16: Acute Compartment Syndrome

Margaret M. McQueen, Andrew D. Duckworth

Introduction to Acute Compartment Syndrome
Acute compartment syndrome (ACS) occurs when pressure rises within a confined space in
the body, resulting in a critical reduction of the blood flow to the tissues contained within the
space.7,8,69,105,106,114 Without urgent fasciotomy and decompression of the affected
compartments,43,54,78,114 tissue ischemia and necrosis will lead to permanent functional
disability.110,116,159,173 The ACS should be differentiated from other related conditions, so
awareness of the different definitions associated with a compartment syndrome is important.
ACS is defined as the elevation of intracompartmental
pressure (ICP) to a level and for a duration that without
decompression will cause tissue ischemia and necrosis.
Exertional compartment syndrome is the elevation of ICP
during exercise, causing ischemia, pain, and rarely
neurologic symptoms and signs. It is characterized by
resolution of symptoms with rest but may proceed to ACS
if exercise continues.
Volkmann's ischemic contracture is the end stage of
neglected ACS with irreversible muscle necrosis leading
to ischemic contractures.190
The crush syndrome is the systemic result of muscle
necrosis commonly caused by prolonged external
compression of an extremity. In crush syndrome, muscle
necrosis is established by the time of presentation, but
ICP may rise as a result of intracompartmental edema,
causing a superimposed ACS.
History
Well over a century has passed since the first description of ischemic muscle contractures
was published in the medical literature. The first report of the condition was attributed to
Hamilton in 1850 by Hildebrand,77 but Hamilton's original description has never been found.
The credit for the first full description belongs to Richard Von Volkmann who published a
summary of his views in 1882.190 He stated that paralysis and contractures appeared after too
tight bandaging of the forearm and hand, were ischemic in nature, and were caused by
prolonged blocking of arterial blood. He recognized that muscle cannot survive longer than 6
hours with complete interruption of its blood flow and that 12 hours or less of too tight
bandaging were enough to result in “dismal permanent crippling.” In 1888,
Peterson149 recognized that ischemic contracture could occur in the absence of bandaging but
did not postulate a cause.
The first major reports appeared in the English-speaking literature in the early 20th century.
At this time, it was suggested that swelling after removal of tight bandaging might contribute
to the contracture and that the contracture was caused by “fibrous tissue–forming elements”
or a myositic process.39,162,195 By the early part of the 20th century, published accounts of the
sequence of events in ACS were remarkably similar to what is known today, with
differentiation between acute ischemia caused by major vessel rupture, acute ischemia
caused by “subfascial tension,” the late stage of ischemic contracture, and the separate
concept of nerve involvement.11 This paper was the first description of fasciotomy to relieve
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the pressure. The importance of early fasciotomy was suggested at this time11,135 and
confirmed by prevention of the development of contractures in animal experiments. 83
During the Second World War, attention was directed away from these sound conclusions. A
belief arose that ischemic contracture was caused by arterial injury and spasm with reflex
collateral spasm. Successful results from excision of the damaged artery46,60 were
undoubtedly owing to the fasciotomy carried out as part of the exposure for the surgery. An
unfortunate legacy of this belief persists today in the dangerously mistaken view that an ACS
cannot exist in the presence of normal peripheral pulses.
The arterial injury theory was challenged by Seddon in 1966. 167 He noted that in all cases of
ischemic contracture, there was early and gross swelling requiring prompt fasciotomy, and
that 50% of his cases had palpable peripheral pulses. He was unable to explain muscle
infarcts at the same level as the injury on the basis of arterial damage. He recommended early
fasciotomy.
In their classic paper, McQuillan and Nolan121 reported on 15 cases complicated by “local
ischemia.” They described the vicious cycle of increasing tension in an enclosed
compartment causing venous obstruction and subsequent reduction in arterial inflow. Their
most important conclusion was that delay in performing a fasciotomy was the single cause of
failure of treatment.
Epidemiology
The epidemiology of ACS is invaluable for identifying high-risk patients who benefit from
increased clinical vigilance and ICP monitoring, with the aim to decrease the time to
definitive diagnosis and fasciotomy.37 Areas of the body commonly involved are the lower
leg20,64,116,161 and forearm.19,52,86,148 The incidence in the Western World is 3.1/100,000
population per year,120 with males more frequently affected than females (10:1; males
7.3/100,000, females 0.7/100,000).86,120 The mean age is approximately 32 years, with males
being younger than females (30 years vs. 44 years).120,128,181 Youth has been found to be the
most important risk factor for developing ACS, possibly due to the relatively high muscle
bulk in a fixed compartment, and thus a reduced capacity for swelling in these patients. Older
patients often have reduced muscle bulk secondary to sarcopenia, with an associated
increased perfusion pressure due to hypertension, which could potentially explain the
protective effects of increasing age. The age- and gender-specific incidences are illustrated
in Figure 16-1, demonstrating a type B pattern or the L-shaped pattern described by Buhr and
Cooke.24 The mean age for the whole group was 32 years; the median age for males was 30
years and for females 44 years.
Figure 16-1 The annual age- and gender-specific incidence of acute compartment
syndrome.

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The underlying condition causing ACS is most commonly a fracture (69% of cases) (Table
16-1). Similar figures have been reported in children, with 76% of cases caused by fracture,
predominantly tibial diaphyseal, distal radius, and forearm. 10 The most common fracture
associated with ACS in adults is tibial diaphyseal fracture. Fractures of the tibial diaphysis
make up a third of all presentations,120 with the prevalence of ACS found to range from 2.7%
to 15%,3,17,30,44,117,120,134,175,201 with the differences in prevalence likely to be because of
different diagnostic techniques and selection of patients. Although initial studies suggested
that intramedullary tibial nailing could be associated with an increased rate of
ACS,92,125,134,185,186,201 this has since been disproved115,186 with large studies in patients with
fracture of the tibia suggesting that youth, males, and diaphyseal fractures are key risk factors
for developing ACS.114,147 However, recent data have reported a high rate of ACS following
fractures of the tibial plateau (12% vs. 3% for shaft fractures),5 with the Schatzker VI
fracture type particularly high risk.5,208
TABLE 16-1
Conditions Associated with Injury Causing Acute Compartment Syndrome Presenting to an
Orthopedic Trauma Unit
Underlying Condition % of Cases
Tibial diaphyseal fracture 36
Soft tissue injury 23.2
Distal radius fracture 9.8
Crush syndrome 7.9
Diaphyseal fracture forearm 7.9
Femoral diaphyseal fracture 3.0
Tibial plateau fracture 3.0
Hand fracture(s) 2.5
Tibial pilon fractures 2.5
Foot fracture(s) 1.8
Ankle fracture 0.6
Elbow fracture dislocation 0.6
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Underlying Condition % of Cases
Pelvic fracture 0.6
Humeral diaphyseal fracture 0.6
The second most common cause of ACS is soft tissue injury, which when added to tibial
diaphyseal fracture makes up almost two-thirds of the cases. The second most common
fracture to be complicated by ACS is the distal radius fracture. It occurs in approximately
0.25% of cases. Forearm diaphyseal fractures are complicated by ACS in 3% of cases. The
prevalence of ACS in other anatomic locations is rarely reported. Other less common causes
of ACS are listed in Table 16-2.
TABLE 16-2
Causes of Acute Compartment Syndrome
Conditions Increasing the Volume of Compartment Contents
Fracture
Soft tissue injury
Crush syndrome (including use of the lithotomy position)84
Revascularization
Exercise94
Bleeding diathesis/anticoagulants66,124
Fluid infusion (including arthroscopy)10,132
Arterial puncture133
Ruptured ganglia/cysts30
Osteotomy45
Snake bite152
Nephrotic syndrome146
Leukemic infiltration151
Viral myositis78
Acute hematogenous osteomyelitis144
Conditions Reducing Compartment Volume
Burns
Repair of muscle hernia4
Medical Comorbidity
Diabetes21
Hypothyroidism67
From adolescence, younger patients are at more risk of compartment syndrome. In tibial
diaphyseal fracture, the prevalence of ACS was reported as being three times greater in the
under 35-year-old age group, and in distal radial fractures, the prevalence is 35 times less in
the older age group.120 Adolescents have been recognized as having a high rate (8.3%) of
compartment syndrome after tibial fracture. 30 More recently, in a cohort of 212 children with
tibial diaphyseal fractures and a median age of 13 years, a prevalence of 11.4% was reported.
In the group older than 14 years who were injured in a motor vehicle accident, the prevalence
was 48%.175
In a retrospective case series from the Edinburgh Orthopaedic Trauma Unit of 1,388 patients
who sustained an acute tibial diaphyseal fracture and a rate of ACS of 11.5% (n = 160),
multivariate regression analysis revealed that age was the strongest factor associated with the
development of ACS, with the highest prevalence in the second and third decades, and with
all other factors strongly confounded by age.119 This is supported by other studies that have
found that the prevalence of ACS is three times greater in patients <35 years of age, 120 and
that adolescents have an increased rate of ACS following a fracture of the tibia, 30 particularly
after high-energy mechanisms such as a motor vehicle accident. 175 The only exception to
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youth being a risk factor in ACS is in cases with soft tissue injury only. These patients have
an average age of 36 years and are significantly older than those with a fracture. 79
Despite the commonly held perception that open fractures and high-energy injuries are
associated with a diagnosis of ACS, the literature supports a high rate of ACS following
closed low-energy fractures of the tibial diaphysis. 17,34,117,120 High-energy injury is generally
believed to increase the risks of developing an ACS. Nevertheless, in tibial diaphyseal
fracture in adults complicated by ACS, the proportion of high- and low-energy injury shows
a slight preponderance of low-energy injury (59%).120 In the same population, there are an
equal number of high- and low-energy injuries in tibial diaphyseal fractures uncomplicated
by ACS.31 Adolescents may be an exception to this because of the high prevalence of 48%
reported in teenagers after road accidents.175 In the larger Edinburgh series, there was an
increased risk of ACS in closed compared with open fractures (p < 0.05). This suggests ACS
may be more prevalent after low-energy injury, possibly because in low-energy injury the
compartment boundaries are less likely to be disrupted and an “autodecompression” effect is
avoided.
High-energy injuries such as sports, a fall from height, and a motor vehicle accident account
for less than 50% of all ACS cases secondary to a fracture of the tibial diaphysis, 120with these
modes of injury accounting for ~50% of tibial diaphyseal fractures that do not develop
ACS.31 Similar findings in the literature are found for closed versus open fractures of the
tibia, with not only closed fractures but lower Gustilo and Anderson grade fractures more
commonly associated with ACS.120 It is important to note that open tibial diaphyseal
fractures remain at risk of ACS, which occurs in approximately 3%, 120 but it appears that the
lower Gustilo types are at more risk, again possibly because of the lack of disruption of the
compartment boundaries. Despite this, the literature does support an increased rate of ACS
following high-energy fractures of the femur and forearm, likely because of the higher rate of
young males who have these types of injuries.86,120,151,166
Other fractures associated with developing ACS are forearm diaphyseal fractures (prevalence
3%) and fractures of the distal radius (prevalence 0.25%). Distal radial and forearm
diaphyseal fractures associated with high-energy injury are more likely to be complicated by
ACS, probably because of the high preponderance of young males who sustained these types
of injuries. This is illustrated by a comparison of the age- and gender-related incidence of
distal radius fractures complicated by ACS (Fig. 16-2). The likely explanation for the
preponderance of young patients with ACS is that the young have relatively large muscle
volumes, whereas their compartment size does not change after growth is complete. Thus,
younger patients may have less space for swelling of the muscle after injury. Presumably, the
older person has smaller hypotrophic muscles allowing more space for swelling. There may
also be a protective effect of hypertension in the older patient.
Figure 16-2 The annual age-specific incidence of all distal radius fractures compared
with the annual age-specific incidence of acute compartment syndrome in distal radial
fractures.

