Current Orthopaedics (2004)18, 468–476
EMERGENCY CARE
Acute compartment syndrome
S. Singha,, S.P. Trikhab
, J. Lewisc
a
7 Ardmay Gardens, Surbiton, Surrey, KT6 4SW, UK
b
Flat 3, 9 Grange Road, Kingston-upon-Thames, Surrey, KT1 2QU, UK
c
Worthing and Southlands NHS Trust, West Sussex, UK
Summary Compartment syndrome can occur in any myofascial muscle compart-
ment. If left untreated it can lead to ischaemic contractures and severe disabilities.
A high index of suspicion is required in at risk cases. Compartment pressure
monitoring is a useful adjunct in the diagnosis of raised compartment pressure
especially when clinical assessment is difficult. The key to a successful outcome is
early diagnosis and decompression of affected compartments.
2005 Elsevier Ltd. All rights reserved.
Introduction
Compartment syndrome has been defined as ‘a
condition in which the circulation and function of
tissues within a closed space are compromised by
an increased pressure within that space’.1
The
muscles and nerves of the extremity are enclosed in
fascial spaces or compartments and are therefore
susceptible to this condition. It is a surgical
emergency which if not recognised and treated
early can lead to ischaemic contractures, neurolo-
gical deficit, amputation, renal failure and even
death. Richard von Volkmann was the first to report
this complication.2
He reported post-traumatic
muscle contracture of acute onset with increasing
deformity despite splinting and passive exercises.
Compartment syndrome is most commonly seen
following trauma, but may occur after ischaemic
reperfusion injuries,3
burns4
and positioning during
surgery 5
Fractures of the tibial shaft and the
forearm account for 58% of compartment syn-
dromes.6
A high index of suspicion is required and
early decompression of all at risk compartments is
the treatment of choice.7–9
Pathophysiology
The common pathogenic factor in compartment
syndrome is increased pressure within a fascial
compartment. Three theories have been proposed
to explain the development of tissue ischaemia:
(1) The increased compartmental pressure may
lead to arterial spasm.10
ARTICLE IN PRESS
www.elsevier.com/locate/cuor
KEYWORDS
Compartment
syndrome;
Volkmanns ischaemic
contracture;
Fasciotomy;
Compartment
pressure monitoring
0268-0890/$ - see front matter 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cuor.2004.12.006
Corresponding author. Tel.:+44 07968 013803;
fax: +44 208 390 7029.
E-mail addresses: [email protected] (S. Singh),
[email protected] (S.P. Trikha), [email protected]
(J. Lewis).
2.
(2) The criticalclosing pressure theory states that
because of the small luminal radius and the high
mural tension of arterioles there must be a
significant transmural pressure difference (ar-
teriolar pressure minus tissue pressure) to
maintain patency. If tissue pressure rises or
arteriolar pressure drops so that this critical
pressure difference does not exist then the
arterioles will close.11
(3) If tissue pressure rises then the veins will
collapse due to their thin walls. If blood
continues to flow from the capillaries the
venous pressure will rise until it exceeds tissue
pressure and patency of the veins is re-
established. This leads to an increase in venous
pressure and therefore reduces the arteriove-
nous gradient and as a result reduces tissue
blood flow.12
The response of skeletal muscle to ischaemia or
trauma is similar regardless of the mechanism of
injury.13
When muscles become anoxic histamine-
like substances are released and these dilate the
capillary bed and increase endothelial permeabil-
ity. Transudation of plasma occurs into the intra-
muscular compartment and this increases the
pressure within the muscular compartment. To
compensate the lymphatic drainage increases,
however when this reaches a maximum the
intracompartmental pressure (ICP) causes collapse
of lymphatic vessels.14
Due to the high pressure in
the arterial system there is continuing blood flow
into the compartment and this increases the
swelling and oedema. It is only in the late stages
of compartment syndrome that arterial flow into
the compartment is compromised.
The amount of pressure required to produce a
compartmental syndrome depends on many fac-
tors, including the duration of pressure elevation,
metabolic rate of tissues, vascular tone and the
mean arterial pressure.
