Chapter 29: Acute Compartment Syndrome

Margaret M. McQueen

Chapter Outline

Introduction to Acute Compartment Syndrome

Acute compartment syndrome 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. Without urgent decompression, tissue ischemia, necrosis, and functional impairment occur. The acute compartment syndrome should be differentiated from other related conditions, so awareness of the different definitions associated with a compartment syndrome is important. 
Acute compartment syndrome 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 intracompartmental pressure during exercise, causing ischemia, pain, and rarely neurologic symptoms and signs. It is characterized by resolution of symptoms with rest but may proceed to acute compartment syndrome if exercise continues. 
Volkmann ischemic contracture is the end stage of neglected acute compartment syndrome with irreversible muscle necrosis leading to ischemic contractures. 
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 acute compartment syndrome. 

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,64 but Hamilton’s original description has never been found. The credit for the first full description belongs to Richard Von Volkmann155 who published a summary of his views in 1882. 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 Peterson118 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 twentieth 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.30,129,159 By the early part of the twentieth century published accounts of the sequence of events in acute compartment syndrome 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.9 This paper was the first description of fasciotomy to relieve the pressure. The importance of early fasciotomy was suggested at this time9,110 and confirmed by prevention of the development of contractures in animal experiments.70 
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 artery36,47 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 acute compartment syndrome cannot exist in the presence of normal peripheral pulses. 
The arterial injury theory was challenged by Seddon132 in 1966. 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 Nolan101 reported on 15 cases complicated by “local ischemia”. They described the vicious circle 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

Knowledge of the epidemiology of acute compartment syndrome is important in defining the patient at risk of developing acute compartment syndrome. The epidemiology of acute compartment syndrome has been described in a cohort of 164 patients drawn from a defined population in the United Kingdom.100 
The incidence of acute compartment syndrome in a westernized population is 3.1 per 100,000 of the population per annum.100 The annual incidence for males is 7.3 per 100,000 compared with 0.7 per 100,000 for females, a tenfold increase in risk for males. The age- and gender-specific incidences are illustrated in Figure 29-1, showing a type B pattern (see Chapter 3) or the L-shaped pattern described by Buhr and Cooke.18 The mean age for the whole group was 32 years; the median age for males was 30 years and for females 44 years. 
Figure 29-1
The annual age- and gender-specific incidence of acute compartment syndrome.
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The underlying condition causing acute compartment syndrome was most commonly a fracture (69% of cases) (Table 29-1). Similar figures have been reported in children, with 76% of cases caused by fracture, predominantly tibial diaphyseal, distal radius, and forearm.8 The most common fracture associated with acute compartment syndrome in adults is tibial diaphyseal fracture. The prevalence of acute compartment syndrome in tibial diaphyseal fractures is reported as 2.7% to 15%,3,16,24,34,98100,109,141,163 with the differences in prevalences likely to be because of different diagnostic techniques and selection of patients. 
Table 29-1
Conditions Associated with Injury Causing Acute Compartment Syndrome Presenting to an Orthopaedic 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
Pelvic fracture 0.6
Humeral diaphyseal fracture 0.6
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The second most common cause of acute compartment syndrome 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 acute compartment syndrome is the distal radius fracture. It occurs in approximately 0.25% of cases. Forearm diaphyseal fractures are complicated by acute compartment syndrome in 3% of cases. The prevalence of acute compartment syndrome in other anatomic locations is rarely reported. Other less common causes of acute compartment syndrome are listed in Table 29-2
 
Table 29-2
Causes of Acute Compartment Syndrome
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Table 29-2
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/anticoagulants66,125
Fluid infusion (including arthroscopy)10,133
Arterial puncture134
Ruptured ganglia/cysts31
Osteotomy45
Snake bite153
Nephrotic syndrome147
Leukemic infiltration152
Viral myositis78
Acute hematogenous osteomyelitis145
Conditions Reducing Compartment Volume
Burns
Repair of muscle hernia4
Medical Comorbidity
Diabetes21
Hypothyroidism67
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From adolescence younger patients are at more risk of compartment syndrome. In tibial diaphyseal fracture the prevalence of acute compartment syndrome 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.100 Adolescents have been recognized as having a high rate (8.3%) of compartment syndrome after tibial fracture.24 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%.141 Analysis of 1,403 tibial diaphyseal fractures presenting to the Edinburgh Orthopaedic Trauma Unit over the period from 1995 to 2007 shows that there were 160 cases of acute compartment syndrome (11.4%). Using univariate analysis, significant risk factors for the development of acute compartment syndrome were youth (p < 0.001) and male gender. Males were almost six times more likely to develop acute compartment syndrome if aged between 20 and 29 years compared with those aged over 40 years. Youth, regardless of gender, is therefore a significant risk factor for the development of acute compartment syndrome after tibial fracture. The only exception to youth being a risk factor in acute compartment syndrome 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.66 
High-energy injury is generally believed to increase the risks of developing an acute compartment syndrome. Nevertheless, in tibial diaphyseal fracture in adults complicated by acute compartment syndrome the proportion of high- and low-energy injury shows a slight preponderance of low-energy injury (59%).100 In the same population there is an equal number of high-energy and low-energy injury in tibial diaphyseal fractures uncomplicated by acute compartment syndrome.25 Adolescents may be an exception to this because of the high prevalence of 48% reported in teenagers after road accidents.141 In the larger Edinburgh series there was an increased risk of acute compartment syndrome in closed compared with open fractures (p < 0.05). This suggests acute compartment syndrome 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. The concept of patients with lower-energy injury being at higher risk is supported by the distribution of severe open fractures. In those complicated by acute compartment syndrome, 20% are Gustilo type III.100 In the whole population of tibial fractures, 60% were type III.25 It is important to note that open tibial diaphyseal fractures remain at risk of acute compartment syndrome, which occurs in approximately 3%,100 but it appears that the lower Gustilo types are at more risk, again possibly because of the lack of disruption of the compartment boundaries. 
Distal radial and forearm diaphyseal fractures associated with high-energy injury are more likely to be complicated by acute compartment syndrome, probably because of the high preponderance of young males who sustained these types of injury. This is illustrated by a comparison of the age- and gender-related incidence of distal radius fractures complicated by acute compartment syndrome (Fig. 29-2). The likely explanation for the preponderance of young patients with acute compartment syndrome 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 29-2
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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The second most common type of acute compartment syndrome is that arising in the absence of fractures. The majority of these arise subsequent to soft tissue injury, particularly a crushing type injury, but some arise with no preceding history of trauma.66 In children 61% of cases of acute compartment syndrome in the absence of fracture are reported as being iatrogenic.120 Patients with acute compartment syndrome 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 use of anticoagulants also seems to be a risk factor for the development of acute compartment syndrome. 
Patients with polytrauma are at particular risk of delay in the diagnosis of their acute compartment syndrome, so identification of at-risk factors in this group is of particular importance.37 Kosir et al.75 examined risk factors for lower limb acute compartment syndrome in 45 critically ill trauma patients with the institution of an aggressive screening protocol. The prevalence of acute compartment syndrome was 20%. High base deficits, lactate levels, and transfusion requirements were significant risk factors in this group. 
The possible risk factors for the development or late diagnosis of acute compartment syndrome are listed in Table 29-3. As well as demographic risk factors, altered pain perception can delay diagnosis. This can occur if the patient has an altered conscious state or with certain types of anesthesia or analgesia.55,81,108 
Table 29-3
Risk Factors for Development or Late Diagnosis of Acute Compartment Syndrome
Demographic Altered Pain Perception
Youth Altered conscious level
Tibial fracture Regional anesthesia
High-energy forearm fracture Patient-controlled analgesia
High-energy femoral diaphyseal fracture Children
Bleeding diathesis/anticoagulants Associated nerve injury
Polytrauma with high base deficit, lactate levels, and transfusion requirement
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Pathogenesis