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 Although fracture is the most common cause, it is key to appreciate that almost a quarter of
all cases follow an isolated soft tissue injury,79,86,120 with some cases having no clear history
of preceding injury. The majority of these arise subsequent to soft tissue injury, particularly a
crushing-type injury, but some arise with no preceding history of trauma. 79 In children, 61%
of cases of ACS in the absence of fracture are reported as being iatrogenic. 152 Potential
precipitating causes include crush syndrome, crush injuries, a drug overdose, and
anticoagulation medications, for example, warfarin
therapy.40,47,51,52,120,123,124,128,130,154,166 Patients with ACS without fracture tend to be older and
have more medical comorbidities than those with a fracture. They are more evenly
distributed between the genders with a male to female ratio of five to one.
The possible risk factors for the development or late diagnosis of ACS are listed in Table 16-
3. A delay in the time to diagnosis of ACS has been associated with inexperience, regional or
general anesthesia (GA), polytrauma cases, injuries to the soft tissues, as well as relying
solely on the clinical symptoms and signs to make the diagnosis of
ACS.33,67,101,114,124,133,155,156,188 Patients with polytrauma are at particular risk of delay in the
diagnosis of their ACS, so identification of at-risk factors in this group is of particular
importance.48
TABLE 16-3
The Risk Factors for the Development or Late Diagnosis of ACS
Risk Factors for Developing ACS
Age (youth)
Fracture of the tibia
High-energy femoral shaft fracture
High-energy fracture(s) of the forearm
Clotting abnormalities, e.g., warfarin
• Polytrauma patients
↑ Lactate/base deficit
Transfusion
Risk Factors for a Delay in the Diagnosis of ACS
Reliance on clinical signs alone
Children
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Patients with learning disabilities
Associated neurologic injury
Reduced/altered conscious level
Regional anesthesia
Patient-controlled analgesia

Adapted with permission from Duckworth AD, McQueen MM. The diagnosis of acute
compartment syndrome: a critical analysis review. JBJS Rev. 2017;5(12):e1 .
Kosir et al. reported a rate of 20% for lower limb ACS in 45 critically injured patients and
found that a high lactate level, an increased base deficit, and a requirement for transfusion
were associated with the development of the condition. 91 A systematic review on the use of
regional anesthesia or patient-controlled analgesia and ACS found no clear delay in the time
to diagnosis, although the literature was very limited in terms of size and design and further
data in this area is clearly needed. 36
Pathogenesis
There remains uncertainty about the exact physiologic mechanism of the reduction in blood
flow in the ACS, although it is generally accepted that the effect is at small vessel level,
either arteriolar, capillary, or venous levels.
The critical closing pressure theory states that there is a critical closing pressure in the small
vessels when the transmural pressure (TM) (the difference between intravascular pressure
and tissue pressure) drops.25 TM is balanced by a constricting force (TC) consisting of active
and elastic tension derived from smooth muscle action in the vessel walls. The equilibrium
between expanding and contracting forces is expressed in a derivation of Laplace law: TM =
RC ÷ r, where r is the radius of the vessel.
If, because of increasing tissue pressure, the TM drops to a level such that elastic fibers in the
vessel wall are no longer stretched and therefore cannot contribute any elastic tension, then
there will be no further automatic decrease in the radius. TC ÷ r then becomes greater than
TM and active closure of the vessel will occur. This concept has been verified in both animal
and human local vascular beds.7,141,158,206 Ashton8 was the first to relate these findings to ACS
and concluded that whatever the cause of the raised tissue pressure, blood flow will be
decreased and may temporarily cease altogether as a result of a combination of active
arteriolar closure and passive capillary compression, depending on vasomotor tone and the
height of the total tissue pressure. Critics of this theory doubt the possibility of maintaining
arteriolar closure in the presence of ischemia, which is a strong local stimulus for
vasodilatation.106 Ashton noted that flow resumes after 30 to 60 seconds of maintained tissue
pressure and attributes this to vessel reopening possibly because of an accumulation of
vasodilator metabolites.7
A second theory is the arteriovenous (AV) gradient theory. 106,111 According to this theory, the
increases in local tissue pressure reduce the local AV pressure gradient and thus reduce the
blood flow. When flow diminishes to less than the metabolic demands of the tissues (not
necessarily to zero), then functional abnormalities result. The relationship between AV
gradient and the local blood flow (LBF) is summarized in the equation: LBF = (Pa − Pv) ÷ R,
where Pa is the local arterial pressure, Pv is the local venous pressure, and R is the local
vascular resistance. Veins are collapsible tubes and the pressure within them can never be
less than the local tissue pressure. If tissue pressure rises as in the ACS, then the Pv must also
rise, thus reducing the AV gradient (Pa − Pv) and therefore the LBF. At low AV gradients,
compensation from R is relatively ineffective74 and LBF is primarily determined by the AV
gradient. Matsen et al. presented results on human subjects demonstrating reduction of the
AV gradient with elevation of the limb in the presence of raised tissue pressure.111 This
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theory has been supported by work that demonstrated that with external pressure applied,
simulating ACS, venous and capillary flow ceased, but arterioles were still capable of
carrying flow.191 This disproves the critical closing theory but supports the hypothesis of
reduced AV gradient as the mechanism of reducing blood flow.
A third theory, the microvascular occlusion theory, postulates that capillary occlusion is the
main mechanism reducing blood flow in ACS.65 Measurement of capillary pressure in dogs
with normal tissue pressures revealed a mean level of 25 mm Hg. Hargens et al. suggested
that a tissue pressure of similar value is sufficient to reduce capillary blood flow.65 Resultant
muscle ischemia leads to increased capillary membrane permeability to plasma proteins,
increasing edema and obstruction of lymphatic by the raised tissue pressure. Nonetheless, the
authors admitted that reactive hyperemia and vasodilatation both tend to raise the critical
pressure level for microvascular occlusion. However, this work was done in the presence of
normal tissue pressures and it has also been pointed out that capillaries are collapsible
tubes106 and their intravascular pressure ought to rise in the presence of raised tissue pressure.
Hargens' theory65 is supported by work demonstrating reduction of the number of perfused
capillaries per unit area with raised tissue pressures. 69
Effects of Raised Tissue Pressure on Muscle
Regardless of the mechanism of vessel closure, reduction in blood flow in the ACS has a
profound effect on muscle tissue. Skeletal muscle is the tissue in the extremities most
vulnerable to ischemia and is therefore the most important tissue to be considered in ACS.
Both the magnitude and duration of pressure elevation have been shown experimentally to be
important influences in the extent of muscle damage.
There is now universal agreement that rising tissue pressure leads to a reduction in muscle
blood flow. A number of experimental studies have highlighted the importance of perfusion
pressure as well as tissue pressure in the reduction of muscle blood flow. MR measurements
of cellular metabolic derangement (pH, tissue oxygenation, and energy stores) and histologic
studies, including electron microscopy and videomicroscopy studies of capillary blood flow,
have shown that critical tissue pressure thresholds are 10 to 20 mm Hg below diastolic blood
pressure or 25 to 30 mm Hg below mean arterial pressure.69,72,76,103 Increased vulnerability in
previously traumatized or ischemic muscle has been demonstrated when the critical threshold
may occur at tissue pressures more than 30 mm Hg below mean arterial pressure. 13
The ultimate result of reduced blood flow to skeletal muscle is ischemia followed by
necrosis, with general agreement that increasing periods of complete ischemia produce
increasing irreversible changes.71,93,150 Evidence indicates that muscle necrosis is present in
its greatest extent centrally in the muscle, and that external evaluation of the degree of
muscle necrosis is unreliable. The duration of muscle ischemia dictates the amount of
necrosis, although some muscle fibers are more vulnerable than others to ischemia. For
example, the muscles of the anterior compartment of the leg contain type I fibers or red slow
twitch fibers, whereas the gastrocnemius contains mainly type II or white fast twitch fibers.
Type I fibers depend on oxidative metabolism of triglycerides for their energy source and are
more vulnerable to oxygen depletion than type II fibers whose metabolism is primarily
anaerobic.97 This may explain the particular vulnerability of the anterior compartment to
raised ICP.
Effects of Raised Tissue Pressure on Nerve
There is little dispute about the effects of raised tissue pressure on neurologic function. All
investigators note a loss of neuromuscular function with raised tissue pressures but at varying
pressure thresholds and duration.53,66,105,174 In a study on human neurologic function, Matsen
et al. found considerable variation of pressure tolerance that could not be attributed to

