A 20 year old male arrives ambulatory to the ED at 
12:30 pm accompanied by friends.  He is complaining 
of pain in his left forearm and hand.  He states that he 
became drunk the previous night and fell off a bar 
stool.  He does not remember the event well.  He 
awoke in the morning with pain in his left arm, from the 
mid-upper arm to his wrist.   He complains that he 
cannot move his elbow, wrist, or fingers.  He also 
complains that he has the sensation of pinpricks in his 
arm with decreased sensation, and numbness in his left 
hand.

Consider some of the possible diagnoses:
     Fracture
     Peripheral nerve palsy
     Compartment syndrome
     Cellulitis
     Rhabdomyolysis
     Vascular injury
     Deep venous thrombosis
     Gas gangrene
     Necrotizing fasciitis

     Exam: VS  T 37.3 degrees C, P 96, R 20, BP 
158/89.  He is generally alert, cooperative and in no 
acute distress.  HEENT unremarkable.  Heart regular 
without murmurs.  Lungs clear.  Abdomen soft and 
non-tender.  No hepatosplenomegaly.  Left upper 
extremity:  AC joint and shoulder non-tender.  His 
ability to move his fingers and wrist is minimal.  His 
radial pulse is good.  Capillary refill in the nailbeds is 
good.  Pulse oximetry on all the fingers of his left hand 
demonstrates a good perfusion pulsation waveform.  
His forearm appears to be modestly swollen.  The skin 
from his elbow to wrist is tense and warm with slight 
erythema and superficial peeling.  No pallor is noted.  
Sensation in his wrist and hand is minimal.  He also has 
a large patch of necrotic skin in the shape of a polygon 
over his left flank.

     Radiographs of his left forearm are obtained.

View his forearm radiographs.


     After viewing his radiographs, what work-up would 
you recommend?

     Initially, it was believed that the patient had suffered 
a fracture of his left forearm (during the fall from the 
bar stool) complicated by a nerve injury.  However, 
radiographs of his left forearm returned normal.  The 
possibility of cellulitis and sepsis in his forearm was 
raised.  The necrotic lesion on his back suggested 
disseminated infection, but its polygon shape was 
inconsistent with sepsis.  Upon further questioning, the 
patient; however, denied any history of fever.  The 
superficial peeling of his forearm resembled a possible 
chemical or heat burn, but the patient could not 
remember any such event occurring.  
     The diagnosis of compartment syndrome (CS) was 
considered, but no fracture was present and his distal 
pulses were normal, including pulse oximetry perfusion 
waveforms in his fingers.  Some bloodwork was drawn, 
including a CBC and blood culture.  An IV was started 
and he was immediately given some antibiotics.

     Given that the patient demonstrated good distal 
pulses and the absence of pallor, is a compartment 
syndrome possible?

     An orthopedic surgeon was consulted.  A pressure 
transducer measured the patient's forearm 
compartment pressure to be 72 mmHg.  This is 
diagnostic of a compartment syndrome.

     Does the presence of normal distal pulses rule out a 
compartment syndrome?  Absolutely NOT!!  Avoid this 
pitfall.  A compartment syndrome occurs when venous 
outflow is impeded, thus arterial pulsation is still 
present in many compartment syndrome cases.


     What compartment pressure is diagnostic of 
compartment syndrome?  What is the definitive 
treatment for compartment syndrome?

     The patient was immediately taken to the operating 
room for a fasciotomy.  Large areas of muscle necrosis 
were noted.  The patient also developed renal 
insufficiency secondary to severe rhabdomyolysis.  
After multiple debridement procedures, he was able to 
regain some forearm, wrist, and hand function, but it 
was apparent that he suffered permanent 
neuromuscular deficits.

     What are the complications of compartment 
syndrome?  What was the etiology for his compartment 
syndrome?

