Acute Compartment Syndrome

Compartment syndrome may develop wherever a compartment is present. Possible sites include the lower leg, forearm, wrist, and hand.

Lower leg

The lower leg is divided into 4 compartments. A fifth compartment has been documented, but the clinical significance of this compartment has yet to be established. The 5 compartments are as follows:

• Anterior

• Lateral

• Superficial posterior

• Deep posterior

• Tibialis posterior

Anterior compartment

Muscles in the anterior compartment are as follows:

• Tibialis anterior

• Extensor digitorum longus

• Extensor hallucis longus

• Peroneus tertius

The borders of the anterior compartment are as follows:

• Tibia

• Fibula

• Interosseous membrane

• Anterior intermuscular septum

Lateral compartment

The lateral compartment includes the peroneus longus and brevis. Within the compartment lies the common peroneal nerve superficial branch. The borders of this compartment are as follows:

• Anterior intermuscular septum

• Fibula

• Posterior intermuscular septum

• Deep fascia

Superficial posterior compartment

The superficial posterior compartment contains the gastrocnemius, soleus, and plantaris. It is surrounded by the deep fascia of the leg.

Deep posterior compartment

The muscles within the deep posterior compartment are as follows:

• Flexor digitorum longus

• Flexor hallucis longus

• Popliteus

• Tibialis posterior

Also within this compartment lie the posterior tibial artery and vein and the tibial nerve.

The borders of the deep posterior compartment are as follows:

• Tibia

• Fibula

• Deep transverse fascia

• Interosseous membrane

Tibialis posteriorcompartment

The tibialis posterior compartment is a more recently described subdivision of the deep posterior compartment. It consists of the tibialis posterior, which has been shown to have its own fascial layer.

Forearm

Four interconnected compartments of the forearm are recognized, as follows:

• Superficial volar (flexor)

• Deep volar

• Dorsal (extensor) compartment

• Compartment containing the mobile wad of Henry

The deep volar compartment contains the flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles and tendons. The mobile wad of Henry comprises the brachioradialis, extensor carpi radialis brevis (ECRB), and extensor carpi radialis longus muscles and tendons.

Elevated pressures most commonly affect the volar compartments, but the dorsal and mobile wad compartments may also be involved, alone or in addition to the volar compartments. It is usually difficult to clinically differentiate isolated or combined involvement of the deep and superficial volar compartments.

Wrist

In the wrist, most of the soft tissues are bound within rigid compartments. The volar wrist tendons, for the most part, are tightly constrained within the carpal tunnel (thumb and finger long flexor tendons), except for the flexor carpi radialis, flexor carpi ulnaris, and palmaris longus tendons, which are in separate compartments. The dorsal compartments are primarily channels for tendons and are rarely afflicted by compartment syndrome.

The dorsal extensor tendons pass under an extensor retinaculum and are divided into 6 compartments, as follows:

• Radial wrist abductor (abductor pollicis longus tendon) and thumb extensor (extensor pollicis brevis tendon) dorsal to the trapezium bone

• Radial wrist extensors (extensor carpi radialis longus and ECRB tendons) dorsal and radial to the trapezoid bone

• Extensor pollicis longus tendon

• Common finger extensors (extensor digitorum communis [EDC] tendon) dorsal to the capitotrapezoid articulation

• Extensor digiti minimi tendon to the fifth digit

• Ulnar wrist extensor (extensor carpi ulnaris tendon) in a groove adjacent to the ulnar styloid

Hand

The hand has 10 compartments, as follows:

• Dorsal interossei (4 compartments)

• Palmar interossei (3 compartments)

• Adductor pollicis compartment

• Thenar compartment

• Hypothenar compartment

Compartment syndrome results primarily from increased intracompartmental pressure. The mechanism involved in the development of increased pressure depends on the precipitating event.

Two distinct types of compartment syndrome have been recognized. The first type is associated with trauma to the affected compartment, as seen in fractures or muscle injuries. The second form, called exertional compartment syndrome, is associated with repetitive loading or microtrauma related to physical activity.[15, 16, 17, 18, 19, 20, 21, 22, 23] Thus, compartment syndrome may be acute or chronic in nature.

Tissue perfusion is proportional to the difference between the capillary perfusion pressure (CPP) and the interstitial fluid pressure, which is stated by the following formula:

LBF = (PA - PV)/R

In the formula above, LBF is local blood flow, PA is local arterial pressure, PV is venous pressure, and R is local vascular resistance.

Normal myocyte metabolism requires a 5-7 mm Hg oxygen tension, which can readily be obtained with a CPP of 25 mm Hg and an interstitial tissue pressure of 4-6 mm Hg.[24]

When fluid is introduced into a fixed-volume compartment, tissue pressure increases and venous pressure rises. When the interstitial pressure exceeds the CPP (a narrowed arteriovenous [AV] perfusion gradient), capillary collapse and muscle and tissue ischemia occur.

Skeletal muscle responds to ischemia by releasing histaminelike substances that increase vascular permeability. Plasma leaks out of the capillaries, and relative blood sludging in the small capillaries occurs, worsening the ischemia. The myocytes begin to lyse, and the myofibrillar proteins decompose into osmotically active particles that attract water from arterial blood.

One milliosmole (mOsm) is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment attracts sufficient fluid to cause a further rise in intramuscular pressure. When tissue blood flow is diminished further, muscle ischemia and subsequent cell edema worsen. This vicious cycle of worsening tissue perfusion continues to propagate.

