Acute Compartment Syndrome

Article Author:
Allison Torlincasi
Article Editor:
Muhammad Waseem
Updated:
11/18/2018 5:16:57 PM
PubMed Link:
Acute Compartment Syndrome

Introduction

Acute compartment syndrome (ACS) is a condition that involves increased pressure within a confined tissue space, which results in ischemia. It is an urgent diagnosis and can be a devastating condition if the diagnosis is delayed or missed. The extremities are divided into compartments separated by connective tissue called fascia. The compartments are composed of muscle fibers, nerves, and blood vessels. Acute compartment syndrome occurs when there is an increased pressure within a compartment and a disruption in circulation, which can lead to ischemia and eventually to necrosis.[1][2][3]

Etiology

Acute compartment syndrome can be caused by an increase in pressure within the compartment. It occurs either by increasing the content or reducing the volume of a compartment. The most common cause is trauma associated with a fracture. Examples include bicondylar plateau fractures and segmental or comminuted tibial shaft fractures. Other causes include arterial injury, occlusions, reperfusion injury, crush injuries, burns (especially circumferential burns), electrocutions, snake venom exposure, stressful athletic activity, contusions and infiltrations from intravenous (IV) sites. Constrictive casts and military anti-shock trousers (MAST) can also cause acute compartment syndrome. Beware that a compartment syndrome can occur with or without any known trauma. Certain conditions such as hemophilia or rhabdomyolysis can cause compartment syndrome without direct trauma. Since open fractures may not necessarily decompress increased compartment pressures, acute compartment syndrome can also occur with open fractures.[4][5]

Epidemiology

Acute extremity compartment syndrome usually occurs following trauma, and the most common cause is a fracture. When the fracture is comminuted, there is a higher probability of its occurrence. Acute compartment syndrome occurs more commonly in males than females and is also more common in people younger than the age of 35.

Pathophysiology

In the setting of acute extremity compartment syndrome regardless of mechanism, the compartment pressure increases, causing hypoxia of tissues. There is normally an equilibrium between venous outflow and arterial inflow. When there is an increase in compartmental pressure, there is a reduction in venous outflow. This causes a build-up of venous pressure and an increased venous capillary pressure. If the intra-compartmental pressure becomes greater than arterial pressure, a decrease in arterial inflow will also occur. The decrease of venous outflow and arterial inflow result in decreased oxygenation of tissues causing ischemia. If the deficit of oxygenation becomes great enough then, irreversible necrosis may occur.[6][7][8]

The normal pressure within a compartment is less than 10 mmHg, and a pressure of more than 30 mmHg is described as acute compartment syndrome.

Although the four compartments of the leg are most frequently involved, acute compartment syndrome can occur at other sites including the arm, forearm, hand, foot, shoulder, buttocks and thigh.

The lower leg consists of following compartments:

  1. Anterior compartment: This is the most common site for acute compartment syndrome. The anterior compartment of the leg contains the four extensor muscles of the foot, the anterior tibial artery, and the deep peroneal nerve. Loss of sensation between the first and second toes and weakness of foot on dorsiflexion are the initial signs when the anterior compartment is involved.
  2. Lateral compartment: This contains peroneus longus and peroneus brevis muscles, and the peroneal artery. The superficial and the proximal segment of the deep peroneal nerve are also found here. Acute compartment syndrome involving lateral compartment presents as weakness in inversion and dorsiflexion of the foot, as well as sensory loss in the web space between the great toe and the adjacent toe.
  3. Deep posterior compartment: This compartment is comprised of the muscles that enable plantar flexion of the foot, as well as the posterior tibial artery, peroneal artery, and the tibial nerve. Acute compartment syndrome involving deep posterior compartment may result in decreased sensation over the plantar aspect of the foot, weakness of toe flexion, and pain with passive extension of the toes. Acute compartment syndrome of this compartment is frequently missed.
  4. Superficial posterior compartment: This compartment contains gastrocnemius and soleus muscles which are involved in plantar flexion. Since this does not contain any major arteries or nerves, Acute compartment syndrome is least likely to develop in this compartment.

