A summary of CS etiologies is as follows:

* External restriction of the muscle compartment

o Military antishock trousers (MAST) (CS in the lower extremity)

o Tight splints, casts, dressings

o Burns15

o Tight fascial closure during ORIF (open reduction and internal fixation)

o Lithotomy position (CS in the lower extremity)

o Malfunctioning sequential compression devices (SCDs)

o Tight ski boots (CS in the lower extremity)

o Localized external pressure

* Internal increase in compartment volume/content

o Hemorrhage (due to trauma, warfarin [Coumadin], tissue plasminogen activator [t-PA])16,17

o Hemophilia

o Postischemic swelling

o Fractures9

o Postoperative hematoma/muscle edema

o Gunshot wounds to the thigh (CS in the lower extremity)

o Massive hypertonic IV fluid infusion

o Drug/alcohol abuse and coma

o Compartment fluid injection18

o Snake envenomation

o Nephrotic syndrome

o Crush injuries, burns

o Rhabdomyolysis19

o Gastrocnemius or peroneus muscle tear (CS in the lower extremity)

o Weight lifting, overuse of weights, exercise

o Androgen abuse/muscle hypertrophy

o Knee arthroscopy (CS in the lower extremity)

o Ruptured Baker cyst

o Influenza myositis

o Seizure and eclampsia

o Autoimmune vasculitis20

Pathophysiology

Compartment syndrome (CS) occurs when an elevated intrafascial compartment pressure results in ischemia of muscle and nerve tissue. Although the inciting pathogenic factor in CS is increased tissue pressure, 3 theories have been proposed to explain the development of tissue ischemia, as follows:

* A critical closing pressure of the arterioles is reached, similar to the West zones in the lung, and the arterioles snap shut.21

* Arterial spasm occurs from inflammatory mediators, from a nitric oxide pathway, or from elevated pressure alone.22

* Thin-walled veins close when compartment pressure rises, but the veins reopen if blood continues to flow from the capillaries and elevates local venous pressure. The resulting narrowed arterial-venous perfusion gradient progresses until, eventually, muscle ischemia occurs.

Ashton examined the effect of increased compartment pressure on regional blood flow and concluded that at least 2 mechanisms were involved, as follows22 :

* Active closure of the arterioles when the transmural pressure is lowered, either by a decrease in intravascular pressure or by a rise in tissue pressure

* Collapse of soft-walled capillaries when tissue pressure rises

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 as the blood flows inward. One milliosmole is estimated to exert a pressure of 19.5 mm Hg; therefore, a relatively small increase in osmotically active particles in a closed compartment can attract sufficient fluid to cause a further rise in intramuscular pressure. With diminished blood flow, muscle ischemia and subsequent cell edema worsens. This vicious cycle of worsening tissue perfusion continues until eventual compartment tamponade occurs. The transmural pressure at which blood flow ceases depends on adrenergic tone, volume status, and other factors.

Within 6-10 hours, muscle infarction and nerve injury result. Muscle has considerable ability to regenerate by forming new muscle cells; therefore, it is extremely important to decompress ischemic muscle as early as possible. Cellular destruction and alterations in vascular membrane permeability lead to the release of myoglobin into the circulation. Advanced CS may result in rhabdomyolysis, or rhabdomyolysis may result in CS. For uncertain reasons, CS that is associated with surgical positioning may present later, with a mean time to presentation of 15-24 hours or longer postoperatively.23

Reneman described the pathogenesis of chronic CS (CCS) in the leg.24 Muscle bulk increases 20% during exercise and contributes to the transient increase in intracompartmental pressure. As the intracompartmental pressure rises, arterial flow during muscle relaxation decreases, and the patient experiences muscle cramping.

Presentation

The patient afflicted by compartment syndrome (CS) may experience crescendo pain that is out of proportion to the original injury. The pain is deep and aching in nature and is worsened by passive stretching of the fingers. The patient may also describe a tense feeling in the extremity. Pain, however, should not be a sine qua non of CS. The forearm is often tender and tense, and the sensibility/sensitivity of the fingertips may be diminished.

