Compartment Syndromes

Introduction

Acute compartment syndrome (ACS) can be a devastating injury if diagnosis and treatment are delayed or missed. Physicians evaluating patients with acute long bone fractures, especially of the tibia, should keep ACS in the forefront of their mind when examining the traumatized patient. Although the ability to define ACS has become clearer, much controversy and confusion still remain regarding when ACS exists and when intervention is required. As with many conditions associated with severe loss of function, ACS is a highly litigious topic. Because fasciotomies are not benign procedures, both failing to treat ACS and unnecessary treatment when ACS is not present can lead to significant dysfunction. The goal of this chapter is to provide a review of the pathophysiology of ACS, its diagnosis, and the methods for performing fasciotomy to various areas of the limbs.

In addition, this chapter provides lessons learned and a military perspective on ACS, which is a disease process that has been defined in war. Due to the sheer volume (density of exposure) of injuries, as well as the severity of injury, associated with the recent conflicts throughout the world, much has been learned about the diagnosis, treatment, management, and mismanagement of ACS, but unfortunately, much remains to be learned about this condition. This chapter discusses lessons learned on the management of ACS in both the civilian and military setting and highlights areas requiring further research and understanding.

History

In 1881, Richard von Volkmann published an article in which he attempted to relate the state of irreversible contractures of flexor muscles of the hand to an ischemic process occurring in the forearm. In 1906, Hildebrand first used the term Volkmann's ischemic contracture to describe the endpoint of untreated compartment syndrome and suggested that elevated tissue pressure may be causally related to the ischemic contracture. In 1914, Murphy was the first to suggest that fasciotomy, if done before the development of the contracture, may prevent the contracture from occurring. After almost 100 years of investigation, advancements have been made in the field of ACS, but the ability to definitively and objectively diagnose and treat ACS still remains a challenge.

During and after World War II (WWII), high-velocity gunshot wounds and their concomitant soft tissue injuries were identified as causes for residual muscle contractures of both the upper and lower extremities ( Fig. 17.1 ). Although the existence of arterial trauma complicating a fracture was well known, the concomitant need for fasciotomy at the time of arterial repair was not generally appreciated. During the Korean War, the advancements in vascular surgery allowed for the better restoration of blood flow to ischemic limbs, but the insight into reperfusion injuries was limited. Similar observations were made in 1967 during the Vietnam War by Chandler and Knapp, who also suggested that had more fasciotomies been performed after arterial repair to the extremities, the long-term results might have been better.

In 1958, Ellis brought attention to the existence of ACS in the lower extremity by describing a 2% incidence of ACS associated with tibial fractures. In 1966 and 1967, two different reports described the existence of four separate compartments within the lower leg and the need for addressing each injured compartment. After helping describe the compartments of the lower leg, Whitesides and colleagues went on to postulate a perfusion model for ACS as well as guidelines for decompression, which have been the basis for our understanding of ACS for nearly four decades.

Pathophysiology

Compartment syndrome is a condition that involves increased pressure within a confined tissue space, resulting in ischemia. This increased pressure can come through adding volume to the compartment or by decreasing the volume through external forces. There are many causes of compartment syndrome, yet ultimately, all lead to the increased pressure within a closed compartment resulting in ischemia. The excess tissue pressure within the compartment leads to venous obstruction. If the pressure is left untreated, prolonged muscle and nerve ischemia will lead to irreversible damage to the compartment components.

