crush injuries and rhabdomyolysis

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Rhabdomyolysis …a big word for big problEMS Reappropriated from the internet… SORT OF

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Rhabdomyolysis…a big word for big problEMS

Reappropriated from the internet… SORT OF

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

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.

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%

Myocyte Injury

Hours of ischemia

0 2 4 6

Tolerable-no permanent histological

changes

Irreversible anatomic and

functional changes

Muscle necrosis

Cell Ion Physiology

intracellular

extracellular

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

Patient Will Develop:

• Hypovolemia• Hyperkalemia (too much Potassium)• Hyperphosphatemia • Hypocalcemia

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

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

Pathophysiology of ARF

Not reabsorbed

Binds Tamm-Horsfell proteins

Kidneys just cannot handle it !

Myoglobin – 1-3% of wet mm weight

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

Malinoski, et al. (2004)

Treatment Algorithm for

preventing renal failure

WAY ABOVE MY PAY GRADE

EMS TREATMENT• Rapid Transport• Airway Mgmt / ECG • Normal Saline (not LR)• Sodium Bicarb?• Calcium Chloride?• D50/Insulin?• Albuterol neb treatment?• Diuretics?

Hyperkalemia = peaked T-waves

LCEMS CRUSH INJURY PROTOCOLALS LEVEL 1: PARAMEDIC ONLYPRE-EXTRICATION1. 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 IMb. Morphine 4 mg initial then 2 mg increments prn up to 10 mg

3. IMMEDIATELY PRIOR TO EXTRICATION: Give Sodium Bicarbonate1 mEq/kg up to 100 mEq IVP

4. ExtricationPOST-EXTRICATION5. Continue cardiac monitoring and assess for hyperkalemia; i.e. widening of

QRS (>0.12 seconds) and peak T waves, hypotension6. If hyperkalemic changes on monitor, give; Calcium Chloride 1 gm IV slow

(over 5 minutes)7. Give an Albuterol (only) Neb 2.5 mg8. Dress/splint wound/extremity9. Call Trauma Alert if criteria are met

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

Late Treatment

• Dialysis –– intermitted preferred

to continuous• Reduce use of

anticoagulants in trauma patients

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