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differences in systemic pressure.107 The mechanism of damage to nerve is yet to be
definitively determined and could result from ischemia, ischemia plus compression, toxic
effects, or the effects of acidosis.
Effects of Raised Tissue Pressure on Bone
Nonunion is recognized as a complication of ACS. 32,34,87,117,125 It was first suggested by Nario
in 1938 that “Volkmann's disease” caused obliteration of the “musculodiaphyseal” vessels
and caused frequent pseudarthrosis.139 McQueen observed a reduction in bone blood flow
and bone union in rabbit tibiae after an experimentally induced ACS.114 It is likely that
muscle ischemia reduces the capacity for development of the extraosseous blood supply on
which long bones depend for healing.
Reperfusion Injury
The reperfusion syndrome is a group of complications following reestablishment of blood
flow to the ischemic tissues and can occur after fasciotomy and restoration of muscle blood
flow in the ACS. Reperfusion is followed by an inflammatory response in the ischemic tissue
that can cause further tissue damage. The trigger for the inflammatory response is probably
the breakdown products of muscle.16 Some breakdown products are procoagulants that
activate the intrinsic clotting system. This results in increasing microvascular thrombosis,
which in turn increases the extent of muscle damage.
If there is a large amount of muscle involved in the ischemic process, the inflammatory
response may become systemic. In ACS, this is most likely to occur in the crush syndrome.
Procoagulants escape into the systemic circulation and produce systemic coagulopathy with
parallel activation of inflammatory mediators. These then damage the vascular endothelium,
leading to increased permeability, transcapillary fluid leakage and subsequent worsening of
ICP,59 and eventually multiple organ failure. Systemic clotting and the breakdown products
of dead and dying cells also lead to activation of white blood cells, with the release of
additional inflammatory mediators such as histamine, interleukin, oxygen-free radicals,
thromboxane, and many others.16 This is the basis for the use of agents such as antioxidants,
antithromboxanes, antileukotrienes, and antiplatelet-activating factors that modify the
inflammatory process. Some of these agents have been shown in the laboratory to be capable
of reducing muscle injury.1,88,89,193
Diagnosis of Acute Compartment Syndrome
Prompt diagnosis of ACS is the key to a successful outcome. Delay in diagnosis has long
been recognized as the single cause of failure of the treatment of ACS. 104,121,159,161 A delay in
the time to diagnosis of ACS has been associated with relying solely on the clinical
symptoms and signs to make the diagnosis of ACS, among a range of other
factors.33,67,101,114,124,133,155,156,188 Despite this, many centers still utilize clinical symptoms and
signs alone for the diagnosis. One series from a level 1 trauma center found ICP monitoring
was employed as the primary diagnostic instrument in 11.7% of 386 fractures of the tibial
diaphysis.142 Furthermore, a very recent survey of US trauma surgeons also found that
physical examination should be utilized in the awake patient, with monitoring useful in the
obtunded or unconscious patient.27
Delay in treatment of the ACS can be catastrophic, leading to serious complications such as
permanent sensory and motor deficits, contractures, infection, and at times, amputation of the
limb.134,152,161 In serious cases, there may be systemic injury from the reperfusion syndrome.
A clear understanding of the clinical techniques necessary to make an early diagnosis is
therefore essential to any physician treating ACS to avoid such complications. As well as
improving outcome, early recognition and treatment of ACS are associated with decreased
indemnity risk in potential malpractice claims. 15
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Clinical Diagnosis
The symptoms and signs indicative of an ACS are swelling, pain on passive stretch, pain out
of proportion to the injury, paresthesia, and paralysis. Peripheral pulses and capillary return
are always intact in ACS. Absent peripheral pulses, pallor, and reduced capillary return are
late clinical signs of ACS and will be associated with a vascular injury requiring an
angiogram, or an established ACS where amputation is often inevitable. 114 Conversely, it is
dangerous to exclude the diagnosis of ACS because distal pulses are present.
Pain
Pain is the first symptom of ACS in the awake and alert patient. 188 The pain experienced by
the patient is by nature ischemic and usually severe and out of proportion to the clinical
situation and the apparent extent of the injury, with increasing analgesia requirements
common. However, pain is very subjective and can be an unreliable symptom, with cases
documented in the literature of ACS occurring in the absence of pain.9 Pain can be
influenced by psychosocial factors such as anxiety,192 is almost universal following injury, is
of variable intensity,40,106 for example, when it involves the deep posterior
compartment,104,106 and could be even nonexistent with an associated nerve
injury.78,205 Assessment can be very difficult in children or patients with learning disabilities
where agitation and analgesia requirements are important to asssess, 10 and cannot be assessed
at all in the presence of regional anesthesia or in the unconscious patient.33,67,133
Pain has been found to have a very low sensitivity (13%) with a good specificity (97%),
which equates to a large percentage of false-negative or missed cases, although with a small
percentage of false-positive cases.40,104,116,188,205 There is general agreement, however, that
pain, if present, is a relatively early symptom of ACS in the awake alert patient. 188 Increasing
requirements for opiates should also be considered in assessing the severity of pain.
Pain with passive stretch of the muscles involved is recognized as a symptom of ACS. Pain
is increased, for example, in an anterior compartment syndrome when the toes or foot are
plantarflexed. This symptom is no more reliable than rest pain because the reasons for
unreliability quoted above apply equally to pain on passive stretch. Pain on passive stretch of
the muscle compartment involved has analogous diagnostic performance characteristics as
the same confounding factors listed above also apply (see Table 16-3).9,188,205
Paresthesia
Paresthesia and hypesthesia may occur in the territory of the nerves traversing the affected
compartment and are usually the first signs of nerve ischemia, although sensory abnormality
may be the result of concomitant nerve injury. 201,205 Some authors have advocated that
paresthesia or hypesthesia could be the optimal sign for diagnosing ACS132 but it is now
established as a late sign161 with a very low sensitivity (13%) despite very good specificity
(98%).188 This rate of false negatives excludes paresthesia as an accurate diagnostic indicator.
Reduced or absent sensation could be associated with nerve ischemia within the involved
compartment or concomitant injury.157,205
Paralysis
Paralysis of muscle groups affected by the ACS is recognized as being a late sign of
established ACS where irreversible injury to the soft tissues has occurred. Paralysis prior to
fasciotomy is a poor prognostic indicator in ACS, 20,34,38,159,166,203 with Bradley reporting that
only 13% of patients fully recovered.20 The literature also suggests it is the worst clinical
symptom or sign in terms of combined sensitivity and specificity, 188 probably because of the
difficulty of interpreting the underlying cause of the weakness, which could be inhibition by
pain, direct injury to muscle, or associated nerve injury. 41
Swelling
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Palpable swelling in the compartment affected may be a further sign of compartment
syndrome and visible swelling is almost universally seen, although the degree of swelling is
difficult to assess accurately, making this sign very subjective. Assessment is routinely
inadequate because of cast immobilization, as well as deep compartments being difficult to
assess.104,132 Although sensitivity is higher than for other clinical symptoms and signs (54%),
the specificity (76%) and negative predictive value (63%) are far inferior.
Diagnostic Performance Characteristics
Although the literature is clear that employing a combination of clinical symptoms and signs
raises the sensitivity for diagnosing ACS,188 this is not practical. Ulmer et al. carried out a
systematic review of four studies (132 cases) to determine the diagnostic performance
characteristics of the four commonly quoted symptoms and signs associated with ACS
including pain on passive stretch, pain, paralysis, and paresthesia. He found that the
sensitivity of each of the four symptoms and signs was low and that all were better at
discounting rather than corroborating the diagnosis. One positive sign resulted in the odds of
a case of confirmed ACS to be less than 26%. To achieve a probability of over 90% of ACS
being present, however, three clinical findings must be noted. The third clinical finding is
paresis; thus, to achieve an accurate clinical diagnosis of ACS, the condition must be allowed
to progress until a late stage. This is clearly unacceptable and has led to a search for earlier,
more reliable methods of diagnosis. Kosir et al. abandoned clinical examination as part of
their screening protocol for critically ill trauma patients because of the difficulty in eliciting
reliable symptoms and signs in this group,91 while both Shereff172 and Myerson137 state that
clinical diagnosis of ACS in the foot is so unreliable that other methods should be used.
Compartment Pressure Monitoring
Several techniques were developed to measure ICP once it was appreciated that ACS was
caused by increased tissue pressure within the affected compartment (Table 16-4). Because
raised tissue pressure is the primary event in ACS, changes in ICP will precede the clinical
symptoms and signs.96,115
TABLE 16-4
The Advantages and Disadvantages of the Currently Available ICP Monitoring Techniques
Used in the Diagnosis of Acute Compartment Syndrome
Method Advantages Disadvantages
Accuracy limited with false
positives/negatives
Invasive indirect measure
Continuous measurement
unfeasible
Needle tip may block
Simple technique Fluid infusion can cause clinical
Needle manometer Low cost picture to deteriorate
Good accuracy with high Invasive indirect measure
surface area Blockage at air/fluid junction
Blockage of catheter possible
uncommon Wick material retention possible
Continuous monitoring Transducer must be at catheter
Wick catheter feasible level
Good accuracy
Transducer-tip Continuous monitoring Increased costs
intracompartmental catheter feasible Resterilization necessary
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Method Advantages Disadvantages
Transducer level not
important
Invasive indirect measure
Catheter may block
Good accuracy with high Air bubble can lead to false low
surface area reading
Continuous monitoring Transducer must be at catheter
Slit catheter feasible level
Good accuracy and
correlation Increased costs
Continuous monitoring Not yet clearly validated for ACS
feasible Measurement dependent on soft
Near-infrared spectroscopy Noninvasive technique tissue depth