     Upon questioning one of the patient's friends, it was 
revealed that the patient had taken 20 or 30 shots of 
liquor the previous night.  After falling off the bar stool, 
his friends carried him into the back of a pick-up truck 
where he slept until he awoke the next day.  His 
compartment syndrome was due to him sleeping on his 
arm in an intoxicated state and compressing it for an 
extended period of time.  Because of his ethanol 
intoxication, normal body protective reflexes that 
stimulate the body to move and roll while sleeping were 
blunted.  In retrospect, it was believed that the necrotic 
lesion on his back was probably due to pressure 
necrosis resulting from something (in the back of the 
pick-up truck) pressing upon his flank while he was 
unconscious.  

Discussion
     Compartment syndrome is the result of increased 
pressure within a closed anatomical space.  As such, 
any area of the body which contains a compartment 
can be affected, namely the hand, forearm, upper arm, 
entire lower extremity, abdomen, and buttocks.  As the 
intracompartmental pressures increase and exceed the 
perfusion pressure, tissues become ischemic and may 
become necrotic without timely intervention.  
Compartment Syndrome is a thus a limb- (and even 
life-) threatening condition.  Patient prognosis depends 
upon the timeliness of diagnosis.  Therefore, time is 
critical.  It is generally accepted that 6 hours is the 
upper limit of tissue viability (1).
     Traditionally, the "6 Ps" (pain, paresthesia, paresis, 
pallor, poikilothermia, and pulselessness) were used to 
clinically diagnose compartment syndrome.  In an effort 
to generate as many Ps as possible, this series of 6 Ps 
is really a pitfall because pulselessness and pallor are 
usually NOT present in a compartment syndrome.  
Additionally, poikilothermia is not a term which is 
commonly used.  Thus, only 3 Ps remain.  Learn the 
three important Ps of pain, paresthesia and paresis and 
do not rely on the other three.
     Currently, it is generally accepted that pallor and 
pulselessness are no longer reliable criteria for CS.  In 
the pathophysiology of CS, venous outflow resistance 
is increased, ultimately leading to a cessation in blood 
flow.  CS is really a venous infarction rather than an 
arterial infarction.  Venous outflow is impeded when the 
compartment pressure exceeds about 30 mmHg.  As 
the compartment pressure rises, all the veins are 
compressed and venous outflow is blocked.  Since 
venous outflow is blocked, perfusion of the tissues 
within the compartment ceases.  There may still be 
arterial pulsation of the larger arteries within the 
compartment and distal to the compartment because 
the systolic pressure still exceeds the compartment 
pressure.  In addition, arterial blood may continue to 
flow through arteriolo-arteriolar shunts (1, 2, 3).  Thus, 
distal pulses may still be present.  Pulsation within 
larger arteries, however, will not result in any capillary 
circulation, because venous outflow is blocked.  Avoid 
this pitfall.  Pulselessness is NOT present in early 
cases of compartment syndrome.  Do not use the 
presence of pulses to rule out a compartment 
syndrome, because this will cause the diagnosis to be 
delayed beyond the point of salvage.
     Similarly, pallor may not be evident in a 
compartment syndrome.  The skin outside the 
compartment may be normally perfused since only 
intracompartmental perfusion may be affected.  Even if 
the venous outflow of the skin is impeded, the 
appearance of the skin would be that of venous 
congestion and NOT pallor.
     Pain, however, is a reliable indicator of 
compartment syndrome.  CS should be suspected if the 
patient complains of severe pain following any injury to 
an extremity.  Often, the pain is more severe than one 
would expect from the injury.  Severe pain after 
splinting or casting should raise the possibility of 
compartment syndrome.  The pain may occur at rest or 
with certain movements, such as passive stretching of 
the muscles or active flexion/extension.  The pain can 
be described as a burning sensation, and it is not 
usually relieved by pain medication or splinting.
     Paresthesia will ultimately develop as nerve 
conduction slows in hypoxic/ischemic conditions.  A 
later finding in CS, paresis or paralysis may set in as 
motor neurons start to dysfunction.  The extremity may 
also feel tense or hard (1, 3). 