The data on effects of ischaemia to tissues are
derived from research in which sudden, total
ischaemia was imposed. Neural tissues demonstrate
functional abnormalities (parasthesia and hyper-
esthesia) within 30 min of the onset of ischaemia,
and irreversible functional loss after 12 h.12,15–17
Muscle shows functional changes after 2–4 h and
irreversible changes beginning at 4–12 h.16–18
Ischaemia of 4 h gives rise to significant myoglobi-
nuria, reaching a maximum at about 3 h although it
can persist up to 12 h.19–22
Compartment syndromes
lasting longer than 12 h produce chronic functional
deficits, such as contractures, motor weakness and
sensory disturbance.23,24
Any cause of increased
compartmental pressure can result in a compart-
ment syndrome. See Table 1 for a list of aetiologies
as described by Matsen1
.
Diagnosis
Clinical
The key to successful treatment of acute compart-
ment syndrome is early diagnosis and decompres-
sion of the affected compartments.1,7,9,23,24
The classical signs of impending compartment
syndrome are pain, pallor, parasthesia, paralysis
and pulselessness (The 5 p’s). However by the time
all these symptoms have developed (especially
pulselessness) the limb will be non-viable.
A high index of suspicion is required to make the
diagnosis. Clinical diagnosis is made on a combina-
tion of physical signs and symptoms. These include
pain out of proportion to the stimulus, pain on
passive stretch of the affected muscle compart-
ment, altered sensation, muscle weakness and
tenderness over the muscle compartment. The
symptoms and signs which are the most reliable in
making the diagnosis are increasing pain, and pain
on passive stretching of the muscle within the
affected compartment.25–28
However these symp-
toms are subjective and impossible to elicit in the
unconscious, non-cooperative patient and those
ARTICLE IN PRESS
Table 1 Aetiology of compartment syndrome as
described by Matsen.
Decreased compartment size
Closure of fascial defects
Tight dressings
Localised external pressure
Increased compartment content
Bleeding
Vascular injury
Bleeding disorder
Increased capillary permeability
Post Ischaemic swelling
Exercise
Seizure and eclampsia
Trauma
Burns
Orthopaedic surgery
Increased capillary pressure
Exercise
Venous obstruction
Muscle hypertrophy
Infiltrated infusion
Nephrotic syndrome
Acute compartment syndrome 469
3.
who have hadregional blocks. There has been
concern raised with the use of patient controlled
analgesia and regional anaesthesia in high risk
cases.28,29
Intracompartmental pressures
Pain can be unreliable especially in the trauma
patient. It can range from being mild to severe, and
in the unconscious patient important clinical
symptoms and signs can be difficult to elicit.
Techniques have been developed to measure ICPs.
Technique for monitoring intracompartmental
pressures
Whitesides 30
introduced a method for measuring
ICP that required simple equipment available in
most hospitals (Fig. 1). Using a needle, plastic
tubing filled with saline and air attached to a
mercury manometer they established tissue pres-
sure measurement criteria as determinants of the
need for fasciotomy. However this technique
involved the injection of saline into the compart-
ment and this may aggravate an impending com-
partment syndrome.
The slit and wick techniques require a polyethy-
lene tubing connected to a pressure transducer.
The tubing is filled with water and it is important
that there are no air bubbles present within the
tubing. The wick and slit catheter allow continuous
monitoring of compartments, and have been shown
to be more accurate than the needle manometer
technique.31
However the end of the tubing in the
fascial compartment may become blocked with
blood leading to inaccurate readings. Due to these
potential draw backs a solid-state transducer (STIC)
intracompartment catheter has been developed.32
This has a multiperforated polyethylene tip with a
STIC which can remain patent for up 16h. The STIC
catheter has been shown to be functionally superior
to conventional systems (needle, wick and slit) and
easier to assemble, calibrate, maintain and interpret.
The wick, slit and STIC methods require specia-
lised equipment which may not be readily avail-
able, while the needle system as proposed by
Whitesides30
can be constructed from equipment
which is readily available in most hospitals.
If on clinical examination an obvious compart-
ment syndrome is present pressure measurement
may not be necessary. However it can be useful
adjunct in the diagnosis of compartment syndrome
especially in children, unconscious patients and
those with equivocal clinical findings.