Any condition increasing the content or reducing the volume of a compartment could lead to compartment syndrome, but the most prevalent cause of compartment syndrome is trauma associated with a fracture. In the cases of fracture, energy from the trauma is dissipated into the bone and muscle, inducing intracellular swelling at the site of the trauma. The fracture site is also susceptible to hematoma after the injury, further amplifying the problem by increasing the volume and, therefore, the pressure of the compartment. High-energy tibial fractures are the most common type of injury associated with compartment syndrome, more specifically, bicondylar plateau fractures and segmental or comminuted tibial shaft fractures ( Figs. 17.2 and 17.3 ). ACS has been reported to complicate tibia fractures in as few as 1% to 9% of all cases and as high as 24% of polytrauma patients. However, it is important to consider that compartment syndrome can also develop secondary to arterial injury, occlusions, reperfusion injury, crush injuries, prolonged malposition, burns, electrocutions, snake venom, stressful athletic activity, contusions, and infiltrations from intravenous (IV) sites. There is also the potential for a compartment syndrome to arise from postresuscitation systemic inflammatory response syndrome after massive blood and fluid resuscitation.

Compartment syndrome may result from a complication of an arterial injury ( Fig. 17.4 ). When it occurs, it is often observed after the restoration of arterial inflow to the compartment, termed reperfusion injury. Before the restoration of arterial inflow, there is a period of nerve and muscle ischemia. During hypoxia, transudation of fluid through the capillary basement membranes and the capillaries of striated muscle can occur. Once arterial inflow has been reestablished, the fluid continues to leak through the basement membrane into the interstitial space, subsequently raising the pressure because of increased content within the compartment.

The pathophysiology of compartment syndrome was poorly understood during the Korean War, and misdiagnosis would often lead to poor outcomes. At the time, the five or six “Ps” (pain, pallor, pulselessness, paralysis, paresthesia, and poikilothermia) were most commonly used to identify compartment syndrome. However, in most cases, all of the “Ps” except pain are signs and symptoms associated with severe ischemia and occur too late in the process to serve as the trigger for optimal intervention and recovery. A series of tourniquet studies by Whitesides et al. in 1971 improved our understanding of the condition. By using a long cuff tourniquet and radioactive xenon imaging, the study evaluated blood reabsorption at different pressures. When the cuff pressure was at or above diastolic pressure, there was no reabsorption of xenon in the calf. However, once the cuff pressure was lowered below the diastolic pressure, xenon reabsorption was recovered. This study established the relevance of perfusion pressure (i.e., perfusion pressure = diastolic blood pressure − intracompartmental pressure) when considering compartment syndrome.

There has been significant controversy over the pressure threshold for the diagnosis of ACS. Two theories have been proposed. One is based on an absolute value of 30 mm Hg for intracompartmental pressure, and the other theory is based on a differential value of pressure, also termed perfusion pressure or Δp. As the body of evidence has grown, the theory of perfusion pressure has been shown to be the more reliable and diagnostically accurate threshold for determining ACS.

Initially proposed by Whitesides and colleagues, the perfusion pressure theory was based on the fact that decreased blood flow occurs as intracompartmental pressures near the diastolic blood pressure. Dahn et al. showed that flow measured with xenon clearance stops as the cuff pressure reaches diastolic pressure. Clayton and colleagues showed similar findings in a rabbit model using xenon washout.

McQueen and Court-Brown reported on 116 diaphyseal tibia fractures with continual prospective monitoring of the anterior compartment. Within the first 12 hours, 53 patients had absolute intracompartmental pressures higher than 30 mm Hg, 30 patients had pressures higher than 40 mm Hg, and 4 patients had pressures higher than 50 mm Hg. However, only one patient had a perfusion pressure of less than 30 mm Hg, and he underwent fasciotomy without complication. Similar elevated absolute pressures were observed over the following 12 hours out to 24 hours after injury, with only two patients requiring fasciotomy for perfusion pressures less than 30 mm Hg. No sequelae associated with missed ACS were reported. Previously, this group had shown that continual anterior compartment pressure monitoring leads to earlier diagnosis of ACS (diagnosed on average 16 hours from injury) and substantially less (none in their series) long-term sequelae of ACS compared with a group of patients who were not monitored and who were diagnosed much later (average, 32 hours from injury). These long-term sequelae include weakness, stiffness and contracture, and negative effects on bone healing (delayed and increased risk of nonunion). Based on this work, McQueen and Court-Brown recommended a perfusion pressure of less than 30 mm Hg as the threshold for diagnosing ACS in the leg.