In children, supracondylar fractures of the humerus and both bone forearm fractures may be associated with compartment syndrome.

History and Physical

Five P’s: pain, pallor, pulselessness, paresthesias, paralysis

Pain is only the initial finding. Usually, it is out of proportion to the apparent injury. However, this symptom may be absent in advanced acute compartment syndrome. Also, pain with passive stretch of muscles in the affected compartment is also reported as an early finding. Beware that pain can be nonspecific. In the initial stages, more subtle signs such as burning sensation over the involved compartment, nonspecific sensory deficits or poorly localized deep muscular pain may be present.

The tenseness of compartments may be palpated early in the examination and may also suggest developing compartment syndrome. These symptoms typically develop rapidly from the first 30 minutes of injury but may develop within two hours. As pain can increase in severity over time, periodic assessments of pain are vital, in addition to assessment of sensation and pulse rate. Pulse is usually intact with compartment syndrome, but findings can include the “Ps” of arterial insufficiency, pulselessness, paresthesia, poikilothermia, paralysis, and pallor. These symptoms may indicate irreversible necrosis.

Beware that the presence or absence of a palpable arterial pulse may not accurately indicate relative tissue pressure or predict the risk for compartment syndrome. In some patients, a pulse is still present, even in a severely compromised extremity.

As these clinical features are important in identifying compartment syndrome, they are neither sensitive nor specific to the diagnosis and other factors, such as compartment pressures, can be helpful in making the diagnosis.

Evaluation

A diagnosis of acute compartment syndrome is not always obvious. Therefore, serial examinations and frequent assessments are necessary to make such a diagnosis.[9][10][11]

  • Assess tenderness in the muscle compartment
  • Evaluate motor and neurologic function
  • Radiographs should be obtained if a fracture is suspected

In an appropriate setting, measurement of intra-compartmental pressure can aid in a diagnosis. Compartment pressures are often measured with the use of a manometer since this makes it a simple and easy procedure to perform. A manometer is a device that can detect compartment pressure by determining the resistance when the device injects a saline solution into the compartment. Another method employs a slit catheter, whereby a catheter is placed within the compartment, and the pressure can be measured with an arterial line transducer. This method is more accurate and allows for continuous monitoring. Its use is also recommended to measure all the surrounding compartments, thereby minimizing any error in diagnosis.

The normal pressure within the compartment is between 0 mmHg to 8 mmHg (i.e., less than 10 mmHg).

An intra-compartmental pressure greater than 30 mmHg indicates compartment syndrome and a need for fasciotomy. When intra-compartmental pressure increases to within 10 mmHg to 30 mmHg of the patient's diastolic blood pressure, inadequate perfusion occurs and resulting in relative ischemia of the involved extremity.

The perfusion pressure of a compartment, also known as the compartment delta pressure, is defined as the difference between the diastolic blood pressure and the intra-compartmental pressure:

  • Acute compartment syndrome delta pressure = mean arterial pressure - measured compartment pressure 

This difference (delta pressure) is directly related to blood flow to the tissue. As compartment pressure approaches the mean arterial pressure, delta pressure decreases. Once delta pressure falls below 30 mmHg, tissue ischemia may occur.

Non-invasive techniques are sometimes used to detect the extent of ischemia. Ultrasound with Doppler flowmetry can be used to determine if there is any occlusion of blood flow. Near infra-red spectroscopy has been found to be useful in studies in developing compartment syndrome. It can be used to assess tissue oxygenation, and studies have found that decreased tissue oxygenation has a high probability of developing into compartment syndrome. Laboratory studies, however, are not helpful in confirming the diagnosis of compartment syndrome, but, they may be valuable in identifying other, alternate diagnoses.

