Crush Injury and

Crush Syndrome
Jim Holliman, M.D., F.A.C.E.P.
Professor of Military and Emergency Medicine
Uniformed Services University of the Health
Sciences
Clinical Professor of Emergency Medicine
George Washington University
Bethesda, Maryland, U.S.A.

Crush Injury and Crush

Syndrome
Lecture Outline
Epidemiology
Pathophysiology
Treatment
Controversies
Prognosis

in management

Causes of Crush Syndrome

Immobility

against firm surface for > one

hour :
Drug or alcohol intoxication
Carbon monoxide poisoning
Cerebrovascular accident
Head trauma with coma
Elderly with hip fracture
Improper positioning of surgical patient
Assault with beating
Pneumatic Antishock Garment (PASG or
MAST)

Causes of Mass Casualties

with Crush Syndrome
Building

collapse

Earthquakes
Landslides
Bombings
Construction accidents
Heavy snow on roof
Mine

or trench collapse

Crush Syndrome
Official Definitions
From

recent consensus meeting :

"A crush injury is a direct injury resulting from
crush. Crush syndrome is the systemic manifestation
of muscle cell damage resulting from pressure or
crushing."
Better (mine) :
Crush syndrome is the clinical condition caused by
compression of muscle with subsequent
rhabdomyolysis which can then cause the
complications of electrolyte disturbances, fluid
sequestration, & myoglobinuria.
Another :
"A form of traumatic rhabdomyolysis that occurs
after prolonged continuous pressure & is
characterized by systemic involvement".

Historical Reports of Crush

Syndrome
Old

Testament Book of Numbers

Deaths from illness involving muscle pain &
weakness (rhabdomyolysis)
Due to eating quail which had consumed
hemlock seeds
Larrey (Napoleon's army surgeon) in 1812
described limb gangrene in carbon monoxide
victims
Bywaters & Beal in 1941 reported 5 patients from
the London Blitz who died of renal failure
Later reports (both clinical & animal studies)
by Bywaters identified myoglobinuria as the
cause for the renal failure

Major Mass Casualty Events

with Reports of Crush
Syndrome
Earthquakes

:
Tangshan, China 1976
Armenia 1988
Iran 1990 and 2003
Northridge, California 1994
Kobe, Japan 1995 ("Hanshin-Awaji")
Turkey 1992 (Izmit, "Marmara" 1999)
Terrorist bombings :
Israel
Lebanon
Saudi Arabia

Buildings damaged in the 1999 Marmara

earthquake

Incidence of Crush
Syndrome in Mass Casualty
Events
10

to 60 % of survivors extricated from

collapsed buildings
Up to half may develop renal failure
At least half of these require
dialysis
Typically about 20 % of injured are
hospitalized, and 5 to 20 % of these
have crush injury, and 0.5 to 1 % end
up needing dialysis
Incidence less in quakes where most
residences are adobe or one story

Pathophysiology of Crush
Syndrome
Not

usually directly due to ischemia

Main cause is stretch of the muscle sarcolemma
Sarcolemma permeability increases
Influx of sodium, water, & extracellular calcium
into the sarcoplasm
Results in cellular swelling, increased
intracellular calcium, disrupted cellular
function & respiration, decreased ATP
production, & subsequent myocytic death
Muscle swelling can then cause early or even days
delayed compartment syndrome

Systemic Sequelae of
Crush Injury
Result

from death of muscle cells

and leak of intracellular
metabolites into the systemic
circulation ("reperfusion injury"

Superoxide anions (free radicals)

then cause further membrane
injury

May

not manifest until just after

entrapped part of body is
extricated

Metabolic Derangements
from Crush Syndrome
Hypovolemia

(fluid sequestration
in damaged muscle)
Hyperkalemia
Hypocalcemia (due to calcium
deposition in muscle)
Hyperphosphatemia
Metabolic acidosis
Myoglobinemia / myoglobinuria

Effects of Myoglobinuria in
Crush Syndrome
Myoglobin

can precipitate
(particularly with hypovolemia and
acidosis) and directly obstruct
renal tubular flow
Myoglobin is also directly toxic to
the renal tubular cells

