Current Orthopaedics (1999) 13, 113-119

1999 Harcourt Brace & Co. Ltd

Mini-symposium: Tibial fractures

(v) Acute compartment syndrome in tibial fractures

M.M. McQueen

INTRODUCTION

an abrupt drop occurring when intracompartmental

pressure reaches 60 mmHg even for a short time.
Clayton and his colleagues6 have studied muscle
blood flow clinically and found that muscle blood
flow reduced as the difference between compartment
pressure and diastolic pressure reduced.
The length of time for which pressure has been
applied also has a significant influence on muscle
ischaemia. A pressure which is tolerated over a period
of a few hours may lead to significant muscle
ischaemia over a longer period. 7 Other factors which
reduce the tolerance of muscle to raised compartment
pressure are hypotension, hypoxia, arterial occlusion
and halothane anaesthesia?
All authors agree that loss of neuromuscular function occurs in the acute compartment syndrome,
although there remains debate about the level and
duration of applied pressure which causes irreversible
damage/1-I3 Matsen and his co-authors examined the
effects of raised pressure on peripheral nerve function
in human subjects and noted considerable variation
of pressure tolerance. Recommended pressure levels
for decompression vary from 30mmHg TM to 55
mmHg ~3in normotensive patients to prevent permanent neuromuscular deficit.
Bone union after fracture is also affected by raised
compartmental pressures. Karlstrom and his coauthors ~ and DeLee and Stiehl ~6noted a high incidence of delayed or non-union in tibial fractures
complicated by acute compartment syndrome. In a
retrospective study/7 a series of tibial fractures in
adults complicated by acute compartment syndrome
took an average of 34 weeks to unite compared to 15
weeks in a matched uncomplicated group. A recent
prospective study of 25 tibial fractures complicated
by acute compartment syndrome has confirmed this
finding TM with cases of acute compartment syndrome
with sequelae taking twice as long to unite their tibial

Acute compartment syndrome is a condition in which

the circulation and function of tissues within a closed
space are compromised by increased pressure within
that space. If untreated, this condition leads to
ischaemia of muscle and nerve and eventually to
disabling contractures, sensory changes and muscle
weakness. Neglect of acute compartment syndrome
leads to devastating complications for the patient and
is one of the commonest reasons for orthopaedic
surgeons being accused of negligence. It is of the
utmost importance that the possibility of this complication arising be appreciated at all times during the
treatment of tibial fractures.

PATHOGENESIS
Acute compartment syndrome reduces blood flow to
all the tissues in the compartment including muscle,
nerve and bone. Although it is accepted that muscle
blood flow is reduced, there remains considerable
debate as to the mechanism of vessel shut-down. This
includes proponents of a critical closing pressure with
a combination of active arteriolar closure and passive
capillary compression/ reduction of local arteriovenous pressure 2 and capillary occlusion?
Regardless of the mechanism of vessel shut-down,
the effect is to cause acute tissue ischaemia. Muscle
blood flow has been studied extensively4-~and there is
universal agreement that increasing compartmental
pressure results in decreasing muscle blood flow with

Margaret M. McQueen MD FRCSEd(Orth), Consultant

Orthopaedic Surgeon, Edinburgh Orthopaedic Trauma Unit,

Royal Infirmary of Edinburgh, Lauriston Place, Edinburgh EH3
9YW, UK

113

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Current Orthopaedics

fractures as those without sequelae. Increasing the

delay to fasciotomy significantly increased the union
time of tibial diaphyseal fractures. This is attributed
to an effect on bone blood flow?9

E P I D E M I O L O G Y OF ACUTE COMPARTMENT
SYNDROME
There are many underlying causes of the acute compartment syndrome. The commonest reported cause is
fracture, with incidences ranging from 30% 20to 70%. 21
In a recent prospective study of 164 acute compartment syndromes presenting to the Edinburgh
Orthopaedic Trauma Unit, 69% of the cases were due
to fractures, approximately half of these being tibial
fractures.
In Edinburgh, in the period from January 1988 to
December 1995, there were 58 acute compartment
syndromes in tibial fractures, giving an incidence of
4.3% in all tibial fractures and 3.3% in open tibial
fractures. Of the 58 patients, there were 54 males and
4 females with an average age of 29 years. The average
annual age and sex-specific distribution shows a large
peak of young males (Fig. 1).
In the under-35-year-old age group, the incidence is
6% compared with 2% in the over-35-year-old age
group. This difference is statistically significant. The
younger patient is therefore at greater risk of acute
compartment syndrome after tibial fracture. This may
be because younger muscle tends to be larger than
older muscle while compartments presumably remain
the same size throughout life after growth is complete.
Thus, young patients have less available space for their
muscle to swell, putting them at more risk of acute
compartment syndrome developing.
In the whole group, the majority of the fractures
had been caused by sporting injuries (47%) and 22%