There remains uncertainty about the exact physiologic mechanism of the reduction in blood flow in the acute compartment syndrome, 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.19 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:   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.6,115,124,168 Ashton7 was the first to relate these findings to acute compartment syndrome 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.85 Ashton6 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. 
A second theory is the arteriovenous (AV) gradient theory.85,92 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:   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 acute compartment syndrome, then the Pv must also rise, thus reducing the AV gradient (PaPv) and therefore the local blood flow. At low AV gradients compensation from R is relatively ineffective62 and local blood flow is primarily determined by the AV gradient. Matsen et al.92 presented results on human subjects demonstrating reduction of the AV gradient with elevation of the limb in the presence of raised tissue pressure. This theory has been supported by work that demonstrated that with external pressure applied, simulating acute compartment syndrome, venous and capillary flow ceased, but arterioles were still capable of carrying flow.156 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 acute compartment syndrome.52 Measurement of capillary pressure in dogs with normal tissue pressures revealed a mean level of 25 mm Hg. Hargens et al.52 suggested that a tissue pressure of similar value is sufficient to reduce capillary blood flow. 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 tubes85 and their intravascular pressure ought to rise in the presence of raised tissue pressure. Hargens’ theory52 is supported by work demonstrating reduction of the number of perfused capillaries per unit area with raised tissue pressures.57 

Effects of Raised Tissue Pressure on Muscle

Regardless of the mechanism of vessel closure, reduction in blood flow in the acute compartment syndrome 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 acute compartment syndrome. 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.57,60,63,83 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.12 
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.59,77,119 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.79 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.40,54,87,140 In a study on human neurologic function, Matsen et al.89 found considerable variation of pressure tolerance that could not be attributed to differences in systemic pressure. 
The mechanism of damage to nerve is as yet uncertain and could result from ischemia, ischemia plus compression, toxic effects, or the effects of acidosis. 

Effects of Raised Tissue Pressure on Bone

Nonunion is now recognized as a complication of acute compartment syndrome.23,27,71,98,103 It was first suggested by Nario in 1938 that “Volkmann’s disease” caused obliteration of the “musculodiaphyseal” vessels and caused frequent pseudarthrosis.113 McQueen95 observed a reduction in bone blood flow and bone union in rabbit tibiae after an experimentally induced acute compartment syndrome. 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 re-establishment of blood flow to the ischemic tissues and can occur after fasciotomy and restoration of muscle blood flow in the acute compartment syndrome. 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.15 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 acute compartment syndrome 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 intracompartmental pressure,46 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.15 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.1,72,73,157 

Diagnosis of Acute Compartment Syndrome

Prompt diagnosis of acute compartment syndrome is the key to a successful outcome. Delay in diagnosis has long been recognized as the single cause of failure of the treatment of acute compartment syndrome.86,101,126,128 Delay in diagnosis may be because of inexperience and lack of awareness of the possibility of acute compartment syndrome, an indefinite and confusing clinical presentation,102,151 or anesthetic or analgesic techniques that mask the clinical signs.26,55,81,108 
Delay in treatment of the acute compartment syndrome can be catastrophic, leading to serious complications such as permanent sensory and motor deficits, contractures, infection, and at times, amputation of the limb.109,120,128 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 acute compartment syndrome to avoid such complications. As well as improving outcome, early recognition and treatment of acute compartment syndrome is associated with decreased indemnity risk in potential malpractice claims.14 

Clinical Diagnosis

Pain is considered to be the first symptom of acute compartment syndrome. The pain experienced by the patient is by nature ischemic and usually severe and out of proportion to the clinical situation. Pain may, however, be an unreliable indication of the presence of acute compartment syndrome because it can be variable in its intensity.32,88,162 Pain may be absent in acute compartment syndrome associated with nerve injury65,167 or minimal in the deep posterior compartment syndrome.86,88 Pain is present in most cases because of the index injury but cannot be elicited in the unconscious patient or where regional anesthesia is used.26,55,108 Kosir at al.75 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. Children may not be able to express the severity of their pain, so restlessness, agitation, and anxiety with increasing analgesic requirements should raise the suspicion of the presence of an acute compartment syndrome.8 Both Shereff139 and Myerson112 state that clinical diagnosis of acute compartment syndrome in the foot is so unreliable that other methods should be used. 
Pain has been shown to have a sensitivity of only 19% and a specificity of 97% in the diagnosis of acute compartment syndrome (i.e., a high proportion of false-negative or missed cases but a low proportion of false-positive cases).151 There is general agreement, however, that pain, if present, is a relatively early symptom of acute compartment syndrome in the awake alert patient.151 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 acute compartment syndrome. Thus 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. The sensitivity and specificity of pain on passive stretch are similar to those for rest pain.151 
Paresthesia and hypoesthesia 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.163,167 Ulmer151 reports a sensitivity of 13% and specificity of 98% for the clinical finding of paresthesia in acute compartment syndrome, a false-negative rate that precludes this symptom from being a useful diagnostic tool. 
Paralysis of muscle groups affected by the acute compartment syndrome is recognized as being a late sign.151 This sign has equally low sensitivity as others in predicting the presence of acute compartment syndrome, 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. If a motor deficit develops, full recovery is unusual.17,27,29,126,131,165 
Bradley17 reported full recovery in only 13% of patients with paralysis as a sign of their acute compartment syndrome. 
Palpable swelling in the compartment affected may be a further sign of compartment syndrome, although the degree of swelling is difficult to assess accurately, making this sign very subjective. Casts or dressings often obscure compartments at risk and prevent assessment of swelling.75 Some compartments such as the deep posterior compartment of the leg are completely buried under the muscle compartments, obscuring any swelling. 
Peripheral pulses and capillary return are always intact in acute compartment syndrome unless there is major arterial injury or disease or in the very late stages of acute compartment syndrome when amputation is inevitable. If acute compartment syndrome is suspected and pulses are absent, then arteriography is indicated. Conversely, it is dangerous to exclude the diagnosis of acute compartment syndrome because distal pulses are present. 
Using a combination of clinical symptoms and signs increases their sensitivity as diagnostic tools.151 To achieve a probability of over 90% of acute compartment syndrome being present, however, three clinical findings must be noted. The third clinical finding is paresis; thus, to achieve an accurate clinical diagnosis of acute compartment syndrome 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. 