Paraesthesia, or numbness, is an unreliable early complaint of CS5 ; 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.25 Correlation has also been reported between diminished vibration sense (256 cycles/s) and increasing compartment pressure.

On physical examination, evidence of trauma and gross deformity should alert the physician to the possibility of an evolving CS. Comparison of the affected limb to the unaffected limb is useful. Pulselessness is a late and unreliable finding, and the presence of a radial pulse does not exclude the possibility of a CS. 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 CS. As the pressure increases, pallor and loss of pulses are late findings. If objective evidence of a motor deficit is found, the CS is far advanced. Laboratory testing that reveals a creatine kinase (CK) of 1000-5000 U/mL or greater or the presence of myoglobinuria can suggest CS.

CS in the hand most often occurs following iatrogenic injury in a patient who is obtunded in an intensive care unit. Symptoms may be nonspecific compared with those in other CS cases. Early recognition of this complication is based on physical examination and a high index of suspicion. Unlike elsewhere, CS in the hand lacks 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).

Chronic CS (CCS) is clinically distinct from the acute CS; it often occurs bilaterally, and pain may be reproducible at a specific workload or time interval. Most athletes cannot play through the severe pain, but symptoms tend to resolve within an hour of terminating the activity. Bilateral CCS should be suspected in patients who complain of bilateral exercise-induced pain in the anconeus muscle, the forearms, the thenar and hypothenar regions, and the first dorsal interosseous muscle. The symptoms are usually minimal during normal daily activities.

Indications

In the setting of the classic compartment syndrome (CS) presentation and physical examination findings, no further diagnostic studies are needed. No uniform consensus exists on the minimum pressure for which fasciotomy should be performed. Whitesides et al noted 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).4 Since then, many surgeons have used 30 mm Hg as a cutoff for fasciotomy. Mubarak and Hargens recommended that fasciotomy be performed for the following patients26 : (1) 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; (2) those who are uncooperative or unconscious, with a compartment pressure of greater than 30 mm Hg; and (3) those with low blood pressure and a compartment pressureof 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.5 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 compartmental 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 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.

Relevant Anatomy

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

* Superficial volar (flexor) compartment

* Deep volar (flexor digitorum profundus, flexor pollicis longus, and pronator quadratus muscles and tendons) compartment

* Dorsal (extensor) compartment

* Compartment containing the mobile wad of Henry (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.

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. Consideration of a carpal tunnel release is warranted when performing a volar release. Mostly, the dorsal compartments are channels for tendons and rarely are afflicted by CS.

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

The hand has 10 compartments, as follows:

* Dorsal interossei (4 compartments)

* Palmar interossei (3 compartments)

* Adductor pollicis compartment

* Thenar compartment

* Hypothenar compartment

Contraindications

If compartment syndrome (CS) is diagnosed late, fasciotomy is of no benefit. In fact, fasciotomy probably is contraindicated after the third or fourth day following the onset of CS. 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, in the setting of an unclear syndrome duration, the surgeon should elect to decompress the indicated compartments.

Laboratory Studies

* CK (creatine kinase)- Used to determine the level of muscle necrosis

o Serial CK measurements may show rising levels indicative of a developing compartment syndrome (CS).

o High CK levels should alert the physician to possible rhabdomyolysis.

* Blood urea nitrogen (BUN)/creatinine levels - Used to assess kidney function in cases of rhabdomyolysis

o Purines released from cell nuclei result in hyperuricemia and nephrotoxicity.

o Coexisting oliguria, aciduria, and uricosuria worsen nephrotoxicity.

o Assessment of BUN/creatinine levels allows for assessment of the patient's hydration status.

o An anion gap may indicate other underlying etiologies (eg, drug overdose) for the CS.

* Sodium, potassium, bicarbonate, phosphate levels

o These measurements are used to assess lactic acidosis and other metabolic acids.

o The potassium level needs to be assessed, as severe hyperkalemia may result in a wide complex and possibly fatal arrhythmia.

o Hyperphosphatemia aggravates hypocalcemia.

o Metastatic calcification is possible.