White and colleagues compared two groups with continual pressure monitoring. The control group consisted of 60 tibia fractures with absolute intracompartmental pressures that remained below 30 mm Hg. The study group consisted of tibial fractures with pressures greater than 30 mm Hg for at least 6 hours. No fasciotomies were performed, and there were no differences at final follow-up between groups with regard to recovery and strength. The work of these different groups provided a clinical evidence base for the superiority of perfusion pressures over absolute pressures in assessing for ACS; yet, absolute pressure thresholds remain commonly applied and commonly described in texts and articles.

Accepting perfusion pressure as the optimal means for applying information obtained from intracompartmental pressure (ICP) monitoring, subsequent clinical and basic science research has aimed at defining the most diagnostically accurate perfusion pressure threshold. Prayson and colleagues continually monitored 19 alert patients with tibial fractures. All remained asymptomatic for ACS and showed no signs of missed ACS. Of these patients, 95% had pressures higher than 30 mm Hg, 84% had pressures that were within 30 mm Hg from diastolic pressure, and 58% had intracompartmental pressures within 20 mm Hg of diastolic. The clinical study by Prayson et al. is consistent with animal studies that suggest the threshold for ischemia and irreversible muscle damage occurs between perfusion pressures of 10 and 20 mm Hg based on diastolic blood pressure. Despite these findings, 30 mm Hg has remained the most commonly recommended perfusion pressure threshold. This more conservative threshold increases sensitivity (i.e., maximizes the chance of finding all true positives) in an attempt to ensure that a fasciotomy will be performed before permanent muscle and tissue damage. Because pressure measurements are typically performed as a single measurement, the goal in setting the threshold of 30 mm Hg was to allow for enough time to perform an appropriate fasciotomy after a critical perfusion pressure has been recorded.

The culmination of ACS research to date was a validation that perfusion pressure is the best means for using ICP data in the diagnosis of ACS. Although perfusion pressure seemed to have been a leap forward in our understanding of how best to objectively diagnose ACS, we still have more to learn. The ambiguity in clinical and basic science research findings highlights the fact that pressure monitoring is ultimately an indirect measure or surrogate of the physiologic parameter that is at the source of ACS—perfusion.

At this point, based on the current evidence, the utility of an absolute threshold of 30 mm Hg can be considered historical. Although the exact effects of moderately elevated intracompartmental pressures on muscle tissue are unknown, it seems evident that this condition does not result in significant permanent dysfunction consistent with ACS. The necessity of interpreting the ICP in the setting of the patient's blood pressure is vital. Understanding that blood flow is significantly decreased between a perfusion of 20 and 10 mm Hg will assist the surgeon in managing a potentially catastrophic disorder. By using the perfusion method in conjunction with available clinical examination, the clinician can attempt to minimize unnecessary fasciotomies while preventing missed compartment syndromes.

Diagnosis: Clinical Assessment

The clinical diagnosis of ACS is not always obvious. Typically, the patient is polytraumatized, and ascertaining which injury is causing pain can be difficult. In many cases, the patient may be obtunded or sedated. Because of these conditions, frequent delays in ACS diagnosis can occur. The subjective nature of this decision process was highlighted by O'Toole and colleagues, who examined the rate of ACS diagnosis associated with tibia fractures at a single level I trauma center. The rate of ACS, as well as the use of ICP measurements, varied based on the surgeon. The attending surgeons were all fellowship-trained faculty at an orthopaedic trauma fellowship program, yet the rate of ACS diagnosis in essentially the same patient population, with the same injury, varied from 2% to 24% between surgeons.

The first feature of the clinical assessment is serial examination. ACS does not occur instantaneously, and pressures can increase for up to 48 hours after injury or surgical procedure. Identifying a change in clinical findings over time can be key to the accurate and timely diagnosis of ACS. Outcomes are directly correlated to the prompt diagnosis and treatment of ACS. If treatment is not instituted within 12 hours of symptoms, the clinical outcomes are substantially reduced.