Compartment Pressure Monitoring

Several techniques were developed to measure ICP once it was appreciated that acute compartment syndrome was caused by increased tissue pressure within the affected compartment. Because raised tissue pressure is the primary event in acute compartment syndrome, changes in ICP will precede the clinical symptoms and signs.96 
There are a number of methods available to measure ICP. One of the first to be used was the needle manometer method, using a needle introduced into the compartment and connected to a column filled partly with saline and partly with air.162 A syringe filled with air is attached to this column, as is a pressure manometer or transducer. The ICP is the pressure that is required to inject air into the tubing and flatten the meniscus between the saline and the air. This method was modified by Matsen et al. to allow infusion of saline into the compartment.90,91 The ICP is the pressure resistance to infusion of saline. These methods, although simple and inexpensive, have some drawbacks. A danger exists of too large a volume being infused, possibly inducing acute compartment syndrome. It is probably the least accurate of the measurement techniques available, with falsely high values having been recorded in comparison with other techniques104 and falsely low values in cases of very high ICP.146 A needle with only one perforation at its tip also can become easily blocked. 
The wick catheter was first described for use in acute compartment syndrome by Mubarak et al.105 This is a modification of the needle technique, in which fibrils protrude from the bore of the catheter assembly. This allows a large surface area for measurement and prevents obstruction of the needle; it is 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.127 This operates on the same principle as the wick catheter in that 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. 29-3). The interstitial pressure is measured through a column of saline attached to a transducer. Patency can be confirmed by gentle pressure over the catheter tip; an immediate rise in the pressure should be seen. Care must be taken to avoid the presence of air bubbles in the system as this can, like the wick catheter, result in falsely low readings. The slit catheter is more accurate than the continuous infusion method104 and is as accurate as the wick catheter.138 
Figure 29-3
The tip of a slit catheter, which can be made easily from standard equipment by cutting two slits in the tip of the catheter.
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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 1984 and measurements were correlated with conventional pressure monitoring systems.93 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.166 These systems are more expensive, however, and are a potential problem for resterilization. 
All the methods above measure ICP, which is an indirect way of measuring muscle blood flow and oxygenation. Near-infrared spectroscopy measures tissue oxygen saturation noninvasively by means of a probe placed on the skin. This has proved to correlate to tissue pressures experimentally5 and in human volunteers.42 In patients with acute compartment syndrome 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.143 It has also been used to demonstrate the hyperemic response to injury in tibial fracture.144 The technique has promise but requires further validation in humans subjected to injury. 
ICP is usually monitored in the anterior compartment because this is most commonly involved in acute compartment syndrome and is easily accessible.98 There is a risk of missing an acute compartment syndrome in the deep posterior compartments and some authors recommend measurement of both,61 but measuring two compartments is much more cumbersome. If the anterior compartment alone is monitored, the surgeon must be aware of the small chance of deep posterior acute compartment syndrome and measure the deep posterior compartment pressures if there are unexplained symptoms in the presence of anterior compartment pressures with a safe difference between the diastolic pressure and the tissue pressure P). It is important to measure the peak pressure within the limb, which usually occurs within 5 cm of the level of the fracture.61 Recommended catheter placement for each of the anatomic areas is summarized in Table 29-4
Table 29-4
Recommended Catheter Placements for Compartmental Pressure Monitoring
Anatomic Area Catheter Placement
Thigh Anterior compartment
Leg Anterior compartment
Deep posterior if clinically suspected
Foot Interosseous compartments
Consider calcaneal compartment in hindfoot injuries
Forearm Flexor compartment
Hand Interosseous compartment
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Threshold for Decompression in Acute Compartment Syndrome

Much debate has occurred about the critical pressure threshold, beyond which decompression of acute compartment syndrome is required. After appreciation of the nature of acute compartment syndrome being raised ICP, debate centered around the use of tissue pressure alone as indication of the need for decompression. One level believed to be critical was 30 mm Hg of ICP because this is a value close to capillary blood pressure.53,107 Some authors felt that 40 mm Hg of tissue pressure should be the threshold for decompression,50,90,93,131 although some recognized a significant variation between individuals in their tolerance of raised ICP.50,92 In a series of patients with tibial fractures, a tissue pressure of 50 mm Hg was recommended as a pressure threshold for decompression in normotensive patients.51 
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.162 were the first to suggest the importance of the difference between the diastolic blood pressure and tissue pressure, or ΔP. 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. There is now good evidence from experimental work to support this concept60,83 or the similar concept that the difference between mean arterial pressure and tissue pressure should not be less than 30 mm Hg in normal muscle or 40 mm Hg in muscle subject to trauma63 or antecedent ischemia.12 
This concept was tested in a clinical study designed to test the hypothesis of the differential pressure as a threshold for decompression.98 One hundred and sixteen patients with tibial diaphyseal fractures underwent continuous ICP monitoring both perioperatively and for at least 24 hours postoperatively. The differential pressure between the diastolic blood pressure and the ICP was recorded. Mean pressures over a 12-hour period were calculated to include the duration of elevated pressure in the analysis. Three patients had ΔP of less than 30 mm Hg for more than 2 hours and underwent fasciotomy. Of the remaining patients, all maintained a ΔP greater than 30 mm Hg despite a number of those having an ICP greater than 40 mm Hg. None of these patients underwent fasciotomy and none had any sequelae of acute compartment syndrome at final review. The authors concluded that a ΔP of 30 mm Hg is a safe threshold for decompression in acute compartment syndrome. This has been validated by the same group who examined the outcome in terms of muscle power and returned to function in two groups of patients with tibial fractures.161 The first group of patients all had an ICP of greater than 30 mm Hg and the second all had an ICP less than 30 mm Hg. Both groups maintained a ΔP of greater than 30 mm Hg. There were no differences in the outcomes between the two groups. The concept of the use of ΔP is also supported by Ovre et al.,117 who found an unacceptably high rate of fasciotomies (29%) using an ICP of 30 mm Hg as a threshold for decompression. 
The sensitivity and specificity of continuous compartment pressure monitoring has recently been reported.99 Using a pressure threshold of a ΔP of 30 mm Hg for more than 2 hours in 850 patients there were 11 false positives and 9 false negatives giving a sensitivity of 94% and a specificity of 98.4%. The positive predictive value was 92.8% and the negative predictive value was 98.7%. To achieve similar accuracy with clinical symptoms and signs three signs need to be present with the third being paralysis.151 The authors 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 acute compartment syndrome the risk should be weighted slightly toward false positives or so-called unnecessary fasciotomy which was felt to be preferable to false negatives or missing the acute compartment syndrome.99 
To derive the full benefit of monitoring for acute compartment syndrome, the diagnosis should be made on the basis of sequential differential pressure measurements rather than awaiting the development of clinical symptoms and signs. It has been demonstrated that this approach reduces both the delay to fasciotomy and the development of sequelae97 and that the appearance of clinical symptoms and signs lags behind the pressure changes.98 This is well illustrated in a study in which the authors claimed to compare intracompartmental pressure monitoring with clinical findings in a randomized trial of178 tibial fractures,56 but their threshold for fasciotomy in both groups was the appearance of clinical signs regardless of the pressure measurement. Not surprisingly, the authors found no differences in the outcome of the two groups but had a total of 27 complications of neglected acute compartment syndrome excluding nonunions. 
All of the work quoted above was 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 Hadley82 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 the development of muscle necrosis and sequelae.29,77,79,83,98,119,120,163 Continuous pressure monitoring allows a clear record of the trend of the tissue pressure measurements. 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. Fasciotomy should not be performed based on a single pressure reading except in extreme cases. Using this protocol, delay to fasciotomy and the sequelae of acute compartment syndrome are reduced without unnecessary fasciotomies being performed.98 
Overtreatment has been cited as a problem with continuous monitoring,69 but this study did not consider the importance of the duration of raised ICP in the diagnosis of acute compartment syndrome. Some authors have found compartment pressure monitoring less useful but used clinical symptoms and signs as their indication for fasciotomy with pressure monitoring only as an adjunct.3,56 For ICP monitoring to be most effective in reducing delay, it must be used as the primary indication for fasciotomy. 

Surgical and Applied Anatomy

Thigh

The thigh is divided into three main compartments, both of which are bounded by the fascia lata and separated by the medial and lateral intermuscular septa (Fig. 29-4). Their contents and the clinical signs of compartment syndrome in each compartment are summarized in Table 29-5. Involvement of the adductor compartment is rare. 
A, anterior; Ad, adductor; P, posterior.
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Figure 29-4
A cross section of the thigh demonstrating the three compartments and the access to them.
A, anterior; Ad, adductor; P, posterior.
A, anterior; Ad, adductor; P, posterior.
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Table 29-5
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
Obturator nerve Sensory changes rare
Weakness—hip adduction
X

Leg

There are four compartments in the leg—anterior, lateral, superficial posterior, and deep posterior (Fig. 29-5). 
Figure 29-5
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.
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.
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Figure 29-5
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.
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.
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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 acute compartment syndrome are listed in Table 29-6
Table 29-6
Compartments of the Leg, Their Contents, and Clinical Signs of Acute Compartment Syndrome
Compartment Contents Signs
Anterior Tibialis anterior Pain on passive flexion—ankle/toes
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
Plantaris
Sural nerve
Weakness—plantar flexion
Deep posterior Tibialis posterior Pain on passive ankle/toe extension/foot eversion
Flexor digitorum longus
Flexor hallucis longus Numbness—sole of foot
Posterior tibial nerve Weakness—toe/ankle flexion, foot inversion
X
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 septum. Its contents and the clinical signs of involvement in acute compartment syndrome are detailed in Table 29-6. The deep peroneal nerve may rarely be affected as it passes through the lateral compartment en route to the anterior compartment. 
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 acute compartment syndrome are summarized in Table 29-6
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 29-6 lists the contents of the deep posterior compartment and the likely clinical signs in acute compartment syndrome. 