* Complete blood cell count and coagulation studies

o These studies should be part of the preoperative lab studies obtained.

o Anemia worsens tissue oxygenation.

o Disseminated intravascular coagulation is a possible complication.

* Urinalysis

o This study is used to determine myoglobin and CK (if available).

o Urinalysis may be used to help identify causes of acute renal failure (eg, acute tubular necrosis, prerenal).

o A urine dip may reveal blood but no red blood cells, which indicates the presence of myoglobin.

Imaging Studies

* Imaging studies are usually not helpful in making the diagnosis of compartment syndrome (CS). However, such studies are used in part to eliminate disorders in the differential diagnosis.

o Standard radiographs are obtained to determine the occurrence and nature of fractures.

o Computed tomography (CT) scanning may be useful if pelvic or thigh CS is part of the differential diagnosis.

o Doppler ultrasound may be used 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.27

Diagnostic Procedures

* Direct pressure measurement: Various products are commercially available for direct pressure measurements (ACE Medical Equipment Inc, Clearwater, Fla; Stryker Corp).

o Supplies needed to make your own pressure transducer are as follows:

+ 1 sterile 20-mL Luer-Lok tip syringe (BD Medical Systems, Sandy, Utah)

+ 1 4-way stopcock

+ 1 18-gauge 1.25-in Angiocath IV catheter (BD Medical Systems)

+ 2 89-cm-long extension tube sets

+ 2 18-gauge needles

+ 1 Telfa adhesive dressing pad (Kendall Healthcare Products Co, Mansfield, Mass)

o Instructions for measuring intracompartmental pressure2 :

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 saline bag, 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.

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

o Laser Doppler ultrasound

o Methoxy isobutyl isonitrile enhanced magnetic resonance imaging (MRI)

o Phosphate-nuclear magnetic resonance (NMR) spectroscopy

o Thallous chloride-201 (201 Tl ) and technetium-99 (99m Tc) sestamibi scanning

o Xenon scanning

Treatment

Medical Therapy

If a developing compartment syndrome (CS) 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. Releasing 1 side of a plaster cast can reduce compartment pressure by 30%, bivalving can produce an additional 35% reduction,2 and complete removal of the cast reduces the pressure by another 15%, for a total decrease of 85% from baseline.28 Cutting Webril (Kendall Healthcare Products Co) may decrease compartmental pressure by 10-30%.29 Hence, when CS is identified or suspected, all bandages and casts must be removed. In cases of snake envenomation, administration of antivenin may reverse a developing CS.

In the setting of an acute CS, 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.30,31 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/h. Contractures are produced after 12 hours of total ischemia. Relative hypertension and correction of acute anemia may help prevent the development of an impending acute CS. Ongoing research continues to examine the role of nitric oxide.

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 the crush syndrome and acute renal failure almost always recover renal function, even those patients who require prolonged hemodialysis. Current recommendations are as follows:

* Combat hypovolemia with crystalloid solution.

* Infuse 500 mL/h of crystalloid solution and 22.4 mEq bicarbonate (12 L/d, forcing diuresis of approximately 8 L/d).

* If diuresis is less than 300 mL/h, 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 Undersea and Hyperbaric Medical Society (UHMS) Hyperbaric Oxygen (HBO) Committee reported 13 major syndromes amenable to HBO, of which fourth on the list is crush injury, CS, and other acute traumatic ischemias.32 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. At the time of surgical debridement, previous treatment with HBO aids in the demarcation of nonviable tissue. The best results are obtained when therapy is begun early. Twice-daily treatments at 2.0-2.5 atmosphere absolute (ATA) for 90-120 minutes are recommended for 5-7 days, with frequent examinations of the affected area.

Despite the recommendation for hyperbarics, most authors strongly advise caution in employing this modality. The treatment of choice for CS is early decompression. If the tissue pressure remains elevated in a patient with any other signs or symptoms of a CS, adequate decompressive fasciotomy must be performed as an emergency procedure.