Some reduction in the local AV gradient can be compensated for by changes in local vascular resistance (autoregulation). However, compartment tamponade occurs as arterial blood flow is occluded. Shrier and Magder questioned this traditional hypothesis for the pathophysiology of compartment syndrome and postulated that within muscle compartments, a critical closing pressure exists (similar to West zone II in lung physiology).[25] These authors showed that the increase in this critical closing pressure, which they called Pcrit, rather than an increase in arterial resistance, results in decreased blood flow.

The transmural pressure at which blood flow ceases depends on adrenergic tone as well as the interstitial pressure; the pressure at which this occurs is still under debate. However, in general, compartmental pressures higher than 30 mm Hg require surgical intervention. If such high compartmental pressures are left untreated, within 6-10 hours, muscle infarction, tissue necrosis, and nerve injury occur. For unclear reasons, compartment syndrome that is associated with surgical positioning may manifest later, with a mean time to presentation of 15-24 hours or longer postoperatively.[26]

Pressure-induced functional deficits are likely caused by decreased tissue perfusion rather than a direct mechanical effect. Therefore, the amount of pressure a limb can tolerate depends on limb elevation, blood pressure, hemorrhage, and arterial occlusion. In addition to local morbidity caused by muscle necrosis and tissue ischemia, cellular destruction and alterations in muscle cell membranes lead to the release of myoglobin into the circulation. This circulating myoglobin results in renal injury. Advanced compartment syndrome may result in rhabdomyolysis, and conversely, rhabdomyolysis may result in compartment syndrome.[27] Mortality is usually due to renal failure or sepsis from difficult wound management.

The mechanism of compartment syndrome following vascular trauma may differ slightly from the above scenario because most cases occur with reperfusion. This reperfusion syndrome is likely related to the ischemic depletion of high-energy phosphate forms and ischemic muscle injury.

Muscle has considerable ability to regenerate by forming new muscle cells. Therefore, it is extremely important to decompress ischemic muscle as early as possible. Compartment pressures return to normal after a fasciotomy.[28]

Any internal or external event that increases pressure within a compartment can cause compartment syndrome. Thus, increased fluid content or decreased compartment size can lead to the condition.[29]

Increased fluid content can be caused by the following:

• Intensive muscle use (eg, tetany, vigorous exercise, seizures)[30]

• Everyday exercise activities (eg, stationary bicycle use, horseback riding[31] )

• Burns[32]

• Envenomation

• Decreased serum osmolarity (eg, nephrotic syndrome)

• Hemorrhage (particularly from a large vessel injury)[33, 34]

• Postischemic swelling

• Drug/alcohol abuse and coma

• Rhabdomyolysis[35]

• Gastrocnemius or peroneus muscle tear (lower extremity)

• Ruptured Baker cyst

• Influenza myositis[36]

• Autoimmune vasculitis[37]

• Androgen abuse/muscle hypertrophy

• Deep venous thrombosis[38]

Fractures or gunshot wounds may be the source of hemorrhage underlying compartment syndrome.[4] Upper extremity fractures most frequently associated with compartment syndrome are supracondylar fractures of the humerus, but cases have also been reported in conjunction with fractures of the radial or ulnar diaphysis, fractures of the surgical neck of the humerus, and Colles fractures.

Although trauma is the most common etiology, compartment syndrome has been shown to occur in neonates from intrauterine malposition or strangulation of the extremity by the umbilical cord.

Lying on a limb can cause compartment syndrome. In 1979, Owen et al published a landmark study in which researchers measured intracompartmental pressures in various positions common in drug overdoses.[10] Average pressures were 48 mm Hg with the head resting on the forearm; 178 mm Hg when the forearm was under the ribcage; and 72 mm Hg when one leg was folded under the other.

A study by Shadgan et al indicated that in adult patients with tibial diaphyseal fractures, younger age is a risk factor for acute compartment syndrome. The study, of 1125 patients, found that the mean age of those who developed the syndrome was significantly below that of the rest of the cohort (33.08 years vs 42.01 years). Patient sex, whether the fracture was open or closed, and the use of intramedullary nailing were not found to be risk factors.[39]

In contrast, in a retrospective study by Robertson et al of pediatric patients with supracondylar humerus fractures, regression analysis indicated that compartment syndrome is more likely to occur in patients who are older or male, as well as in those who exhibit a floating elbow fracture pattern or have neurovascular injury.[40]

Another pediatric study, a literature review by Mortensen et al, indicated that in children, risk factors for the development of acute compartment syndrome include open radius/ulna fractures (odds ratio [OR]: 3.56), high-energy trauma (OR: 3.51), humerus fractures sustained concurrently with forearm fractures (OR: 3.49), open tibia fractures (OR: 2.29), and male gender (OR: 2.06).[41]

A literature review by Mortensen et al involving adult patients indicated that risk factors for acute compartment syndrome include age 18-64 years (pooled OR: 1.34), male gender (pooled OR: 2.18), gunshot wound with fracture and vascular injury (pooled OR: 12.5), combined forefoot and midfoot injury (pooled OR: 3.3), an Injury Severity Score (ISS) of 0-9 compared with an ISS of greater than 9 (pooled OR: 1.58), Orthopaedic Trauma Association (OTA)/AO Foundation (AO) type C fracture (pooled OR: 2.75), vascular injury (pooled OR: 9.05), and high-energy trauma (pooled OR: 3.10).[42]