At what pressure to decompress?
The normal tissue pressure within closed compart-
ments is about 0–10 mmHg. This pressure markedly
increases in compartment syndrome. There is
inadequate perfusion and relative ischaemia when
the tissue pressure within a closed compartment
rises to within 10–30 mmHg of a patient’s diastolic
blood pressure. Whitesides believed that fasciot-
omy is indicated when the tissue pressure rises to
40 mmHg in a patient with a diastolic pressure of
70 mmHg. Using these criteria no functional deficits
developed in patients, and all showed conclusive
ARTICLE IN PRESS
Figure 1 Apparatus for measuring compartment pressure.
S. Singh et al.
470
4.
evidence of compartmentsyndrome at the time of
operation.30
McQueen 33
recommended a differential
pressure (diastolic pressure minus ICP) of 30 mmHg
as a threshold for fasciotomy in tibial fractures.
ICPs between 30 and 50 mmHg have been
suggested that a fasciotomy should be performed.34
The lower level of 30 mmHg is most commonly used
as when the tissue pressure rises above this the
capillary pressure is insufficient to maintain capil-
lary blood flow. It has also been shown that fascial
compliance decreases sharply at an ICP of 33 mmHg
as the fascia has reached its maximum stretch.35
It is important to state that tissue viability is
dependant on adequate perfusion and blood flow
within the microcirculation. Setting an absolute
pressure ignores the role that blood pressure plays
in maintaining adequate blood flow within a
compartment. It has been shown that muscle
damage occurring at a specific level relative to
the blood pressure is more consistent that relying
on a fixed compartment pressure.36
The diastolic pressure minus the ICP is called the
delta pressure. The critical level has been found to
range from 10 to 35 mmHg. The most commonly
used delta pressure is 30 mmHg or less.1,10,33
In
tibial fractures it has been shown that by using a
delta pressure of 30 mmHg unnecessary fascio-
tomies can be avoided. No clinically significant
complications were identified in patients with a
delta pressure greater than 30 mmHg.
The ICP or delta pressure at one point in time
does not necessarily confirm that a compartment
syndrome is present. During intramedullary nailing
there are short increases in ICP, however these are
not always associated with clinical signs of com-
partment syndrome.37
The higher the ICP and the
longer it is maintained the greater the muscle
damage, however an ICP of 30 mmHg maintained
for 8 h caused significant muscle necrosis in canines
35
and biochemical changes have been observed in
the experimental situation with a delta pressure of
20 mmHg for 4 h. When the delta pressure ap-
proached zero these changes were present in 2 h.38
As stated earlier the sooner the decompression
the better the outcome. If decompression is
delayed for more than 12 h permanent disability
may occur, however if decompression is performed
under 6 h of making the diagnosis a full recovery
can be expected.24,25,39,40,41
However confirming
the exact time of the start of compartment
syndrome can be difficult.
Problems with interpreting pressures
The majority of compartment syndromes occur in
the lower limb and hence the majority of the
clinical studies relate to this region of the body.
The site at which the compartment pressure is
measured should be within a few centimetres of
the maximal pressure as it cannot be assumed that
the ICP equilibrates throughout the compart-
ment.42
The pressure is always highest 5 cm from
the fracture in tibial fractures, and therefore it is
recommended that ICP should be measured as close
to the site of injury as possible.43
In the lower leg there are four fascial compart-
ments and one or all of these may be involved in
compartment syndrome. The highest pressures are
recorded in the anterior compartment then the
deep posterior compartment.9,42
It would seem
logical therefore in tibial fractures to measure the
pressure within 5 cm of the fracture and to monitor
the pressure in the anterior tibial compartment.
However other compartments may need to be
monitored depending on the clinical picture.
Within the UK practices for monitoring ICP vary.
In a postal questionnaire 46% of trauma centres had
equipment available for monitoring compartment
pressures, and 42% of respondents were unsure at
what ICP they would perform fasciotomies. Only 9%
used a delta pressure of 30 mmHg as a guide to
perform fasciotomies as suggested by Whitesides 30
and McQueen.33
Failing to diagnose and treat a compartment
syndrome urgently can be disastrous for patients.