Surgical Therapy

The fasciotomy technique is a matter of surgical choice. The goal is salvage of a functional extremity. In no way should the adequacy of decompression be compromised due to concern over cosmesis. It is essential to decompress all tight compartments, and the skin must be considered a potentially significant limiting structure.33,34

Decompression fasciotomy of the forearm is performed through a volar approach, a dorsal approach, or both. In the forearm, unlike the fascial compartments of the leg, the volar compartment, dorsal compartment, and mobile wad compartment (containing the brachioradialis and radial wrist extensors) are interconnected. Thus, fasciotomies of all 3 compartments may be unnecessary.

Superficial fasciotomy is usually adequate to decompress the entire forearm.35 The flexor digitorum profundus and flexor pollicis longus muscles (deep volar compartment) are among the most severely affected muscles, due to their deep location adjacent to the radius and ulna. Prefasciotomy and postfasciotomy pressures often are obtained from all compartments of the volar forearm, and if deep compartment pressures remain high after superficial fasciotomy, an additional release is indicated.

Forearm fasciotomy requires decompression from the wrist to mid arm, including the lacertus fibrosus fascia, the fascial compartments over the flexor carpi ulnaris, and the edge of the flexor superficialis muscles. With median nerve involvement, in addition to carpal tunnel release, the surgeon must explore the nerve in the proximal forearm. The median nerve is decompressed throughout its course, including high-risk areas that are deep to the bicipital aponeurosis (lacertus fibrosus); between the humeral and ulnar heads of the pronator teres, the proximal arch, and deep fascial surface of the flexor digitorum superficialis; and the carpal tunnel.25

In the surgical treatment of hand CS, anatomically, 10 separate osteofascial compartments can typically be released with a carpal tunnel release and 1 or 2 dorsal incisions. The transverse carpal ligament also requires release. In the digits, 2 dorsal longitudinal incisions are usually made. Schnall et al, however, reported the use of an alternative approach for fasciotomy in cases of pyogenic flexor tenosynovitis36 ; this approach involved irrigation of the tendon sheath and leaving the lateral incision open, which allowed early active mobilization of the finger.

Preoperative Details

Prophylactic antibiotics against Staphylococcus aureus are generally recommended.

Intraoperative Details

After standard surgical preparation and draping, no tourniquet should be used.

Fasciotomy for acute compartment syndrome of the forearm: Volar Henry approach for superficial and deep flexors

1. Make a volar curvilinear incision medial to the biceps tendon, crossing the elbow flexion crease at an angle. Carry the incision distally into the palm to allow for a carpal tunnel release (similar to the McConnell combined exposure of the median and ulnar nerves), but avoid crossing the wrist flexion crease at a right angle.

2. Divide the lacertus fibrosis proximally.

3. Expose the brachial artery, and determine whether there is a normal flow.

4. Release the superficial volar compartment throughout its length under direct vision.

5. Identify the flexor carpi ulnaris, and retract it with its underlying ulnar neurovascular bundle medially.

6. Retract the flexor digitorum superficialis and median nerve laterally to expose the flexor digitorum profundus in the deep compartment. If its overlying fascia is tight, incise it longitudinally.

7. Continue the dissection distally by incising the transverse carpal ligament along the ulnar border of the palmaris longus tendon and median nerve. Inspect and examine the median nerve to ensure that it is not injured or entrapped.

8. If an associated fracture is present, reduce and stabilize the fracture and obtain hemostasis.

9. In the distal forearm, if the median nerve is exposed, suture the distal forearm skin flap loosely over the nerve. Leave the rest of the incision open.

10. Check the dorsal compartments. The volar fasciotomy should decompress the dorsal musculature sufficiently. If not, release them also.

11. Apply a sterile moist dressing and a long arm splint. The elbow should not be left flexed beyond 90°.

Volar ulna approach (similar to Henry approach) for extensor mechanism

This approach is used to release the flexor carpi ulnaris and flexor digitorum superficialis. Watch the proximal edge of the flexor digitorum superficialis, and decompress the ulnar nerve at the wrist.

