Fasciotomy of the Leg for Acute Compartment Syndrom.

DEFINITION

Compartment syndrome remains one of the most devastating orthopaedic conditions if not treated appropriately. The potential clinical sequelae and medicolegal implications of possible missed

compartment syndrome make it one of the most important entities in all of orthopaedic surgery.5

Compartment syndrome is a condition, with numerous causes, in which the pressure within the osteofascial compartment rises to a level that exceeds intramuscular arteriolar pressure, resulting in decreased blood flow to the capillaries, decreased oxygen diffusion to the tissue, and, ultimately, cell death. This is the rare orthopaedic emergency for which evidence indicates that delay in treatment

results in worse outcomes.101329303134

The clinical sequelae of missed compartment syndrome can be life- and limb-threatening. Myonecrosis can lead to acute renal failure and multiorgan failure if not appropriately managed.24

Any situation that leads to increased pressure within the compartment can result in compartment syndrome.

The impermeable fascia prevents fluid from leaking out of the compartment and also prevents an increase in volume that could reduce pressure within the compartment.

The incidence of compartment syndrome is 7.3 per 100,000 male patients and 0.7 per 100,000 female patients.

This chapter describes acute compartment syndrome (ACS), in contrast to exertional compartment syndrome.

Exertional compartment syndrome is a transient chronic condition brought on by exercise. Unlike ACS, exertional compartment syndrome is not an emergency, and its treatment is beyond the scope of this chapter.

 

FIG 1 • Cross-section of the lower leg at midtibial level.

 

 

 

ANATOMY

 

The lower leg has four compartments: anterior, lateral, superficial posterior, and deep posterior (FIG 1Table 1).

 

The anterior compartment is bound anteriorly by fascia, laterally by the anterior intermuscular septum, and posteriorly by the interosseous membrane between the fibula and tibia.

 

 

The four muscles in this compartment are the tibialis anterior, extensor digitorum longus, extensor hallucis longus, and peroneus tertius.

 

The neurovascular bundle includes the deep peroneal nerve and the anterior tibial artery.

 

The deep peroneal nerve provides sensation to the first dorsal web space of the foot and motor function to all the muscles in the anterior compartment.

 

The anterior tibial artery travels in this compartment just anterior to the tibiofibular interosseous membrane and continues in the foot as the dorsalis pedis artery.

 

The lateral compartment is bordered anteriorly by the fascia, posteriorly by the posterior intermuscular septum, and medially by the fibula.

 

 

The lateral compartment has only two muscles: the peroneus longus and the peroneus brevis.

 

The major nerve supply to the lateral compartment is the superficial peroneal nerve, which supplies the two muscles

 

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of the compartment. The nerve supplies sensation to the dorsum of the foot, except the first dorsal web space.

Table 1 Compartments of the Lower Leg

Compartment

Muscles

Major

Arteries

Nerves

Anterior

Tibialis anterior

Extensor hallucis longus Extensor digitorum longus

Peroneus tertius

Anterior tibial

Deep peroneal

Lateral

Peroneus brevis

Peroneus longus

None

Superficial peroneal

Deep peroneal (proximal in leg)

Deep posterior

Posterior tibialis

Flexor hallucis longus Flexor digitorum longus

Posterior tibial Tibial

Peroneal

Superficial

posterior

Gastrocnemius

Soleus

None

None

 

 

Because the deep peroneal nerve courses proximally around the fibular head, both the deep and superficial peroneal nerves travel proximally within this compartment.

 

No main vessels are present in this compartment, and the muscles receive their blood supply from the peroneal and anterior tibial arteries.

 

The deep posterior compartment contains the flexor digitorum longus, tibialis posterior, and flexor hallucis longus muscles. Popliteus is thought to lie within this compartment proximally.

 

 

Although it is not considered a separate compartment, the tibialis posterior muscle can have its own fascial covering.

 

The deep posterior compartment contains the main neurovascular bundle of the posterior compartment, which consists of the tibial nerve, posterior tibial artery and vein, and peroneal artery and vein.

 

The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris muscles, which are supplied by branches of the tibial nerve, posterior tibial artery, and peroneal arteries.

 

 

No major artery travels in this compartment.

 

PATHOGENESIS

 

Although the exact pathophysiology is not completely understood, the syndrome is thought to be the result of either a decrease in the space available for the tissues within the fixed compartment or an increase in the size of the tissues within the compartment.

 

 

Either case can result in an increase in pressure above a critical value.