[] Males 1
LI Females]

9"[I
8

6
4
3r
2

l,

all
<20 2029

.m
3039

4049

5059

6069

n
7079

80- >90
89

Fig. 1 Averageannual age-andsex-specificincidencefor acute

compartment syndromecomplicatingtibial diaphysealfractures
1988-1994.

were caused by road accidents. The incidence of acute

compartment syndrome was slightly higher after lowenergy injury. This may be because compartment
boundaries are less likely to be disrupted after lowenergy injury.

CLINICAL DIAGNOSIS
The clinical symptoms and signs of acute compartment syndrome are those of muscle and nerve
ischaemia. The commonest and most reliable symptom is pain which is out of proportion to the clinical
situation. 16,22,23Rollins and his co-authors 24found pain
to be present in 83% of their patients requiring fasciotomy while in the Edinburgh series 95% of conscious patients had significant pain? 9 However, pain
can be an unreliable symptom as it can be very variable in degree. 22,25,26 Acute compartment syndrome
may be painless either in association with nerve
injury27,;8or in its early stages?9 In the deep posterior
compartment syndrome, pain may be minimal 26,3
while pain is not a useful symptom in the unconscious
patient. Pain is normally increased by passive stretching of the affected muscle group, but this may often be
confused by muscle injury, which will cause similar
findings.
Sensory symptoms and signs are usually the first
indication of nerve ischaemia with paraesthesia or
anaesthesia in the territory of the nerves running
through the affected compartments. 23'26Sensory deficit
is reported in 42%-100% of cases, j6'24'3~ In the
Edinburgh series, 30% had sensory deficits prior to
fasciotomy.19
Progression of nerve ischaemia causes paralysis of
muscles, which is reported in varying frequency in different series. It is generally believed that motor deficit
is a late finding and is associated with irreversible
damage to muscle and nerve. 32 Fifteen per cent of
patients had developed motor weakness at the time of
fasciotomy in the Edinburgh series. There was a statistically significant increase in permanent sequelae in
these patients.19
A potentially disastrous error in the clinical diagnosis of the acute compartment syndrome is to underestimate the severity of the condition because
peripheral pulses are present. Compartment pressure
is only rarely high enough to occlude a major vessel
and the acute compartment syndrome often occurs
with pressure lower than the diastolic pressure. 18.23.25.33,34
The only exception to this is in associated arterial
injury, where the absent pulse is due to arterial damage rather than high compartment pressure. Distal
ischaemia and absent pulses are an indication for arteriography.
Swelling or tenseness is a common sign of acute
compartment syndrome, provided it is possible to palpate the compartment. However, in cases where the
leg is encased in plasters or dressings or where there is

Acute compartment syndrome in tibial fractures

marked peripheral oedema, this sign may be difficult
to elicit.
The early diagnosis of the acute compartment
syndrome is of paramount importance. Delay in
diagnosis is often due to either inexperience and insufficient awareness of the condition or to an indefinite
and confusing clinical presentation with unreliable
clinical signs. Delay in treatment can lead to catastrophic consequences, including contracture, infection
and occasionally amputation, and is cited as the single
most important cause of failure. ~6,3,31,35

M O N I T O R I N G OF I N T R A - C O M P A R T M E N T A L
PRESSURE
Because of the unreliability of the clinical diagnosis of
the acute compartment syndrome, methods of measuring pressure within the muscle compartment have
been developed. The first method reported was the
needle manometer method 25 but this technique has
been criticized by several authors because of the
potential for falsely high readings caused by injection
of saline, 36 the impossibility of continuous pressure
readings 37 and the awkwardness of observing an air
fluid meniscus and a manometer simultaneously with
possible inter-observer error. 33
Matsen et aP 3 described a continuous infusion
method of monitoring pressure, which relies on measurement of the pressure required to infuse fluid
slowly into the muscle compartment. Matsen and his
colleagues concluded that the method is simple to use
and accurate to within 2 mmHg. The main disadvantages are a slow response time and the risk of aggravating swelling by continuous infusion? 9
The wick catheter technique 36 depends on braided
Dexon wicks which protrude from the end of an
epidural catheter and provide an extensive contact
area, preventing obstruction of the catheter tip.
Mubarak and his co-authors found the method to be
accurate and reproducible and to allow continuous
long-term measurement. A possible disadvantage of
this technique is the risk of leaving part of the
catheter in situ.
The slit catheter technique 39depends on slits being
cut at the tip of a catheter resulting in a large surface
area preventing occlusion by muscle. A continuous
infusion is therefore not required but a disadvantage
of this technique is its susceptibility to the presence of
an air bubble at the tip of the catheter reducing
catheter response to changes in intracompartmental
pressure. 33

