4. Extrication POST-EXTRICATION 5. Continue cardiac monitoring and assess for hyperkalemia; i.e. widening of QRS (>0.12 seconds) and peak T waves, hypotension 6. If hyperkalemic changes on monitor, give; Calcium Chloride 1 gm IV slow (over 5 minutes) 7. Give an Albuterol (only) Neb 2.5 mg 8. Dress/splint wound/extremity 9. Call Trauma Alert if criteria are met
  17. 17. Early Treatment: HOSPITAL • FLUIDS – Begin early, even on the field • Damaged muscles attract a lot of fluid – Up to 10L/day • Ideally ½ NS with 100mmol/L bicarb – prevents tubular precipitation – reduces risk of hyperkalemia from damaged mm – corrects acidemia – not proven beneficial however not deleterious • 10ml/h 15% mannitol – renal vasodilator – free radical scavenger – Forced diuresis w/in 6 hrs of admission
  18. 18. Late Treatment • Dialysis – – intermitted preferred to continuous • Reduce use of anticoagulants in trauma patients
  19. 19. Studies • Many done after earthquakes, mass beatings, other natural disasters – Spitak earthquake of 1988 in Armenia 600 required dialysis – Marmara earthquake Turkey 1999 n=462 on dialysis, 19% mortality which was much better than before – 1995 International Society of Nephrology created Disaster Relief Task Force to prev/treat crush injury-induced ARF The causes of death in 50 patients with the crush syndrome following the Hanshin–Awaji Earthquake. Deaths from hypovolemia and hyperkalemia were the most common in the early period, while sepsis leading to multiple organ failure was responsible for most of the late deaths

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