Foot

Until recently, most authorities believed that there were four compartments in the foot—medial, lateral, central, and interosseous (Fig. 29-6). 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 29-7
Figure 29-6
A cross section of the foot showing access from the dorsum of the foot to the compartments.
I, interosseous.
I, interosseous.
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Table 29-7
Compartments of the Foot and Their Contents
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Table 29-7
Compartments of the Foot and Their Contents
Compartment Contents
Medial Intrinsic muscles of the great toe
Lateral Flexor digiti minimi
Abductor digiti minimi
Central
• Superficial Flexor digitorum brevis
• Deep (calcaneal) Quadratus plantae
Adductor hallucis Adductor hallucis
Interosseous × 4 Interosseous muscles
Digital nerves
X
Manoli and Weber challenged the concept of four compartments using cadaver infusion techniques.80 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. 29-7) 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 lie 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 acute compartment syndrome.49 The clinical diagnosis of acute compartment syndrome should be suspected in the presence of severe swelling, but differentiating the affected compartments is extremely difficult. 
Figure 29-7
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.
The medial approach for release of the calcaneal compartment is shown. FHL, flexor hallucis longus.
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Figure 29-7
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.
The medial approach for release of the calcaneal compartment is shown. FHL, flexor hallucis longus.
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Arm

There are two compartments in the arm: anterior and posterior (Fig. 29-8). 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 acute compartment syndrome are detailed in Table 29-8. In late cases paralysis of the muscles innervated by the median, ulna, and radial nerves is seen. 
Figure 29-8
A cross section of the arm showing the anterior compartment containing biceps (B) and brachialis (Br), and the posterior compartment containing triceps (T).
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Table 29-8
Compartments of the Arm, Their Contents, and Clinical Signs of Acute Compartment Syndrome
Compartment Contents Signs
Anterior Biceps
Brachialis
Coracobrachialis
Median nerve
Ulnar nerve
Musculocutaneous nerve
Lateral cutaneous nerve
Antebrachial nerve
Radial nerve (distal third)
Pain on passive elbow extension
Numbness—median/ulnar distribution
Numbness—volar/lateral distal forearm
Weakness—elbow flexion
Weakness—median/ulnar motor function
Posterior Triceps
Radial nerve
Ulnar nerve (distally)
Pain on passive elbow flexion
Numbness—ulnar/radial distribution
Weakness—elbow extension
Weakness—radial/ulnar motor function
X
The posterior compartment has the same boundaries as the anterior but lies posterior to the humerus. Its contents and the clinical signs of acute compartment syndrome are listed in Table 29-8

Forearm

The forearm contains three compartments: volar, dorsal, and “the mobile wad” (Fig. 29-9). The volar compartment has the ulna, radius, and interosseous membrane as its posterior limit and the antebrachial fascia as its anterior limit. Table 29-9 lists the contents and clinical signs of acute compartment syndrome 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,43 but in practice it is not usually necessary to distinguish between these at fasciotomy.20 
Figure 29-9
A cross section of the midforearm.
 
The pronator quadratus compartment is not shown as it lies in the distal forearm. D, dorsal; V, volar.
The pronator quadratus compartment is not shown as it lies in the distal forearm. D, dorsal; V, volar.
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Figure 29-9
A cross section of the midforearm.
The pronator quadratus compartment is not shown as it lies in the distal forearm. D, dorsal; V, volar.
The pronator quadratus compartment is not shown as it lies in the distal forearm. D, dorsal; V, volar.
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Table 29-9
Compartments of the Forearm, Their Contents, and the Clinical Signs of Acute Compartment Syndrome
Compartment Contents Signs
Volar Flexor carpi radialis longus and brevis
Flexor digitorum superficialis and profundus
Pronator teres
Pronator quadratus
Median nerve
Ulnar nerve
Pain on passive wrist/finger extension
Numbness—median/ulnar distribution
Weakness—wrist/finger flexion
Weakness—median/ulnar motor function in hand
Dorsal Extensor digitorum
Extensor pollicis longus
Abductor pollicis longus
Extensor carpi ulnaris
Pain—passive wrist/finger flexion
Weakness—wrist/finger flexion
Mobile wad Brachioradialis
Extensor carpi radialis
Pain on passive wrist flexion/elbow extension
Weakness—wrist extension/elbow flexion
X
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 acute compartment syndrome are summarized in Table 29-9

Hand

General agreement exists that the hand has ten muscle compartments: one thenar, one hypothenar, one adductor pollicis, four dorsal interosseous, and three volar interosseous compartments (Fig. 29-10). 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.48 The contents of the hand compartments are detailed in Table 29-10
Figure 29-10
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.
The adductor pollicis lies more distally. CP, central palmar; H, hypothenar; I, interosseous; T, thenar.
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Figure 29-10
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.
The adductor pollicis lies more distally. CP, central palmar; H, hypothenar; I, interosseous; T, thenar.
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Table 29-10
The Compartments of the Hand and Their Contents
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Table 29-10
The Compartments of the Hand and Their Contents
Compartment Contents
Thenar Abductor pollicis brevis
Flexor pollicis brevis
Opponens pollicis
Hypothenar Abductor digiti minimi
Flexor digiti minimi
Opponens digiti minimi
Dorsal interosseous × 4 Dorsal interossei
Volar interossei × 3 Volar interossei
Adductor pollicis Adductor pollicis
X

Treatment

The single most effective treatment for acute compartment syndrome is fasciotomy, which if delayed can cause devastating complications. Nevertheless, other preliminary measures should be taken in cases of impending acute compartment syndrome. 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.38 The split and spread cast is the only method that can accommodate increasing limb swelling.161 The limb should not be elevated above the height of the heart as this reduces the AV gradient.92 Hypotension should be corrected because this will reduce perfusion pressure. Oxygen therapy should be instituted to ensure maximum oxygen saturation. 

Fasciotomy

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 acute compartment syndrome. It is essential to visualize all contained muscles in their entirety (Fig. 29-11) 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.39 
Figure 29-11
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.
Note that the incision extends the whole length of the muscle compartment allowing inspection of all muscle groups.
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Figure 29-11
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.
Note that the incision extends the whole length of the muscle compartment allowing inspection of all muscle groups.
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In the leg, all four compartments should be released. One of the most commonly used techniques is the double incision four-compartment fasciotomy.106 The anterior and lateral compartments are released through a lateral skin incision over the intermuscular septum between the compartments (Fig. 29-5). 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 (Fig. 29-11). 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 (Fig. 29-5). 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. 29-12). 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 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.121 
Figure 29-12
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.
The superficial posterior compartment is being retracted to display the deep compartment. The scissors are deep to the fascia overlying the deep posterior compartment.
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Figure 29-12
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.
The superficial posterior compartment is being retracted to display the deep compartment. The scissors are deep to the fascia overlying the deep posterior compartment.
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Single incision fasciotomy of all four compartments was first described using excision of the fibula,74 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.22 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.106,154 
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. 29-13),148 although a medial incision can be used over the adductors if considered necessary (Fig. 29-4). 
Figure 29-13
Fasciotomy of the thigh through a single lateral incision.
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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 (Fig. 29-6). 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 (Fig. 29-7).111,130 
Fasciotomy of the arm is performed through anterior and posterior incisions (Fig. 29-8) when the compartments are easily visualized. On rare occasions the deltoid muscle should also be decompressed.28 
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 biceps tendon at the elbow to the palm of the hand to allow carpal tunnel decompression that is usually necessary (Fig. 29-14). Fascial incision then allows direct access to the compartment (Fig. 29-9). The deep flexors must be carefully inspected after fascial incision. Separate exposure and decompression of pronator quadratus may be necessary.20 Usually volar fasciotomy is sufficient to decompress the forearm,29 but if ICP remains elevated in the dorsal compartment perioperatively, then dorsal compression is easily performed through a straight dorsal incision (Fig. 29-9). 
Figure 29-14
Fasciotomy of the forearm in a case of crush syndrome.
 