Pressure monitoring can be a useful adjunct to help
confirm the diagnosis. McQueen et al. 37
suggest
monitoring all patients at risk as an aid to clinical
diagnosis. Others have suggested that this can lead
to over treatment.44
Certainly pressure monitoring
should be used in unconscious patients, those who
are difficult to assess and when equivocal clinical
findings are present. All centres involved in trauma
should have equipment available for monitoring
compartment pressures and clinicians involved in
trauma need to be aware of interpretation of these
results.
Other methods for measuring compartment
pressures
Near-Infrared Spectroscopy (NIRS)
NIRS is an optical technique that allows tracking of
variations in the oxygenation of muscle tissue.45
The technique involves monitoring the absorption
of light transmitted through muscle tissue at two
distinct wavelengths. A change in the oxygenation
state of haemoglobin results in opposite changes in
the absorption of light. By calculating the differ-
ences in the absorption signal the device provides a
continuous index of tissue oxygenation. It can be of
ARTICLE IN PRESS
Acute compartment syndrome 471
5.
use in investigatingchronic compartment syndrome
in adults, as it can detect changes in relative
oxygenation, but it is of little value in acute
compartment syndrome as changes in the relative
oxygenation may have already occurred.46
Laser Doppler flowmetry
This uses a flexible fibre optic wire which is
introduced into the muscle compartment. The
signals from this wire are recorded on a computer.
It can be used as an adjunct in the diagnosis of
chronic compartment syndrome,47
however it was
suggested that further work needs to be carried out
into the pathophysiology of chronic compartment
syndrome and laser Doppler flowmetry needs
analysis in larger population groups.
Treatment
Raised ICP threatens the viability of the limb and
this represents a true management emergency. As
stated earlier early diagnosis is the key to a
successful outcome.
Removal of all dressing down to skin, followed by
open extensive fasciotomies with decompression of
all muscle compartments in the limb is the
treatment of choice.
Experimental evidence shows that the circular
cast can substantiate the adverse effects of raised
ICP.48
Splitting of the cast on one side led to an
average fall in ICP 30%, and 65% if split on both
sides. Splitting of the padding led to a further fall in
ICP by 10%. Complete removal of the cast reduced
the pressure by another 15%.
In patients whom the diagnosis is being consid-
ered and in those in whom resuscitation is
proceeding the following steps should be per-
formed:14
(1) Ensure the patient is normotensive, as hypoten-
sion reduces perfusion pressure and facilitates
tissue injury,
(2) Remove any circumferential or constricting
bandages as these may increase ICP,
(3) Maintain the limb at heart level as elevation
reduces the arterio-venous pressure gradient.
(4) Give supplemental oxygen to ensure optimal
saturation.
Fasciotomies
If the tissue pressure remains elevated despite the
above, and the clinical scenario indicates increased
ICP adequate decompressive fasciotomies should be
performed.
Several surgical approaches have been tried in
the leg. The surgical goal is the prevention of
permanent disability, and the adequacy of decom-
pression should not be compromised by cosmesis or
the number and lengths of incisions. It is essential
to decompress all compartments at risk.
In the lower limb fibulectomy via a single lateral
incision has been suggested, however this only
allows limited views and an adequate release may
not be achieved. A two incision approach allows
safe access to all four compartments of the lower
leg and is the treatment of choice. The deep
posterior compartment has been neglected in
descriptions of fasciotomies however this is the
2nd most commonly involved compartment and
access can be gained behind the posteromedial
border of the tibia in the distal third of the leg
where the belly of flexor digitorum longus is
exposed.
The technique of double incision fasciotomy is
described below. It is important to perform a
complete decompression and incisions less than
15 cm may result in inadequate decompression.49
In
the emergency treatment of compartment syn-
drome there is no place for short cosmetic
incisions.
Lower limb fasciotomy (Fig. 2)
Anterolateral incision. This incision allows ap-
proach to the anterior and lateral compartments of
the leg. A 15–20 cm incision is placed halfway
ARTICLE IN PRESS
Figure 2 The safe incisions. These are designed to avoid
the perforating arteries. The antero-lateral incision is
2 cm lateral to the medial border of the tibia. The
postero-medial incision is 1 or 2 cm prosterior to the
medial border of the tibia.