TISSUE PRESSURE THRESHOLDS FOR

DECOMPRESSION

There is considerable debate about the pressure level at

which muscle compartments should be decompressed.

115

Whitesides and his co-authors 25 stress the importance

of relating the tissue pressure to the systemic blood
pressure and stated that ischaemia begins when the
tissue pressure rises to within 10 30 m m H g of the
diastolic pressure. This statement was supported by
Heckmann and his co-authors 4who studied the effect
of varying differences between the compartment pressure and the diastolic pressure (Ap) on canine muscle
and concluded that a Ap of 10-20 m m H g was an indication for fasciotomy. Other authors have quoted
critical tissue pressures of 30 mmHg, 41'4240 m m H g 38,~3~s
to 4 5 m m H g . 46 Some of this variation may be
explained by differing techniques and some by failure
to take the patient's blood pressure into account. It is
recognized that there is considerable variation in the
individual's tolerance of increased tissue pressure <46
and that the use of a single absolute pressure as an
indication for fasciotomy may result in unnecessary
decompressions. 47
A series of 116 patients with tibial diaphyseal fractures underwent continuous compartment monitoring
in the Edinburgh Orthopaedic Trauma Unit? 8
Continuous pressure monitoring of the anterior compartment was carried out for at least 24 hours using
the slit catheter method. Review was carried out at an
average of 15 months after injury to document the
incidence of late contracture. There were three acute
compartment syndromes with Ap levels of 15 mmHg,
1 0 m m H g and 1 5 m m H g respectively. The third
patient illustrates the use of continuous compartment
pressure monitoring. He was a 19-year-old male with
a Tscherne Grade CP 9 tibial diaphyseal fracture sustained whilst playing football. Six hours after injury,
the fracture was reduced and stabilized with an
intramedullary nail and compartment monitoring was
commenced: His compartment pressure immediately
postoperatively was 45 m m H g (Ap 45 mmHg). The
patient was symptom-free after recovery from anaesthetic. Over the following 12 hours, the pressure rose
to 75 m m H g (Ap 15 mmHg) (Fig. 2) and the patient
developed some stretch pain. Fasciotomy was
performed and the surgical findings confirmed the
diagnosis (Fig. 3) with a marked reduction in compartment pressure (Fig. 2). Recovery was uneventful
and no sequelae of the acute compartment syndrome
were found 13 months after injury. This case illustrates that compartment monitoring allows the early
diagnosis of compartment syndrome.
In the group of 116 patients, a Ap of less than 30
mmHg was taken as an indication for decompression.
Fifty-three patients had compartment pressures of
greater than 30 m m H g and 30 of these had pressures
higher than 40 m m H g in the first 12 hours after injury,
but only one had a Ap of less than 30 m m H g and he
had a fasciotomy.
During the second 12 hours after injury, 28 patients
had pressures over 30 m m H g and seven had pressures
over 40 mmHg. Two patients had Ap levels of less
than 30 m m H g and underwent fasciotomy. None of

116 Current Orthopaedics

Fig. 2 Compartment monitoring trace of a patient with acute compartment

syndrome. Note the pressure of 75 mmHg in the anterior compartment,which
reduces to 15 mmHg after fasciotomy.

INDICATIONS FOR PRESSURE MONITORING

Fig. 3 Fasciotomyof the anterior and lateral compartmentsof

the patient in Figure 2 showingescape of the muscle groups, which
confirms the clinicaldiagnosis and monitoring findings.
the patients with a Ap of more than 30 m m H g had any
sequelae of the acute compartment syndrome at final
review. Had a compartment pressure of 3 0 m m H g
been the threshold for decompression, 50 patients
would have had an unnecessary fasciotomy. Even if a
higher threshold of 40 m m H g were used, 27 patients
would have had an unnecessary decompression.
Decompression of involved compartments should
be performed if the Ap level drops to less than 30
mmHg. It is safe to observe relatively high compartment pressures provided there is the protection of a
Ap level of greater than 30 mmHg. Continuous monitoring is essential until the Ap is steadily rising and the
compartment pressure is dropping, as there may be a
lag period between injury and the onset of muscle
ischaemia.