A study by Bouklouch et al of over 200,000 patients with tibial fractures indicated that, regarding fracture location, proximal and midshaft tibial fractures increase the risk of acute compartment syndrome by the greatest amount. Moreover, open fractures were found to carry twice the risk of acute compartment syndrome, the OR being 2.20-2.42. Other reported risk factors included complex fractures, substance abuse disorders, cirrhosis, and smoking. The likelihood of discovering significant muscle necrosis was determined to be greater with fasciotomies for open tibial fractures than for closed fractures.[43]

A study by Allmon et al of radiographic predictors of compartment syndrome in patients with tibial fractures found that each 10% increase in the ratio of fracture length to tibial length increased the odds of compartment syndrome by 1.67. The report also found that the likelihood of compartment syndrome after plateau fracture was 12%, compared with 3% and 2% for shaft and pilon fractures, respectively. In addition, patients with Schatzker VI fractures were at greater risk for compartment syndrome than were those with other types of Schatzker fractures, while in patients with plateau fractures, accompanying fibular fractures also raised the likelihood of compartment syndrome.[44]

A retrospective cohort study by Wuarin et al indicated that risk factors for the development of acute compartment syndrome during the treatment of tibial shaft fractures include a distance of 15 cm or more from the center of the tibial fracture to the talar dome, associated tibial plateau or pilon fracture, closed fracture, and polytrauma.[45]

In a study of nonfracture acute compartment syndrome in pediatric patients (37 children, 39 cases total), Livingston et al found that vascular causes were the most prevalent (28% of cases), followed by trauma (26%), postoperative causes (21%), exertion (15%), and infection (10%). The study also reported that pediatric nonfracture acute compartment syndrome was associated with a high rate of myonecrosis at surgery and with diagnostic delay (average of 48 h from symptom onset to diagnosis).[46]

Iatrogenic causes

Iatrogenic causes of compartment syndrome include the following:

• Military antishock trousers[47]

• Tight splints, casts, dressings[48]

• Lithotomy position (lower extremity cases)[49]

• Malfunctioning sequential compression devices

• Intramuscular, intra-arterial, or intracompartmental injection[50]

• Intraosseous infusion

• Massive hypertonic IV fluid infusion

• Pressurized intravenous (IV) infusion of parenteral hypertonic contrast agent

• Attempts at cannulating veins and arteries of the arm in patients on systemic anticoagulants or patients treated with thrombolytic drugs

• Intraoperative use of a pressurized pulsatile irrigation system

• Use of a pump for infusion of fluids into the joint during an arthroscopic procedure

Chemotherapy drugs can produce true compartment syndrome. Alternatively, extravasation of these drugs can cause pain and swelling that mimics compartment syndrome.

Compartment syndrome may follow operations for orthopedic fixation (eg, open reduction and internal fixation). These cases may result from postoperative hematoma, muscle edema, or tight closure of the deep fascia. These risks can usually be minimized by releasing the tourniquet before wound closure to ensure that hemostasis is adequate and by closing only the subcutaneous tissue and skin.

In rare cases, acute compartment syndrome can develop in the lower leg after coronary artery bypass grafting (CABG), with systemic and local factors increasing the risk, according to a report by Te Kolste et al. The study, which involved five patients who developed acute compartment syndrome as a result of CABG, as well as a literature review, noted such risk factors as cardiopulmonary bypass, which can increase microvascular permeability; cardiac-assist devices, which can produce arterial occlusion and reperfusion injury; harvesting of the greater saphenous vein, which can result in hematoma; and, in patients with peripheral vascular disease, use of the lithotomy position and the employment of elastic bandages, which can reduce arterial blood flow.[51]

Abdominal surgery can lead to well-leg compartment syndrome (WLCS), with a study by Christoffersen et al finding that of 40 prospectively collected cases of WLCS and 124 retrospectively collected cases, 68% of legs had under-knee support during the abdominal operation. The investigators also found that in 56% of cases, WLCS symptoms presented within 2 hours postsurgery.[52]

The anterior distal lower extremity is the most common studied site of compartment syndrome. Tibial fracture is the most common precipitating event, accounting for 2-12% of all compartment syndrome cases, according to the literature. In a retrospective study by McQueen and Court-Brown in 164 patients with diagnosed compartment syndrome, 69% of cases were associated with a fracture, and half of those involved the tibia. In the study, compartment syndrome was diagnosed more often in men than in women. This finding likely represents selection bias, however, because most patients with traumatic injuries are male.[53] In a 10-year study, McQueen et al studied 850 patients and concluded that continuous intracompartmental pressure monitoring should be considered following tibial diaphyseal fracture because these patients are at risk for acute compartment syndrome.[54]

The incidence of acute compartment syndrome varies depending on the inciting event. DeLee and Stiehl found that 6% of patients with open tibial fractures developed compartment syndrome, compared with only 1.2% of patients with closed tibial fractures.[55] The reported incidence of compartment syndrome may underestimate the true incidence because the syndrome may go undetected in severely traumatized patients.

In the aforementioned study by Robertson et al of pediatric patients with supracondylar humerus fractures, acute traumatic compartment syndrome developed in approximately 2-3 fractures per 1000.[40]

The frequency of compartment syndrome is much higher in patients who have an associated vascular injury. Feliciano et al reported that 19% of patients with vascular injury required fasciotomy[56] ; an incidence of 30% has also been suggested, but this figure is not well documented and is most likely an estimate. The true incidence of cases associated with vascular trauma may not be known because many vascular surgeons perform a prophylactic fasciotomy at the time of the vascular repair in high-risk patients.