 

Increased fluid content and swelling of damaged muscles can be caused by the following:

 

 

Bleeding into the compartment (from fractures, large vessel injury, or bleeding disorders)

 

 

Fractures are the most common cause of compartment syndrome. It is estimated that 9.1% of tibial plateau fractures develop compartment syndrome.7

 

Blunt trauma is the second most common cause, accounting for 23% of cases.19

 

Increased capillary permeability (eg, burns, ischemia, exercise, snake bite, drug injection, intravenous fluids)

 

Decreased compartment size can be caused by the following:

 

 

Burns

 

Tight circumferential wrapping, dressings, casts

 

Localized external pressure, such as lying on the limb for an extended period of time or from pressure on the “well leg” in the lithotomy position on the fracture table

 

Elevated pressure prevents perfusion of the tissue from the capillaries and results in anoxia and necrosis.

 

 

The impermeable fascia prevents fluid from escaping, causing a rise in compartment pressure, such that it exceeds the pressure within the veins, resulting in collapse of the veins or an increase in venous

pressure.22

 

The final event is cellular anoxia and necrosis.24

 

During necrosis, an increase in intracellular calcium concentration occurs, coupled with a subsequent shift of water into the tissue, causing the tissue to swell further, adding to the pressure.12 This “capillary

leakage” adds to the increased pressure in the compartment, thus creating a vicious cycle. Lindsay et al17 reported that prolonged ischemia of the muscle results in adenosine triphosphate breakdown and that the amount of energy depletion during ischemia determines the extent of the ischemic damage.

 

The effects on muscle and nerve function are time-dependent.

 

 

Prolonged delay results in greater loss of function.

 

Red muscle fibers (eg, anterior compartment of the leg), which rely predominantly on aerobic metabolism, are far more vulnerable to ischemia than “white” muscle fibers (eg, gastrocnemius muscle), which rely on anaerobic metabolism.14

 

After sustained elevation of compartment pressures for more than 6 to 8 hours, nerve conduction is blocked.10 In animal studies,1330 irreversible muscle damage occurred after 8 to 12 hours.

 

The exact pressure at which change within the compartment occurs has been the subject of debate and has evolved over time.

 

 

Initially, the pressure of 30 mm Hg was reported to be the maximum pressure above which irreversible muscle damage occurred.40

 

Currently, clinicians have recognized the importance of the patient's blood pressure when considering the compartment pressure and use an absolute difference between diastolic blood pressure and compartment

pressure of less than 30 mm Hg as an indicator of ACS.18

 

 

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Animal studies have highlighted the importance of the systemic pressures relative to the compartment pressure.

 

 

Whiteman and Heckman40 found that irreversible ischemic changes occurred when the compartment

pressure was elevated within 30 mm Hg of the mean arterial pressure and within 20 mm Hg of the diastolic pressure.

 

Research4 on limb ischemia at the University of Pennsylvania led to similar conclusions. Bernot et al4 coined the term delta P, referring to the difference between the mean arterial pressure minus the

compartment pressure, with a lower number reflecting less blood flow. The authors4 found that cellular anoxia and death occur with pressure within 20 mm Hg of the mean arterial pressure; however, at pressures within 40 mm Hg, oxygen tension was reduced, but anoxia was not indicated and aerobic metabolism persisted.

 

McQueen et al18 used the cutoff of compartment pressure within 30 mm Hg of the diastolic blood pressure as a fasciotomy threshold. No adverse clinical outcomes occurred as a result of not releasing compartments with pressures that were more than 30 mm Hg from the diastolic blood pressure, and this has come to be the value currently used most often as a threshold for compartment syndrome.

 

NATURAL HISTORY

 

The outcome of compartment syndrome depends on location, trauma to the tissue, and time to intervention.

 

 

Six hours of ischemia currently is the accepted upper limit of viability. Rorabeck and Macnab31 reported almost complete recovery of the limb function when fasciotomies were performed within 6 hours of the onset of symptoms.

 

Muscle undergoes irreversible change after 8 hours of ischemia, whereas nerves can incur irreversible damage in 6 hours.10

 

Compartment syndrome can have broad effects on multiple systems.

 

 

As muscle necrosis occurs, myoglobin, potassium, and other metabolites are released into circulation.

 

As a result, several metabolic conditions can arise, including myoglobinuria, hypothermia, metabolic acidosis, and hyperkalemia. In turn, these biochemical phenomena can cause renal failure, cardiac arrhythmias, and, potentially, death.

 

PATIENT HISTORY AND PHYSICAL FINDINGS

 

Diagnosis of compartment syndrome is a clinical challenge, and significant variation among clinicians likely

exists.25 Studies of diagnosis in patients are limited by lack of a reliable gold standard other than “fasciotomy was performed,” which is what typically is used in the literature.

 

Compartment syndrome is, for the most part, still a clinical diagnosis. However, the use of physical examination findings to diagnose compartment syndrome has not been well validated.38

 

The key to successful handling of compartment syndrome is early diagnosis and treatment. Therefore, the orthopaedic surgeon must be familiar with the risk factors and signs and symptoms of the diagnosis, obtain a detailed documented history, and perform a thorough physical examination.