S. Singh et al.
472
6.
between the fibulaand the tibial crest. The skin
edges are undermined. A short longitudinal incision
is made over the muscle bellies allowing palpation
of the intramuscular septum between the anterior
and lateral compartments. By identifying the
septum the superficial peroneal nerve can be
identified adjacent to the septum where it crosses
the junction of the middle and distal thirds of the
leg. The anterior compartment fascia is opened
throughout the leg by extending the first incision in
the fascia (Fig. 3). It is important not to damage
the superficial peroneal nerve in the distal third of
the wound. The peroneal compartment is decom-
pressed by incising the fascia in line with the fibular
shaft posterior to the intermuscular septum.
Proximally the incision is directed to the fibular
head and distally to the lateral malleolus remaining
posterior to the superficial peroneal nerve.
Posteromedial incision. This incision is used to
decompress the superficial and deep posterior
compartments of the leg. It is placed 2 cm posterior
to the posterior tibial margin and is about 15–20 cm
long. Care should be taken to avoid damage to the
saphenous nerve and vein and they should be
retracted anteriorly. The superficial posterior com-
partment is decompressed first, and the fascia is
incised throughout its length (Fig. 4). The Achilles
tendon helps to identify this compartment. The
fasciotomy is extended distally as far as the medial
malleolus. The deep posterior compartment is then
released by incising the fascia distally and then
proximally under the bridge of soleus. It may be
necessary to detach the soleus from the back of
the tibia.
A technique for forearm fasciotomy is now
described.
Forearm fasciotomy
A single incision can be used to decompress the
volar aspect of the forearm (Fig. 5). It is similar to
the volar approach to the radius as described by
Henry.50
It begins 1 cm proximal and 2 cm lateral to
the medial epicondyle. It is carried obliquely across
the antecubital fossa and over the volar aspect of
the mobile wad of three muscles (brachioradialis,
extensor carpi radialis longus and extensor carpi
radialis brevis). It is curved medially reaching the
midline at the junction of the middle and distal
third of the forearm. It is continued straight distally
to the proximal skin crease over palmaris longus.
The incision is curved across the wrist crease to the
mid palm area. The median nerve should be
decompressed at the carpal tunnel. In cases of
median nerve symptoms the median nerve should
also be explored in the proximal forearm. The
median nerve can be constricted at the proximal
end of pronator teres and at the proximal edge of
flexor digitorum superficialis.
The dorsal muscle compartment can be released
by a single incision. This begins 2 cm distal to the
lateral epicondyle and carried distally to the wrist.
The skin edges are undermined and the dorsal
fascia incised directly in line with the skin incision.
Foot fasciotomies
Excessive bleeding and oedema can produce com-
partment syndromes in the closed spaces of the
foot. Foot compartment syndrome should be
suspected in all crushing and high energy foot
ARTICLE IN PRESS
Figure 3 Anterior and peroneal compartment decom-
pression (ac—anteriror compartment; Ic—lateral com-
partment). The fascia is shown in dark grey.
Figure 4 Decompression of the posterior compartments
(s—soleus; g—gastrocneumius; tp—tibialis posterior).
Acute compartment syndrome 473
7.
injuries. With crushinjuries of the foot Myerson
found acute compartment syndrome in 16 of 58
patients.51
Tense swelling of the foot should alert
the clinician to this possibility, particularly because
pain on passive stretch of the toes and the presence
or absence of pedal pulses are less reliable
indications of compartment syndrome in the foot.
There are a number of different approaches to
decompress foot compartments. A dorsal approach
along the 2nd and 4th metatarsals is simple to
perform and provides effective decompression of
all four compartments.52
Associated Lisfranc in-
juries and metatarsal fractures can also be stabi-
lised via this approach.
Closure of fasciotomy wounds
After decompression of fascial compartments the
wounds are left open and sterile dressings are
applied. Delayed primary closure can be performed
when swelling has subsided, however this may be
difficult due to skin retraction and oedema. If the
wound edges cannot be approximated without
tension, skin grafting may be required.