Compartment syndrome outcome depends on both the diagnosis and the time from injury to intervention. Rorabeck and Macnab reported almost complete recovery of limb function if fasciotomy was performed within 6 hours.[57] Matsen found necrosis after 6 hours of ischemia, which currently is the accepted upper limit of viability.[58]

When fasciotomy was performed within 12 hours after the onset of acute compartment syndrome, Sheridan and Matsen reported that normal limb function was regained in 68% of patients.[59] However, when fasciotomy was delayed 12 hours or longer, only 8% of patients had normal function. Thus, little or no return of function can be expected when the diagnosis and treatment are delayed. Tendon transfers and stabilization may be indicated as late treatment for CS.

Long-term follow-up of patients who have undergone fasciotomies has shown good results, with a return to premorbid activity level. Pain also has been found to significantly improve.

In the lower leg, the results of fasciotomies for posterior compartment syndrome are not as good as those for the anterior compartment. A possible explanation is that it is difficult to do a complete decompression of the deeper posterior compartment, because of the morbidity associated with this procedure. In general, however, early diagnosis, with institution of the appropriate treatment, results in a good outcome.

With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve damage, along with chronic pain, may occur. In the lower leg, peroneal nerve palsy, in particular, may develop.

Volkmann contracture is the residual limb deformity that results over weeks to months following untreated acute compartment syndrome or ischemia from an uncorrected arterial injury. Approximately 1-10% of patients develop a Volkmann contracture.[60] Calcific myonecrosis of lower extremity muscles has been identified as an uncommon late complication of posttraumatic compartment syndrome.

Recurrent compartment syndrome has been reported in athletes. It is thought to be related to severe scarring and the subsequent closing of the initial compartment release.

Infection is a serious complication of compartment syndrome. In a retrospective review by Matsen et al, 11 of 24 extremities that had late surgical decompression developed infections, and 5 of these infections led to an amputation.[61] Infection after fasciotomy may become chronic. Patients, especially those with multiple traumatic injuries, may die because of infections or metabolic complications. Renal failure or multiple organ failure may occur preoperatively or postoperatively. Most fatalities are due to prolonged intensive care admissions with sepsis and multisystem organ failure.

Patients with compartment syndrome typically present with pain whose severity appears out of proportion to the injury. The pain is often described as burning. The pain is also deep and aching in nature and is worsened by passive stretching of the involved muscles. The patient may describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of the diagnosis. In severe trauma, such as an open fracture, it is difficult to differentiate between pain from the fracture and pain resulting from increased compartment pressure.

Paresthesia or numbness is an unreliable early complaint[11] ; however, decreased 2-point discrimination is a more reliable early test and can be helpful to make the diagnosis. Botte and Gelberman reported that 4 of 9 awake patients with compartment pressures higher than 30 mm Hg had median nerve 2-point discrimination of more than 1 cm.[19] Correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure. Importantly, note that these symptoms assume a conscious patient who did not suffer any additional injury that hinders sensory input (eg, spinal cord injury). In young children, the ability to gather a history of complaints is limited.[62]

Determine the mechanism of injury. High-velocity injuries are particularly worrisome, as are long-bone fractures and crush injuries. Penetrating injuries (eg, gunshot wounds, stabbings) can cause arterial injury, which can quickly lead to compartment syndrome. Venous injury may also cause compartment syndrome, however, so the clinician should not be misled by the presence of palpable pulses.

Anticoagulation therapy and bleeding disorders (eg, hemophilia) significantly increase the likelihood of compartment syndrome. Remember to ask if patients are anticoagulated for any reason. Compartment syndrome requiring fasciotomy has been observed after simple venipuncture in an anticoagulated patient.

Vigorous exertion may lead to compartment syndrome. Compartment syndrome has been found in soldiers and athletes without any trauma. This can be acute or chronic, with acute compartment pressures as high as those found in severe trauma. If compartment syndrome is suspected, check intracompartmental pressure, even in the absence of any trauma history.[63]

Hand compartment syndrome

Compartment syndrome in the hand most often occurs following iatrogenic injury in a patient who is obtunded in an intensive care unit. Symptoms may be nonspecific when compared with those in other cases of compartment syndrome. Early recognition of this complication is based on physical examination and a high index of suspicion. Compartment syndrome in the hand, unlike cases elsewhere in the body, does not cause abnormalities in the sensory nerves, as no nerves are found within the compartments.

Consider the diagnosis when nonspecific aching of the hand, increased pain, loss of digital motion, and continued swelling are present. A tight, swollen hand in an intrinsic minus position—with the digits in metacarpophalangeal (MCP) extension and proximal interphalangeal (PIP) flexion—is highly indicative. Intrinsic tightness becomes evident on examination because motion of the PIP joint becomes dependent on the position of the MCP joint (more PIP motion is possible with MCP flexion than with MCP extension).

On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of a developing compartment syndrome. Comparison of the affected limb to the unaffected limb is useful. Excessively vigorous examination of a tibial fracture should be avoided because this may exacerbate irritation of the deep posterior compartment.

Common symptoms observed in compartment syndrome include a feeling of tightness and swelling. Pain with certain movements, particularly passive stretching of the muscles, is the earliest clinical indicator of compartment syndrome. A patient may report pain with active flexion.

The traditional 5 P's of acute ischemia in a limb (ie, pain, paresthesia, pallor, pulselessness, poikilothermia) are not clinically reliable; they may manifest only in the late stages of compartment syndrome, by which time extensive and irreversible soft tissue damage may have taken place. Peripheral pulses and capillary refill remain normal in most cases of upper extremity acute compartment syndrome.