There is necrosis of the forearm flexors proximally. The carpal tunnel has been decompressed.
There is necrosis of the forearm flexors proximally. The carpal tunnel has been decompressed.
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Figure 29-14
Fasciotomy of the forearm in a case of crush syndrome.
There is necrosis of the forearm flexors proximally. The carpal tunnel has been decompressed.
There is necrosis of the forearm flexors proximally. The carpal tunnel has been decompressed.
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Decompression of the hand can usually be adequately achieved using two dorsal incisions that allow access to the interosseous compartments (Fig. 29-10). This may often be 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.58 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.29 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.68 A further disadvantage is the prolonged time required to achieve closure, which may be up to 10 days.11,68 
Split skin grafting, although offering immediate skin cover, has the disadvantage of a high rate of long-term morbidity.35 The recent introduction of vacuum-assisted closure (VAC) systems is likely to be a significant advantage in this area and may reduce the need for split skin grafting with a low complication rate.160 

Management of Associated Fractures

As is now generally accepted, fractures, especially of the long bones, should be stabilized in the presence of acute compartment syndrome treated by fasciotomy.40,44,126,150 In reality the treatment of the fracture should not be altered by the presence of an acute compartment syndrome, although cast management of a tibial fracture is contraindicated in the presence of acute compartment syndrome. 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 acute compartment syndrome.76,103 This was refuted by other studies examining intercompartmental pressures during and after tibial nailing. McQueen et al.97 studying reamed intramedullary nailing and Tornetta and French149 studying unreamed intramedullary nailing agreed that the ICP increased perioperatively and dissipated postoperatively, and that nailing did not increase the likelihood of acute compartment syndrome. Nassif et al.114 found no differences in ICP between reamed and unreamed nailing. 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 acute compartment syndrome.141 
Several factors may raise ICP during stabilization of tibial fractures. These include traction which raises pressure in the deep posterior compartment by approximately 6% per kilogram of weight applied.137 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.89 Thus excessive traction, poor positioning of the thigh bar, and high elevation of the leg should be avoided in patients at risk of acute compartment syndrome. 

Complications of Acute Compartment Syndrome

Complications of acute compartment syndrome 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 acute compartment syndrome.101 Delay to fasciotomy of more than 6 hours is likely to cause significant sequelae,128 including muscle contractures, muscle weakness, sensory loss, infection, and nonunion of fractures.23,27,41,54,59,71,79,87,89,98,103,123,140 In severe cases amputation may be necessary because of infection or lack of function.33 

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 acute compartment syndrome 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.122 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.122 
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 circumstances a thorough debridement of necrotic muscle is mandatory. 

Author’s Preferred Method of Management

 
 

Early diagnosis of acute compartment syndrome is essential, and it is important to be aware of the patients at risk of developing acute compartment syndrome. Good clinical examination techniques in the alert patient will help to identify the compartments at risk. Compartment monitoring should be used in all “at risk” patients as defined in Table 29-3. 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.

 

Fasciotomy is performed on the basis of a persistent differential pressure of less than 30 mm Hg (Fig. 29-15). 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.

 
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Figure 29-15
Compartment pressure monitoring.
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I 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 should then be applied. A “re-look” 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. I 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.

Future Directions

Acute compartment syndrome remains a potentially devastating complication of fracture that continues to be a significant cause of disability and successful litigation.14,136 In a review of Canadian legal cases relating to ACS between 1998 and 2008 55% of cases had an unfavorable outcome for doctors or judgement 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.136 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.14 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.158,164 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. 
Other future developments are likely to center on methods of measuring blood flow directly rather than indirectly by ICP measurement. Noninvasive methods of diagnosing acute compartment syndrome are being examined.135 One such example is near-infrared spectroscopy, which measures the amount of oxygenated hemoglobin in muscle tissues transcutaneously.5,42,64,142 
Methods of reducing the effects of acute compartment syndrome 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 acute compartment syndrome with promising results.72 This work should be extended to human studies in an attempt to reduce the effects of acute compartment syndrome in the clinical situation. 
Prevention of acute compartment syndrome is the ultimate goal in its management. Attempts have been made to reduce ICP with the administration of hypertonic fluids intravenously,13 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.116 Whether this technique can be useful clinically remains to be seen. 