Various methods have been described using the
elastic properties of the skin to aid fasciotomy
closure.
An elastic vessel shoelace can be applied with
the staples at the side of the wound. This can be
gradually tightened without the need for anaes-
thesia, providing gradual closure of the fasciotomy
wound.53
Closure of the wound takes about 10 days.
There are some commercially available devices to
aid fasciotomy closure.54
The Suture Tension
Adjustment Reel (STAR) is placed parallel to the
wounds at the time of fasciotomy, and when the
swelling has subsided the reels are tightened to
gradually close the wound. This method requires
2–4 days of bedside tightening for wound closure.
Split skin grafting can lead to a poor cosmetic
result, with insensate skin and donor site morbidity.
Delayed primary closure using the skin’s elasticity
provides a more cosmetically acceptable outcome
for the patient but requires greater nursing care.
However a poor cosmetic result is preferable to the
outcome of a missed compartment syndrome.
Intramedullary nailing
Over the last 2 decades intramedullary nailing of
tibial fractures has increased. Initially there was
concern that nailing may increase ICPs and pre-
cipitate compartment syndrome and it was thought
that nailing should be delayed for up to 7 days to
allow the swelling to subside.55
Further research in
this area has shown that during reaming the
pressure may rise to 180 mmHg,37
however this
high ICP fell back to normal after removing the
reamer. The application of traction also increases
ICPs but these immediately dropped with release of
the traction. Despite high pressures being reached
during the reduction of tibial fractures and during
reaming no patients in the study developed any
sequelae of compartment syndrome. Transient
increases in compartment pressures seam to be
well tolerated and return back to normal after the
stimulus is removed.
Controversy still exists if monitoring should be
performed during intramedullary nailing. McQu-
een9,33
advocates routine monitoring of all patients
with tibial fractures if facilities are available.
Others have suggested that this may lead to over
treatment44
and unnecessary fasciotomies.
Conclusion
Compartment syndrome can have disastrous con-
sequences if not recognised and treated appro-
priately. In conscious patients the diagnosis can be
made by careful examination of the patient.
Invasive monitoring is a useful adjunct especially
in unconscious patients and those who are difficult
to assess. As the tissue pressure rises the viability of
the cells are threatened. The tissue pressure level
at which perfusion threatens cell viability varies
ARTICLE IN PRESS
Figure 5 The incision for decompression of the volar
aspect of the forearm. If posterior compartment pressure
doesn’t concomitantly fall then the posterior compart-
ment requires to be opened by an additional linear
posterior incision.
S. Singh et al.
474
8.
according to theage and circulatory status of the
patient. A delta pressure (Diastolic pressure-Tissue
pressure) of 30 mmHg or less is an accepted level
that fasciotomy should be performed.
References
1. Matsen FA. Compartment Syndrome. Clin Orthop
1975;113:8–14.
2. Volkmann R. Die ischaemischem Muskellamungen und
Kontrakturen. Zentralbl. Chir 1881;8:801.
3. Perry MO, Thal E R, Shires G T. Management of arterial
injuries. Ann Surg 1971;173:402–8.
4. Brown RL, Greenhalgh DG, Kagan RJ, Warden GD. The
adequacy of limb escharotomies-fasciotomies after referral
to a major burns centre. J Trauma 1994;37:916–20.
5. Goldsmith AL, MacCallum MID. Compartment syndrome as a
complication of the prolonged use of the Lloyd–Davies
position. Anaesthesia 1996;51:1048–52.
6. McQueen MM, Gatson P, Court-Brown CM. Acute compart-
ment syndrome: who is at risk? J Bone Joint Surg 2000;
82-B:200–3.
7. Rorabeck CH. The treatment of compartment syndromes of
the leg. J Bone Joint Surg 1984;66-B:93–7.
8. Matsen FA, Winquist RA, Krugmire RB. Diagnosis and
management of compartment syndromes. J Bone Joint Surg
1980;62-A:286–91.
9. McQueen MM, Christie J, Court-Brown CM. Acute compart-
ment syndrome in tibial diaphyseal fractures. J Bone Joint
Surg 1996;78-B:95–8.