Clinical signs of an impending ACS include pain on palpation of the swollen, tense compartment, and reproduction of pain with passive muscle stretch ( Fig. 17.5 ). Later findings include sensory deficit in the territory of the nerves traversing the compartment and muscle weakness ( Fig. 17.6 ). Pallor, pulselessness, paralysis, and poikilothermia (decreased temperature) are all late-stage signs that may or may not be present. If present, these symptoms indicate complete ischemia and should be considered a sign of poor prognosis.

ACS is typically encountered within the first 36 to 72 hours after a traumatic injury. Peak pressures were measured between 24 and 48 hours after injury, and initial pressure measurements did not correlate with maximum pressures. ACS is 10 times more common in men than women and has a propensity for younger subjects, with the average age being 30 years in men and 44 years in women. In addition, noncontiguous tibia fractures, knee dislocations, and higher Arbeitsgemeinschaft für Osteosynthesefragen (AO)/Orthopaedic Trauma Association (OTA) classification injuries were found to be more closely correlated to ACS. These injuries should prompt the clinician to be particularly suspicious in obtunded, sedated, or intubated patients in whom clinical signs and symptoms are more unreliable. High-energy injuries of the tibia followed by those of the forearm are the fractures most commonly associated with ACS. Bleeding disorders or anticoagulation are also risk factors for ACS.

ACS should be considered in any traumatized patient. Although clinical findings are considered the gold standard, these signs cannot always be relied on. Sensitivity (13% to 19%) and positive predictive value (11% to 15%) are quite low in the traumatized patient, whereas specificity (97%) and negative predictive values (98%) are much better. In other words, if the patient has all the clinical signs, you can be fairly certain the patient has ACS, but the absence of signs does not necessarily imply the absence of ACS. Additionally, in many instances, the patient may be obtunded or sedated, leaving minimal information to gain from the clinical examination.

The earliest clinical signs associated with ACS are typically a tense compartment or extremity with increasing pain at rest and with passive stretch ( Fig. 17.7 ). The term “pain out of proportion” is commonly used to describe symptoms associated with ACS; however, in advanced ACS, this symptom may be absent. Additionally, it can be difficult to assess what is “out of proportion” for any single individual. A more worrisome pain finding is progressive pain, especially when it is not well controlled by pain medications. Pulses and capillary refill are not reliable signs. They should be examined but not used to determine the existence of an ACS. Shunting can occur through vessels outside the affected compartment(s), allowing for distal pulses and capillary refill. Further, alteration in pulse or, in the extreme case, pulselessness is an end-stage sign of ACS, and its presence may indicate a delayed diagnosis.

Despite the clinical signs that are commonly quoted in the literature to help make a diagnosis of ACS, several sources cite that these clinical findings are of poor diagnostic value in adult patients with ACS. In fact, Ulmer found the probability of ACS to be above 90% when three clinical signs and symptoms are present; the third sign was paralysis, at which time full recovery is already unlikely. The study by McQueen et al. used continuous ICP monitoring as the primary tool for diagnosis of ACS in a cohort of tibial diaphyseal fractures. A slit catheter was inserted into the anterior compartment of the affected leg, and a diagnosis of ACS was made if the differential pressure remained less than 30 mm Hg for more than 2 hours. It is important to note that diagnosis was made based on multiple (continuous) measurements, not a single measurement, which may by itself lead to overtreatment. The results from their cohort of 850 patients revealed a sensitivity of 94%, a specificity of 98%, a positive predictive value of 93%, and a negative predictive value of 99% for continuous ICP monitoring in the diagnosis of ACS.

Any evaluation of an injured extremity, especially penetrating injuries, should include an assessment of the vascular status. Arterial injuries can be confused with or associated with ACS. Johansen and colleagues demonstrated the value of measuring the Doppler-assessed ankle-brachial index (ABI; the systolic arterial pressure in the injured extremity divided by the arterial pressure in the uninvolved arm). A value less than 0.90 necessitates further arterial investigation; 94% of patients with an index this low have positive arteriographic findings. No major arterial injuries were missed using these criteria (see Fig. 17.4 ).

