Crush Injuries and Rhabdomyolysis

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Crush Injuries Crush Injuries and and Rhabdomyolysis Rhabdomyolysis Tracy So Tracy So Trauma/ICU conference Trauma/ICU conference

Transcript of Crush Injuries and Rhabdomyolysis

Page 1: Crush Injuries and Rhabdomyolysis

Crush Injuries andCrush Injuries and RhabdomyolysisRhabdomyolysis

Tracy SoTracy SoTrauma/ICU conferenceTrauma/ICU conference

Page 2: Crush Injuries and Rhabdomyolysis

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.

RhabdomyolysisRhabdomyolysis• Release of intracellular components from injured

myocytes into the circulation

Poison hemlock was used to execute Socrates.

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Causes of RhabdomyolysisCauses 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

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Myocyte InjuryMyocyte Injury

Hours of ischemia

0 2 4 6

Tolerable-no permanent histological

changes

Irreversible anatomic and

functional changes

Muscle necrosis

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Cell Ion PhysiologyCell Ion Physiology

intracellular

extracellular

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Pathogenesis of Myocyte InjuryPathogenesis 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

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When to Suspect RhabdoWhen 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: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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Pathophysiology of ARFPathophysiology 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%

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Pathophysiology of ARFPathophysiology 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

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Diagnosis Diagnosis • 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

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Malinoski, et al. (2004)

Treatment Algorithm for

preventing renal failure

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Early TreatmentEarly Treatment• 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

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Late TreatmentLate Treatment

• Dialysis –– intermitted preferred

to continuous• Reduce use of

anticoagulants in trauma patients

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StudiesStudies• 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