Reproduced with permission from Duckworth AD, McQueen MM. The diagnosis of acute
compartment syndrome: a critical analysis review. JBJS Rev. 2017;5(12):e1 .
Noninvasive Techniques
The common invasive methods of measuring ICP are an indirect way of measuring muscle
blood flow and oxygenation. Assessment of the ICP using modern noninvasive techniques
has undeniable advantages and potential, but the use of these methods is still to be adequately
validated in the literature. Near-infrared spectroscopy uses a probe placed on the skin to
measure tissue oxygen saturation noninvasively. This has been shown to correlate well with
the tissue pressure in both experimental6,23 and human55,178 studies, with recent data from a
case-control study of 109 patients demonstrating some positive results, but with further
validation required.180 In patients with ACS, the reduction in oxygenation values compared to
the opposite uninjured leg has been shown to correlate with reducing perfusion pressures but
a critical level has not yet been established. 178 It has also been used to demonstrate the
hyperemic response to injury in tibial fractures. 179
Ultrasound scanning detects waveforms secondary to fascial displacement by the arterial
pulse, leading to efforts to try and correlate with ICP readings ranging greater than 30 mm
Hg with fascial displacement in healthy volunteers. The sensitivity of this technique has been
reported at 77%, with a specificity of 93%.98 The primary limitation of this technique is the
reduction in sensitivity with a hypotensive patient.
Invasive Techniques
The pros and cons of each invasive monitoring technique are found in Table 16-4. One of the
first invasive techniques used a needle manometer,108,110,198 where a needle is introduced into
the compartment and connected to a column filled partly with saline and partly with
air.199 The ICP is calculated through the accompanying manometer and is the pressure that is
required to inject air into the tubing and flatten the meniscus between the saline and the air.
Matsen et al. developed a modified technique using an infusion of saline into the
compartment, with the ICP measured as the pressure resistance to the infusion of the
saline.108 The needle manometer is a simple and inexpensive method but has some
drawbacks. A danger exists of too large a volume being infused, possibly inducing ACS. It is
probably the least accurate of the measurement techniques available, with falsely high values
having been recorded in comparison with other techniques126 and falsely low values in cases
of very high ICP.183 A needle with only one perforation at its tip also can become easily
blocked.

892
The wick catheter was first described for use in ACS by Mubarak et al.129 This is a
modification of the needle technique, in which fibrils protrude from the bore of the catheter
assembly.129,132 This allows a large surface area for measurement and prevents obstruction of
the needle, as well as being ideal for continuous measurement. A disadvantage of this
technique is the possibility of a blood clot blocking the tip or air in the column of fluid
between the catheter and the transducer, which will dampen the response and give falsely
low readings. There is a theoretical risk of retention of wick material in the tissues.
The slit catheter was first described by Rorabeck et al. and is similar to the wick catheter
technique.126,160,171 It is designed to increase the surface area at the tip of the catheter by
means of being cut axially at the end of the catheter (Fig. 16-3).160 The interstitial pressure is
measured through a column of saline attached to a transducer. The patency of the catheter
can be tested once it is in situ by applying light pressure to the compartment, which should
result in an immediate elevation of the ICP reading. Care must be taken to avoid the presence
of air bubbles or any blockage in the system as this can, like the wick catheter, result in
falsely low readings. The literature would suggest that the slit catheter has superior accuracy
to the continuous infusion method,126 with comparable accuracy to the wick catheter. 171
Figure 16-3 The tip of a slit catheter, which can be made easily from standard
equipment by cutting two slits in the tip of the catheter.

Attempts to improve the reliability of ICP measurement led to the placement of the pressure
transducer directly into the compartment by siting it within the lumen of a catheter. The solid
state transducer intracompartmental catheter (STIC) was described in 1984112,113,204 and
utilizes a pressure transducer located directly within the catheter lumen, with good
correlations reported when compared to the conventional techniques.112 This device is now
commercially available and widely used, although to retain patency of the catheter for
continuous monitoring, an infusion must be used with its attendant problems. The alternative
is intermittent pressure measurements, which is likely to cause significant discomfort to
patients and is more labor intensive. Newer systems with the transducer placed at the tip of
the catheter do not depend on a column of fluid and therefore avoid the problems of
patency.204
The Stryker ICP monitor (Stryker, Kalamazoo, MI) is a commercially available device for
compartment pressure monitoring, although the accuracy of the device has been shown to be
somewhat limited in a study analyzing interobserver variability in four above-knee cadaveric
lower leg ACS models.94 Boody et al. analyzed the accuracy of three ICP monitoring
apparatuses (Whitesides' apparatus, ICP pressure monitor by Stryker©, arterial line
893
manometer) using an in vitro ovine muscle model18 and found that all three had a good
correlation between the computed and measured ICPs.
One study assessed 26 patients with suspected ACS (97 compartments) to contrast the STIC
technique with the modified Whitesides' needle and an electronic transducer–tipped
catheter.28 The authors reported a correlation coefficient of 0.83 and determined that despite
the techniques being similar in terms of ICP readings, reliability for ICP monitoring in the
trauma setting was not established, particularly when utilized for one-off ICP
measurements.28
Catheter Placement
Recommended catheter placement for each of the anatomic areas is summarized in Table 16-
5. Careful placement of the catheter within the affected compartment is carried out using a
strict aseptic technique.197 The literature would suggest that when there is an associated
fracture, the catheter tip should lie within 5 cm of the level of the fracture to obtain the peak
measure of the ICP reading within the compartment (Fig. 16-4).73,103,114,163 Conversely, some
authors have suggested that tip placement at the fracture level results in inaccurately high
ICP readings due to the fracture hematoma.68 It is important that the level of the transducer is
secured at the level of the compartment being measured due to changes in the reading with
height.
TABLE 16-5
Recommended Catheter Placements for Compartmental Pressure Monitoring
Anatomic Area Catheter Placement
Thigh Anterior compartment
Anterior compartment
Leg Deep posterior if clinically suspected
Interosseous compartments
Foot Consider calcaneal compartment in hindfoot injuries
Forearm Flexor compartment
Hand Interosseous compartment
Figure 16-4
Estimation of the entry point (arrow) on the anteroposterior radiograph of a midshaft
tibial diaphyseal fracture.
The entry point should be proximal to the fracture site and 1 to 2 cm lateral to the lateral
subcutaneous border of the tibia.
(Reproduced with permission from Duckworth AD, McQueen MM. Continuous
intracompartmental pressure monitoring for acute compartment syndrome. JBJS Essential
Surg Techn. 2013;3(3):e13 .)

894
The leg anterior compartment is recommended due to evidence suggesting it is the most
commonly involved compartment and is readily accessible, 3,117 although placement here will
not detect an increased ICP in the other compartments. Concomitant ICP monitoring in the
deep posterior compartment is suggested by some to reduce the chance of missing an isolated
deep ACS, although this is difficult and cumbersome for the patient.73,104 A more rational
approach is to monitor the deep compartment when the clinical picture is suggestive of that
compartment being involved. As with the leg, monitoring the anterior compartment of the
thigh is advised due to frequent involvement,122–124,166,184 with isolated posterior thigh ACS
documented in the literature.99 For cases of suspected foot ACS, ICP monitoring of the
interosseous compartments is advocated by some, with the calcaneal compartment being
monitored in hindfoot injuries.47,136,138 For the upper limb, the forearm is one of the most
commonly involved sites, with volar compartment placement
recommended.19,40,52,80,86,151,182 The rare isolated dorsal ACS requires placement in the
extensor compartment.86 The anterior compartment of the arm and the hand interosseous
compartments are the other recommended sites in the upper limb.35,63,114,151
Threshold for Decompression in Acute Compartment Syndrome
Much debate has occurred about the critical pressure threshold, beyond which decompression
of ACS is required, with the debate centered around using either the ICP alone, or the
differential pressure or perfusion pressure (ΔP). The literature would suggest that the normal
resting ICP in adult muscle is around 10 mm Hg.58 One level believed to be critical was 30
895
mm Hg of ICP because this is a value close to capillary blood pressure, while other authors
felt that 40 mm Hg of tissue pressure should be the threshold for
decompression.4,17,63,65,108,132,159 In one series of patients with tibial fractures, a tissue pressure
of 50 mm Hg was recommended as a pressure threshold for decompression in normotensive
patients.64 However, it has been recognized there is a significant variation between
individuals in their tolerance of raised ICP and is intrinsically linked with the systemic blood
pressure or perfusion pressure.72,76,103,111,117,199
It is now recognized that apparent variation between individuals in their tolerance of raised
ICP is because of variations in systemic blood pressure. Whitesides et al. were the first to
suggest the importance of employing the differential pressure or delta pressure ( ΔP) that is
equal to diastolic pressure – intra-compartmental pressure.199 They stated that there is
inadequate perfusion and relative ischemia when the tissue pressure rises to within 10 to 30
mm Hg of the diastolic pressure. Since then, the literature has suggested aΔP of 10 to 35
mm Hg to be diagnostic,22,72,103 but with good clinical and experimental data now advocating
a pressure difference ≤30 mm Hg should be used as a safe threshold for diagnosing
ACS.116,117,146,197 However, the critical ΔP will likely be increased in traumatized or
ischemic muscle.
The concept of the use of ΔP is also supported by Ovre et al.,145 although they did report a
higher than expected rate of fasciotomies (29%) using an ICP of 30 mm Hg as a threshold for
decompression. In one study from Edinburgh, 116 patients with an acute fracture of the tibial
diaphysis117 underwent immediate continuous anterior compartment ICP monitoring, which
continued for a minimum of 24 hours. When employing a ΔP of ≤30 mm Hg for more than
2 hours as the differential pressure threshold for proceeding to fasciotomy, three patients
underwent fasciotomy, there were no unnecessary fasciotomies (overtreatment), no missed
cases of ACS, as well as no sequelae at a final mean follow-up of 15 months.117 This protocol
was validated by the same group in 101 patients with a tibial diaphyseal fracture. 197 There
were 41 patients with an absolute ICP reading greater than 30 mm Hg for more than 6 hours
continuously (but with normal ΔP of >30 mm Hg). These patients were compared with 60
patients where there was an absolute ICP reading of less than 30 mm Hg throughout. In the
following 1-year period, there was no statistically significant difference in isometric muscle
analysis or in the return to function.
Much of the literature to date has been performed in adults and with reference to leg
compartment syndrome. The threshold may differ for children who have a low diastolic
pressure and are therefore more likely to have a ΔP less than 30 mm Hg. Mars and
Hadley102 recommend the use of the mean arterial pressure rather than the diastolic pressure
to obviate this problem. It has been assumed that these pressure thresholds apply equally to
anatomic areas other than the leg, although this has not been formally examined.
Timing
Time factors are also important in making the decision to proceed to fasciotomy. It is well
established experimentally and clinically that both the duration and severity of the pressure
elevation influence muscle ischemia and thus patient outcome, 4,65,66,75 so it is necessary to
contemplate the trend and timing of ICP readings when deciding whether to proceed to
fasciotomy.104,116,134,161,173 A limitation of the current literature is the definition of the time of
onset of ACS and thus it is difficult to determine the time to fasciotomy. In the acute setting,
it is suggested that the duration to fasciotomy is best defined as the point from admission as
this is most consistently defined.37,79,114,117 Crush syndrome is the one exception to this, as the