Dorsal approach

1. Pronate the arm.

2. Begin the incision distal to the lateral epicondyle between the EDC and ECRB, extending approximately 10 cm distally toward the midline of the wrist.

3. Gently undermine the subcutaneous tissue, and release the fascia overlying the mobile wad of Henry and the extensor retinaculum (extensor digitorum communis [EDC] and extensor carpi radialis brevis [ECRB]). Do not close the skin at this time, but anticipate secondary closure later. Apply a sterile moist dressing and a long arm splint. The elbow should not be left flexed beyond 90º.

Fasciotomy for acute compartment syndrome of the hand

1. Make 2 longitudinal dorsal hand incisions over the second and fourth metacarpals.

2. Retract the extensor tendons to provide access to the dorsal and volar compartments.

3. Open the dorsal and volar compartments by longitudinal releases.

4. The dorsal incisions are generally left open but may be closed primarily. Closure that is delayed primarily, with or without skin grafting, is required for the volar incision.

Image 2 shows the incision and relevant anatomy of a volar release.

(Click Image to enlarge.) Volar release in the fo...

(Click Image to enlarge.) Volar release in the forearm. The upper illustration shows the incision that is used. The lower left picture depicts the relevant incisional anatomy. The lower right picture depicts the cross-sectional anatomy.

[ CLOSE WINDOW ]

(Click Image to enlarge.) Volar release in the fo...

(Click Image to enlarge.) Volar release in the forearm. The upper illustration shows the incision that is used. The lower left picture depicts the relevant incisional anatomy. The lower right picture depicts the cross-sectional anatomy.

Surgical anatomy of the volar forearm. Photo cour...

Surgical anatomy of the volar forearm. Photo courtesy of Dr. Smith, Harborview/UW Medical Center, Department of Orthopaedics, Seattle, Wash.

[ CLOSE WINDOW ]

Surgical anatomy of the volar forearm. Photo cour...

Surgical anatomy of the volar forearm. Photo courtesy of Dr. Smith, Harborview/UW Medical Center, Department of Orthopaedics, Seattle, Wash.

Image 3 shows the surgical anatomy of the volar forearm.

Postoperative Details

The postoperative details depend on the etiology of the CS and on the overall clinical condition of the patient. Elevate the affected extremity for 24-48 hours after surgery. If necrotic muscle develops, excise it. Tendinous attachments are retained if possible. Delayed primary closure of the skin can usually be accomplished at 5 days. If closure is not possible within 5 days, a split-thickness skin graft should be applied instead. The rehabilitation protocol is dependent upon the underlying mechanism of injury and the stability of the fracture reduction.

Follow-up

Standard suture removal and postoperative wound checks are indicated. Patients may require skin grafting if the skin defect is large.

Complications

Volkmann contracture (VC) is the residual limb deformity that results over weeks to months following untreated acute compartment syndrome (CS) or ischemia from an uncorrected arterial injury. Approximately 1-10% of CS cases develop a VC.2 Treatment of VCs can be found elsewhere.

Recurrent exertional CS has occurred in athletes and is thought to be related to severe scarring and subsequent closing of the compartment release.

Outcome and Prognosis

If fasciotomy is performed within 12 hours after the onset of acute compartment syndrome (CS), the prognosis is good; Sheridan and Matsen reported that normal limb function was regained in 68% of patients in such cases.37 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 for CS are delayed. Tendon transfers and stabilization may be indicated as late treatment for CS.

Future and Controversies

Controversy still exists regarding the treatment of compartment syndrome (CS) that presents more than 3 days after the injury. Most authors suggest that fasciotomy is contraindicated due to the near universal occurrence of severe infection and the difficulty in managing necrotic muscle. Additionally, many authors remark that no generally accepted pressure threshold exists and that fasciotomy should be performed whenever the clinical impression favors the diagnosis of CS.