Risk Factors for Compartment Syndrome

 

The patient's history is critical. Certain aspects of the patient's history render the syndrome more likely.

 

Risk factors for compartment syndrome include age younger than 35 years, male gender, and mechanism of sport injury.192643

 

The most common cause of ACS is fracture, and the second most common cause is soft tissue injury.

 

Tibial fractures are associated with a high rate of compartment syndrome, with rates for shaft fractures ranging from 1% to 11%.2538 Proximal tibial fractures are at particular risk, especially high-energy tibial plateau fractures, with rates of approximately 15% to 28%3933 and fracturedislocations reported to be as high as

53%.2036 Ballistic proximal fibular fractures20 also have been shown to be at particular risk for developing compartment syndrome.

 

 

It should be noted that open fractures can still develop ACS, and some authors have found no difference in incidence of ACS with open compared with closed fractures.1819

 

The existence of any of the following characteristics should heighten the surgeon's suspicion: high-energy injury mechanism, a patient receiving anticoagulation medication, or a patient with a tight circumferential dressing.

 

Physical Examination of Acute Compartment Syndrome

 

Little rigorous data exist regarding the validation of clinical examination findings. The most widely cited review of the literature on this topic includes only four patients with compartment syndrome.38

 

The classic “Ps” taught in medical schools (pain out of proportion, pain with passive range of motion, paresthesias, pulselessness, pallor, paralysis, and pressure on palpation) for diagnosing compartment

syndrome are not equally useful, and little validation work has been conducted.38

 

Pain out of proportion to the injury is a classic symptom of the diagnosis. Patient injury severity and perception and expression of pain vary substantially, rendering this judgment difficult in clinical practice. The amount of

pain medicine needed by the patient is a useful predictor of compartment syndrome in a pediatric setting.2

 

Patients in whom pain might be difficult to ascertain include those with head injuries; those using ethanol or drugs; those who are intubated or sedated; those who have major distracting injuries, such as long bone fracture; those receiving large amounts of pain medicine; and those with any other factor that might alter the patient's ability to accurately sense and communicate pain levels.

 

 

Pain perception can also be altered by anesthesia, and some work suggests that patients receiving epidural anesthesia are four times more likely to develop compartment syndrome than those receiving other forms of pain control.23

 

This type of anesthesia results in a sympathetic nerve blockade, thereby increasing the blood flow, compounding the local tissue pressures and extremity swelling.

 

Similarly, local anesthesia combined with narcotics has been shown to increase the risk of compartment syndrome.823

 

Pulselessness typically is not helpful because the presence of a pulse does not rule out compartment syndrome. Most patients with ACS have normal pulses.

 

Pallor typically is not helpful either. Pallor also reflects loss of arterial flow and rarely is present during physical examination.

 

 

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Pain with passive range of motion of the muscles of the compartment is another classic sign of compartment syndrome.12 For tibial fractures, for example, motion of the toes does not typically cause substantial pain.

 

Zones of paresthesia can be a useful, but confusing, s ymptom of compartment syndrome.

 

 

It has been shown, however, that nerve function is altered after only 2 hours of ischemia; therefore, paresthesia represents a potential early symptom.11

 

Light touch is a better indicator because it indicates change in the ability of the nerves to detect a threshold force, as opposed to two-point discrimination. Two-point discrimination is a test of nerve density, which might not change until later in the process.

 

 

With increased pressure in a compartment, the sensory nerves are affected first and then the motor nerves (eg, in the anterior compartment, the deep peroneal nerve is affected quickly and patients report loss of sensation between the first two toes).

 

Considering that small fiber nerves are affected first, light touch will be affected before pressure and proprioception.

 

Decreased motor function of muscles in the compartment is another classic sign. However, it can be caused by ischemia, guarding, pain, or a combination of these factors, particularly in patients with distracting extremity injuries, such as tibial shaft fracture.

 

 

Muscle force should be documented in all compartments when ruling out compartment syndrome. Documenting that the patient “wiggles toes” is not adequate because that indicates only that either the flexors or extensors are firing. “NVI” is not useful either because it does not state the exact muscle groups that were tested.

 

Palpation of tight compartments has been thought to be an important indicator of compartment syndrome. The deep posterior compartment cannot be directly palpated because of its location deep to the superficial posterior compartment. Recent data have questioned clinicians' ability to evaluate pressure based on

palpation alone.35

 

Serial examinations are critical. All complaints should be thoroughly investigated, and all findings should be carefully documented in the chart such that subsequent examiners can refer to the record as a tool for diagnosis.

 

IMAGING AND OTHER DIAGNOSTIC STUDIES

 

The diagnosis of compartment syndrome typically is made clinically. Intracompartmental pressure measurements are the most common data used to aid in diagnosis, particularly in patients with limited physical examinations.