The most important diagnostic physical finding is a firm, wooden feeling on deep palpation. Bullae may also be seen; however, so-called fracture blisters are common in the absence of compartment syndrome. In cases involving the leg, a soft tissue mass may be noticed as a result of herniation of fat and/or muscle tissue from the fascial defect that is often found in the lower third of the leg. In cases of trauma and gross deformity, a claw-toe deformity might occur; therefore, the patient should be evaluated for such a condition.

If a patient complains of pain, determine whether any neural compromise is present. Sensory nerves tend to be affected before the motor nerves, and selected nerves may be more susceptible than others in the same compartment. For example, in acute anterior lower leg compartment syndrome, the first sign to develop may be numbness between the first 2 toes (superficial peroneal nerve).

Decreased 2-point discrimination is the most consistent early finding, and correlation has also been reported between diminished vibration sense (as measured with a 256 cycle per second tuning fork). If objective evidence of a major sensory deficit, a motor deficit, or loss of peripheral pulse is found, the syndrome is far advanced.

In a patient with the classic compartment syndrome presentation and physical examination findings, no laboratory workup is needed. Laboratory results are often normal, are not necessary to diagnose compartment syndrome, and are not helpful to rule out compartment syndrome. However, in acute compartment syndrome, especially with trauma, consider performing a workup for rhabdomyolysis, with measurement of the following:

• Creatine phosphokinase (CPK)

• Renal function studies

• Urinalysis

• Urine myoglobin

A CPK concentration of 1000-5000 U/mL or greater or the presence of myoglobinuria can suggest compartment syndrome. Serial CPK measurements may show rising levels indicative of a developing compartment syndrome. Urinalysis may be used to help identify causes of acute renal failure.

Patients with rhabdomyolysis should have serum chemistry studies done. Complete blood cell count and coagulation studies should be part of the preoperative workup. Anemia worsens tissue oxygenation. Disseminated intravascular coagulation is a rare but possible complication.

Measurement of intracompartmental pressures remains the standard for diagnosis of compartment syndrome. Perform this procedure as soon as a diagnosis of compartment syndrome is suspected.

Imaging studies are usually not helpful in making the diagnosis of compartment syndrome. However, such studies are used in part to eliminate disorders in the differential diagnosis. Standard radiographs are obtained to determine the occurrence and nature of fractures. Stress fractures and periostitis can be diagnosed with plain radiographs, bone scans, computed tomography (CT) scans, or magnetic resonance imaging (MRI) scans.[64] CT scanning may be useful if pelvic or thigh compartment syndrome is part of the differential diagnosis.

Muscle tears can be observed using MRI or ultrasonography.[12] MRI may show increased signal intensity in an entire compartment on T2-weighted, spin-echo sequences. Doppler ultrasound may be used to evaluate arterial flow and to rule out deep venous thrombosis, particularly in the lower extremities. In addition, the loss of normal phasic patterns of tibial venous blood flow has been shown to accurately predict the need for surgical fasciotomy.[65] Ultrasonography alone is not useful in diagnosing compartment syndrome, but it aids in the exclusion of other disorders.

In the lower leg, partial vascular occlusion may cause a pseudo–compartment syndrome. Angiography may be needed to exclude adductor canal compression syndrome and popliteal artery entrapment. Pulse oximetry is helpful in identifying limb hypoperfusion. However, it is not sensitive enough to exclude compartment syndrome. In unusual cases, muscle biopsies may be necessary in primary muscle disorders. Histology is usually not helpful, but if necrotizing fasciitis is in the differential diagnosis, intraoperative cultures and a Gram stain may be of benefit.

Blood urea nitrogen (BUN) and creatinine levels are used to assess the patient's hydration status in cases of rhabdomyolysis. Measurement of the potassium level is needed in cases of rhabdomyolysis, as severe hyperkalemia may result in a wide-complex, possibly fatal arrhythmia. Purines released from cell nuclei result in hyperuricemia and nephrotoxicity. Coexisting oliguria, aciduria, and uricosuria worsen nephrotoxicity.

An anion gap (see the Anion Gap calculator) may indicate other underlying etiologies (eg, drug overdose) for the compartment syndrome. Sodium, potassium, bicarbonate, and phosphate levels are used to assess lactic acidosis and other metabolic acids. In addition, hyperphosphatemia aggravates hypocalcemia. Metastatic calcification is possible.

Various methods and equipment can be used for compartment pressure measurement. A transducer connected to a catheter usually is introduced into the compartment to be measured. This is the most accurate method of measuring compartment pressure and diagnosing compartment syndrome. Measurement of the compartment pressure then can be performed at rest, as well as during and after exercise. With the acute syndrome, the exact pressure threshold is controversial, but typical ranges are from 30-45 mm Hg at rest. Some sources state that it is better to associate this pressure to diastolic pressure (that is, within 10-30 mm Hg of diastolic pressure).

Injection technique of direct pressure measurement

Direct compartment-pressure measurement is the diagnostic criterion standard and should be the first priority if the diagnosis is in question. A number of handheld devices are available. The Stryker pressure tonometer is widely used, and pressure measurements from the Stryker device are within 5 mm Hg of the slit catheter for 95% of all readings (direct communication with Stryker Corporation, April 2007). The Stryker STIC device is shown in the image below.

Stryker STIC Monitor. Image courtesy of Stryker Corporation, used with permission.

If a commercial device is unavailable, it is possible to assemble a device to measure intracompartment pressure. The device measures the pressure that is necessary to inject a small quantity of fluid. This technique often overestimates low pressures but is generally reliable.