Currently accepted indications for pressure monitoring are the unconscious patient, 2s'41'42'46patients difficult
to assess such as young children, 25'32 patients with
equivocal symptoms and signs, especially in the presence of concomitant nerve injury, 28'5and patients with
multiple injury. 23 Compartment monitoring has also
been recommended for assessing the adequacy of
decompressive fasciotomy41and in patients 'at risk' of
compartment syndrome. Some author 1consider that
pressure monitoring should not replace clinical assessment, despite stating that clinical findings are wellknown to be unreliable, while others 24 feel that the
usefulness of pressure monitoring is limited because
most surgeons would find pressure monitoring cumbersome and the need for fasciotomy is readily apparent clinically. Despite this statement, this series had
five patients with complications of acute compartment syndrome caused by delay in decompression.
Of 25 tibial fractures complicated by acute compartment syndrome presenting to the Edinburgh
Orthopaedic Trauma Unit over a four-and-a-half-year
period, TM 13 patients underwent early continuous compartment monitoring and 12 either had no monitoring
performed or had a single pressure measurement carried out immediately before fasciotomy to confirm the
clinical diagnosis. The choice was dictated by surgeon
preference. The severity of injury was not statistically
different on comparing the two groups. At review
almost one year after injury, the monitored group
demonstrated no complications of acute compartment
syndrome. In contrast, in the non-monitored group,

Acute compartment syndrome in tibial fractures

there were 10 patients with complications of acute
compartment syndrome. There was an associated
dramatic reduction in delay in fasciotomy in the
monitored group.
This clearly demonstrates the effectiveness of compartment pressure monitoring in tibial fractures.
Compartment monitoring heightens awareness
amongst medical and nursing staff of the possibility
of the syndrome developing and acts as an 'early
warning system' for cases of impending compartment
syndrome. These factors combine to reduce delay and
to reduce the long-term sequelae.
Ideally, all tibial fractures should undergo compartment pressure monitoring and this is currently
part of the routine management of tibial fractures in
Edinburgh. It is recognized, however, that compartment monitoring may be a limited resource in some
centres and in these circumstances patients most at
risk should be monitored. In the context of tibial fractures, the younger patient is at risk of acute compartment syndrome and should undergo continuous
pressure measurements to reduce the incidence of
disabling consequences.

MANAGEMENT
The only reliable method of treating an established
acute compartment syndrome is surgical decompression by incision of overlying fascia or fasciotomy. No
other method has been documented which is either
sufficiently reliable or rapid in reducing compartment
pressures.
Impending acute compartment syndromes may on
occasions be aborted by release of external limiting
envelopes such as dressings or plaster casts.
Volkmann52 in 1881, was the first to note that tight
bandaging could cause paralysis and contractures in
the hands. Garfin and his colleagues53demonstrated a
65% reduction in intracompartmental pressure by
splitting and spreading a cast in experimentally elevated compartment pressures and a further 10%
reduction by splitting the underlying dressings. The
split-and-spread cast has also been shown to be the
only method of casting which can expand to accommodate increasing swelling in a limb24 In most cases,
however, splitting of a cast or dressings will not prevent progression from impending to established acute
compartment syndrome and fasciotomy is required.
Several techniques are available but whichever is
employed all authors agree that exposure of all four
compartments is necessary. 24,3~,5558
The double-incision, four-compartment fasciotomy58 is one of the most commonly used techniques in clinical practice. The anterior and lateral
compartments are approached through a longitudinal
incision placed just anteriorly to the fibular shaft and
the two posterior compartments through a longitudinal incision medial to the medial border of the tibia.