 

Once a patient is diagnosed with compartment syndrome, fasciotomies should be performed emergently. Any workup that could substantially delay this process should be undertaken with great caution.

 

Intracompartmental Pressure Measurements

 

If the patient cannot provide clinical clues because he or she is sedated or for other reasons, or if the diagnosis is in question, compartment pressures can be measured.

 

The exact pressure that defines compartment syndrome is still debated, although a pressure measurement should be obtained with reference to the diastolic blood pressure.18

 

Some authors have argued that using single pressure measurements alone might result in high rates of false-positive diagnoses using the standard delta P of 30 mm Hg threshold.2741 Therefore, in our opinion, compartment pressure checks should not be performed on patients in whom there is no clinical concern for

ACS.

 

The technique of measuring compartment pressures must be mastered by the surgeon.

 

Inexperience with the technique can lead to inaccurate data and potentially missed compartment syndrome.

 

When measuring the pressure, the surgeon must be familiar with the local anatomy and able to accurately measure all the compartments.

 

Location of the measurement is important.

 

 

Whitesides and Heckman40 reported that the highest pressures were within 5 cm of the fracture site; pressures decreased as the measurements were obtained distally and proximally to the fracture.

 

Measurement of the Compartment Pressure

 

Several techniques to measure compartment pressure have been described, including the Whiteside infusion technique, the Stic technique, the Wick catheter technique, and the slit catheter technique. The two most commonly used instruments are the Whiteside side port needle and the slit catheter device.

 

Numerous digital pressure monitors are commercially available and frequently used. The Stryker pressure monitor is in common clinical use (FIG 2).

 

Inserting an arterial line (16- to 18-gauge needle) is easy to do in the operating room, but the pressure measured with a simple needle is thought to be 5 to 19 mm Hg higher than the pressure measured with a side port or wick catheter.21

 

Pressure values should be recorded for all four compartments. Typically, each compartment is checked twice.

If a fracture is present, the value will be highest within 5 cm of the fracture.40 The contralateral limb can be checked as a control. Normal resting internal compartment pressure is approximately 8 mm Hg in adults and 13 to 16 mm Hg in children.

 

Delta P (diastolic blood pressure minus intracompartmental pressure) is measured.

 

 

A delta P of less than 30 mm Hg generally is accepted as an indication for fasciotomy based on the work

conducted by McQueen et al19 that showed that all patients with a delta P greater than 10 mm Hg in whom fasciotomy was not performed had normal function at follow-u Clinicians should interpret this study with caution considering it used continuous pressure measurement values averaged over 12 hours (not one-time pressure measurements, as are obtained in common clinical practice) and considering only three patients in that study had compartment syndrome.

 

Although some animal data indicate that lower thresholds might be safe and although some concern might exist that this threshold leads to a high false-positive rate,2741 clinicians should be reassured that delta P of 30 mm Hg seems to be highly sensitive to avoid missing any compartment syndromes.

 

Unless the patient will be in the operating room for a prolonged time period, preoperative values of diastolic

 

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pressure should typically be used because diastolic blood pressure decreases 20 points, on average, with anesthesia.15

 

 

 

FIG 2 • Stryker intracompartmental pressure monitor. A. Quick pressure monitoring kit containing the intracompartmental pressure monitor, a prefilled saline syringe, a diaphragm chamber (transducer), and a needle. B. The assembled pressure monitor. To assemble the monitor kit, the needle is attached to the tapered end of the tapered chamber stem (transducer). The blue cap from the prefilled syringe is removed and the syringe is screwed into the remaining end of the transducer, which is a Luer-lock connection. The cover of the monitor is opened. The transducer is placed inside the well (black surface down). The snap cover is closed. Next, the clear end cap is pulled off the syringe end, and the monitor is ready to use. To prime the monitor, the needle is held 45 degrees up from the horizontal and the syringe plunger is pushed slowly to purge air from the syringe. The monitor is then turned on. The assembled monitor is tilted at the approximate intended angle of insertion of the needle into the skin. The zero button is pressed to set the display at zero.

The needle is then inserted into the appropriate location in the compartment. C. The intracompartmental pressure monitor needle has side ports to prevent soft tissue from collapsing around the needle opening. This is different from a regular needle that has only one opening at the end.

 

 

McQueen et al19 have advocated routine continuous pressure monitoring in the anterior compartment of tibial fractures. It is their center's technique for continuous monitoring that has been extrapolated to determine our current threshold of 30 mm Hg delta P even though the measurement technique used does not currently include continuous measurement. Continuous monitoring of routine tibial shaft fractures has not gained clinical popularity in North America as of yet, likely because of logistical difficulties in setting up the monitoring and

some clinicians' concerns regarding the false positives associated with monitoring.2741

 

Near-infrared spectroscopy is a noninvasive and continuous method that determines tissue oxygenation by comparing the light emitted when comparing the concentration of venous blood oxyhemoglobin and deoxyhemoglobin. It might ultimately be a tool to monitor patients with evolving compartment syndrome,

making it useful in the setting of critically ill patients.128 This technology has not been validated and is not currently in routine clinical use.