10. Ashton H. The effect of Increased Tissue pressure on Blood
flow. Clin Orthop 1975;113:15–26.
11. Burton AC. On the physical equilibrium of small blood
vessels. Am J Physiology 1951;164:319–29.
12. Parkes AR. Traumatic Ischaemia of peripheral nerves with
some observations on Volkmann’s Ischaemic Contracture. Br
J Surg 1944;32:403–13.
13. Sanderson RA, Foley RK, McIvor G, Kirkaldy-Willis WH.
Histological Response on Skeletal Muscle to Ischaemia. Clin
Orthop 1975;113:27–35.
14. Mars M, Hadley GP. Raised intracompartmental pressure and
compartment syndromes. Injury 1998;29:403–11.
15. Bowden REM, Gutmann E. The fate of voluntary muscle after
vascular injury in man. J Bone Joint Surg 1949;31-B:356.
16. Holmes W, Highet WB, Seddon HJ. Ischaemic nerve lesions
occurring in Volkmanns Contracture. Br J Surg 1944;32:259.
17. Malan E, Tattoni G. Physiological and anatomopathology of
acute ischaemia of the extremities. J Cardiovasc Surg
1963;17:212.
18. Whitesides TE, Hirada H, Morimoto K. The response of
skeletal muscle to temporary ischaemia: an experimental
study. J Bone Joint Surg 1971;53A:1027.
19. Klock JC, Sexton MJ. Rhabdomyolysis and acute myoglobi-
nuric renal failure following herion use. Calif Med 1973;
119:5.
20. Montagnani CA, Simeone FM. Observations on the liberation
of myoglobin and haemoglobin after release of muscle
ischaemia. Surgery 1953;34:169.
21. Schreiber SN, Liebowitz MR, Bernstein LH. Limb compression
and renal impairment (crush syndrome) following narcotic
overdose. J Bone Joint Surg 1972;54A:1683.
22. Spinner M, Mache A, Silver L, Barsky AJ. Impending
ischaemic contracture of the hand. Plast Reconstruct Surg
1972;50:341.
23. McQuillan WM, Nolan B. Ischaemia complicating injury.
J Bone Joint Surg 1968;50B:482.
24. Matsen FA, Clawson DK. The deep posterior compartmental
syndrome of the leg. J Bone Joint Surg 1975;57A:34.
25. Rorabeck CH, Macnab I. Anterior tibial compartment
syndrome complicating fratures of the shaft of the tibia.
J Bone Joint Surg 1976;58A:549–50.
26. Halpern AA, Nagel DA. Anterior compartment pressures in
patients with tibial fractures. J Trauma 1980;20:786–90.
27. Ellis H. Disabilities after tibial shaft fractures: with special
reference to Volkmanns ischaemic contracture. J Bone Joint
Surg 1958;40B:190–7.
28. Thonse R, Ashford RU, Williams IR, Harrington P. Differences
in attitudes to analgesia in post-operative limb surgery put pati-
ents at risk of compartment syndrome. Injury 2004;35:290–5.
29. Richards H, Langston, Kulkarni R, Downes EM. Does patient
controlled analgesia delay the diagnosis of compartment
syndrome following intramedullary nailing of the tibia.
Injury 2004;35:296–8.
30. Whitesides TE, Haney TC, Morimoto K, Harada H. Tissue
pressure measurements as a determinant for the need of
fasciotomy. Clin Orthop 1975;113:43–51.
31. Rorabeck CH, Castle GSP, Hardie R, Logan J. Compartment
pressure measurements: an experimental investigation using
the Slit Cathter. J Trauma 1981;21:446–9.
32. McDermott AGP, Marble AE, Yabsley RH. Monitoring Acute
Compartment Pressures with the STIC Catheter. Clin Orthop
1984;190:192–8.
33. McQueen MM, Court-Brown CM. Compartmet monitoring in
tibial fractures. The pressure threshold for decompression.
J Bone Joint Surg 1996;78-B:99–104.
34. Elliot KGB, Johnstone AJ. Diagnosing acute compartment
syndrome. J Bone Joint Surg 2003;85-B:625–32.