References

Adams JG Jr, Dhar A, Shukla SD, et al. Effect of pentoxifylline on tissue injury and platelet-activating factor production during ischemia-reperfusion injury. J Vasc Surg. 1995;21:742–748.
Adkison DP, Bosse MJ, Gaccione DR, et al. Anatomical variations in the course of the superficial peroneal nerve. J Bone Joint Surg Am. 1991;73:112–114.
Al-Dadah OQ, Darrah C, Cooper A, et al. Continuous compartment pressure monitoring vs. clinical monitoring in tibial diaphyseal fractures. Injury. 2008;39:1204–1209.
Almdahl SM, Due J Jr, Samdal FA. Compartment syndrome with muscle necrosis following repair of hernia of tibialis anterior. Case report. Acta Chir Scand. 1987;153:695.
Arbabi S, Brundage SI, Gentilello LM. Near-infrared spectroscopy: a potential method for continuous, transcutaneous monitoring for compartmental syndrome in critically injured patients. J Trauma. 1999;47:829–833.
Ashton H. Critical closing pressure in human peripheral vascular beds. Clin Sci. 1962;22:79–87.
Ashton H. The effect of increased tissue pressure on blood flow. Clin Orthop Relat Res. 1975;15–26.
Bae DS, Kadiyala RK, Waters PM. Acute compartment syndrome in children: contemporary diagnosis, treatment, and outcome. J Pediatr Orthop. 2001;21:680–688.
Bardenheuer L. Die Anlang und Behandlung der ischaemische Muskellahmungen und Kontrakturen. Samml Klin Vortrage. 1911;122:437.
Belanger M, Fadale P. Compartment syndrome of the leg after arthroscopic examination of a tibial plateau fracture. Case report and review of the literature. Arthroscopy. 1997;13:646–651.
Berman SS, Schilling JD, McIntyre KE, et al. Shoelace technique for delayed primary closure of fasciotomies. Am J Surg. 1994;167:435–436.
Bernot M, Gupta R, Dobrasz J, et al. The effect of antecedent ischemia on the tolerance of skeletal muscle to increased interstitial pressure. J Orthop Trauma. 1996;10:555–559.
Better OS, Zinman C, Reis DN, et al. Hypertonic mannitol ameliorates intracompartmental tamponade in model compartment syndrome in the dog. Nephron. 1991;58:344–346.
Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment syndrome. J Bone Joint Surg Am. 2004;86-A:864–868.
Blaisdell FW. The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review. Cardiovasc Surg. 2002;10:620–630.
Blick SS, Brumback RJ, Poka A, et al. Compartment syndrome in open tibial fractures. J Bone Joint Surg Am. 1986;68:1348–1353.
Bradley EL III. The anterior tibial compartment syndrome. Surg Gynecol Obstet. 1973;136:289–297.
Buhr AJ, Cooke AM. Fracture patterns. Lancet. 1959;1:531–536.
Burton AC. On the physical equilibrium of small blood vessels. Am J Physiol. 1951;164:319–329.
Chan PS, Steinberg DR, Pepe MD, et al. The significance of the three volar spaces in forearm compartment syndrome: a clinical and cadaveric correlation. J Hand Surg Am. 1998;23:1077–1081.
Chautems RC, Irmay F, Magnin M, et al. Spontaneous anterior and lateral tibial compartment syndrome in a type I diabetic patient: case report. J Trauma. 1997;43:140–141.
Cooper GG. A method of single-incision, four compartment fasciotomy of the leg. Eur J Vasc Surg. 1992;6:659–661.
Court-Brown C, McQueen M. Compartment syndrome delays tibial union. Acta Orthop Scand. 1987;58:249–252.
Court-Brown CM, Byrnes T, McLaughlin G. Intramedullary nailing of tibial diaphyseal fractures in adolescents with open physes. Injury. 2003;34:781–785.
Court-Brown CM, McBirnie J. The epidemiology of tibial fractures. J Bone Joint Surg Br. 1995;77:417–421.
Davis ET, Harris A, Keene D, et al. The use of regional anaesthesia in patients at risk of acute compartment syndrome. Injury. 2006;37:128–133.
DeLee JC, Stiehl JB. Open tibia fracture with compartment syndrome. Clin Orthop Relat Res. 1981;160:175–184.
Diminick M, Shapiro G, Cornell C. Acute compartment syndrome of the triceps and deltoid. J Orthop Trauma. 1999;13:225–227.
Duckworth AD, Mitchell SE, Molyneux SG, et al. Acute compartment syndrome of the forearm. J Bone Joint Surg Am. 2012;94:e63.
Dudgeon LS. Volkmann’s Contracture. Lancet. 1902;1:78–85.
Dunlop D, Parker PJ, Keating JF. Ruptured Baker’s cyst causing posterior compartment syndrome. Injury. 1997;28:561–562.
Eaton RG, Green WT. Volkmann’s ischemia. A volar compartment syndrome of the forearm. Clin Orthop Relat Res. 1975;113:58–64.
Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma. 1996;40:342–344.
Finkemeier CG, Schmidt AH, Kyle RF, et al. A prospective, randomized study of intramedullary nails inserted with and without reaming for the treatment of open and closed fractures of the tibial shaft. J Orthop Trauma. 2000;14:187–193.
Fitzgerald AM, Gaston P, Wilson Y, et al. Long-term sequelae of fasciotomy wounds. Br J Plast Surg. 2000;53:690–693.
Foisie PS. Volkmann’s Ischemic Contracture. N Engl J Med. 1942;226:679.
Frink M, Klaus AK, Kuther G, et al. Long term results of compartment syndrome of the lower limb in polytraumatised patients. Injury. 2007;38:607–613.
Garfin SR, Mubarak SJ, Evans KL, et al. Quantification of intracompartmental pressure and volume under plaster casts. J Bone Joint Surg Am. 1981;63:449–453.
Gaspard DJ, Kohl RD Jr. Compartmental syndromes in which the skin is the limiting boundary. Clin Orthop Relat Res. 1975;113:65–68.
Gelberman RH. Upper extremity compartment syndromes. In: Mubarak SJ, Hargens AR, eds. 1st ed. Philadelphia, PA: Saunders WB.; 1981.
Gelberman RH, Szabo RM, Williamson RV, et al. Tissue pressure threshold for peripheral nerve viability. Clin Orthop Relat Res. 1983;178:285–291.
Gentilello LM, Sanzone A, Wang L, et al. Near-infrared spectroscopy versus compartment pressure for the diagnosis of lower extremity compartmental syndrome using electromyography-determined measurements of neuromuscular function. J Trauma. 2001;51:1–8, discussion.
Gerber A, Masquelet AC. Anatomy and intracompartmental pressure measurement technique of the pronator quadratus compartment. J Hand Surg Am. 2001;26:1129–1134.
Gershuni DH, Mubarak SJ, Yaru NC, et al. Fracture of the tibia complicated by acute compartment syndrome. Clin Orthop Relat Res. 1987;217:221–227.
Gibson MJ, Barnes MR, Allen MJ, et al. Weakness of foot dorsiflexion and changes in compartment pressures after tibial osteotomy. J Bone Joint Surg Br. 1986;68:471–475.
Gillani S, Cao J, Suzuki T, et al. The effect of ischemia reperfusion injury on skeletal muscle. Injury. 2012;43:670–675.
Griffiths DL. Volkmann’s ischemic contracture. Br J Surg. 1940;28:239–260.
Guyton GP, Shearman CM, Saltzman CL. Compartmental divisions of the hand revisited. Rethinking the validity of cadaver infusion experiments. J Bone Joint Surg Br. 2001A;83:241–244.
Guyton GP, Shearman CM, Saltzman CL. The compartments of the foot revisited. Rethinking the validity of cadaver infusion experiments. J Bone Joint Surg Br. 2001B;83:245–249.
Halpern AA, Nagel DA. Compartment syndromes of the forearm: early recognition using tissue pressure measurements. J Hand Surg Am. 1979;4:258–263.
Halpern AA, Nagel DA. Anterior compartment pressures in patients with tibial fractures. J Trauma. 1980;20:786–790.
Hargens AR, Akeson WH, Mubarak SJ, et al. Fluid balance within the canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg Am. 1978;60:499–505.
Hargens AR, Akeson WH, Mubarak SJ, et al. Kappa Delta Award paper. Tissue fluid pressures: from basic research tools to clinical applications. J Orthop Res. 1989;7:902–909.
Hargens AR, Romine JS, Sipe JC, et al. Peripheral nerve-conduction block by high muscle-compartment pressure. J Bone Joint Surg Am. 1979;61:192–200.
Harrington P, Bunola J, Jennings AJ, et al. Acute compartment syndrome masked by intravenous morphine from a patient-controlled analgesia pump. Injury. 2000;31:387–389.
Harris IA, Kadir A, Donald G. Continuous compartment pressure monitoring for tibia fractures: does it influence outcome? J Trauma. 2006;60:1330–1335.
Hartsock LA, O’Farrell D, Seaber AV, et al. Effect of increased compartment pressure on the microcirculation of skeletal muscle. Microsurgery. 1998;18:67–71.