The presence of an open wound associated with the fracture should not eliminate the possibility of ACS. Between 6% and 9% of open tibial fractures are complicated by compartment syndrome, with the incidence being directly proportional to the severity of the soft tissue injury ( Fig. 17.8 ). Special consideration should be given to patients after fracture stabilization. In most cases, initial fracture stabilization aims to restore alignment for definitive management or for temporary management with permanent stabilization once the soft tissues are ready. It is common for ACS to develop after alignment has been restored in fractured extremities ( Fig. 17.9 ). Intramedullary compartment pressures have been shown to increase with manipulation during intramedullary nailing of a tibia. Although this study showed a rapid return to lower levels of pressure, a reduction of overlapping bones will typically elongate the compartment. With elongation (i.e., distraction), a potential decrease in compartment volume can occur, placing a limb at risk for ACS.

In addition to trauma patients, a high index of suspicion for ACS is necessary in patients on anticoagulation or with hemophilia conditions. Diagnosis is difficult in this patient population given their propensity for bleeding with seemingly minor trauma. Care is first aimed at hemostatic maneuvers before surgical intervention; this includes the substitution of absent clotting factor along with input from a hematology specialist. If such maneuvers fail to control the signs and symptoms of ACS, fasciotomies should be performed. However, greater caution is required in these patients because bleeding risk is high, and as a result, there is a higher-than-average amputation rate in hemophiliacs.

Postoperative increases in pain medicine should be monitored, and patients, as well as floor staff, should be warned to monitor the injured extremity closely. The use of epidural and regional anesthetic techniques, such as pain catheters, in these patients has been a subject of debate, with case reports of delayed ACS diagnosis after the use of each of these techniques, but a systematic review of the literature calls into question the putative role of regional anesthetics in the diagnostic delays. Postoperative blocks and pain pumps should be used with caution in patients for whom ACS may be concerning, specifically, upper extremity injuries such as both-bone forearm fractures. The fear is that regional or epidural anesthetics will decrease the patient's ability to detect the increasing pain associated with ACS. That being said, ischemic pain tends to overcome nerve blockade, and the presence of pain (especially breakthrough pain) over a functional pain catheter should be viewed as very worrisome for ACS. Over the past decade of war, the need to transport combat-injured patients great distances by land and ground transport in the initial 72 hours after injury has progressed the use of regional pain catheters in patients with injury patterns that are considered prone to ACS (e.g., tibial shaft fractures) without an observed increase of ACS diagnosis delay related to this pain modality. Finally, a thorough postoperative evaluation or multiple evaluations in the obtunded patient should be performed to detect early signs of ACS.

Crush Syndrome

Crush syndrome is a medical term used specifically to describe a type of injury that can ultimately lead to devastating consequences, including death, if not managed appropriately. Crush injury is typically produced by continuous and prolonged pressure and is most prevalent in the setting of mass casualties, such as with earthquakes or military conflict. Crush syndrome is the second most common cause of death in these situations, behind direct injury from the catastrophe. Additionally, this syndrome can occur in persons who are trapped in one position for a prolonged period or who have collapsed or fallen asleep in one position for an excessive period when under the influence of alcohol or drugs. Careful consideration should be made based on the timeline of the injury, as well as the resources available, before administering any medical treatments.

The first step in managing the patient is to administer intravascular support. Typically, the patient experiences significant systemic hemodynamic complications such as acute renal failure and cardiac arrhythmias or collapse because of the influx of toxins and myoglobin secondary to large muscle damage. If possible, IV catheters should be begun before releasing the compressive force because once the force is released, the damaged muscle will begin to release cellular metabolites into the bloodstream. It is important to remember that although elevated pressures cause muscle damage in ACS, the elevated pressures in crush syndrome are a result of already damaged muscle resulting in leaky vasculature.