Renal Toxicity of Myoglobin

Bywaters'

studies showed acid

urine is required for myoglobin to
cause renal injury
At pH < 5.6, myoglobin dissociates
into its 2 components :

Globin (shown nontoxic if infused)

Ferrihemate (probably the toxic
component)

Other Clinical Syndromes with

Similar Effects as Crush
Syndrome
Tumor

lysis syndrome
Heatstroke
Exertional rhabdomyolysis
High voltage (> 1000 volts)
electrical injury

Field Rescue Considerations

for Patients with Crush
Syndrome
Apply

facemask to protect from dust

inhalation
Oxygen (if no risk of fire at the scene)
If building unstable, then equipment
stabilization may be needed before
medical treatment can be given
Start IV normal saline early if possible
Ventilate well near gas or diesel powered
generators to avoid CO poisoning

Hyperkalemia in Crush
Syndrome
Can

occur soon after extrication

Can be quickly fatal
May occur before manifestations
of renal failure
May occur without obvious signs
of compartment syndrome
May require emergent prehospital
treatment

Emergent Treatment of
Hyperkalemia from Crush
Syndrome
Normal

saline IV fluid bolus

IV NaHCO3 50 to 100 meq
Aerosolized albuterol (2.5 mg in 3 cc)
Less effective or practical :

IV dextrose (25 grams) & insulin (5

units IV)
PO or PR kayexalate
Note

that IV calcium is controversial (as it

may just worsen intramuscular
hypercalcemia)
Emergent hemodialysis may be needed

Main Treatment for Crush

Syndrome : IV Fluid
Resuscitation
Normal

saline (0.9 %) preferred

(lactated Ringers contains 4 meq /

liter of potassium, & so may
worsen hyperkalemia, & also has
calcium)

If

started early, may prevent later

development of renal failure
Best if IV fluids can be started
even prior to extrication

Recommended IV Fluid
Infusion Rates for Crush
Syndrome
1

to 1.5 liters per hour for young

adults
20 cc per kg per hour for children
10 cc per kg per hour for elderly
Insert foley catheter as early as
possible

Target urine output should be > 50 cc

per hour for adults, and > 2 cc per kg

per hour for children
Some references advocate 150 to 200

Use of IV Bicarbonate for

Crush Syndrome
Goal

is to have alkaline urine

(check with pH paper)
Can bolus supplement the normal
saline with 50 meq (1 amp) doses

Up to 300 meq per 24 hours may

be needed

Or

add 3 amps (150 meq) to one

liter D5W and infuse as first or
second IV bolus

Use of Mannitol for Crush

Syndrome
May

help eliminate myoglobin

from the kidney & prevent renal
failure
May be useful to initiate diuresis
in a patient who has adequate
normal saline on board but whose
urine output is still < 2 cc per kg
per hour, or if adequate urine
output is still not achieved 4 hours
after treatment started

Mannitol Dosage for Crush

Syndrome
Mannitol

20 % solution 0.25 grams per

kg IV over 10 to 30 minutes

Diuresis should start in 15 to 30

minutes
If urine output thereafter drops again,
hypovolemia should be assumed, and
only after aggressive rehydration
should a second dose of mannitol be
given
Maximum

dose : 2 grams per kg per

day (or 200 grams per day)

Contraindications to
Mannitol
Established

anuric renal failure

Severe congestive heart failure

These patients may require

pressors such as dopamine in order

to tolerate the fluid load required
for treatment, or may need early
dialysis

Other Advantages of
Mannitol for Treating Crush
Syndrome
May

scavenge free radicals in

muscle thus limiting necrosis
Positive inotropic effect on the
heart
Most important : may help
decompress compartment
syndrome by mobilizing fluid from
damaged muscle (thereby
preventing need for fasciotomy)

Compartment Syndrome in
Crush Injury
Normal

muscle compartment pressure is < 15 mm Hg

Pressure > 30 mm Hg produces muscle ischemia, so
fasciotomy indicated if pressure is persistent above
this
Irreversible muscle damage occurs after 6 hours, &
irreversible nerve damage may occur after 4 hours of
ischemia
Patients with higher diastolic pressure can tolerate
higher tissue pressure without ischemia, so
fasciotomy recommended when compartment
pressure approaches 20 mm Hg below diastolic
pressure
However, if patient is hypotensive, they can have
significant ischemia at lower compartment pressures