Havig MT, Leversedge FJ, Seiler JG III. Forearm compartment pressures: an in vitro analysis of open and endoscopic assisted fasciotomy. J Hand Surg Am. 1999;24:1289–1297.
Hayes G, Liauw S, Romaschin AD. Separation of reperfusion injury from ischemia induced necrosis. Surg Forum. 1988;39:306–308.
Heckman MM, Whitesides TE Jr, Grewe SR, et al. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993;7:199–210.
Heckman MM, Whitesides TE Jr, Grewe SR, et al. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of the fracture. J Bone Joint Surg Am. 1994;76:1285–1292.
Henriksen O. Orthostatic changes of blood flow in subcutaneous tissue in patients with arterial insufficiency of the legs. Scand J Clin Lab Invest. 1974;34:103–109.
Heppenstall RB, Sapega AA, Scott R, et al. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988;226:138–155.
Hildebrand O. Die Lehre von den ischamischen Muskellahmungen und Kontrakturen. Zeitschrift fur Chirurgie. 1906;108:44–201.
Holden CE. The pathology and prevention of Volkmann’s ischaemic contracture. J Bone Joint Surg Br. 1979;61-B:296–300.
Hope MJ, McQueen MM. Acute compartment syndrome in the absence of fracture. J Orthop Trauma. 2004;18:220–224.
Hsu SI, Thadhani RI, Daniels GH. Acute compartment syndrome in a hypothyroid patient. Thyroid. 1995;5:305–308.
Janzing HM, Broos PL. Dermatotraction: an effective technique for the closure of fasciotomy wounds: a preliminary report of fifteen patients. J Orthop Trauma. 2001A;15:438–441.
Janzing HM, Broos PL. Routine monitoring of compartment pressure in patients with tibial fractures: Beware of overtreatment! Injury. 2001B;32:415–421.
Jepson PN. Ischaemic contracture: experimental study. Ann Surg. 1926;84:785–795.
Karlstrom G, Lonnerholm T, Olerud S. Cavus deformity of the foot after fracture of the tibial shaft. J Bone Joint Surg Am. 1975;57:893–900.
Kearns SR, Daly AF, Sheehan K, et al. Oral vitamin C reduces the injury to skeletal muscle caused by compartment syndrome. J Bone Joint Surg Br. 2004;86:906–911.
Kearns SR, Moneley D, Murray P, et al. Oral vitamin C attenuates acute ischaemia-reperfusion injury in skeletal muscle. J Bone Joint Surg Br. 2001;83:1202–1206.
Kelly RP, Whitesides TE. Transfibular route for fasciotomy of the leg. J Bone Joint Surg Am. 1967;49:1022–1023.
Kosir R, Moore FA, Selby JH, et al. Acute lower extremity compartment syndrome (ALECS) screening protocol in critically ill trauma patients. J Trauma. 2007;63:268–275.
Koval KJ, Clapper MF, Brumback RJ, et al. Complications of reamed intramedullary nailing of the tibia. J Orthop Trauma. 1991;5:184–189.
Labbe R, Lindsay T, Walker PM. The extent and distribution of skeletal muscle necrosis after graded periods of complete ischemia. J Vasc Surg. 1987;6:152–157.
Lam R, Lin PH, Alankar S, et al. Acute limb ischemia secondary to myositis-induced compartment syndrome in a patient with human immunodeficiency virus infection. J Vasc Surg. 2003;37:1103–1105.
Lindsay TF, Liauw S, Romaschin AD, et al. The effect of ischemia/reperfusion on adenine nucleotide metabolism and xanthine oxidase production in skeletal muscle. J Vasc Surg. 1990;12:8–15.
Manoli A, Weber TG. Fasciotomy of the foot: an anatomical study with special reference to release of the calcaneal compartment. Foot Ankle. 1990;10:267–275.
Mar GJ, Barrington MJ, McGuirk BR. Acute compartment syndrome of the lower limb and the effect of postoperative analgesia on diagnosis. Br J Anaesth. 2009;102:3–11.
Mars M, Hadley GP. Raised compartmental pressure in children: a basis for management. Injury. 1998;29:183–185.
Matava MJ, Whitesides TE Jr, Seiler JG III, et al. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma. 1994;37:50–58.
Mathews PV, Perry JJ, Murray PC. Compartment syndrome of the well leg as a result of the hemilithotomy position: a report of two cases and review of literature. J Orthop Trauma. 2001;15:580–583.
Matsen FA III. Compartmental Syndromes. 1st ed. New York, NY: Grune and Stratton; 1980.
Matsen FA III, Clawson DK. The deep posterior compartmental syndrome of the leg. J Bone Joint Surg Am. 1975;57:34–39.
Matsen FA III, King RV, Krugmire RB Jr, et al. Physiological effects of increased tissue pressure. Int Orthop. 1979;3:237–244.
Matsen FA III, Krugmire RB Jr. Compartmental syndromes. Surg Gynecol Obstet. 1978;147:943–949.
Matsen FA III, Mayo KA, Krugmire RB Jr, et al. A model compartmental syndrome in man with particular reference to the quantification of nerve function. J Bone Joint Surg Am. 1977;59:648–653.
Matsen FA III, Mayo KA, Sheridan GW, et al. Monitoring of intramuscular pressure. Surgery. 1976;79:702–709.
Matsen FA III, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartmental syndromes. J Bone Joint Surg Am. 1980;62:286–291.
Matsen FA III, Wyss CR, Krugmire RB Jr, et al. The effects of limb elevation and dependency on local arteriovenous gradients in normal human limbs with particular reference to limbs with increased tissue pressure. Clin Orthop Relat Res. 1980;187–195.
McDermott AG, Marble AE, Yabsley RH. Monitoring acute compartment pressures with the S.T.I.C. catheter. Clin Orthop Relat Res. 1984;190:192–198.
McKee MD, Jupiter JB. Acute exercise-induced bilateral anterolateral leg compartment syndrome in a healthy young man. Am J Orthop (Belle Mead NJ). 1995;24:862–864.
McQueen MM. The effect of acute compartment syndrome on bone blood flow and bone union [Thesis] University of Edinburgh; 1995.
McQueen MM, Christie J, Court-Brown CM. Compartment pressures after intramedullary nailing of the tibia. J Bone Joint Surg Br. 1990;72:395–397.
McQueen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibial diaphyseal fractures. J Bone Joint Surg Br. 1996;78:95–98.
McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 1996;78:99–104.
McQueen MM, Duckworth AD, Aitken SA, et al. The estimated sensitivity and specificity of compartment pressure monitoring for acute compartment syndrome. J Bone Joint Surg Am. 2013;95:673–677.
McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br. 2000;82:200–203.
McQuillan WM, Nolan B. Ischaemia complicating injury. A report of thirty-seven cases. J Bone Joint Surg Br. 1968;50:482–492.
Mithoefer K, Lhowe DW, Vrahas MS, et al. Functional outcome after acute compartment syndrome of the thigh. J Bone Joint Surg Am. 2006;88:729–737.
Moed BR, Strom DE. Compartment syndrome after closed intramedullary nailing of the tibia: a canine model and report of two cases. J Orthop Trauma. 1991;5:71–77.
Moed BR, Thorderson PK. Measurement of intracompartmental pressure: a comparison of the slit catheter, side-ported needle, and simple needle. J Bone Joint Surg Am. 1993;75:231–235.
Mubarak SJ, Hargens AR, Owen CA, et al. The wick catheter technique for measurement of intramuscular pressure. A new research and clinical tool. J Bone Joint Surg Am. 1976;58:1016–1020.
Mubarak SJ, Owen CA. Double-incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg Am. 1977;59:184–187.
Mubarak SJ, Owen CA, Hargens AR, et al. Acute compartment syndromes: diagnosis and treatment with the aid of the wick catheter. J Bone Joint Surg Am. 1978;60:1091–1095.
Mubarak SJ, Wilton NC. Compartment syndromes and epidural analgesia. J Pediatr Orthop. 1997;17:282–284.
Mullett H, Al-Abed K, Prasad CV, et al. Outcome of compartment syndrome following intramedullary nailing of tibial diaphyseal fractures. Injury. 2001;32:411–413.
Murphy JB. Myositis. JAMA. 1914;63:1249–1255.
Myerson M, Manoli A. Compartment syndromes of the foot after calcaneal fractures. Clin Orthop Relat Res. 1993;290:142–150.
Myerson MS. Management of compartment syndromes of the foot. Clin Orthop Relat Res. 1991;271:239–248.
Nario CV. La enfermedad de Volkman experimental. Ann Fac Med Montivideo. 1938;10:87–128.
Nassif JM, Gorczyca JT, Cole JK, et al. Effect of acute reamed versus unreamed intramedullary nailing on compartment pressure when treating closed tibial shaft fractures: a randomized prospective study. J Orthop Trauma. 2000;14:554–558.