     The anterior distal lower extremity is cited as the 
most common site of compartment syndrome.  The 
reason for this location is probably due to its high 
frequency of injury.  The usual cause of CS is a 
fracture.  However, the incidence of CS following a 
fracture is actually very small.  In the setting of a 
fracture, compartment syndrome is therefore a 
diagnosis of low probability but high morbidity.  It is 
also estimated that 30% of limbs will develop CS 
following vascular injury (1).
     According to one study, young men appear to be at 
higher risk for developing CS.  Compared to other 
patient profiles, young men have relatively larger 
muscle volume confined to an osseofascial space 
which ceases to expand after growth is complete.  
Young men are also more likely to be engaged in 
activities (for example, sports or fights) which are 
associated with these injuries (4).
     There are two main pathways to increasing 
intracompartmental pressure: 1) Increasing the fluid 
content within the compartment, either by hemorrhage 
or from edema; and 2) Decreasing the compartment 
size, either by tissue constricture or by external 
compression (1, 5).

I. Increased fluid content
   A. Hemorrhage
      a. Vascular injury
      b. Fracture
      c. Surgical
      d. Bleeding disorder
      e. Blunt trauma
   B. Edematous conditions
      a. Long bone fractures
      b. Crush injuries
      c. Burns
      d. Decreased serum osmolarity
         1. Liver disease
         2. Nephrotic syndrome
      e. Rhabdomyolysis (cause or consequence)
      f. Infiltrated infusion
      g. Intraarterial injection (iatrogenic)
      h. Envenomation
      i. Intensive muscle activity
         1. Vigorous exercise
         2. Tetany
         3. Seizures

II. Decreased compartment size
   A. Constricture
      a. Burn eschar
      b. Frostbite eschar
   B. External compression
      a. Casts/tight bandages
      b. Lying on limb
         1. Drug overdose
         2. Unconsciousness
      c. Compression stockings
      d. MAST (military anti-shock) trousers
      e. Tourniquets


     Based on the findings of one orthopedic trauma unit 
in Edinburgh, Scotland, the following outline reveals the 
underlying condition and mode and cause of injury of 
164 cases of CS between 1988 and 1995, inclusive, 
with percentage of cases in parentheses (4):

I. Underlying Condition
   A. Tibial diaphyseal fracture (36%)
   B. Soft-tissue injury (23%)
   C. Distal radial fracture (10%)
   D. Crush syndrome (8%)
   E. Diaphyseal fracture of radius and/or ulna (8%)
   F. Other (15%)
II. Mode of Injury
   A. Sport (20%)
   B. MVA pedestrian (12%)
   C. Crushing injury (10%)
   D. MVA driver (9%)
   E. Fall from standing height (9%)
   F. Other (40%)
III. Cause of Injury
   A. Direct blow (26%)
   B. Crushing injury (20%)
   C. Penetrating injury (13%)
   D. Spontaneous (13%)
   E. MVA pedestrian (10%)
   F. Other (18%)

     Osseofascial compartments are relatively 
nondistensible and have a fixed volume. Thus, the 
introduction of fluid into or external compression of the 
compartment will undoubtedly raise the 
intracompartmental pressure.  There are several 
theories which attempt to explain the exact mechanism 
of the resulting decrease in tissue perfusion.  One 
popular theory states that the increase in 
intracompartmental pressure leads to a compression of 
the venous system.  As the pressure in the venous 
system rises, the arteriovenous pressure gradient 
decreases.  Hence, blood has a decreased tendency to 
flow into the capillaries.  The body's compensatory 
mechanisms to increase perfusion pressure are 
eventually overwhelmed by increasing 
intracompartmental pressures.  The increased venous 
outflow resistance ultimately causes a retrograde blood 
stasis.  Blood ceases to perfuse the cells and the 
tissues become ischemic (2).
     A further complication is that hypoxic cells will 
release vasoactive substances such as histamine and 
serotonin which serve to increase capillary 
permeability.  As protein leaks into the interstitial 
space, water is pulled along with it.  Thus, the 
intracompartmental pressures continue to rise.
     Prolonged ischemia (over 6 hours) will result in 
rhabdomyolysis and potential loss of limb.  
Rhabdomyolysis may lead to acute renal failure and 
eventual death. 