 

 

Laboratory studies should include a complete metabolic profile, a complete blood count with differential, creatine phosphokinase (CPK), urine myoglobin, serum myoglobin, urinalysis (which might be positive for blood but negative for red blood cells, indicating myoglobin in the urine caused by rhabdomyolysis), and a coagulation profile (prothrombin time, partial thromboplastin time, international normalized ratio).

 

Obtaining a complete laboratory panel should not delay operative treatment in a diagnosed case of compartment syndrome.

 

Elevated CPK or creatine kinase in an intubated trauma patient might be a sign of compartment syndrome. Typical CPK values are 1000 to 5000 μg/L or higher in cases of ACS. One recent study proposed a CPK

value of 4000 μg/L as indicative of ACS.39 Myoglobinemia can also be observed in some cases.

 

 

DIFFERENTIAL DIAGNOSIS

Compartment syndrome is diagnosed in a patient with either of the following: Suspicious clinical findings as discussed earlier

Pressure in a compartment within 30 mm Hg of the diastolic blood pressure

Other diagnoses to consider

Normal pain response secondary to fracture or other trauma Low pain tolerance secondary to preoperative substance abuse Muscle rupture

Deep venous thrombosis and thrombophlebitis Cellulitis

Coelenterate and jellyfish envenomations

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Necrotizing fasciitis Peripheral vascular injury Peripheral nerve injury Rhabdomyolysis

Of special note, recent studies have shown that in the case of envenomations, compartment syndrome is multifactorial and fasciotomy might not prevent myonecrosis, which can be caused by the direct toxic effect of the venom and the inflammatory response.

In these cases, antivenom should be administered; this has been shown to decrease limb hypoperfusion.

 

 

NONOPERATIVE MANAGEMENT

 

All patients suspected of having ACS should undergo emergent fasciotomies performed in the operating room or at the bedside.

 

Nonoperative treatment of ACS is almost never appropriate unless operative treatment would risk the patient's life. ACS is a life- and limb-threatening injury; the successful treatment of which is based on limiting the time

until fasciotomy is performed.

 

Considering that ischemic injury is the basis for c ompartment syndrome, additional oxygen should be administered to the patient diagnosed with compartment syndrome because it will slightly increase the blood partial pressure of oxygen.

 

 

The surgeon must ensure that the patient is normotensive because hypotension reduces perfusion pressure and leads to further tissue injury.

 

Any circumferential bandages or casts should be removed from patients at risk for development of compartment syndrome.

 

 

Compartment pressure falls by 30% when a cast is split on one side and by 65% when a cast is spread after splitting. Splitting the padding reduces the pressure by an additional 10% and complete removal of the

cast by another 15%. A total of 85% to 90% reduction in pressure can be achieved by removing the cast.42

 

Elevating the limb above the heart decreases mean arterial pressure in the limb without changing the intracompartmental pressure. Thus, the affected extremity should not be elevated.

 

 

As shown by Wiger et al,42 after an elevation of 35 cm, the mean perfusion pressure decreased by 23 mm Hg but the intracompartmental pressure stayed the same.

 

Intravenous fluids should be administered to decrease the chance of kidney damage from myoglobin.

 

 

The “crush syndrome” is a sequela of muscle necrosis (ie, high CPK level, above 20,000 IU) that manifests as nonoliguric renal failure, myoglobinuria, oliguria, shock, acidosis, hyperkalemia, and cardiac arrhythmia.

 

Treatment is supportive, with ventilatory support, hydration, correction of acidosis, and dialysis.

 

It is important in this situation to decrease the metabolic load by preventing ongoing tissue necrosis and performing débridement of all dead tissue.

 

The use of narcotics should be closely recorded and monitored for any patient suspected of having compartment syndrome.

 

 

The use of local, spinal, or epidural anesthesia for postoperative pain control generally is discouraged in patients at high risk for compartment syndrome because it limits the ability of the clinician to perform serial examinations.

 

Late Presentation of Acute Compartment Syndrome

 

Nonoperative treatment of missed compartment syndrome is reserved for patients presenting very late after missed compartment syndrome who already have irreversible muscle necrosis.

 

 

One school of thought is that these patients should not be treated operatively because doing so would increase the chance of infection and lead to amputation.

 

It often is difficult to know when compartment syndrome has occurred, however, so in situations in which it is unclear, it is probably wise to release the compartments.