Appropriate management will require an understanding of both the timeline of the injury and the medical resources available. Surgical treatment in crush syndrome should mirror that of ACS with regard to timelines. Surgical release should be performed if the crush period was less than 6 to 12 hours. After 6 hours but before 12 hours of compression, the benefit of surgical release is controversial because significant muscle damage will have already occurred. Surgical release after 12 hours of compression is considered contraindicated because irreversible muscle death has already occurred, and surgical release only increases the likelihood of infection by exposing necrotic tissue to the outside environment. Additionally, if the compression period was less than 6 to 12 hours but elevated pressures have persisted for extended periods (greater than 6 hours), consideration for nonoperative management should be given. When in doubt and if possible, a discussion with the patient or family members regarding the potential need for revision surgery and amputation if significant necrotic muscle is encountered should take place.

In the case of a mass-casualty setting, management from a surgical perspective should again center on the timeline, the time of crush, and the availability of continued care and medical resources. Typical humanitarian responses can be delayed by several hours to days. In these settings and when resources are limited for continued management such as wound care and surgical closure of fasciotomies, surgical intervention should not be performed. In the setting of a patient found unresponsive, an attempt at determining an accurate timeline is critical to managing the patient. If compression is alleviated within a 6-hour time frame, release of the affected compartments should be performed in an urgent manner, assuming the patient is stable to undergo surgical intervention ( Figs. 17.10 and 17.11 ). Releases after 12 hours of ischemia should be avoided because of the increased risk for infection and amputation.

The clinical examination in crush syndrome can be very similar to that for ACS. The patient usually suffers no pain initially and may have no physical complaints. Initially, there is flaccid paralysis of the injured limb and a patchy sensory loss. Over the course of hours, swelling rapidly ensues, often far more dramatically than would be seen in compartment syndrome. The swelling is caused by rapid release of fluid because of the failure of intracellular mechanisms that allow cells to retain water. The result is clinical evidence of muscle damage with darkening of the urine related to myoglobinuria and rapid deterioration of renal function. In summary, the viability of the muscle and the ability to provide follow-up wound care and management should guide surgical intervention when managing crush syndrome.

Compartment Syndrome in Combat

Although Volkmann (1881) is credited with the initial description of the aftermath of a missed compartment syndrome (the eponym for which is a Volkmann contracture ), ACS has and will always remain a disease of the military surgeon. Since the Napoleonic era, when Desault and others coined the term débridement to describe the “unbridling” of the swollen soft tissues under the nonelastic fascia after severe traumatic injury, compartment syndrome and its diagnosis and management have been a constant bane of combat casualty care. Fast-forward 200 years or more to the conflicts in Southwest Asia (Iraq and Afghanistan); military surgeons continue to struggle with the ideal method for diagnosing this condition.

A review of the Joint Theater Trauma Registry (JTTR), which is a prospectively maintained trauma registry that collects data from all echelons of care (i.e., from the battlefield support medical facilities to the major medical centers in the United States), reveals that between September 1, 2011, and March 18, 2013, 31% of soldiers with tibia fractures (65 out of 211) were recorded as having undergone fasciotomy. Ritenour and colleagues found that in the lead-up to the “surge” in Operation Iraqi Freedom, 336 soldiers in a similar length of time (January 1, 2005, to August 21, 2006) underwent fasciotomy, with 49% being in the leg. This rate of fasciotomy, a surgery whose only indication is the treatment or prophylaxis of compartment syndrome, is substantially higher than that reported in the civilian Level I trauma setting. For example, O'Toole and colleagues reported a rate of 2% to 24% for tibial shaft fractures at a single major trauma center in the United States. There are several explanations for this increase in fasciotomy rate in the combat setting. In some cases, the amount of energy imparted by military wounding mechanisms (e.g., improvised explosive device [IED] blasts) is simply substantially greater than that seen in the civilian setting ( Fig. 17.12 ). Additionally, two primary reasons for the difference in fasciotomy rates between combat and civilian casualties are the concept of a “completion” fasciotomy and the concern for transit times between echelons of care.