     CPK and serum myoglobin levels may be elevated, 
indicating rhabdomyolysis.  Dipstick urinalysis may be 
positive for blood, but on microscopic review be 
negative for RBCs, indicating the presence of 
myoglobin in the urine (1).
     Radiographs of the extremity may show the 
presence of an underlying fracture, but the absence of 
a fracture does not rule out a compartment syndrome 
since there are other etiologies for compartment 
syndrome.  A CT scan may reveal areas of muscle 
necrosis.  A CT scan, however, should not delay the 
treatment of a compartment syndrome.  Once it is 
suspected, it should be acted upon immediately to 
maximize the patient's chance of recovery.
     A measurement of the compartment pressure 
should be obtained as soon as a diagnosis of CS is 
suspected.  Commercial pressure measurement 
devices are available.  If none is available, three 
generic procedures for measuring the 
intracompartmental pressure are suggested at the end 
of this case.
     The level of intracompartmental pressure which 
serves as the cutoff point for diagnosing CS is under 
debate.  Some cite 30 mmHg as indicative of CS, 
whereas others claim that 45 mmHg is an appropriate 
cut-off (1).
     The threshold for developing compartment 
syndrome is directly affected by the amount of blood 
flow to that area.  As such, hypotensive patients may 
develop CS at lower intracompartmental pressures.  
Thus, some advocate the use of perfusion pressure, 
rather than just intracompartmental pressure, in 
determining CS.  Perfusion pressure = Diastolic BP 
minus the intracompartmental pressure (7, 8).  
McQueen used perfusion pressure measurements of 
less than 30 mmHg as diagnostic of CS and an 
indication for fasciotomy (1).

     TREATMENT:  Since the pathophysiology of CS 
involves an ischemic event, it may be helpful to give 
the patient oxygen to increase pO2.  The patient should 
be hydrated intravenously to prevent acute renal failure 
secondary to rhabdomyolysis (1, 5).  The involved 
extremity should kept at body level so that arterial 
blood flow is not compromised and venous drainage is 
unhindered (3).
     The definitive therapy for CS is fasciotomy to 
relieve the intracompartmental pressure.  The 
emergency physician should seek immediate surgical 
consultation, usually with orthopedics.

     COMPLICATIONS: Prognosis ultimately depends 
upon the speed of diagnosis and treatment.  However, 
even with timely intervention, the patient may still 
suffer some permanent neuromuscular dysfunction.  
Volkmann's ischemic contracture is the functionless, 
claw-hand deformity that results from untreated 
forearm ischemia.  Rhabdomyolysis will occur after 
approximately 6 hours of warm ischemia and may 
escalate into a bacterial gangrene infection, loss of 
limb, and sepsis.  Acute renal failure may result from 
rhabdomyolysis, and if left untreated, will lead to death 
(6).  Following a fasciotomy, there is a risk of infection.  
The procedure will also leave some cosmetic deformity 
(1).
 
CLINICAL PEARLS:

     1) CS can occur without any trauma.   Prolonged 
external compression of an extremity can occur in the 
setting of drug/alcohol overdose and lead to CS.
     2) Prognosis depends upon the speed of diagnosis 
and treatment.
     3) Severe pain (especially with passive stretching of 
the muscles) followed by increasing neuromuscular 
deficits are the key clinical manifestations of CS.
     4) The traditional sign of pulselessness is not a 
definitive criteria of CS.  Pulses may still be palpable in 
CS due to arteriolo-arteriolar shunts.  Do not be fooled 
by palpable pulses.
     5) CS is mainly a clinical diagnosis, but can be 
confirmed by measuring intracompartmental pressures
     6) Critically-ill patients may present with a myriad of 
complicating factors.
     a) Shock:  Hence, a lower intracompartmental 
pressure is needed to overcome a lower perfusion 
pressure.  Additionally, patients who require large 
volume resuscitation are at risk for developing 
interstitial edema and subsequent CS (7).
     b) Altered mental/neurological status:  Thus, the 
patient may not complain of pain and/or paresthesia.  
Examples include patients with CNS injury or patients 
on narcotics (5).
     c) Hypoxia and/or Anemia:  In which case ischemia 
will occur more quickly following smaller compromises 
in capillary perfusion pressure (8).
     7) Treatment of rhabdomyolysis involves aggressive 
IV hydration to prevent acute renal failure.
     8) Fasciotomy is the definitive treatment for 
compartment syndrome

Intracompartmental pressure measurement methods:

     The Stryker Stic device is a commercially available 
product made specifically for measuring 
intracompartmental pressures.  It is fast and accurate, 
but it is modestly expensive and it is possible that your 
hospital does not have it.
     If you don't have access to a Stryker Stic device, 
there are three generic alternatives which will probably 
work with equipment that is available in most hospitals.  
The three methods described below are:
     1) Mercury column manometer method
     2) Electronic pressure transducer method
     3) The IV infusion pump method

1.  Mercury column manometer method (6,9,10)

The following equipment is needed:
     18-gauge needle
     10-mL syringe
     Intravenous extension tubing (two)
     Vial bacteriostatic normal saline
     Mercury column manometer
     Three-way stopcock

     This three-way stopcock is a stopcock that must be 
able to communicate with three ports simultaneously.  
Most stopcocks have three ports and only communicate 
two of these ports at a time (this is confusing because 
these may also be called 2-way or 4-way stopcocks).  
However, most such stopcocks can communicate all 
three ports at a time.  If the stopcock is positioned such 
that the three ports point to 9 o'clock, 12 o'clock and 3 
o'clock, the position of the stopcock lever and ports can 
be described.  

View the diagram of the stopcock for clarification.


     The stopcocks on the top row have a single lever 
which always points to the port that is off.  The 
stopcocks on the bottom have a different design with 
four levers, one of which is labeled "off" and the other 
three which communicate with each other.
     In normal use, the "off" stopcock lever can be 
placed in any position between 9, 12 and 3 o'clock (the 
first three positions from left to right on the stopcock 
diagram).  In these positions, the stopcock 
communicates with two ports at a time, with one port 
off.  However, by forcing the stopcock "off" lever over 
the hump to the 6 o'clock position, the stopcock will 
usually communicate all three ports simultaneously (the 
position on the right of the stopcock diagram).

View a diagram of this mercury manometer method.



Follow this procedure:
     1) Clean the site of needle insertion with a 
povidone-iodine solution. 
     2) If necessary, anesthetize the site of insertion.  BE 
CAREFUL not to inject into the suspected 
compartment.  If the site is already numb, then no local 
anesthesia is necessary.
     3) Connect intravenous extension tubing to the front 
and rear ports of the three-way stopcock (as shown in 
the mercury manometer method diagram).
     4) Connect the 10-ml syringe, with the plunger at the 
3-ml mark, to the upper port (as shown in the diagram)
     5) Connect the sterile 18-gauge needle to the end of 
the IV extension tubing.  Then turn the stopcock so that 
the other IV extension tubing is "off" (3 o'clock position 
on the diagram).
     6) Put the needle into a bottle of bacteriostatic 
saline then use the syringe to draw up some 
bacteriostatic saline through this needle through the IV 
tubing attached to the needle so that saline fills the 
tubing from the tip of the needle to a halfway point in 
the tubing (refer to the mercury manometer method 
diagram).  The other half of the tubing (nearest to the 
stopcock) and the syringe should contain only air.
     7) Attach the IV extension tubing (from the 3 o'clock 
port) to the mercury manometer as shown in the 
diagram.
     8) Insert the needle into the designated muscle 
compartment.
     9) Turn the stopcock "off" lever to the 6 o'clock 
position as shown in the diagram so that all three ports 
are open simultaneously.
     10) Depress the plunger SLOWLY, causing a rise in 
the pressure within the system.  The mercury column in 
the manometer will rise until the pressure within the 
system is equivalent to the pressure within the 
compartment.  As the pressure within the system 
exceeds the pressure in the compartment, the saline in 
the connection tubing will slowly move towards the 
needle.  The reading on the manometer at the time that 
the saline first begins to move represents the 
compartment pressure (Be careful not to inject the 
saline into the compartment).  Some have 
recommending reading the shape of the meniscus in 
the tubing.  If the meniscus is concave or convex, then 
the pressure on the saline column is too high or too low.  
When the meniscus is flat, then the pressure is 
perfectly balanced and the mercury manometer's 
reading should accurately reflect the pressure in the 
compartment. 