 

One school of thought is that if compartment syndrome has run its course, fasciotomies should not be performed unless the pressure in the compartment is within 30 mm Hg of diastolic pressure, but this recommendation is controversial and without support in the literature.

 

SURGICAL MANAGEMENT

 

All patients with ACS should be treated with emergent fasciotomies of the affected compartments because compartment syndrome is limb-threatening and potentially lifethreatening if allowed to progress to myonecrosis and renal failure.

 

Time to diagnosis and surgical treatment of compartment syndrome is critical; nerve damage after 6 hours of ischemia might be irreversible.

 

Patients with compartment syndrome should be given the highest priority, and the condition should be treated as an operative emergency.

 

Fasciotomy of the involved compartment is the standard of care for ACS.

 

 

In a trauma setting, typically all four compartments of the leg are released, regardless of evidence of involvement of the other compartments.

 

Fasciotomies ideally should be performed in the operating room.

 

 

If the patient is too ill to be transported to the operating room or if no operating room is available, fasciotomies can be performed at the bedside in as sterile an environment as possible.

 

The only common contraindication to fasciotomy in the face of compartment syndrome is delayed presentation, in which a patient with missed compartment syndrome presents late, after irreversible injury has set in (see Nonoperative Management section).

 

Fasciotomies are also often performed in a prophylactic manner for any patient with an ischemic limb for more than 6 hours to prevent reperfusion injury.

 

Preoperative Planning

 

Once compartment syndrome is diagnosed, every effort should be directed at getting the patient to the operating room as quickly as possible for fasciotomies.

 

 

All further workup should be deferred until fasciotomies are complete, except workup that is needed for a potential life-threatening injury.

 

Little preoperative planning is required for this component of the patient's treatment.

 

 

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Radiographs should be reviewed to rule out fractures and dislocations; however, additional radiographs can be obtained in the operating room after fasciotomies have been completed.

 

Only essential preoperative workup should be conducted before the patient is taken to the operating room. The case should not be delayed for additional, nonessential radiographic worku

 

Positioning

 

The patient usually is positioned supine on the operating room table to facilitate fasciotomies. A small bump can be placed under the hip on the affected side.

 

The leg is prepared in a sterile fashion, and a thigh tourniquet is applied but not inflated.

 

Approach

 

Two separate techniques have been used for decompression of the lower leg compartments.

 

 

The two-incision technique is the most commonly used method, but a one-incision technique involving a lateral (perifibular) approach also exists.

 

The two-incision technique is more straightforward and requires less experience to ensure a complete compartment release and is therefore typically advocated. Draw both planned incisions on the skin before making them to avoid a narrow skin bridge.

 

Some have argued that the one-incision technique can be useful in cases of defined anterior tibial artery injuries to help prevent loss of anterior skin.

 

TECHNIQUES

  • Double-Incision Technique

Anterolateral Incision

 

The anterolateral incision decompresses the anterior and lateral compartments.

 

The anterolateral incision is made halfway between the fibula and the crest of the tibia and lies just above the intermuscular septum dividing the anterior and lateral compartments (TECH FIG 1A).

 

Fasciotomies have also been accomplished through small incisions. However, we prefer using generous incisions to allow for full decompression of the compartments.

 

We recommend incisions that typically are at least 15 to 20 cm both medially and laterally.

 

A small transverse incision is made to identify the intermuscular septum, after which scissors are used to split the fascia of the anterior and lateral compartments.

 

Care must be taken to avoid injuring the superficial peroneal nerve by making separate incisions in each compartment and not cutting the intermuscular septum (TECH FIG 1B-F).

 

 

 

TECH FIG 1 • Lateral incision of the two-incision technique. A. The anterolateral incision is made halfway between the fibula and the tibial crest overlying the intermuscular septum dividing the anterior and lateral compartments. B. Close-up picture of the fasciotomy site after skin incision before the fascia is open, showing the intermuscular septum between the lateral and anterior compartments and the course of the superficial peroneal nerve. (continued)

Posteromedial Incision

 

 

 

The posteromedial approach decompresses the superficial and deep posterior compartments. The incision lies approximately 2 cm posterior to the posterior tibial margin (TECH FIG 2A). Care is taken to avoid injury to the saphenous vein and nerve, which are retracted anteriorly.

 

Each fascia of the deep and superficial posterior compartments is incised longitudinally in line with the incision (TECH FIG 2B-E).

 

The deep posterior compartment is initially released distally, and then the scissors are oriented proximally through and under the soleus bridge. If the posterior tibia is visualized, the deep posterior compartment has been released.

 

Some surgeons release the soleus attachment to the tibia more than halfway. Also, the fascia over the posterior tibial muscle should be released.

 

One useful tip is to keep the tips of the scissors away from major neurovascular structures.