35. Hargens AR, Akeson WH, Murbarak SJ, et al. Fluid balance
within the canine anterolateral compartment and its
relationship to compartment syndromes. J Bone Joint Surg
1978;60-A:499–505.
36. Heppenstall RB, Sapega A, Scott R, et al. The compartment
syndrome: an experimental and clinical study of muscular
energy metabolism using phosphorus nuclear magnetic
resonance spectroscopy. Clin Orthop 1998;226:138–55.
37. McQueen MM, Court-Brown CM. Compartment pressures
after intramedullary nailing of the tibia. J Bone Joint Surg
1990;72-B:395–7.
38. Heppenstall RB, Sapega A, Izant T, et al. Compartment
syndrome: a quantative study of high energy phosphorus
compounds using 31P-magnetic resonance spectroscopy.
J Trauma 1989;29:1133–9.
39. Sheridean GW, Matsen III FA. Fasciotomy in the treatment of
the acute compartment syndrome. J Bone Joint Surg 1976;
58-A:112–5.
40. McQueen MM, Christie J, Court-Brown CM. Acute compart-
ment syndrome in tibial diaphyseal fractures. J Bone Joint
Surg 1996;78-B:95–8.
41. Mullet H, Al-Abed K, Prasad CVR, O’Sullivan M. Outcome of
compartment syndrome following intramedullary nailing of
tibial diaphyseal fractures. Injury 2001;32:411–3.
42. Heckman MM, Whitesides TE, Grewe SR, Rooks MD.
Compartment pressure in association with closed tibial
fractures: the relationship between tissue pressure, com-
partment and the distance from the site of the fracture.
J Bone Joint Surg 1994;76-A:1285–92.
43. Matava MJ, Whitesides TE, Seiler JG, Hewan-Lowe K, Hutton
WC. Deterioration for the compartment pressure threshold
of muscle ischaemia in a canine model. J Trauma 1994;37:
50–8.
ARTICLE IN PRESS
Acute compartment syndrome 475
9.
44. Janzig HMJ,Broos PLO. Routine monitoring of compartment
pressure in patients with tibial fractures: beware of over
treatment. Injury 2001;32:415–21.
45. Chance B, Nioka S, Kent J, McCully K, Fountain M, Greenfield
R, Holtom G. Time resolved spectroscopy of haemoglobin
and myoglobin in resting and ischaemic muscle. Anal
Biochem 1988;174:698–707.
46. Breit GA, Gross JH, Watenpaugh DE, Chance B, Hargens A.
Near-Infrared Spectroscopy for monitoring of tissue
Oxygenation of Exercising Skeletal Muscle in chronic
compartment syndrome model. J Bone Joint Surg 1997;
79-A:838–43.
47. Abraham P, Leftheriotis G, Saumet JL. Laser Doppler
Flowmetry in the diagnosis of chronic compartment syn-
drome. J Bone Joint Surg 1998;80-B:365–9.
48. Garfin S, Mubark S, Evans K, Hargens A, Akeson W.
Quantification of Intracompartmental pressure and volume
under plaster casts. J Bone Joint Surg 1981;63A:449–53.
49. DeLee JC, Stiehl JB. Open tibia fracture with compartment
syndrome. Clin Orthop 1987;160:175–84.
50. Henry AK. Extensile exposure. Edinburgh and London:
Churchill Livingstone; 1973.
51. Myerson MS, McGarvey WC, Henderson MR, Hakim J.
Morbidity after crush fractures to the foot. J. Orthop
Trauma 1994;8:343–9.
52. Murabak SJ. Hargens AR, Compartment syndromes and
volkmanns contracture. Philadelphia WB: Saunders; 1981.
53. Harris I. Gradual closure of fasciotomy wounds using a vessel
loop shoelace. Injury 1993;24:565–6.
54. McKenney MG, Itzhak N, Fee T, Martin L, Lentz K. A simple
device for closure of fasciotomy wounds. Am J Surg 1996;
172:275–7.
55. Donald G, Seligson D. Treatment of tibial shaft fractures by
percutaneous Kuntscher nailing: Technical difficulties and a
review of 50 consecutive cases. Clin Orthop 1983;178:
64–73.
ARTICLE IN PRESS
S. Singh et al.
476