Supplies needed to make a pressure transducer are as follows:

• One sterile 20-mL Luer-Lok tip syringe (BD Medical Systems)

• One 4-way stopcock

• One 18-gauge 1.25-in Angiocath IV catheter (BD Medical Systems)

• Two 89-cm–long extension tube sets

• Two 18-gauge needles

• One bag of sterile normal saline for intravenous infusion

• One Telfa adhesive dressing pad (Kendall Healthcare Products Co)

• One blood pressure manometer

A diagram of the device is shown in the image below.

Picture of compartment pressure measuring device for use when commercial devices are unavailable.

Instructions for measuring intracompartmental pressure are as follows[60] :

1. Clean and prepare the area.

2. Assemble the 20-mL syringe with the plunger at the 15-mL mark, and connect it to an open end of the 4-way stopcock.

3. Connect the sterile plastic IV extension tube and an 18-gauge needle on 1 end of the stopcock; connect a second IV extension tube at the opposite end of the stopcock to a blood pressure manometer.

4. Insert the tip of the 18-gauge needle into the bag of saline, and open the stopcock to allow flow through the needled IV tubing only. Aspirate the saline solution without bubbles into about half the length of the extension tube. Turn the 4-way stopcock to close off this tube so that the saline solution is not lost during transfer of the needle.

5. Insert the 18-gauge needle into the muscle of the compartment in which the tissue pressure is to be measured.

6. Turn the stopcock so that the syringe is open to both extension tubes, forming a T connection. This produces a closed system in which the air is free to flow into both extension tubes as the pressure within the system is increased.

7. Increase the pressure in the system gradually by slowly depressing the plunger of the syringe while watching the saline/air meniscus. The mercury manometer will rise as the pressure within the system rises. When the pressure in this system has just surpassed the tissue pressure surrounding the needle, a small amount of saline solution is injected into the tissue, and the meniscus will be seen to move. When the column moves, stop the pressure on the syringe plunger and read the level of the manometer. The manometer reading at the time the saline column moves is the tissue pressure in mm Hg.

Wick technique of direct compartment-pressure measurement

The wick technique employs strands of a wettable material that extend from the tissue to a fluid-filled catheter that is connected to a pressure transducer.[66]

As long as the wick catheter patency is checked, the wick method is as reliable as continuous-infusion techniques.

Other measurement techniques

Other less-invasive compartment blood flow measurement techniques that have been studied but are not commonly used in clinical practice include the following:

• Laser Doppler ultrasound

• Methoxy isobutyl isonitrile enhanced magnetic resonance imaging (MRI)

• Phosphate-nuclear magnetic resonance (NMR) spectroscopy

• Thallous chloride-201 (201 Tl ) and technetium-99 (99m Tc) sestamibi, and xenon (Xe) scanning

The treatment of choice for acute compartment syndrome is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a compartment syndrome, adequate decompressive fasciotomy must be performed as an emergency procedure. Following fasciotomy, fracture reduction or stabilization and vascular repair can be performed, if needed.

If a developing compartment syndrome is suspected, place the affected limb or limbs at the level of the heart. Elevation is contraindicated because it decreases arterial flow and narrows the arterial-venous pressure gradient.[13, 14]

In patients with tibial fracture and suspected compartment syndrome, immobilize the lower leg with the ankle in slight plantar flexion, which decreases the deep posterior compartment pressure and does not increase the anterior compartment pressure. (Postoperatively, the ankle is held at 90° to prevent equinus deformity.)

All bandages and casts must be removed. Releasing 1 side of a plaster cast can reduce compartment pressure by 30%, bivalving can produce an additional 35% reduction,[60] and complete removal of the cast reduces the pressure by another 15%, for a total decrease of 85% from baseline.[67] Cutting undercast padding (Webril, Kendall Healthcare Products Co) may decrease compartmental pressure by 10-30%.[68, 60, 10]

Administer antivenin in cases of snake envenomation; this may reverse a developing compartment syndrome. Correct hypoperfusion with crystalloid solution and blood products.

Relative hypertension and correction of acute anemia may help prevent the development of an impending acute compartment syndrome. Ongoing research continues to examine the role of nitric oxide.

In the setting of an acute compartment syndrome, capillary permeability is altered after 3 hours, resulting in postischemia tissue swelling of 30-60%. The role of mannitol in decreasing tissue edema is still under investigation; it may reduce compartment pressures and lessen reperfusion injury.[69, 70, 71] Vasodilator drugs or sympathetic blocking drugs appear to be ineffective, probably because maximal local vasodilatation is already present in this condition.

Observation

A retrospective British study indicated that children under age 12 years with a minimally displaced tibial fracture can be safely treated and discharged without inpatient observation for acute compartment syndrome. Malhotra et al reviewed the clinical and radiographic progress of 159 tibial fractures (81% in the diaphyseal region) in patients under 12 years; in 60% of the injuries, the tibia alone was involved. Most of the 159 fractures (66%) were treated nonoperatively. None of the patients in the study developed acute compartment syndrome.[72]

Based on the study, Malhotra and colleagues advised that children under 12 years with a minimally displaced, tibia-only fracture can be placed in a back-slab cast and discharged from the emergency department with early follow-up, as long as their pain is being effectively addressed and they can mobilize under their parents’ supervision. Inpatient observation for acute compartment syndrome may be advisable, according to the investigators, in patients who have suffered a high-energy injury, who have a displaced fracture, or who also have a fibular fracture.[72]

Ischemia that lasts 4 hours leads to significant myoglobinuria, which reaches a maximum about 3 hours after the circulation is restored but persists for as long as 12 hours. In the face of rhabdomyolysis, IV fluid administration and, potentially, bicarbonate may be used to keep urine output at 1-2 mL/kg/hr.