2.  Electronic transducer method

View a diagram of this electronic transducer 
manometer method.


Follow this procedure:
     1) Clean the site of needle insertion with a 
povidone-iodine solution. 
     2) If necessary, anesthetize the site of insertion.  BE 
CAREFUL not to inject into the suspected 
compartment.  If the site is already numb, then no local 
anesthesia is necessary.
     3) Fill the dome of an electronic pressure transducer 
and the IV tubing extending from it with saline so that 
the saline fills the dome and most of the tubing.  
However, air must be left in the end of the tubing which 
connects to the stopcock (as shown in the electronic 
transducer method diagram).  With the transducer 
connected to the electronic monitor and digital pressure 
readout, calibrate the transducer to "zero" at this time.
     4) Connect the IV tubing to the front and rear ports 
of the three-way stopcock (as shown in the electronic 
transducer method diagram).
     5) Connect the 10-ml syringe, with the plunger at the 
3-ml mark, to the upper port (as shown in the diagram)
     6) Connect the sterile 18-gauge needle to the end of 
the IV extension tubing.  Then turn the stopcock so that 
the other IV extension tubing is "off" (3 o'clock position 
on the diagram).
     7) Put the needle into a bottle of bacteriostatic 
saline then use the syringe to draw up some 
bacteriostatic saline through this needle through the IV 
tubing attached to the needle so that saline fills the 
tubing from the tip of the needle to a halfway point in 
the tubing (refer to the electronic transducer method 
diagram).  The other half of the tubing (nearest to the 
stopcock) and the syringe should contain only air.
     8) Insert the needle into the designated muscle 
compartment.
     9) Turn the stopcock "off" lever to the 6 o'clock 
position as shown in the diagram so that all three ports 
are open simultaneously.
     10) Depress the plunger SLOWLY, causing a rise in 
the pressure within the system.  The digital pressure 
readout on the electronic monitor will rise until the 
pressure within the system is equivalent to the pressure 
within the compartment.  As the pressure within the 
system exceeds the pressure in the compartment, the 
saline in the connection tubing will slowly move towards 
the needle.  The reading on the manometer at the time 
that the saline first begins to move represents the 
compartment pressure (Be careful not to inject the 
saline into the compartment).  Some have 
recommending reading the shape of the meniscus in 
the tubing with the needle.  If the meniscus is concave 
or convex, then the pressure on the saline column is 
too high or too low.  When the meniscus is flat, then the 
pressure is perfectly balanced and the electronic 
transducer's electronic reading should accurately reflect 
the pressure in the compartment.  The shape of the 
meniscus in the tubing connected to the pressure 
transducer should not change much.