896
inevitable long period of compression makes it almost impossible to determine the time of
onset.37
Janzing et al. performed a prospective study of 95 patients with tibial diaphyseal fractures
with a minimum of 1-year follow-up, with every patient undergoing continuous ICP
monitoring.82 With a 14.4% fasciotomy rate, the best combined sensitivity and specificity
was clinical symptoms with a ΔP of <30 mm Hg (61%, 97%), with a ΔP of ≤30 mm Hg
best when using monitoring in isolation (89%, 65%). The authors concluded that an
increased rate of fasciotomy could occur with continuous ICP monitoring, 82 but the study
does not really take into account the trend of the ΔP over time.
Kakar et al. performed a prospective cohort study of 242 tibial diaphyseal fractures that
underwent intramedullary nailing under GA and found that although the preoperative
diastolic blood pressure was associated with the postoperative pressure, a statistically
significant difference was found with the intraoperative pressure (mean difference 18 mm
Hg, p < 0.05).84 This important study highlights the need to utilize serial pressure
measurements when determining whether to proceed to fasciotomy. Intraoperative and
immediate postoperative readings should clearly be interpreted with caution.
Fasciotomy should not be performed based on a single pressure reading except in extreme
cases, as this will likely lead to an increased rate of overtreatment and unnecessary
fasciotomies. Whitney et al. found a false-positive rate of 35% if a one-time ΔP of ≤30 mm
Hg is used without considering the trend over time.200 Continuous pressure monitoring
allows a clear record of the trend of the tissue pressure measurements. The Edinburgh
protocol is well researched in the literature and uses a ΔP of ≤30 mm Hg over a 2-hour
period as the indication for proceeding to urgent fasciotomy. However, the trend of
the ΔP should be considered. In situations where the ΔP drops below 30 mm Hg if the ICP
is dropping and the ΔP is rising, then it is safe to observe the patient in anticipation of
the ΔP returning within a short time to safe levels. If the ICP is rising, the ΔP is dropping
and less than 30 mm Hg, and this trend has been consistent for a period of 2 hours, then
fasciotomy should be performed. Using this protocol, delay to fasciotomy and the sequelae
of ACS are reduced without unnecessary fasciotomies being performed. 117
Clinical Signs Versus ICP Monitoring
McQueen et al. analyzed 25 patients with a tibial diaphyseal fracture that was complicated by
ACS,116 with 13 cases having undergone ICP monitoring and a further 12 patients who
underwent clinical assessment alone. A statistically significant difference in the time from
presentation to fasciotomy was found in the clinical assessment alone cohort (16 hour
difference; p < 0.05), with a significantly higher rate of late ACS sequelae (91% vs. 0%; p <
0.01) and a delay to union (8-week delay; p < 0.05).116
Al-Dadah et al. carried out a study of 218 patients, with 109 consecutive tibial diaphyseal
fractures, who had continuous ICP monitoring and a further 109 historical patients as the
control group that were evaluated for ACS with clinical signs alone. 3 The authors reported
comparable fasciotomy rates (15.6% vs. 14.7%), but no statistically significant difference
was found in either outcome or time to fasciotomy. 3 A limitation of this study is that the
control group had clinical assessment performed on an hourly basis, which many would
argue is difficult to reproduce with accuracy in normal day-to-day clinical practice.
Harris et al. carried out a prospective randomized trial including 200 consecutive tibial
diaphyseal fractures comparing clinical assessment alone (100 patients) with ICP monitoring
(100 patients).68 The primary outcome for this series was the late sequelae of ACS at 6
months following injury, with a total of five patients developing ACS (all in the clinical
897
assessment group). Complications included sensory loss, contracture, toe clawing, muscle
weakness and nonunion. There was no statistically significant difference in the complication
rates between groups (27% vs. 29%). A limitation of this study associated with the indication
to proceed to fasciotomy was the use of clinical symptoms and signs, with monitoring
employed at the discretion of the surgeon. 68 For ICP monitoring to be fairly compared
without bias to clinical assessment alone, the differential pressure over time needs to be the
primary indication for fasciotomy.
Diagnostic Performance Characteristics
The diagnostic performance characteristics of continuous invasive ICP monitoring were
reported in a series from Edinburgh of 850 adult patients with an acute tibial diaphyseal
fracture.118 Our group used a slit catheter technique inserted into the anterior compartment of
the leg and employed diagnostic criteria of a ΔP of less than 30 mm Hg for more than 2
hours. The authors reported a sensitivity of 94% and a specificity of 98.4%, with 11 false-
positive and 9 false-negative cases. The positive predictive value was 92.8% and the negative
predictive value was 98.7% (Table 16-6). In order to attain comparable performance
characteristics to this when using clinical symptoms and signs alone, three signs are needed,
with the third being paresis that is indicative or irreversible injury to the patient.188 The
authors of the study stated that ideally there should be a 100% certainty of the diagnosis but
acknowledged that this is not possible in clinical practice when in most situations, both the
surgeon and the patient have to accept a small amount of risk. With ACS, that risk inevitably
needs to be balanced somewhat in the favor of the unnecessary fasciotomy (false positive)
given the devastating complications associated with a missed ACS (false negative). 118
TABLE 16-6
The Reported Sensitivities and Specificities of the Clinical Symptoms and Signs of ACS,
Along with the Diagnostic Performance Characteristics of ICP Monitoring
Symptom or Sign Sensitivity (%) Specificity (%) PPV (%) NPV (%)
188
Pain 19 97 14 98
Pain on passive stretch188 19 97 14 98
Paresis/motor changes188 13 97 11 98
Paresthesia/sensory
changes188 13 98 15 98
Swelling176 54 76 70 63
ICP monitoring118 94 98 93 99

PPV, positive predictive value; NPV, negative predictive value; ICP, intracompartmental
pressure.
Reproduced with permission from Duckworth AD, McQueen MM. The diagnosis of acute
compartment syndrome: a critical analysis review. JBJS Rev. 2017;5(12):e1 .
Surgical and Applied Anatomy
Thigh
The thigh is divided into three main compartments, all of which are bounded by the fascia
lata and separated by the medial and lateral intermuscular septa (Fig. 16-5). Their contents
and the clinical signs of compartment syndrome in each compartment are summarized
in Table 16-7. Involvement of the adductor compartment is rare.
Figure 16-5 A cross section of the thigh demonstrating the three compartments and the
access to them.
A, anterior; Ad, adductor; P, posterior.

898
Reproduced with permission from Duckworth AD, McQueen MM. Continuous
intracompartmental pressure monitoring for acute compartment syndrome. JBJS Essential
Surg Techn. 2013;3(3):e13 .

TABLE 16-7
Compartments of the Thigh, Their Contents, and Signs of Acute Compartment Syndrome
Compartment Contents Signs
Anterior Quadriceps muscles Pain on passive knee flexion
Sartorius Numbness—medial leg/foot
Femoral nerve Weakness—knee extension
Posterior Hamstring muscles Pain on passive knee extension
Sensory changes rare
Sciatic nerve Weakness—knee flexion
Adductor Adductor muscles Pain on passive hip abduction
Sensory changes rare
Obturator nerve Weakness—hip adduction
Leg
There are four compartments in the leg—anterior, lateral, superficial posterior, and deep
posterior (Fig. 16-6). The anterior compartment is enclosed anteriorly by skin and fascia,
laterally by the intermuscular septum, posteriorly by the fibula and interosseous membrane,
and medially by the tibia. Its contents and the clinical signs of ACS are listed in Table 16-8.
The lateral compartment is enclosed laterally by skin and fascia, posteriorly by the posterior
intermuscular septum, medially by the fibula, and anteriorly by the anterior intermuscular
899
septum. Its contents and the clinical signs of involvement in ACS are detailed in Table 16-8.
The deep peroneal nerve may rarely be affected as it passes through the lateral compartment
en route to the anterior compartment.
Figure 16-6 A cross section of the leg showing the four compartments.
The arrows show the routes for double-incision four-compartment fasciotomy. A, anterior
compartment; DP, deep posterior compartment; L, lateral compartment; SP, superficial
posterior compartment.