The combination of hypovolemia, acidemia, and myoglobinemia may cause acute renal failure. Alkalization of the urine and diuresis appear to be renal-protective, presumably because hemoglobin and myoglobin are more soluble in an alkaline solution. Patients who survive almost always recover renal function, even those patients who require prolonged hemodialysis. Current recommendations are as follows:

• Correct hypovolemia with crystalloid solution

• Infuse 500 mL/hr of crystalloid solution and 22.4 mEq bicarbonate (12 L/day, forcing diuresis of approximately 8 L/day)

• If diuresis is less than 300 mL/hr, administer mannitol dose of 1 g/kg

• If blood pH is greater than 7.45, administer 250 mg acetazolamide

• Monitor vital signs and urine pH level and volume hourly

• Assess osmolarity and electrolytes and arterial blood gas every 6 hours

The definitive surgical therapy for compartment syndrome is emergent fasciotomy to release the involved compartment, with subsequent fracture reduction or stabilization and vascular repair, if needed. When compartment pressures are elevated, especially in acute settings, prompt surgical evaluation should be performed, since elevated pressures can, over a prolonged period, cause irreversible damage.[73, 74] However, no consensus exists regarding the exact pressure at which fasciotomy should be performed.[17, 19, 21, 22, 75, 76, 77]

Whitesides et al advised that fasciotomy should be performed when the compartment pressure rises to within 10-30 mm Hg of the patient's diastolic blood pressure (the so-called delta-P).[78, 79] McQueen and Court-Brown, studying compartment syndrome in dogs, affirmed the difference of 30 mm Hg between the compartment pressure and the diastolic blood pressure as a more reliable measure than absolute pressure measurements.[53]

Currently, many surgeons use a measured compartment pressure of 30 mm Hg as a cutoff for fasciotomy. Multiple pressure readings are often obtained, and the clinician must decide how to incorporate these readings with the clinical picture in the decision-making process.

Mubarak and Hargens recommended that fasciotomy be performed for the following patients[29] :

• Those who are normotensive with positive clinical findings, who have compartment pressures of greater than 30 mm Hg, and whose duration of increased pressure is unknown or thought to be longer than 8 hours

• Those who are uncooperative or unconscious, with a compartment pressure of greater than 30 mm Hg

• Those with low blood pressure and a compartment pressure of greater than 20 mm Hg

The tolerance of tissue to prolonged ischemia varies depending on the type of tissue that is involved. Matsen showed that muscles have functional impairment after 2-4 hours of ischemia and irreversible functional loss after 4-12 hours.[11]

Nerve tissue shows abnormal function after 30 minutes of ischemia, with irreversible functional loss after 12-24 hours. Additional experimental data, however, have shown significant changes in somatosensory potentials as early as 45 minutes after compartment pressure increases up to 30 mm Hg.

If the compartment pressure is greater than 40 mm Hg, a fasciotomy is usually performed emergently, and fasciotomy is indicated if the pressure remains 30-40 mm Hg for longer than 4 hours. As a rule, when in doubt, the compartment should be released.

In a study of patients with clinical signs of compartment syndrome after revascularization surgery for lower limb ischemia, Arato et al reported that measurement of intracompartmental pressure and tissue oxygenation (measured with near-infrared spectroscopy) could be used to determine whether fasciotomy was needed.[80] Patients with pressure below 40 mm Hg and normal tissue oxygen saturation were treated conservatively.

With compartment syndrome in the hand, surgeons should have a lower threshold for decompression; a compartmental pressure of greater than 15-20 mm Hg is a relative indication for release.

If compartment syndrome is diagnosed late, fasciotomy is of no benefit. In fact, fasciotomy probably is contraindicated after the third or fourth day following the onset of compartment syndrome.

When fasciotomy is performed late, severe infection usually develops in the necrotic muscle. However, if the necrotic muscle is left alone and the compartment is not open, it can heal with scar tissue. This may result in a more functional extremity with fewer complications. However, if the duration of compartment syndrome is unclear, the surgeon should elect to decompress the indicated compartments.

A study by Blair et al found that in patients with tibial fractures, four-compartment fasciotomy for acute compartment syndrome is associated with an increased likelihood of infection and nonunion. The study included patients with tibial plateau or shaft fractures with acute compartment syndrome (46 patients) or without acute compartment syndrome (138 patients), with the compartment syndrome patients receiving two-incision four-compartment fasciotomy. Nonunion and deep infection both occurred at a rate of 20% in the compartment syndrome/fasciotomy patients, versus 5% and 4%, respectively, in the other patients.[81]

In the setting of a vascular injury, a fasciotomy should be performed on high-risk patients before arterial exploration. High-risk patients include those with prolonged ischemia time, significant preoperative hypotension, associated crush injury, combined arterial and venous injury, or the need for a major venous ligation in the popliteal or femoral area.

In a survey by Collinge et al of Orthopaedic Trauma Association members, there was a consensus among respondents that wound closure or skin grafting should occur within 1-5 days postfasciotomy. Respondents universally recommended that skin grafting be employed if more than 7 days elapsed before closure.[82]

Studies by Nillius and Rooser, Peek and Haynes, and Fruensgaard and Holm documented the incidence of compartment syndrome following knee arthroscopy and evaluated fasciotomies as treatment.[83, 84, 85] However, Kaper et al have suggested that emergency fasciotomies are not absolutely indicated.[86] Rather, observation of the patient in the recovery room, with serial examinations and repeat compartment pressure measurements, may be considered.