One of the most likely explanations for the divergence is a semantic one. The most common mechanism of injury in today's combat setting is blast related, most commonly from an IED. These blast injuries produce devastating lower extremity trauma, yielding highly contaminated, grade IIIB/C fractures with large “out-to-in” open wounds ( Fig. 17.13 ). The blast wave spontaneously rips open the fascia in many cases, at least at the injury zone. In the process of wound care, extension of the wound margins provides ready access to remaining intact fascia proximal and distal to the zone of injury. This intact fascia can act as a tourniquet, and because the wound and wounding mechanism have introduced all of the negative aspects of fasciotomy, the benefit of completing the fascial release for the length of the compartment comes with little increased risk ( Fig. 17.14 ). Thus “completion” fasciotomy is one of the more common types of fasciotomies performed over the past decade of combat surgery.

Although direct blast injury is the most common mechanism, there are certainly many other injuries, like gunshot wounds ( Fig. 17.15 ), motor vehicle (land and air) accidents, and direct blows. Likewise, IED blasts that hit armored vehicles produce blunt injuries similar to those of civilian high-speed motor vehicle collisions. These mechanisms of injury produce long bone fractures and soft tissue responses that are similar to those in the civilian setting; however, these injuries also receive a higher-than-expected rate of fasciotomy. In this situation, one of the most cited concerns from combat surgeons is the process of aeromedical evacuation, where surgical access to the patient is lost for about 8 hours in the prime window for the development of ACS (i.e., the first 72 hours after injury). In addition, patients are flown at altitude (cabins are typically pressurized to 8000 feet), and access to the patient to complete detailed compartment assessments is diminished. Cognizant of the theoretical potential for aero-evacuation increasing the risk of missed or delayed diagnosis of ACS and based on the results of a study conducted in the US military, the US Army Surgeon General issued an Al l Ar my Act ivities (ALARACT) message in May 2007 directing combat surgeons to apply “liberal use of complete fasciotomy,” especially for those at highest risk. In addition, delay in evacuation of 24 hours should be considered for patients at high risk, to allow for continued serial monitoring. The military retrospective study cited in this ALARACT showed that when complete fasciotomy was delayed until reaching Landstuhl Regional Medical Center in Germany, the rate of amputation doubled (31% vs. 15%), and the rate of mortality quadrupled (19% vs. 5%), compared with the cohort of patients who were successfully released in theater. The effect of this ALARACT was the routine and frequent use of prophylactic fasciotomy for many tibial fractures.

One of the most telling findings of the Ritenour study was that 17% of patients who underwent fasciotomy in theater had a need for revision fasciotomy, most commonly to extend the fascial release (63%) or skin incision (14%). In 41% of these patients, an entire compartment was not released at the index procedure, with the anterior (40%) and deep posterior (37%) being the most commonly missed compartments. Thus the real message was not the lack of diagnosis and fasciotomy performed on soldiers with ACS; instead, the issue was with the adequacy of the surgical technique. Missing a compartment, most commonly in the leg (especially the deep posterior) and forearm, is not unique to the combat setting or surgeon, nor is the severalfold increase in amputation rate when this occurs. The results of this study did prompt the development of a combat extremity surgery course in the US Army that uses didactic and cadaver training to reinforce the proper technique for a double-incision fasciotomy of the leg, as well as fasciotomies of the other extremities, for surgeons preparing to deploy to combat medical treatment facilities.

An important lesson from this pivotal study is that simply making the incisions on the leg or other limb does not ensure that a fasciotomy has been successfully performed. This fact is most important in the setting of prophylactic fasciotomy, where the patient who receives an incomplete fascial release is exposed to all of the risk and morbidity of the procedure without the maximal potential benefit. Although the improved training and attention to detail that have emerged as a result of Ritenour's study have benefited combat casualties, the use of these data to reinforce an exaggerated use of fasciotomies, many of which are prophylactic, is a lasting undesirable effect of this study. Conversely, possibly the most beneficial impact of this study is that it has generated substantial commitment of Department of Defense (DoD) research dollars directed toward finally understanding ACS and developing a gold standard for diagnosis that uses reliable, readily attainable, objective information to define the presence or absence of this purely physiologic disease.