TABLE 16-8
Compartments of the Leg, Their Contents, and Clinical Signs of Acute Compartment
Syndrome
Compartment Contents Signs
Anterior Tibialis anterior
Extensor digitorum longus Numbness—first web space
Extensor hallucis longus
Peroneus tertius
Deep peroneal (anterior tibial) nerve
and vessels Weakness—ankle/toe extension
Lateral Peroneus longus Pain on passive foot inversion
Peroneus brevis Numbness—dorsum of foot
Superficial peroneal nerve Weakness of eversion
Superficial
posterior Gastrocnemius Pain on passive ankle extension
Soleus Numbness—dorsolateral foot

900
Compartment Contents Signs
Plantaris
Sural nerve Weakness—plantar flexion
Pain on passive ankle/toe
Deep posterior Tibialis posterior extension/foot eversion
Flexor digitorum longus
Flexor hallucis longus Numbness—sole of foot
Weakness—toe/ankle flexion, foot
Posterior tibial nerve inversion
The superficial posterior compartment is bounded anteriorly by the intermuscular septum
between the superficial and deep compartments and posteriorly by skin and fascia. Its
contents and the clinical signs of ACS are summarized in Table 16-8. The deep posterior
compartment is limited anteriorly by the tibia and interosseous membrane, laterally by the
fibula, posteriorly by the intermuscular septum separating it from the superficial posterior
compartment, and medially by skin and fascia in the distal part of the leg. Table 16-8lists the
contents of the deep posterior compartment and the likely clinical signs in ACS.
Foot
Until recently, most authorities believed that there were four compartments in the foot—
medial, lateral, central, and interosseous (Fig. 16-7). The medial compartment lies on the
plantar surface of the hallux, the lateral compartment is on the plantar surface of the fifth
metatarsal, and the central compartment lies on the plantar surface of the foot. The
interosseous compartment lies dorsal to the others between the metatarsals. Their contents
are shown in Table 16-9.
Figure 16-7 A cross section of the foot showing access from the dorsum of the foot to the
compartments.
I, interosseous.

TABLE 16-9
Compartments of the Foot and Their Contents

901
Compartment Contents
Medial Intrinsic muscles of the great toe
Flexor digiti minimi
Lateral Abductor digiti minimi
Central
Superficial Flexor digitorum brevis
Deep (calcaneal) Quadratus plantae
Adductor hallucis Adductor hallucis
Interosseous muscles
Interosseous ×4 Digital nerves
Manoli and Weber challenged the concept of four compartments using cadaver infusion
techniques.100 They believe that there are nine compartments in the foot, with two central
compartments, one superficial containing flexor digitorum brevis, and one deep (the
calcaneal compartment) (Fig. 16-8) containing quadratus plantae, which communicates with
the deep posterior compartment of the leg. They demonstrated that each of the four
interosseous muscles and adductor hallucis lies in separate compartments, thus increasing the
number of compartments to nine. The clinical importance of these anatomic findings has
been challenged after the finding that the barrier between the superficial and calcaneal
compartments becomes incompetent at a pressure of 10 mm Hg, much lower than that
required to produce an ACS.62 The clinical diagnosis of ACS should be suspected in the
presence of severe swelling, but differentiating the affected compartments is extremely
difficult.
Figure 16-8 A section through the hindfoot showing the medial, superficial, and deep
central (calcaneal) compartments.
The medial approach for release of the calcaneal compartment is shown. FHL, flexor hallucis
longus.

902
Arm
There are two compartments in the arm: anterior and posterior (Fig. 16-9). The anterior
compartment is bounded by the humerus posteriorly, the lateral and medial intermuscular
septa, and the brachial fascia anteriorly. Its contents and the clinical signs of ACS are
detailed in Table 16-10. In late cases, paralysis of the muscles innervated by the median,
ulna, and radial nerves is seen. The posterior compartment has the same boundaries as the
anterior but lies posterior to the humerus. Its contents and the clinical signs of ACS are listed
in Table 16-10.
Figure 16-9 A cross section of the arm showing the anterior compartment containing
biceps (B) and brachialis (Br), and the posterior compartment containing triceps (T).

903
TABLE 16-10
Compartments of the Arm, Their Contents, and Clinical Signs of Acute Compartment
Syndrome
Compartment Contents Signs
Biceps
Brachialis
Coracobrachialis
Median nerve
Ulnar nerve Pain on passive elbow extension
Musculocutaneous nerve Numbness—median/ulnar distribution
Lateral cutaneous nerve Numbness—volar/lateral distal forearm
Antebrachial nerve Weakness—elbow flexion
Anterior Radial nerve (distal third) Weakness—median/ulnar motor function
Pain on passive elbow flexion
Triceps Numbness—ulnar/radial distribution
Radial nerve Weakness—elbow extension
Posterior Ulnar nerve (distally) Weakness—radial/ulnar motor function
Forearm
The forearm contains three compartments: volar, dorsal, and “the mobile wad” (Fig. 16-10).
The volar compartment has the ulna, radius, and interosseous membrane as its posterior limit
904
and the antebrachial fascia as its anterior limit. Table 16-11 lists the contents and clinical
signs of ACS in the volar compartment of the forearm. A suggestion has been made that the
volar compartment of the forearm contains three spaces, the superficial volar, deep volar, and
pronator quadratus spaces,56 but in practice it is not usually necessary to distinguish between
these at fasciotomy.26 The dorsal compartment of the forearm lies dorsal to the radius, ulna,
and interosseous membrane and contains the finger and thumb extensors, abductor pollicis
longus, and extensor carpi ulnaris. Its contents and the clinical signs of ACS are summarized
in Table 16-11.
Figure 16-10 A cross section of the mid forearm.
The pronator quadratus compartment is not shown as it lies in the distal forearm. D,
dorsal; V, volar.

TABLE 16-11
Compartments of the Forearm, Their Contents, and the Clinical Signs of Acute Compartment
Syndrome
Compartment Contents Signs
Flexor carpi radialis longus and Pain on passive wrist/finger extension
brevis Numbness—median/ulnar distribution
Flexor digitorum superficialis and Weakness—wrist/finger flexion
profundus Weakness—median/ulnar motor
Volar Pronator teres function in hand
905
Compartment Contents Signs
Pronator quadratus
Median nerve
Ulnar nerve
Extensor digitorum
Extensor pollicis longus
Abductor pollicis longus Pain—passive wrist/finger flexion
Dorsal Extensor carpi ulnaris Weakness—wrist/finger flexion
Pain on passive wrist flexion/elbow
extension
Brachioradialis Weakness—wrist extension/elbow
Mobile wad Extensor carpi radialis flexion
Hand
General agreement exists that the hand has 10 muscle compartments: one thenar, one
hypothenar, one adductor pollicis, four dorsal interosseous, and three volar interosseous
compartments (Fig. 16-11). The thenar compartment is surrounded by the thenar fascia, the
thenar septum, and the first metacarpal. The hypothenar compartment is contained by the
hypothenar fascia and septum and the fifth metacarpal. The dorsal interosseous
compartments lie between the metacarpals and are bounded by them laterally and the
interosseous fascia anteriorly and posteriorly. The volar interosseous compartments lie on the
volar aspect of the metacarpals, but it is unlikely that these are functionally separate from the
dorsal interosseous compartments because the tissue barrier between the two cannot
withstand pressures of more than 15 mm Hg. 61 The contents of the hand compartments are
detailed in Table 16-12.
Figure 16-11 A cross section of the hand showing the muscle compartments.
The adductor pollicis lies more distally. CP, central palmar; H, hypothenar; I,
interosseous; T, thenar.

906
TABLE 16-12
The Compartments of the Hand and Their Contents
Compartment Contents
Abductor pollicis brevis
Flexor pollicis brevis
Thenar Opponens pollicis
Abductor digiti minimi
Flexor digiti minimi
Hypothenar Opponens digiti minimi
Dorsal interosseous ×4 Dorsal interossei
Volar interossei ×3 Volar interossei
Adductor pollicis Adductor pollicis
Treatment of Acute Compartment Syndrome
The single most effective treatment for ACS is fasciotomy, delay of which can cause
devastating complications. Nevertheless, other preliminary measures should be taken in cases
of impending ACS. The process may on occasion be aborted by release of external limiting
envelopes such as dressings or plaster casts, including the padding under the cast. Splitting
and spreading a cast has been shown to reduce ICP as has release of dressings. 49 The split
and spread cast is the only method that can accommodate increasing limb swelling.197 The
limb should not be elevated above the height of the heart as this reduces the AV
gradient.111 Hypotension should be corrected because this will reduce perfusion pressure.
Oxygen therapy should be instituted to ensure maximum oxygen saturation.
Fasciotomy
When the diagnosis has been made, urgent fasciotomy should be performed. The basic
principle of fasciotomy of any compartment is full and adequate decompression. Skin
incisions must be made along the full length of the affected compartment. There is no place
for limited or subcutaneous fasciotomy in ACS. It is essential to visualize all contained
muscles in their entirety (Fig. 16-12) to assess their viability and any muscle necrosis must
be thoroughly debrided to avoid infection. Subcutaneous fasciotomy is contraindicated for
these reasons and also because the skin may act as a limiting boundary. 50
Figure 16-12 Fasciotomy of the anterior and lateral compartments of the leg.
Note that the incision extends the whole length of the muscle compartment, allowing
inspection of all muscle groups.