Pressure measurements of the contralateral extremity may be useful as a control to verify the accuracy of the readings. If persistently elevated pressures are recorded or the development of clinical findings consistent with compartment syndrome are noted, the patient can still be returned to the operating room within the 6 hours prior to development of irreversible myonecrosis.

The Hyperbaric Oxygen (HBO) Committee of the Undersea and Hyperbaric Medical Society (UHMS) reported 13 major syndromes amenable to HBO, of which fourth on the list is crush injury, compartment syndrome, and other acute traumatic ischemias.[87] HBO promotes hyperoxic vasoconstriction, which reduces swelling and edema and improves local blood flow and oxygenation. It also increases tissue oxygen tensions and improves the survival of marginally viable tissue.[88]

At the time of surgical debridement, prior treatment with HBO aids in the demarcation of nonviable tissue. The best results are obtained when therapy is started early. Twice-daily treatments at 2.0 atmosphere absolute (ATA) to 2.5 ATA for 90-120 minutes are recommended for 5-7 days, with frequent examinations of the affected area. Despite the recommendation for HBO, most authors strongly advise caution in employing this modality. The treatment of choice for compartment syndrome is early decompression.

Physical Therapy and Occupational Therapy

The patient who undergoes fasciotomy requires a physical therapy program to regain function. Postoperative care and rehabilitation are just as important as the procedure itself.

During the immediate postoperative period, weight bearing is limited, and assistive devices (eg, crutches) are needed. Within a few days and with adequate pain control, the use of crutches can be discontinued. The rehabilitation program then involves range of motion (ROM) and flexibility exercises involving the muscles of the affected compartment. Adjacent joints need to be exercised to maintain their normal ROM.

Once the patient is able to ambulate with a normalized gait pattern, a program of graduated resistive exercises (depending on the person's regular activities or work) is initiated. In the case of athletes, sports-specific exercises are started with the intention of returning to a regular athletic schedule. Cross training is also beneficial for these athletes. Activities such as swimming, pedal exercises, water jogging, and running help athletes regain muscle strength and flexibility without loading the affected compartment.

With surgical intervention for decompression, occupational therapy consultation should be considered early in the postoperative period for assessment of appropriate treatment and of the patient's deficits with regard to activities of daily living (ADL). Therapy for ADL as well as instruction in the use of any necessary assistive device(s) may be indicated.

With late diagnosis, irreversible tissue ischemia can develop in the acute setting. Thus, permanent muscle and nerve damage, along with chronic pain, may occur. Peroneal nerve palsy, in particular, may develop. With muscle damage, muscle contractures may be observed. For more information on management of contractures, see the Medscape Reference article Volkmann Contracture.

Hypesthesia and painful dysesthesia can also result from compartment syndrome. These may resolve slowly with time. Phenytoin (Dilantin), gabapentin (Neurontin), or carbamazepine (Tegretol) may be of some value in making the patient more comfortable.

Opioids, nonopioids, and nonsteroidal anti-inflammatory drugs (NSAIDs) can be used for pain management in compartment syndrome.[89] Side effects and patient profiles should be considered when choosing medications. Acetaminophen can result in liver damage. Narcotics can produce gastrointestinal distress, constipation, and sedation, and they have addictive potential. NSAIDs can result in gastrointestinal upset, gastrointestinal bleeding, renal damage, and impaired coagulation.

Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort, and some have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Acetaminophen (Acephen, Cefaten, Mapap, Tylenol, FeverAll, Aspirin Free Anacin)

Acetaminophen is the drug of choice for pain in patients with documented hypersensitivity to aspirin or NSAIDs, those with upper GI disease, and those who are taking oral anticoagulants.

Class Summary

These medications provide control of moderate to severe pain.

Hydrocodone and acetaminophen (Vicodin, Lorcet, Lortab, Norco, Zolvit)

This drug combination is indicated for moderate to severe pain.

Acetaminophen with codeine (Tylenol-3)

This drug combination is indicated for treatment of mild to moderate pain.

Class Summary

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Naproxen (Naprosyn, Aleve, Naprelan, Anaprox)

Naproxen is indicated for relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Celecoxib (Celebrex)

Celecoxib inhibits primarily cyclooxygenase-2 (COX-2). COX-2 is considered an inducible isoenzyme; it is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, celecoxib does not inhibit the COX-1 isoenzyme; thus GI toxicity may be decreased. The increased cost of celecoxib must be weighed against the benefit of avoidance of GI bleeds. Seek the lowest dose of celecoxib for each patient.

Diclofenac (Voltaren, Cataflam, Cambia, Zipsor)

These nonsteroidal anti-inflammatory drugs inhibit prostaglandin synthesis by decreasing cyclooxygenase activity, decreasing formation of prostaglandin precursors.

Ketorolac

Ketorolac is an intravenously administered NSAID and a very powerful analgesic. It inhibits prostaglandin synthesis by decreasing activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors. In turn, this results in reduced inflammation.

Ibuprofen (Advil, Motrin, Caldolor)

Ibuprofen is usually the drug of choice for treatment of mild to moderate pain, if no contraindications exist. It inhibits inflammatory reactions and pain by decreasing the activity of the enzyme cyclo-oxygenase, resulting in inhibition of prostaglandin synthesis.