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Acute compartment syndrome (ACS) occurs when compartment pressures increase to compromise circulation and tissue function. Human limbs are especially susceptible to ACS due to the separation of muscle groups by fascial membranes. Trauma to a limb, such as a crush injury, fractures, or overuse, can lead to swelling within a compartment that can increase rapidly and result in ACS. This activity reviews the presentation, evaluation, and management of skeletal muscle compartment syndrome and stresses the role of an interprofessional team approach to caring for affected patients. Objectives: Identify the etiology of acute compartment syndrome. Assess the typical presentation of a patient with acute compartment syndrome. Evaluate the management options for acute compartment syndrome. Communicate interprofessional team strategies for improving coordination to advance the management of acute compartment syndrome and optimize outcomes. Access free multiple choice questions on this topic.

Human limbs are composed of muscle groups divided by fascial membranes into anatomic compartments. When a limb sustains trauma (ie, crush injury, fractures, repeated injections or infusions, or overuse), swelling and inflammation within a compartment may increase rapidly. Consequently, acute compartment syndrome (ACS) results when compartment pressures increase to the point that tissue perfusion is compromised.[1][2]

ACS has both traumatic and nontraumatic etiologies. Long bone fractures, especially comminuted fractures, account for the highest proportion of ACS cases. Most ACS syndromes arise from a severe leg injury. In 1 study, 414 acute tibial fractures were evaluated. Mid-shaft tibial fractures had the highest rate of compartment syndrome (10%) and accounted for 40% of all trauma-related ACS. Trauma without fracture can also cause ACS. Examples include crush injury, severe thermal burns, overly constrictive bandages, penetrating trauma, and damage to vascular structures. Nontraumatic causes include vascular occlusion, embolus, ischemia-reperfusion injury, bleeding disorders, vascular disease, nephrotic syndrome, envenomations and bites, extravasation of intravenous fluids, injection of recreational drugs, and prolonged limb compression from tight casts or tourniquets. Younger patients account for the majority of cases.[3][4][5][6]

ACS occurs most often in patients younger than 35 years. The highest incidence is seen in young men, particularly after fractures of the tibial diaphysis and distal radius. Crush injuries among civilians occur most often due to falls or extrication episodes, such as in building collapses, earthquakes, civil unrest, explosions, or high-speed motor vehicle accidents.

ACS occurs when tissue fluid pressure exceeds capillary perfusion pressure to the muscle and nerves within an anatomic compartment. The muscle fascia and other connective tissues are inelastic. As the pressure builds, the venous return eventually is halted, which results in the transudation of fluid. This sets off a cascade of events, leading to an edema-hypoxia cycle. Once edema is severe enough to cause hypoxia, adhesion molecules are activated, leading to the attachment of neutrophils, a release of reactive oxygen species, and severe vasoconstriction. This process results in reperfusion injury and is the basis behind the no-reflow phenomenon. It is estimated that muscle necrosis occurs within 2-3 hours of injury in as many as 35% of patients.[5][3][7]

The patient history should focus on determining if 1 of the traumatic or nontraumatic events mentioned above has occurred, thus placing a patient at risk for ACS. Underlying etiologies such as bleeding diathesis, renal disease, peripheral vascular disease, or cardiac arrhythmias should be explored. Any history of intravenous or intramuscular drug injection should be sought. On physical exam, impending ACS is characterized by the 5 ‘Ps'- increasing pain out of proportion to appearance, paresthesia, paresis, pallor, and distal pulse deficit. Discomfort with passive stretch or tenseness of a muscle compartment is common. The major compartments in the leg are the anterior, lateral, deep, and superficial posterior. The 2 significant compartments of the forearm are the dorsal and volar. Anterior compartment syndrome of the leg is characterized by pain exacerbated by plantarflexion. The muscles of this compartment are the tibialis anterior, the extensor digitorum longus, the extensor hallucis longus, and the peroneus tertius. Lateral compartment syndrome is characterized by pain exacerbated by inversion of the foot. The muscles of this compartment are the peroneus longus and the peroneus brevis. The superficial posterior compartment of the leg contains the soleus, gastrocnemius, and plantar muscles, and the superficial posterior compartment syndrome is characterized by pain on the dorsiflexion of the foot. The deep posterior compartment contains the tibialis posterior, flexor hallucis longus, flexor digitorum longus, and popliteus muscles. Pain exacerbated by extending the toes is characteristic of this compartment syndrome. The volar compartment syndrome of the forearm has pain exacerbated by the wrist extension. The dorsal compartment syndrome has pain worsening on wrist flexion versus resistance.