117

Generous skin incisions are important, as skin has

been reported to act as a limiting boundary for acute
compartment syndromes57,59and for this reason closed
fasciotomy is absolutely contraindicated in the acute
compartment syndrome.
Fasciotomy of all four compartments through a
single incision has been describe@ ~,56'6,~1and has the
advantage of improving the appearance of the leg in
the long term. Excision of the fibula was advocated
initially to expose all four compartments 55,~but this is
unnecessarily destructive, risks damage to the common peroneal nerve and removes and potentially
stabilizing influence of the fibula on a tibial fracture.
Single-incision fasciotomy of all four compartments without fibulectomy is performed through a
lateral incision which allows easy access to the anterior and lateral compartments. Anterior retraction of
the peroneal muscles then allows exposure of the
posterior intermuscular septum overlying the superficial posterior compartment. The deep posterior
compartment is entered by an incision immediately
posterior to the postero-lateral border of the fibula.
Double-incision fasciotomy is faster and, since the
fascial incisions are all superficial, is probably safer
than single-incision methods although both appear to
be equally effective in reducing compartment pressures. 58,62
Whichever technique is employed, it is essential to
obtain a clear and complete view of all four muscle
compartments. There is no indication for decompression of fewer than four compartments in acute compartment syndrome complicating tibial fracture.
Muscle viability must be assessed and necrotic tissue
excised. The skin and fascia must then be left open as
closure would restore a potential limiting envelope.
After 2448 hours, the leg should be inspected for any
further muscle necrosis. At this stage, secondary
closure or skin grafting may be performed.
The method of closure of fasciotomy wounds is a
cause for debate. Clearly, these would must never be
closed primarily. At the second inspection, if the
wounds are healthy, then they may be covered by split
skin graft. Occasionally, delayed closure is possible at
this stage but should never be attempted if there is any
tension on the skin edges.
Criticisms of the use of split skin grafting include
the need to immobilize the patient, and the inevitably
poor cosmetic result with poor sensation in a large
area of the leg. Methods of delayed primary closure
have been reported, most of which employ gradual
re-approximation of the skin edges using a shoe-lace
technique 63'~4and achieve cover within 5-11 days. This
is a longer period with an open wound than would be
expected with split skin graft coverage and raises concern about the possible introduction of hospitalacquired infection. Johnson and his co-authors ~5
found that 51% of patients who had secondary or primary closure of fasciotomy wounds had wound
complications, compared to only 5% who had split

118

Current Orthopaedics

skin graft cover, although they were employing a onestage secondary closure rather than a shoe-lace type
technique. It is recognized in open fractures that delay
in wound coverage leads to poorer results 66,67although
the soft tissue injury of an open fracture is not necessarily analogous to that in acute compartment
syndrome. Further studies need to be performed to
assess the safety of gradual closure of fasciotomy
wounds.
Provided fasciotomy is performed expeditiously
and wound healing is achieved without complications,
there seems to be little support for the possible development of chronic venous insufficiency at a later
stage. 68,69
It is now accepted practice that, in the presence of
an acute compartment syndrome, a tibial fracture
should be stabilized by internal or external fixation. 3~,7
This facilitates wound care and allows early mobilization of surrounding joints, thereby reducing the development of fibrosis and joint stiffness. Internal fixation
using an intramedullary nail where possible is preferable as this causes the least further disturbance to the
soft tissue and avoids the need for pins transfixing the
tissues, which may lead to added difficulty with
wound closure.

COMPLICATIONS
Complications of the acute compartment syndrome
occur when decompression is either late or inadequate
and include muscle contractures and paralysis leading
to deformity, sensory changes including pain, infection and delayed union of the tibial fracture. 17'~9
Muscle necrosis occurs initially and this is then
replaced by scar tissue, which causes the muscle contracture. The resultant deformity depends on the site
of contracture. In the deep posterior compartment,
involvement of the long toe flexors alone can cause
toe clawing but contracture of all the contained muscles can cause a fixed equinovarus deformity. 15'3'71In
the anterior compartment, the initial sign of necrosis
is a foot drop, which may then progress to contracture
of tibialis anterior and subsequent loss of plantarflexion of the ankle. Occasionally, isolated flexor hallucis
longus involvement can result in an extension contracture of the great toe. Deformity from lateral compartment involvement does not seem to occur, 72 while
deformity from superficial posterior contractures is
rare and causes an equinovarus deformity of the foot.
Assessment of the extent of muscle contractures
can be performed by CT 73 or MRI scanning.
Treatment is required in cases of persistent deformity
with disability and consists of a combination of
procedures including excision of scarred m u s c l e , TM tendon lengthening 7w" or tendon transfer. 7~Foot deformities cause serious disability and may require
arthrodesis to achieve a plantigrade foot. Amputation
may be indicated where muscle necrosis is so extensive

that useful function is precluded, in the presence of an

anaesthetic foot or for severe intractable pain.
Treatment of the complications of acute compartment syndrome is unrewarding and it is clear that the
prevention of complications by early diagnosis and
urgent decompression is of prime importance.
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