Paul Barter, FNP, EMT-P, CIC

Crush Injury• MOI in which tissue is locally compressed by

high pressure forces

• May result in permanent disability or death

Therefore…..

early recognition and aggressive treatment are necessary to improve outcome

Crush Syndrome• Also known as Traumatic Rhabdomyolysis

1st reported in 1910 by German authors

Symptoms of muscle pain, weakness and brown-colored

urine in soldiers rescued after being buried in structural

debris

Not well defined until 1940’s

Two nephrologist [Bywaters & Beal] provided descriptions

of victims trapped by their extremities during the London

Blitz

Shock; swollen extremities; tea-colored urine and subsequent

renal failure

Crush Syndrome is areperfusion injury as a

result of traumaticrhabdomyolysis!

What is Rhabdomyolysis??

Rhabdo• "rod-shaped"

Myo• “muscle”

Lysis• refers to decomposition, dissolution, destruction,

loosening, breaking down, separation, or

disintegration

Is the breakdown of muscle fibers resulting

in the release of muscle fiber contents into

the bloodstream

What is this muscle fiber

Myoglobin

-red protein containing heme

-carries and stores oxygen in muscle cells

-structurally similar to a subunit of

hemoglobin

Many known mechanisms• Crush injuries

• Electrocution

• Burns

• Compartment syndrome

• Other that results in muscle damage Natural disasters

• Earthquakes Associated with having up to 20% incidence of crush injuries as do

40% of those surviving to be extricated from structures that collapse

Common events• MVC

• Industrial or mining mishaps

• Farming incidents

According to National Center for Health

Statistics [2005]

• Incidence of traumatic rhabdomyolysis is 0.1 per

10,000 population

“least common traumatic injury pattern”

“if not treated appropriately, it may be lethal”

Occurs when muscle mass is compressed, causing direct injury to muscle fibers• As tissue is compressed, blood flow deprived and

becomes ischemic eventually leading to cellular death

• Time line [varies w/crushing force] skeletal muscle can tolerate ischemia for up to 2 hrs w/o

permanent damage

2-4 hrs

Some reversible cell damage occurs

By 6 hrs

Irreversible tissue necrosis generally sets in

• Crushed tissue undergoes necrosis and cellular

changes with release of metabolic byproducts

• Releases

Myoglobin [muscle protein]

Phosphate & Potassium [from cellular death]

Lactic acid [from anaerobic metabolism]

Uric acid [from protein breakdown]

Causes hypovolemia• Hemorrhagic loss

• Rapid shift of extracellular volume into damage

tissue(s)

• ARF secondary to hypoperfusion

Kidneys normally receive 25% of CO

Compounds the toxicity caused by cast formation and

blockages of nephrons by myoglobin

VIGOROUS volume resuscitation to improve urine flow

Reperfusion • Release of debris from damaged cells into

circulation

Myoglobin

Can lodge in renal tubules leading to ARF

Leading cause of death

Phosphorus

Hyperphosphatemia

Can lead to abnormal calcifications in the vasculatue and

nervous system

Potassium

Once released….• Hyperkalemia may occur

• Signs/Symptoms

Think string

Disseminated Intravascular coagulation

can develop

• Abnormal clumps of thicken blood [clots] form

These occupy the bloods clotting factor resulting in

hemorrhage

• When oxygenated circulation resumes, the aerobic

process by which uric acid is produced can

operate again leading to increasing cellular

acidity and injury

Toxins may continue to leak into body for

as long as 60 hours after release of crush

injury!

The greater the body area compressed

and the longer the time of entrapment

the greater the risk of crush syndrome

Absolutely imperative that an assessment

is made prior to beginning any

extrication activities!

Dually imperative that the rescue team

be made aware of the importance of

treating the patient prior to extrication

As a general rule, requirement for

consideration is based on 3 criteria:

• Involvement of a muscle mass

• Prolonged compression (as little as 1 hour, but

typically 4-6)

– Compromised blood circulation

Example: entrapment of hand is unlikely

to initiate the crush injury syndrome

Compression in excess of 60 minutes Involvement of a large muscle mass Absent pulse and capillary refill return to

distal limb Pale, clammy, cool skin Weak, rapid pulse Usually absence of pain in affected region Onset of shock MAINTAIN HIGH INDEX OF

SUSPICION!

Coordinate time of release with rescue personnel!

Treated as any other multiple trauma victimAirway secured and protected from dust

impaction Adequate oxygenation (NOT necessarily

highflow, maintain SPo2, extended operation)

Maintain body temperature throughout operations!

Rapid transport to Trauma Center

Circulation must be supported and

shock aggressively treated:

– Trendelenburg

– High flow oxygen during transport

– Warm patient! They were just trapped in a

building or soil for extended period!

Aeromedical transport when

available!

Crush Injuries • Result in rhabdomylysis

• Electrolyte abnormalities

• Hypovolemia

Early treatment is rehydration using crystalloids, initiate before extrication

Coordinate time of release with rescue personnel!

Vital signs every 5 minutes ABCs and appropriate oxygen therapy Establish 1 or 2 large bore IVs with NS

• No more than one IO

• One liter fluid

Pain ManagementCardiac monitoring

• 12 lead ECG repeated every 30 minutes

If one complete extremity is crushed >2

hours, or 2 extremities are crushed >1 hour:• Sodium bicarbonate 50 mEq IV slow push every 30

minutes

In addition, one minute prior to extrication give 50 mEq IV

Color Coding:

BLS

Advanced

Critical Care

Paramedic

If hyperkalemia is suspected and ECG changes, calcium chloride 1 gram IV [over 5 minutes]. Repeat in 10 minutes if these is no resolution of the ECG changes of hyperkalemia

Albuterol via nebulizerConsider application of tourniquet for

prolonged entrapment placed as close as possible to the crush injury prior to the release of the extremity

Consider EMS physician response to the scene

A minimum of 50 ml of normal saline should be given between the bolus of calcium chloride and the bolus of sodium bicarbonate

Pain control PRN– Recommend Fentanyl; same as MS but

no vasodilation which might contribute

to hypovolemia

During transport, suspect hyperkalemia if

T waves become peaked, QRS becomes

prolonged, PVC’s ,HTN develops

After extrication, immobilize the

extremity and apply cold therapy; do not

elevate the extremity

Usual trauma treatment• A

• B – avoid succhinylcholine **

• C – early fluid resuscitation No ringers lactate **

Bicarbonate keeps myoglobin floating in circulationpostponing renal casting and heads off

hyperkalemia Early treatment with 2 amps D50 and 10 units Insulin

– As Insulin transports dextrose through cellmembranes pulls Potassium with it

– Few ALS systems carry Insulin, but Docs do!– Monitor BS if this is an option

Albuterol lowers serum Potassium case by driving itback into the cells– Short term, but very effective until other

measuresin place

Calcium chloride• Counteracts life-threatening dysrhythmias

induced by hyperkalemia