Laboratory tests have limited use in ACS but may show arrhythmia, coagulopathy, azotemia, or occult drug use. Abnormalities such as elevated serum creatine phosphokinase (CPK>2000) and myoglobinuria are typically seen as muscle breakdown ensues. Clinical findings and measurement of compartment pressures establish diagnosis. Saline manometry (Whiteside procedure) using pressure transducers is the test of choice. Any intercompartmental pressure above 30mmHg in a symptomatic patient is confirmatory of ACS. Also, any patient with a Delta Pressure (DP) less than 30 is similarly confirmatory. DP = Diastolic Pressure – Compartment Pressure. Any such findings in a symptomatic patient must have a stat surgical consult for possible fasciotomy. Needle placement for saline manometry is specific to the compartment under suspicion. The anterior compartment of the leg is entered approximately one-third the distance down the tibia from the tibial tuberosity (level) and 1 cm lateral to the tibial edge, with the needle going in approximately 1-3cm. The lateral compartment is entered at the same level as above, right at the fibula's edge, and is 1cm in. The superficial posterior compartment is entered at the same level as above and at 3-5cm medial to the mid posterior line, going in 2-4 cm. Finally, at the same level, the deep posterior compartment is entered just medial to the medial tibial edge and aimed in the fibula's direction, going in 2-4 cm. Other modalities, such as ultrasound, laser Doppler flow, and infrared spectroscopy, have been used to measure intercompartmental pressures non-invasively. Other invasive studies such as muscle pH, glucose level, and pO2 have been studied; however, saline manometry remains the gold standard. Interobserver variation has been a problem, and continuous monitoring seems more sensitive and specific than a 1-time measurement.[3]

Any dressing, splint, cast, tourniquet, or other restrictive covering should be removed for a limb at risk for ACS. The limb should be placed at the heart level to avoid both reductions in arterial flow and dependent swelling. Frequent neurocirculatory checks should be performed every few hours in a limb with suspected ACS. There are 3 stages of progression to ACS- ‘suspected,’ ‘impending,’ and ‘established.’ Confirmed (‘established’) cases with symptomatology and abnormal manometrics demand immediate surgical decompression with fasciotomy. However, patients may present with equivocal signs and symptoms and uncertain manometrics. These patients are categorized as ‘suspected.’ The progression of ACS from the ‘suspected stage’ to the ‘impending stage’ is based on the worsening of the clinical findings (5’Ps’) or intermediate compartment pressure measurements. In the ‘impending stage,’ hyperbaric oxygen (HBOT) therapy can be implemented to prevent possible progression to the ‘established stage.’ The typical treatment regimen consists of 3 HBOT treatments at 2.5 Atm for 90-120 minutes (twice daily on day 1, single treatment on day 2). However, the use of HBOT should never delay fasciotomy if a patient has progressed to ‘established’ ACS based on manometric confirmation or severe symptoms. When fasciotomy is performed, HBO2 can be applied for various post-fasciotomy complications, including ischemic muscle, unclear demarcation of viable and non-viable muscle, massive swelling, prolonged ischemia (>6 hours), vascular compromise of flap or graft, and residual neuropathy. HBOT has been shown to increase tissue oxygenation 20-fold. HBOT increases tissue ATP and NADPH oxidase, promoting wound healing by encouraging vascular growth and collagen formation. NADPH also assists in the killing of bacteria by super peroxidation. The 3 main efficacies of HBOT are to reduce edema, increase tissue oxygenation, and reduce post-reperfusion injury. However, to date, no large-scale meta-analysis has been done on the use of HBOT in crush injury and ACS. HBOT is listed as an approved use for ACS from crush injury by the Undersea & Hyperbaric Medical Society(UHMS), but no large concordant double-blind RCTs exist on its use. The European Committee for Hyperbaric Medicine gave HBOT a Grade B recommendation (moderate level of evidence) for open fractures with crush injury and only a Grade C (low level of evidence) for crush injury without fracture.[3][7][8][9][10][11]

The outcomes are favorable if ACS is caught and treated early with a decompressive fasciotomy. One study in 1976 found a fasciotomy done within 12 hours of the onset of clinical symptoms (motor weakness, stretch pain, etc) resulted in the normal function of 68% of patients. If the fasciotomy was delayed beyond 12 hours, only 8% of patients had normal function. Fasciotomies have complications, including additional surgeries for delayed wound closure, skin grafting, pain, cosmetic deformity, nerve injury, muscle weakness, and chronic venous insufficiency.

Muscle necrosis may occur as early as 2-3 hours post-injury. Repeated debridement is performed every 48 to 72 hours for muscle necrosis until the wound remains stable. Nerve deficits with permanent loss may be sustained as early as 1-hour post-injury. Other complications include muscle contractions, sepsis, and amputation. Skin grafts are frequently used to cover large skin loss, and these frequently become ischemic. Associated fractures may harbor osteomyelitis, cause malunion, cause oxygen toxicity, pneumothorax, ruptured tympanic membrane, sinus squeeze, and tooth squeeze, which are some complications of HBOT. Sudden shortness of breath and chest pain should immediately suggest pneumothorax. The ascent from pressurization should be slowed to 1psi/ min. When 1Atm is achieved, the patient should immediately be evaluated for pneumothorax and tension pneumothorax and treated accordingly.[1][3][8][9]

A surgeon should evaluate the patient with compartment syndrome to determine whether urgent fasciotomies and/or other surgical procedures are necessary to save life or limb. A consultation with a hyperbaric physician or orthopedist can be beneficial when the stages of the compartment syndrome are unclear or do not require urgent fasciotomy.

Crush injuries of the extremities are best managed by an interprofessional team that includes a surgeon, HBO specialist, wound specialist, ICU nurses, radiologist, orthopedic surgeon, vascular surgeon, and internist. The key is to resuscitate the patient and salvage viable tissue. Once debridement and fasciotomy have been performed, HBO therapy may help improve the salvage rate of viable tissue. The outcomes of patients with crush injuries are guarded, as many individuals also have other associated injuries.