Nichol J, Girling F, Jerrard W, et al. Fundamental instability of the small blood vessels and critical closing pressures in vascular beds. Am J Physiol. 1951;164:330–344.
Odland R, Schmidt AH, Hunter B, et al. Use of tissue ultrafiltration for treatment of compartment syndrome: a pilot study using porcine hindlimbs. J Orthop Trauma. 2005;19:267–275.
Ovre S, Hvaal K, Holm I, et al. Compartment pressure in nailed tibial fractures. A threshold of 30 mmHg for decompression gives 29% fasciotomies. Arch Orthop Trauma Surg. 1998;118:29–31.
Peterson F. Uber ischamische Muskellahmung. Arch Klin Chir. 1888;37:675–677.
Petrasek PF, Homer-Vanniasinkam S, Walker PM. Determinants of ischemic injury to skeletal muscle. J Vasc Surg. 1994;19:623–631.
Prasarn ML, Ouellette EA, Livingstone A, et al. Acute pediatric upper extremity compartment syndrome in the absence of fracture. J Pediatr Orthop. 2009;29:263–268.
Pyne D, Jawad AS, Padhiar N. Saphenous nerve injury after fasciotomy for compartment syndrome. Br J Sports Med. 2003;37:541–542.
Reis ND, Michaelson M. Crush injury to the lower limbs. Treatment of the local injury. J Bone Joint Surg Am. 1986;68:414–418.
Reverte MM, Dimitriou R, Kanakaris NK, et al. What is the effect of compartment syndrome and fasciotomies on fracture healing in tibial fractures? Injury. 2011;42:1402–1407.
Roddie IC, Shepherd JT. Evidence for critical closure of digital resistance vessels with reduced transmural pressure and passive dilatation with increased venous pressure. J Physiol. 1957;136:498–506.
Rodriguez-Merchan EC. Acute compartment syndrome in haemophilia. Blood Coagul Fibrinolysis. 2013;24:677–682.
Rorabeck CH. The treatment of compartment syndromes of the leg. J Bone Joint Surg Br. 1984;66:93–97.
Rorabeck CH, Castle GS, Hardie R, et al. Compartmental pressure measurements: an experimental investigation using the slit catheter. J Trauma. 1981;21:446–449.
Rorabeck CH, Macnab L. Anterior tibial-compartment syndrome complicating fractures of the shaft of the tibia. J Bone Joint Surg Am. 1976;58:549–550.
Rowlands RP. A case of Volkmann’s contracture treated by shortening the radius and ulna. Lancet. 1905;2:1168–1171.
Sanders R. Displaced intra-articular fractures of the calcaneus. J Bone Joint Surg Am. 2000;82:225–250.
Schwartz JT Jr, Brumback RJ, Lakatos R, et al. Acute compartment syndrome of the thigh. A spectrum of injury. J Bone Joint Surg Am. 1989;71:392–400.
Seddon HJ. Volkmann’s ischaemia in the lower limb. J Bone Joint Surg Br. 1966;48:627–636.
Seiler JG III, Valadie AL III, Drvaric DM, et al. Perioperative compartment syndrome. A report of four cases. J Bone Joint Surg Am. 1996;78:600–602.
Shabat S, Carmel A, Cohen Y, et al. Iatrogenic forearm compartment syndrome in a cardiac intensive care unit induced by brachial artery puncture and acute anticoagulation. J Interv Cardiol. 2002;15:107–109.
Shadgan B, Menon M, O’Brien PJ, et al. Diagnostic techniques in acute compartment syndrome of the leg. J Orthop Trauma. 2008;22:581–587.
Shadgan B, Menon M, Sanders D, et al. Current thinking about acute compartment syndrome of the lower extremity. Can J Surg. 2010;53:329–334.
Shakespeare DT, Henderson NJ. Compartmental pressure changes during calcaneal traction in tibial fractures. J Bone Joint Surg Br. 1982;64:498–499.
Shakespeare DT, Henderson NJ, Clough G. The slit catheter: a comparison with the wick catheter in the measurement of compartment pressure. Injury. 1982;13:404–408.
Shereff MJ. Compartment syndromes of the foot. Instr Course Lect. 1990;39:127–132.
Sheridan GW, Matsen FA III, Krugmire RB Jr. Further investigations on the pathophysiology of the compartmental syndrome. Clin Orthop Relat Res. 1977;123:266–270.
Shore BJ, Glotzbecker MP, Zurakowski D, et al. Acute compartment syndrome in children and teenagers with tibial shaft fractures: incidence and multivariable risk factors. J Orthop Trauma. 2013;27:616–621.
Shuler MS, Reisman WM, Cole AL, et al. Near-infrared spectroscopy in acute compartment syndrome: Case report. Injury. 2011;42:1506–1508.
Shuler MS, Reisman WM, Kinsey TL, et al. Correlation between muscle oxygenation and compartment pressures in acute compartment syndrome of the leg. J Bone Joint Surg Am. 2010;92:863–870.
Shuler MS, Reisman WM, Whitesides TE Jr, et al. Near-infrared spectroscopy in lower extremity trauma. J Bone Joint Surg Am. 2009;91:1360–1368.
Stott NS, Zionts LE, Holtom PD, et al. Acute hematogenous osteomyelitis. An unusual cause of compartment syndrome in a child. Clin Orthop Relat Res. 1995;317:219–222.
Styf JR, Crenshaw A, Hargens AR. Intramuscular pressures during exercise. Comparison of measurements with and without infusion. Acta Orthop Scand. 1989;60:593–596.
Sweeney HE, O’Brien GF. Bilateral anterior tibial syndrome in association with the nephrotic syndrome. Report of a case. Arch Intern Med. 1965;116:487–490.
Tarlow SD, Achterman CA, Hayhurst J, et al. Acute compartment syndrome in the thigh complicating fracture of the femur. A report of three cases. J Bone Joint Surg Am. 1986;68:1439–1443.
Tornetta P III, French BG. Compartment pressures during nonreamed tibial nailing without traction. J Orthop Trauma. 1997;11:24–27.
Turen CH, Burgess AR, Vanco B. Skeletal stabilization for tibial fractures associated with acute compartment syndrome. Clin Orthop Relat Res. 1995;315:163–168.
Ulmer T. The clinical diagnosis of compartment syndrome of the lower leg: are clinical findings predictive of the disorder? J Orthop Trauma. 2002;16:572–577.
Veeragandham RS, Paz IB, Nadeemanee A. Compartment syndrome of the leg secondary to leukemic infiltration: a case report and review of the literature. J Surg Oncol. 1994;55:198–200.
Vigasio A, Battiston B, De FG, et al. Compartmental syndrome due to viper bite. Arch Orthop Trauma Surg. 1991;110:175–177.
Vitale GC, Richardson JD, George SM Jr, et al. Fasciotomy for severe, blunt and penetrating trauma of the extremity. Surg Gynecol Obstet. 1988;166:397–401.
Volkmann RV. Die ischaemischen Muskellahmungen und Kontrakturen. Zentrabl Chir. 1882;8:801–803.
Vollmar B, Westermann S, Menger MD. Microvascular response to compartment syndrome-like external pressure elevation: an in vivo fluorescence microscopic study in the hamster striated muscle. J Trauma. 1999;46:91–96.
Walker PM, Lindsay TF, Labbe R, et al. Salvage of skeletal muscle with free radical scavengers. J Vasc Surg. 1987;5:68–75.
Wall CJ, Richardson MD, Lowe AJ, et al. Survey of management of acute, traumatic compartment syndrome of the leg in Australia. ANZ J Surg. 2007;77:733–737.
Wallis FC. Treatment of paralysis and muscular artophy after the prolonged use of splints or of an Esmarch’s cord. The Practitioner. 1907;67:429–436.
Webb LX. New techniques in wound management: vacuum-assisted wound closure. J Am Acad Orthop Surg. 2002;10:303–311.
White TO, Howell GE, Will EM, et al. Elevated intramuscular compartment pressures do not influence outcome after tibial fracture. J Trauma. 2003;55:1133–1138.
Whitesides TE, Haney TC, Morimoto K, et al. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop Relat Res. 1975;113:43–51.
Williams J, Gibbons M, Trundle H, et al. Complications of nailing in closed tibial fractures. J Orthop Trauma. 1995;9:476–481.
Williams PR, Russell ID, Mintowt-Czyz WJ. Compartment pressure monitoring–current UK orthopaedic practice. Injury. 1998;29:229–232.
Willis RB, Rorabeck CH. Treatment of compartment syndrome in children. Orthop Clin North Am. 1990;21:401–412.
Willy C, Gerngross H, Sterk J. Measurement of intracompartmental pressure with use of a new electronic transducer-tipped catheter system. J Bone Joint Surg Am. 1999;81:158–168.
Wright JG, Bogoch ER, Hastings DE. The ‘occult’ compartment syndrome. J Trauma. 1989;29:133–134.
Yamada S. Effects of positive tissue pressure on blood flow of the finger. J Appl Physiol. 1954;6:495–500.