 

 

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TECH FIG 1 • (continued) C. With a knife, a small transverse incision is made over the intermuscular septum. Care is taken to avoid injury to the superficial peroneal nerve. D. The surgeon inserts the tips of the scissors into the small rent in the fascia, and keeping the tips of the scissors up and away from the superficial peroneal nerve, the surgeon incises the fascia over the anterior compartment distally. E. The scissors are turned with the tips proximally, and the fascia of the anterior compartment is released proximally. F. The tips of the scissors are then inserted into the rent created in the fascia of the lateral compartment. Keeping the tips of the scissors up and away from the superficial peroneal nerve, the surgeon releases the fascia over the lateral compartment proximally and distally.

 

 

 

TECH FIG 2 • Medial incision of the two-incision technique. A. The medial incision lies approximately 2 cm posterior to the posterior tibial margin. B. Care is taken to avoid injury to the saphenous vein. The picture shows the posterior border of the tibia exposed along with the deep and superficial posterior compartments. The tips of the dissecting scissors lie on the deep posterior compartment. (continued)

 

 

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TECH FIG 2 • (continued) C. A small transverse incision is made to identify the intermuscular septum between the deep and superficial posterior compartments. Dissecting scissors are used to release the fascia over the deep posterior compartment proximally and distally. Proximally, the fascia is released under the soleus bridge. Scissors are shown under the fascia of the superficial posterior compartment. D. The deep and superficial compartments are released. The superficial posterior compartment looks healthy, whereas the deep posterior compartment is dusky. The tips of the clamp lie under the soleus bridge, which also needs to be released from its origin on the tibia. E. The surgeon releases the soleus bridge using

electrocautery, taking care to protect the deep structures.

  • One-Incision Technique

     

    The one-incision technique often requires more careful dissection around major neurovascular structures

    and can prove to be more challenging. For this reason, it is less often used. Bible et al6 showed no difference in infection or nonunion rates between a one- and two-incision fasciotomy technique.

     

    A straight lateral incision is created that originates just posterior and parallel to the fibula at the level of the fibular head ( protecting the peroneal nerve) to a point above the tip of the lateral malleolus (TECH FIG 3A).

     

    Posterior to the fibula, access is gained to the deep and superficial posterior compartments (TECH FIG 3B).

     

    The fascia between the soleus and flexor hallucis longus is identified distally and released proximally to the level of the soleus origin (TECH FIG 3C).16

     

    Anterior to the fibula, the anterior and lateral compartments are decompressed, taking care to avoid injury to the superficial peroneal nerve.

     

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    TECH FIG 3 • One-incision technique. A. Schematic shows the incision laterally, just posterior and parallel to the fibula. Again, care is taken to avoid injury to the superficial peroneal nerve. B. Cross-section of the midtibia shows dissection posterior to the fibula, allowing access to the deep and superficial posterior compartments. Here, the fascia between the soleus and flexor hallucis longus is identified distally and released proximally to the level of the soleus origin. C. Schematic showing access to the posterior tibia and thus release of the deep posterior compartment. Dissection anterior to the fibula allows identification of the intermuscular septum between the lateral and anterior compartments. The fascia overlying these two compartments is released proximally and distally with the tips of dissecting scissors, taking care to avoid injury to the superficial peroneal nerve.

  • Muscle Débridement

     

    Regardless of the choice of fasciotomy performed, devitalized muscle undergoes débridement as necessary.

     

    Muscle viability is ascertained by the presence of healthy color and the ability to contract when pinched gently or touched with the electrocautery.

     

    Necrotic muscle serves no function and must eventually be removed because it will form a culture medium for infection after fasciotomy.

     

    Extensive débridement typically is not undertaken until the second look at 36 to 72 hours, when muscle viability is more readily determined.

     

    When fasciotomies are performed in the setting of fractures, the fractures are stabilized with either internal or external fixation, which eliminates the need for constrictive casts and allows access for clinical examination, repeat pressure measurements, and wound care.

     

    Fixation of fractures can trigger compartment syndrome through traction and reaming.

  • Closure of Fasciotomies

 

Fasciotomies typically are not closed acutely because the skin itself can constrict muscle.

 

Most often, fasciotomy wounds are either packed with moist dressings (TECH FIG 4A) or covered with a sterile vacuum sponge and kept under suction until the next débridement procedure (TECH FIG 4B).

 

After a lower leg fasciotomy, a useful technique has been the shoelace closure, which involves using a vessel loop and skin staples to gradually close large areas of gaping skin.

 

This allows gradual approximation of the skin edges over the course of several days, thus potentially obviating the need for a skin graft (TECH FIG 4C).

 

It is our opinion that if two surgical wounds are present, the surgeon should attempt to close the medial wound secondarily before the lateral wound.

 

The lateral side of the leg has better soft tissue coverage and consequently is easier to skin graft over if one of the wounds cannot be closed.