907
Technique
Leg
Double-Incision Four-Compartment Fasciotomy of the Leg: Key
Surgical Steps
Tourniquet on but not inflated
Lateral skin incision approximately 2 cm anterior to
fibula over the intermuscular septum
Skin retracted adequately to allow assessment of fascia
overlying anterior and lateral compartments, which can
then be released
Care taken to avoid superificial peroneal nerve, which has
a variable course but normally pierces fascia
approximately 10 cm above the lateral malleolus
Muscle in anterior and lateral compartments assessed for
viability, with nonviable tissue debrided
Medial skin incision approximately 1 to 2 cm posterior to
the medial border of the tibia, allowing for adequate skin
bridge
Care taken to identify and protect saphenous vein and
nerve
Care also taken to be anterior to the posterior tibial artery
and protect the perforating vessels for any potential local
fasciocutaneous flap that may be needed
Fascia over superficial posterior compartment is
identified and released
Deep posterior compartment is exposed by posterior
retraction of the superficial compartment, with partial
elevation of this compartment of the tibia to allow a full
release
Muscle in superficial and deep posterior compartments
assessed for viability, with nonviable tissue debrided
In the leg, all four compartments should be released. One of the most commonly used
techniques is the double-incision four-compartment fasciotomy.131 The anterior and lateral
compartments are released through a lateral skin incision over the intermuscular septum
between the compartments (see Fig. 16-6). The skin may then be retracted to allow fascial
incisions over both compartments. Care must be taken not to injure the superficial peroneal
nerve that pierces the fascia and lies superficial to it in the distal third of the leg (see Fig. 16-
12). There is considerable variation in its course, with approximately three-quarters of nerves
remaining in the lateral compartment before its exit through the deep fascia and one-quarter
passing into the anterior compartment.2
The two posterior compartments are accessed through a skin incision 2 cm from the medial
edge of the tibia (see Fig. 16-6). This allows a generous skin bridge to the lateral incision but
is anterior to the posterior tibial artery, especially in open fractures, to protect perforating
vessels that supply local fasciocutaneous flaps. The superficial posterior compartment is
easily exposed by skin retraction. The deep posterior compartment is exposed by posterior
retraction of the superficial compartment and is most easily identified in the distal third of
the leg (Fig. 16-13). It is sometimes necessary to elevate the superficial compartment
muscles from the tibia for a short distance to allow release of the deep posterior compartment
908
along its length. Care must be taken to protect the saphenous vein and nerve in this area and
to protect the posterior tibial vessels and nerves.153
Figure 16-13 Decompression of the medial side of the leg.
The superficial posterior compartment is being retracted to display the deep compartment.
The scissors are deep to the fascia overlying the deep posterior compartment.

Single-incision fasciotomy of all four compartments was described using excision of the
fibula,42 but this is unnecessarily destructive and risks damage to the common peroneal
nerve. Single-incision four-compartment fasciotomy without fibulectomy can be performed
through a lateral incision that affords easy access to the anterior and lateral
compartments.29 Anterior retraction of the peroneal muscles 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 posterolateral border of
the fibula. Double-incision fasciotomy is faster and probably safer than single-incision
methods because the fascial incisions are all superficial. Using the single-incision method, it
can be difficult to visualize the full extent of the deep posterior compartment. Both methods
seem to be equally effective at reducing ICP. 131,189
Thigh
In the thigh and gluteal regions, decompression is simple and the compartments are easily
visualized. Both thigh compartments can be approached through a single lateral skin incision
(Fig. 16-14),184 although a medial incision can be used over the adductors if considered
necessary (see Fig. 16-5).
Figure 16-14 Fasciotomy of the thigh through a single lateral incision.

909
Foot
In the foot, there are a number of compartments to decompress, and a sound knowledge of
the anatomy is essential. Dorsal incisions overlying the second and fourth metacarpals allow
sufficient access to the interosseous compartments, and the central compartment that lies
deep to the interosseous compartments (see Fig. 16-7). The medial and lateral compartments
can be accessed around the deep surfaces of the first and fifth metatarsal, respectively. Such a
decompression is usually sufficient in cases of forefoot injury, but when a hindfoot injury,
especially a calcaneal fracture is present, a separate medial incision may be required to
decompress the calcaneal compartment (see Fig. 16-8).85,90,138,164
Arm
Fasciotomy of the arm is performed through anterior and posterior incisions (see Fig. 16-9)
when the compartments are easily visualized. On rare occasions, the deltoid muscle should
also be decompressed.35
Forearm
In the forearm, both volar and dorsal fasciotomies may be performed. In most cases, the
volar compartment is approached first through an incision extending from the proximal
forearm to the palm of the hand to allow carpal tunnel decompression that is usually
necessary (Fig. 16-15). Fascial incision then allows direct access to the compartment (seeFig.
16-10). The deep flexors must be carefully inspected after fascial incision. Separate exposure
and decompression of pronator quadratus may be necessary. 26 Usually, volar fasciotomy is
sufficient to decompress the forearm,38 but if ICP remains elevated in the dorsal
compartment perioperatively, then dorsal compression is easily performed through a straight
dorsal incision (see Fig. 16-10).
Figure 16-15 Fasciotomy of the forearm in a case of crush syndrome.
There is necrosis of the forearm flexors proximally. The carpal tunnel has been
decompressed.

Hand
Decompression of the hand can usually be adequately achieved using two dorsal incisions
that allow access to the interosseous compartments (see Fig. 16-11). This may often be
910
sufficient, but if there is clinical suspicion or raised ICP on measurement, then incisions may
be made over the thenar and hypothenar eminences, allowing fasciotomy of these
compartments.
Management of Fasciotomy Wounds
Fasciotomy incisions must never be closed primarily because this may result in persistent
elevation of ICP.70 The wounds should be left open and dressed, and approximately 48 hours
after fasciotomy, a “second-look” procedure should be undertaken to ensure viability of all
muscle groups. Skin closure or cover should not be attempted unless all muscle groups are
viable.
The type of closure or coverage required is predicted by age and type of injury with split skin
grafting significantly more common in younger patients and crushing-type injuries,
presumably because of the increased muscle bulk in these groups.38 The wounds may then be
closed by delayed primary closure if possible, although this must be without tension on the
skin edges. Commonly, in the leg, this technique is possible in the medial but not the lateral
wound. If delayed primary closure cannot be achieved, then the wound may be closed using
either dermatotraction techniques or split skin grafting. Dermatotraction or gradual closure
techniques have the advantage of avoiding the cosmetic problems of split skin grafting but
may cause skin edge necrosis.81 A further disadvantage is the prolonged time required to
achieve closure, which may be up to 10 days. 12,81
Split skin grafting, although offering immediate skin cover, has the disadvantage of a high
rate of long-term morbidity.45 There is an increasing body of literature supporting the use of
vacuum-assisted closure (VAC) systems which can potentially reduce the need for split skin
grafting with a low complication rate. 95,96,196,207
Management of Associated Fractures
As is now generally accepted, fractures, especially of the long bones, should be stabilized in
the presence of ACS treated by fasciotomy. 57,159,187 In reality, the treatment of the fracture
should not be altered by the presence of an ACS, although cast management of a tibial
fracture is contraindicated in the presence of ACS. Fasciotomy should be performed prior to
fracture stabilization to eliminate any unnecessary delay in decompression. Stabilization of
the fracture allows easy access to the soft tissues and protects the soft tissues, allowing them
to heal.
Reamed intramedullary nailing of the tibia confers excellent stabilization of a diaphyseal
fracture and is now probably the treatment of choice in most centers for tibial diaphyseal
fracture. Some authors, however, have implicated reaming as a possible cause of
ACS.92,125 This was refuted by other studies examining ICPs during and after tibial nailing.
McQueen et al.116 studying reamed intramedullary nailing, and Tornetta and
French186 studying unreamed intramedullary nailing agreed that the ICP increased
perioperatively and dissipated postoperatively, and that nailing did not increase the
likelihood of ACS. Nassif et al. found no differences in ICP between reamed and unreamed
nailing.140 In a group of 212 children and teenagers with tibial fractures treated with casting,
external fixation, and locked and flexible nailing, the fixation type was not predictive of
ACS.175
Several factors may raise ICP during stabilization of tibial fractures. These include traction,
which raises pressure in the deep posterior compartment by approximately 6%/kg of weight
applied.170 Countertraction using a thigh bar can cause external calf compression if the bar is
wrongly positioned and can also decrease arterial flow and venous return, making the leg
more vulnerable to ischemia. Elevation of the leg as in the 90-90 position decreases the
tolerance of the limb to ischemia.107 Thus, excessive traction, poor positioning of the thigh
bar, and high elevation of the leg should be avoided in patients at risk of ACS.
911
Authors' Preferred Treatment for Acute Compartment Syndrome
(Algorithm 16-1)
Early diagnosis of ACS is essential, and it is important to be aware of the patients at risk of
developing ACS. Good clinical examination techniques in the alert patient will help to
identify the compartments at risk. However, given the evidence demonstrating the superior
diagnostic performance characteristics of continuous ICP monitoring when compared to
clinical signs and symptoms alone, we feel continuous ICP monitoring should be employed
as a diagnostic adjunct in all patients defined as being at risk of ACS (Table 16-13). Youth is
the key risk factor for developing ACS, with tibial diaphyseal fractures the most common
precipitating injury. Ultimately, if ACS is suspected, ICP monitoring is recommended.
Algorithm 16-1
Authors' preferred treatment for acute compartment syndrome.