When Should Fasciotomy

be Done for Crush Injury ?
In

most reports of mass casualties from earthquakes,

most of the fasciotomies were done more than 12 hours
after the time of trauma
Reviews of these cases showed high infection rates
with increased mortality and amputations, and poor
long term function
Israeli experience has shown better results with not
routinely performing delayed fasciotomies
So fasciotomy would be indicated if the victim can be
extricated and receive definitive medical care within 6
hours of injury, but not later
If initial compartment pressures are normal, and
delayed compartment syndrome develops, fasciotomy
may be needed

Additional Treatments for

Crush Injury
Don't

forget oxygen suplementation (even

if the patient is not hypoxemic, O2 may
help ischemic muscle)
Don't forget pain medications
Address tetanus immunization status
Acetazolamide (250 mg PO tid) may help
excrete bicarbonate in the urine
Furosemide may initiate diuresis but not
favored since it makes acid urine

Diagnostic Testing in
Patients with Crush Injury
EKG

as early as possible to look for signs of

hyperkalemia
Handheld fingerstick blood analyzer may be useful in
the field to identify hyperkalemia early
Routine labwork to obtain :
CBC, platelets, type and screen, electrolyte panel,
BUN, creatinine, CPK, liver panel, urinalysis
Optional labwork : ABG, myoglobin, PT, PTT
Chest X-ray
Other radiographs, computed tomography, etc. to
evaluate for other injuries

Monitoring the Crush

Syndrome Patient
Urine

output and urine pH (hourly)

Serial electrolytes (particularly potassium)
: every 6 hours initially
CPK, BUN, creatinine : every 8 to 12 hours
ABG (if initially acidotic or on ventilator) :
every 4 hours
May need central IV line or Swan Ganz
catheter for patients with cardiac or
pulmonary disease
Compartment pressures : every 4 hours
initially

Other Injuries in the Crush

Syndrome Patient
High

incidence of associated injuries

Extremity fractures and lacerations are most
common
With crush injury to trunk, can have internal
abdominal injuries in addition to abdominal wall
muscle compression injury
May have "traumatic asphyxia" if chest
compressed
Dust inhalation common in concrete building
collapse
Fires common with earthquakes, so may have
burns, smoke inhalation, and CO poisoning
Hypothermia or hyperthermia

Mortality Related to Crush

Syndrome
In

earthquakes, most of on scene

deaths are due to direct head and
trunk trauma
Of those extricated, mortality
reports vary widely (zero to 60 %)
Mortality increases with :

Age > 50, prior chronic illness

Duration of entrapment (almost no
survivors after 5 days)

Nimitz Freeway
(Interstate highway I880) collapse in
Oakland California from
October 1989
earthquake, causing 42
deaths

Car crushed by 1989 Nimitz Freeway collapse ; one patient

rescued here on the fifth day later died from complications
of crush syndrome

Prognosis Related to Crush

Syndrome
Major

risk factors for renal failure :

2 or more limbs crushed

Insufficient early IV fluid
Delayed in presentation to hospital
Children

at lesser risk to need dialysis

50 % or more may have severe long
term limb disability if fasciotomy done
Patients often need long term
physical therapy and may need
counseling

Disaster Planning Aspects

Related to Crush Syndrome
Need

to have access to increased

number of hemodialysis machines
The Renal Disaster Relief Task Force
of the International Society of
Nephrology has been organized to
bring multiple machines to a disaster
region
Prehospital personnel need to be
supplied with extra facemasks and
respirators
Prehospital personnel will need access
to large amounts of IV fluid and amps

Crush Syndrome
Lecture Summary
Start

IV fluids prior to extrication

if possible
Assess quickly for hyperkalemia
and associated injuries
If extrication > 6 hours after
injury, do not perform fasciotomy
for compartment syndrome
Perform careful monitoring after
admission to hospital