 

Sometimes, small relaxing incisions around the fasciotomy wound can decrease the tension, enhancing the chance of healing (TECH FIG 4D).

 

583

 

 

 

TECH FIG 4 • Closure of fasciotomies. A. Moist dressings covering the fasciotomy wound. B. Sterile vacuum system applied to the fasciotomy site. C. Bootlace technique for approximating the edges of a fasciotomy wound. D. Small relaxing incisions made around the fasciotomy site to release tension and allow easier closure. E. Bootlace technique combined with sterile vacuum system.

 

PEARLS AND PITFALLS

 

 

Medicolegal ▪ When in doubt, the surgeon should measure and document pressure in all pitfalls compartments of the involved extremity. The surgeon should clearly document in

the patient's chart that the patient does not have compartment syndrome at this time if the clinical examination findings and pressures are negative.

 

  • In 1993, the average litigation award was $280,000 for eight cases of missed compartment syndrome (in all eight cases, no compartment pressures had

 

been measured).37

  • The surgeon should consider the possibility of equipment error.

  • Needles can be misplaced in tendons, fascia, or the wrong compartment. All

pressure readings must be interpreted within the context of the clinical presentation.

  • The surgeon should fully release all four compartments along with the soleal

    leash and posterior tibial fascia.

  • No tight postoperative dressings should be used.

  • Skin can cause increased pressure, so the surgeon should not close acutely.

 

 

POSTOPERATIVE CARE

 

Once decompressed, the extremity should be covered in a bulky dressing, splinted with the foot in neutral position, and elevated above the level of the heart to promote venous drainage and reduce interstitial fluid.

 

 

The foot should be splinted in neutral position to prevent equinus contracture.

 

The patient must be closely monitored for the systemic effects of compartment syndrome. See the discussion in the Nonoperative Management section regarding administration of supplemental oxygen, intravenous hydration, mannitol, and hyperbaric oxygen.

 

 

Intravenous hydration is important to help prevent rhabdomyolysis.

 

 

584

 

The timing of skin closure varies depending on the cause and severity of compartment syndrome.

 

 

Most fasciotomies can be closed in 5 to 7 days.

 

If the skin is not easily closed secondarily, a split-thickness skin graft is needed to prevent excessive granulation and to lessen exposure of muscle and tendon. A flap might be needed if nerves, vessels, or bone is exposed.

 

If delayed primary closure is planned, a small relaxing incision can be made.

 

Hyperbaric oxygen has been used because it reduces tissue edema through oxygen-induced vasoconstriction while maintaining and increasing oxygen perfusion.

 

 

However, its opponents argue that hyperbaric oxygen leads to reperfusion injury after compartment syndrome.

 

Other agents that have been found to affect recovery from compartment syndrome include allopurinol and oxypurinol, superoxide dismutase, deferoxamine, and pentafraction of hydroxyethyl starch. These agents are antioxidants that scavenge for damaging free radicals.

 

OUTCOMES

Outcomes generally are poor if compartment syndrome is diagnosed and treated in a delayed fashion.

 

Results are better with earlier treatment.

In a study by Sheridan and Matsen,34 50% of patients underwent decompression within 12 hours and 50% underwent decompression after 12 hours. Sixty-eight percent of the patients who underwent decompression within 12 hours had normal leg function, whereas only 8% of the delayed group had normal function.

If untreated, Volkmann ischemic contractures develop, leading to claw toes, weak dorsiflexors, sensory loss, chronic pain, and, eventually, amputation.

ACS results in hospital stays that are increased threefold and hospital charges that are more than doubled. It is important in this day and age to avoid unnecessary fasciotomies.32.

 

 

 

COMPLICATIONS

Most patients (77%) complain of altered sensation within the margins of the wound.18

Forty percent report dry, scaly skin; 33% pruritus; 30% discolored skin; 25% swollen extremity; 26% tethered scars; 13% recurrent ulcerations; 13% muscle herniation; 10% pain related to the wound; and 7% tethered tendons.

Severe prolonged tissue ischemia resulting in necrosis of the muscles leads to fibrosis of the muscles and contracture that can continue over a period of several weeks.

This is known as Volkmann ischemic contracture.

The late sequelae of compartment syndrome are weak dorsiflexors, claw toes, sensory loss, chronic pain, and, eventually, amputation.

Delayed fasciotomy beyond 12 hours is associated with a reported infection rate of 46% and an amputation rate of 21%.34

The complication rate associated with delayed fasciotomies is also much higher (54%) than that associated with early fasciotomies (4.5%). Therefore, the current recommendation is that if the compartment syndrome has existed for more than 24 to 48 hours and the compartment pressures are not within 30 mm Hg of diastolic pressure, supportive treatment for acute renal failure should be considered, the skin should not be violated, and plans should be made for later reconstruction.

 

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