3.  IV infusion pump method
     This method is very simple, but it requires an IV 
infusion pump with a built in pressure readout.  Most 
modern IV infusion pumps have this feature, which is 
most commonly used to permit nurses to set limits on 
IV infusion pressure so that the pump with alarm if a 
high pressure condition is encountered, usually due to 
an infiltrated IV or a malpositioned IV catheter.  These 
sophisticated pumps reduce the likelihood of an 
undetected infiltrated or obstructed IV catheter.
     Uppal et al, described the use of the IVAC infusion 
pump to measure the intracompartmental pressure 
(11):
     1) Prime the IV infusion pump with saline and 
remove all air bubbles.
     2) Attach an 18-gauge needle to the end of the IV 
tubing.  Infuse saline so that saline is primed through 
the entire needle.
     3) Set the IV infusion pump to 25 cc/hr.
     4) Set the pump to read pressure in mmHg (rather 
than cm H2O).
     5) Adjust the height of the IV infusion pump to be 
roughly level to the patient's extremity which is about to 
be measured.
     6) Turn the pump on to begin infusion, then insert 
the 18-gauge needle with saline flowing through it at 25 
cc/hr into the desired compartment.
     7) Immediately read the infusion pressure on the 
pump when the needle is inserted.  Some pumps have 
a feature to display the pressure continuously.  The 
pressure should have gone from a value near zero to a 
higher value reflecting the pressure within the 
compartment.  The pressure must be read immediately 
to prevent fluid from infusing into the compartment and 
elevating the pressure further.
     8) Remove the needle from the compartment.


References
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www.emedicine.com/emerg/topic739.htm (no date, but 
reviewed online in August 2000).
     2.  Vollmar B, Westermann S, Menger MD.  
Microvascular Reponse to Compartment Syndrome 
Like External Pressure Elevation:  An In Vivo 
Fluorescence Microscopic Study in the Hamster 
Striated Muscle. Journal of Trauma 1999;46(1):91-96.
     3.  Carriere SR, Elsworth T.  Found down: 
Compartment syndrome, rhabdomyolysis, and renal 
failure.  Journal of Emergency Nursing 
1998;24(3):214-217. 
     4.  McQueen MM, Gaston P, Court-Brown CM.  
Acute Compartment Syndrome:  Who is at Risk?  
Journal of Bone & Joint Surgery (Br) 
2000;82-B(2):200-203.
     5.  Cohen RI, Rao R.  A 41-Year-Old Man with 
Thigh Pain and Loss of Sensation in the Toes.  Chest 
1997;111(3):810-812.
     6.  Freedman SH, King BR.  Approach To Fractures 
With Neurovascular Compromise.  In:  Henretig FM,  
King C (eds).  Textbook of Pediatric Emergency 
Procedures, Williams & Wilkins, Baltimore, 1997, 
pp1113-1114.
     7.  Jacobs DG, O'Brien KB, Miles WS.  Unilateral 
Lower Extremity Compartment Syndrome in the 
Quadriplegic Patient:  A Possible Association with the 
Use of Elastic Bandages. Journal of Trauma 
1999;46(2):343-345.
     8.  Arbabi S, Brundage SI, Gentilello LM.  
Near-Infrared Spectroscopy:  A Potential Method for 
Continuous, Transcutaneous Monitoring for 
Compartmental Syndrome in Critically Injured Patients.  
Journal of Trauma 1999;47(5): 829.
     9.  Heppenstall RB.  An Update in Compartment 
Syndrome Investigation and Treatment.  University of 
Pennsylvania Orthopaedic Journal (online at 
http://health.upen.edu/ortho/oj/oj10sp97p49.html) 1997.
     10.  The Leg (Chapter 29).  In: Simon RR, 
Koenigsknecht SJ (eds).  Emergency Orthopedics:  The 
Extremities, third edition.  Appelton & Lange, Norwalk, 
CT, 1995, pp471-478.
     11.  Uppal GS, Smith RC, Sherk HH, Mooar P.  
Accurate Compartment Pressure Measurement Using 
the Intervenous Alarm Control (IVAC) Pump - Report of 
a Technique.  Journal of Orthopedic Trauma 
1992;6(1):87-89.