Elevations in creatine phosphokinase (CPK) and myoglobin may suggest muscle breakdown from rhabdomyolysis which may lead to renal failure. Myoglobinuria may also be present as an indicator of muscle breakdown or rhabdomyolysis. Obtaining a baseline for BUN and creatinine values may be helpful to assess the renal function in patients with compartment syndrome.[12]

Treatment / Management

Acute compartment syndrome is a surgical emergency, so a prompt diagnosis and treatment are important for an optimal outcome. Once the diagnosis is confirmed, immediate emergent surgical fasciotomy is important, since surgical fasciotomy can potentially reduce intra-compartmental pressure.[2][1][13]

  • 15 mmHg to 20 mmHg: Serial compartment pressure measurement
  • 20mmHg to 30 mmHg: Surgical consultation and admit
  • Greater than 30 mm Hg: Surgical fasciotomy

Provide supplemental oxygen.

Remove any restrictive casts, dressings or bandages to relieve pressure.

Keep the extremity at the level of the heart to prevent hypo-perfusion.

Prevent hypotension and provide blood pressure support in patients with hypotension.

Urgent decompression is necessary to reduce the increased compartment pressure. The ideal timeframe for fasciotomy is within six hours of injury to ensure full recovery; it is not recommended after 36 hours following the injury. When tissue pressure remains elevated for that much time, irreversible damage may occur, and fasciotomy may not be beneficial in this situation.

After a fasciotomy is performed and swelling dissipates, a skin graft is most commonly used for closure. Patients must be closely monitored for complications, such as infection, acute renal failure, and rhabdomyolysis.

If necrosis occurs before fasciotomy is performed, there is a high likelihood of infection which may require amputation. If infection occurs, debridement is necessary to prevent the systemic spread or other complications. Renal failure may also occur.

Differential Diagnosis

  • Deep vein thrombosis
  • Cellulitis
  • Gas gangrene
  • Phlegmasia cerulean dolens
  • Rhabdomyolysis

Complications

  • Pain
  • Contractures
  • Rhabdomyolysis
  • Nerve palsy

Pearls and Other Issues

When applying plaster casts, especially following reduction, uni-valving or bi-valving can help to reduce the pressure by about 50%. Beware that once the initial swelling dissipates, the cast can become excessively loose, which can cause loss of reduction.

Enhancing Healthcare Team Outcomes

Compartment syndrome has many causes, and the condition is usually managed by surgeons. However, after the procedure, the role of the nurse and physical therapist are invaluable. All patients who require a fasciotomy will require physical therapy to regain function and strength. The pharmacist will need to be involved to manage the pain and any infection. The nurse is required to perform regular wound care and monitor the leg for any ischemia or gangrene. The patient will need to learn how to use an ambulatory device like a crutch until healing is complete. Even after discharge, the patient will need to enter physical rehabilitation to prevent contractures and stiff muscles. An occupational therapy consult is highly recommended to help teach the patient how to perform daily living activities.[14][15][16] (Level III)

Outcomes

The outcomes after treatment of compartment syndrome depend on the time of diagnosis and rapidity of treatment. When the fasciotomy is done within 6 hours, there is almost 100% recovery of limb function. After 6 hours, there may be residual nerve damage. In very delayed cases, the limb may require an amputation. Data show that when the fasciotomy is done within 12 hours, only 2/3rd of patients have normal limb function. Outcomes for a posterior compartment syndrome are worse than an anterior compartment syndrome, chiefly because it is difficult to perform inadequate decompression of the posterior compartment. Long-term studies on survivors do reveal residual pain, Volkmann contracture, mild neurological deficits and a marked cosmetic defect in the leg. Recurrent compartment syndrome has been known to occur in athletes, chiefly due to scarring. There are some individuals who may die from a compartment syndrome, and these are often due to an infection, leading to sepsis and multiorgan failure.[17][18] (Level V)