Compartment monitoring should be used in all “at-risk” patients as defined in Table 16-3. In
practice, this means that all tibial fractures should be monitored, but if resources to do so are
limited, then younger patients should be selected for monitoring. The anterior compartment
should be monitored, but in rare cases where symptoms are present that cannot be explained
by the tissue pressures in the anterior compartment, the posterior compartment should also be
monitored.

912
The diagnosis of ACS should be made using sequential ΔP readings. The decision to
perform an urgent fasciotomy primarily using ICP monitoring and the differential pressure
(ΔP), with clinical symptoms and signs being used as an adjunct to diagnosis, appears to be
the optimal approach to take. Urgent fasciotomy is recommended in those patients with
symptoms and signs present. In at-risk patients with no or minimal clinical signs, fasciotomy
should be performed with a persistent differential pressure of less than 30 mm Hg for more
than 2 hours (Algorithm 16.1). The threshold for fasciotomy is debated but a
persistent ΔP of less than 30 mm Hg, or which is declining, has been found to prevent a
delay in the diagnosis and reduce long-term complications. If the ΔP is less than 30 mm Hg
but the tissue pressure is dropping, as can happen for instance for a short time after tibial
nailing, then the pressure may be observed for a short period in anticipation of the ΔP rising.
On the other hand, if the ΔP remains less than 30 mm Hg or is reducing, then immediate
fasciotomy is indicated. Delay and complications are minimized by making the decision to
perform a fasciotomy primarily on the level of ΔP, with clinical symptoms and signs being
used as an adjunct to diagnosis.
Once the diagnosis of ACS is confirmed, urgent fasciotomy should be performed. We prefer
four-compartment fasciotomy in the leg because it is simpler and gives an excellent view of
all compartments. If any muscle necrosis is present, this should be thoroughly debrided. At
this stage if a fracture is present, it should be stabilized if this has not been done previously.
Suction dressings if available can be applied. A “relook” procedure should be performed at
48 hours after fasciotomy, with further debridement if necessary. If the wound is healthy,
closure should be undertaken at this stage with either direct closure or split skin grafting. We
do not use gradual closure techniques because of the risk of wound edge necrosis and
prolonged times to coverage. There is no indication to prolong closure beyond 48 hours
unless there is residual muscle necrosis.
TABLE 16-13
Grades of Recommendation for the Diagnosis of Acute Compartment Syndrome
Recommendation Gradea
Youth is the most important risk factor associated with the development of ACS,
with over two-thirds of cases associated with an underlying fracture B
Clinical symptoms and signs alone are inadequate in the diagnosis of ACS due to
well-documented poor sensitivity B
All patients at risk of acute compartment syndrome should undergo continuous
intracompartmental pressure monitoring B
Decompression fasciotomy should be carried out primarily based on a differential
pressure <30 mm Hg for more than 2 hrs B
a
Grade A, good evidence (level I studies with consistent findings) for or against
recommending intervention; grade B, fair evidence (level II or III studies with consistent
findings) for or against recommending intervention; grade C, conflicting or poor-quality
evidence (level IV or V studies), not allowing a recommendation for or against intervention;
grade I, there is insufficient evidence to make a recommendation.
Reproduced with permission from Duckworth AD, McQueen MM. The diagnosis of acute
compartment syndrome: a critical analysis review. JBJS Rev. 2017;5(12):e1 .
Complications of Acute Compartment Syndrome

913
Complications of ACS are unusual if the condition has been treated expeditiously. Delay in
diagnosis has been cited as the single reason for failure in the management of ACS, with a
delay to fasciotomy of more than 6 hours likely to cause significant sequelae. 38,161
The detrimental effects of a delayed diagnosis and treatment for ACS have been known for
over 40 years.121 It is associated with long-term complications, poor patient-reported
outcomes,104,116,134,161,173 increasing medical costs,165 as well as an increased number of
indemnity settlements when compared to the mean for all orthopedic
surgery.15,109 Documented complications include infection, muscle necrosis and contractures,
permanent neurologic injury, chronic pain, and nonunion of associated
fractures.40,79,86,114,124,134,161,173 In severe cases, amputation may be necessary because of
infection or lack of function.43
Late Diagnosis
There is some debate about the place of decompression when the diagnosis is made late and
muscle necrosis is inevitable, whether because of a missed ACS or the crush syndrome. Little
can be gained in exploring a closed crush syndrome when complete muscle necrosis is
inevitable, except in circumstances where there are severe or potentially severe systemic
effects when amputation may be necessary. Increased sepsis rates with potentially serious
consequences have been reported when these cases have been explored. 154 Nonetheless, if
partial muscle necrosis is suspected and compartment monitoring reveals pressures above the
threshold for decompression, there may be an indication for fasciotomy to salvage remaining
viable muscle. In these circumstances, debridement of necrotic muscle must be thorough to
reduce the chances of infection. In rare cases, the ICP may be high enough to occlude major
vessels. This is a further indication for fasciotomy to salvage the distal part of the limb. 154
It is recommended that if there is no likelihood of any surviving muscle and compartment
pressures are low, then fasciotomy should be withheld. If there is any possibility of any
remaining viable muscle or if compartment pressures are above critical levels, fasciotomy
should be performed to preserve any viable muscle. In any circumstance, a thorough
debridement of necrotic muscle is mandatory.
Future Directions for Research
ACS remains a potentially devastating complication of fracture that continues to be a
significant cause of disability and successful litigation. 15,169 In a review of Canadian legal
cases relating to ACS between 1998 and 2008, 55% of cases had an unfavorable outcome for
doctors or judgment for the plaintiff; 77% of plaintiffs had permanent disability. Orthopedic
surgeons were assigned responsibility in the greatest numbers in both of these groups and the
most frequent clinical issue was diagnostic failure or delay. 169 In a study from the United
States, the most prominent risk factor for an indemnity payment was delay in diagnosis, and
the number of hours delayed had a linear relationship to the value of the claim.15 Delay to
diagnosis was cited as the single cause of a poor outcome more than 40 years ago, yet there
remains a remarkable lack of consistency in the methods used to diagnose the
condition.194,202 In light of the published high sensitivity and specificity of continuous ICP
monitoring compared to that for the clinical diagnosis of ACS, clinical diagnosis should no
longer be the gold standard. Continuous ICP monitoring should be instituted in all patients at
risk of ACS. Added to this, universally acceptable, clear, clinical guidelines are required to
improve speed of diagnosis in all units managing trauma and would likely be the single
biggest advance in the management of the condition.
One of the important issues with regard to the current data regarding the diagnosis of ACS is
the lack of a gold-standard reference for the diagnosis of ACS, with the incidence
documented in the current data notably below 30%.120,142,147 In such clinical situations,
914
routine statistical analysis is not robust and other methods including latent class analysis and
Bayes theorem are necessary to accurately determine the diagnostic performance
characteristics. Although the gold standard would be to perform sufficiently powered
prospective randomized controlled trials of clinical signs versus continuous ICP monitoring,
there are important issues of bias due to the inherent risk of modifying routine day-to-day
clinical practice due to the predictable improvement in the frequency and robustness of
clinical assessment.
The current literature would benefit from prospective mid to long-term outcome data on the
efficacy of ICP monitoring, along with reports on the diagnostic performance characteristics
of different ICP-monitoring protocols. Data on ACS in adolescents and other areas of the
body outwith the leg is needed to allow us to determine the indications, thresholds, and
protocols for using ICP monitoring.
Other future developments are likely to center on methods of measuring blood flow directly
rather than indirectly by ICP measurement. Noninvasive methods of diagnosing ACS are
continuing to be developed.168 One such example is near-infrared spectroscopy, which
measures the amount of oxygenated hemoglobin in muscle tissues
transcutaneously.6,55,127,177,180 Methods of reducing the effects of ACS are also likely to play a
part in the future. Some basic science research has already been published on the effects of
antioxidants on the outcome of ACS with promising results.88 This work should be extended
to human studies in an attempt to reduce the effects of ACS in the clinical situation.
Prevention of ACS is the ultimate goal in its management. Attempts have been made to
reduce ICP with the administration of hypertonic fluids intravenously, 14 but these have never
been successful clinically. Nevertheless, an experiment on human subjects using tissue
ultrafiltration to remove fluid from the compartment has been shown to reduce
ICP.143,144 Whether or not this technique can be useful clinically remains to be seen.
Annotated References

Reference Annotation
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Continuous compartment pressure monitoring vs. comparing ICP monitoring with
clinical monitoring in tibial diaphyseal clinical assessment for the diagnosis of
fractures. Injury. 2008;39:1204–1209 . ACS.
Largest series in the literature
Duckworth AD, Mitchell SE, Molyneux SG, et al. documenting the epidemiology and
Acute compartment syndrome of the forearm. J Bone outcome of forearm compartment
Joint Surg Am. 2012;94:e63 . syndrome.
Harris IA, Kadir A, Donald G. Continuous The only prospective randomized
compartment pressure monitoring for tibia fractures: controlled trial comparing ICP
does it influence outcome? J Trauma. 2006;60:1330– monitoring with clinical assessment for
1335 . the diagnosis of ACS.
One of the original studies to refute
Heckman MM, Whitesides TE Jr, Grewe SR, et al. using of absolute tissue pressure as a
Histologic determination of the ischemic threshold of guide to fasciotomy and advocating the
muscle in the canine compartment syndrome use of the differential pressure
model. J Orthop Trauma. 1993;7:199–210 . threshold.
Heckman MM, Whitesides TE Jr, Grewe SR, et al.
Compartment pressure in association with closed A study documenting the importance
tibial fractures: the relationship between tissue of which compartments to monitor in
pressure, compartment, and the distance from the site patients with a closed tibial diaphyseal
915