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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
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