Measurement Techniques

Reliable and accurate intracompartmental pressures can be difficult to obtain in the hands of an experienced clinician. Practice and attention to detail during measurements can help avoid errors in measurement. Measurements taken when pressure is erroneously elevated may prompt a surgeon to act inappropriately and perform an unnecessary fasciotomy; therefore it is critical to obtain accurate measurements.

As described by Heckman and colleagues, the measurement should be performed within 5 cm of the fracture site when evaluating fracture patients. The highest pressures were obtained within 5 cm of the fracture and dissipated as pressures were recorded farther from the fracture site. Additionally, deeper values have been shown to be higher than more superficial values.

At the time of measurement, the foot (in the case of leg ACS) should be maintained in a neutral position without extreme dorsiflexion or plantar flexion. Dorsiflexion will increase posterior compartment pressures, whereas plantar flexion will increase the anterior and lateral compartments. The ideal position is between neutral and the resting position or between 0 and 37 degrees of plantar flexion. Additionally, when measuring the posterior compartments, a rolled sheet or towel should be placed under the heel to remove any pressure associated with the weight of the leg pressing down on the bed ( Fig. 17.16 ). The injured extremity should not be elevated to decrease edema because this maneuver will increase the ICP in, and decrease perfusion to, the extremity.

The injured extremity should have all constrictive or circumferential dressings removed. Garfin and colleagues showed in an animal model that removal of a plaster cast resulted in a 60% reduction in intracompartmental pressures. Cutting the cast, spreading the cast, cutting the cast padding, and ultimately, cast removal all resulted in sequential decreases in intracompartmental pressure.

There have been several studies examining the difference between different pressure measurements. The Stryker Stic and arterial lines have been shown to provide reliable and reproducible readings. Straight needles and smaller-gauge needles have shown a propensity to overestimate the intracompartmental pressure. Wick catheters and side port needles have shown a more reliable reading compared with an 18-gauge needle. Regardless of the instrument used, once the needle is inserted into the limb, a small amount of fluid (roughly 0.1 to 0.2 mL) should be injected through the needle to clear the needle of any soft tissue that may have been trapped in the needle during insertion. If this maneuver is not performed, erroneously high measurements may be obtained.

Needle Manometer

The first direct attempt at measurement of interstitial compartment pressure was by Landerer in 1884. Subsequently, French and Price reported on the usefulness of the technique in the diagnosis of chronic compartment syndrome. Whitesides and colleagues first applied the needle manometer technique to the diagnosis of ACS. In their original description, an 18-gauge needle was connected to a 20-mL syringe by a column of saline and air, and this column was then connected to a standard mercury manometer. After the needle was injected into the compartment, the air pressure within the syringe was raised until the saline–air meniscus was seen to move. The pressure was then read off the mercury manometer ( Fig. 17.17 ). The details of the technique have been well described.

Arterial Line Catheter

A common means of measuring intracompartmental pressures without specialty devices is through the use of an arterial line. An arterial line is attached to any standard critical care or pressure-sensing monitor. The IV tubing is then connected to an IV bag. The tubing is attached to a stopcock valve, and a 10-cc syringe full of saline is attached to the stopcock. A 16-gauge needle is attached to the stopcock needle. The system is then primed and zeroed at the level of the extremity ( Fig. 17.18 ). Care must be taken to have the transducer at the level of the injured extremity as well. Once zeroed, the needle is inserted, and a small amount of saline is injected through the needle with the stopcock opened to the syringe. The stopcock is then switched to allow free flow between the needle tip and the IV tubing and transducer (see Video 17.1 ).