Tibial Anterior Compartment Syndrome

Etiology

Trauma is the most common etiology of compartment syndrome. Other causes of anterior leg compartment syndrome can vary wildly. Some examples include trauma (blunt or penetrating trauma, fracture, hemorrhage, burns), infectious (tetany, myositis), neurogenic (seizures), toxicology (envenomation, drug or alcohol abuse resulting in coma, androgenic steroid abuse), renal (decreased serum osmolarity), musculoskeletal (tear of the muscles of the anterior compartment, everyday activity, muscle hypertrophy, vigorous exercise, chronic repetitive exercise), autoimmune (vasculitis), vascular (deep vein thrombosis, hemorrhage), rhabdomyolysis, and postischemic swelling.[1]

Compartment syndrome can occur during routine medical or surgical care. Causes include dressings, splints or casts which are too tight, lying in the lithotomy position, malfunctioning sequential compression devices, intramuscular or intracompartmental injections, intraosseous line or infusion of hypertonic intravenous (IV) fluid or contrast agent, bleeding into compartments from attempted cannulation of vein or artery, intraoperative use of pressurized pulsatile irrigation, and military antishock trousers. Compartment syndrome can occur as the sequelae of orthopedic procedures and may be the result of post-operative bleeding, muscle edema, or tight closure of fascial layers.

Epidemiology

Tibial fracture is the most common cause of compartment syndrome accounting for up to 12% of all compartment syndrome cases. Open tibial fractures are more likely to cause compartment syndrome (6%) than closed fractures (1.2%). In patients with tibial diaphyseal fractures, younger age is associated with an increased risk of developing compartment syndrome.[2] Increased fracture length relative to the length of the tibia is associated with increased risk. Tibial plateau fracture increases risk, especially Schatzker VI, as compared to shaft or pilon fractures. Accompanying fibular fracture also increases a patient's risk.

Traumatic compartment syndrome may be more common in men. The use of an intramedullary rod is not associated. The frequency of compartment syndrome is much higher in patients with associated vascular insults. One study suggested 19% of patients with vascular injuries required a fasciotomy.

The incidence of chronic exertional compartment syndrome is a relatively common cause of leg pain in athletes ranging from 27% to 33%. Risk factors include running athletes. Also, fascia defects occur in up to 40% of athletes compared to 5% in asymptomatic athletes. Symptoms are frequently bilateral. Males and females are affected equally.

Compartment syndrome in children without a fracture is rare and not well understood. The leg is also the most common location of compartment syndrome in children. In one study of 39 cases of compartment syndrome in kids, vascular was the most common etiology (28%), followed by trauma (26%), postoperative (21%), exertion (15%), and infection (10%).

Pathophysiology

Compartment syndrome results from increased compartment pressure. When the systemic blood pressure is inadequate to overcome the pressure within a compartment, ischemia of its contents occurs.[3] This disease state can be acute or chronic depending on the mechanism.

When there is increased fluid in a fixed volume compartment, such as with bleeding or soft tissue swelling, tissue and venous pressure rise. When the interstitial pressure exceeds the capillary perfusion pressure (CPP), capillary collapse can occur.[4] This leads to decreased blood flow, anoxia, and eventually soft tissue ischemia. Muscle response to this is to release histamine-like substances which increase vascular permeability and fluid in the compartment thereby worsening the ischemia. As cells begin to lyse, their osmotic activity can also attract water from the vascular supply.[5]

Tissue perfusion is proportional to the difference between systolic blood pressure and compartment pressure. Stated differently, it is the difference between the interstitial fluid pressure and capillary perfusion pressure. One equation to measure this is local blood flow (LBF) = [local arterial (LA) pressure - venous pressure (PV)] / local vascular resistance. Under normal conditions, the difference between diastolic blood pressure and compartmental pressure should be more than 30 mmHg although controversy exists over the precise cutoff. As the compartmental pressure increases, this difference will decrease. Compartment pressures greater than 30 mmHg should raise suspicion for compartment syndrome.

Chronic exertional compartment syndrome (CECS) is reversible ischemia caused by repetitive physical activity and resolves with cessation of the offending activity. In rare cases where the athlete continues to exercise, irreversible acute compartment syndrome can develop. Normal physiologic response to activity can lead to a 20% increase in muscle volume. Intramuscular pressure can remain elevated even after fasciotomy suggesting other pathophysiology contributing to CECS. The pathogenesis is not well understood but may include a lower capillary density, lower number of capillaries, and abnormal arteriolar regulation.

History and Physical

History is critical in establishing the etiology and likelihood of compartment syndrome. Past medical and surgical history must be reviewed. In the trauma setting, it is important to distinguish the mechanism. Both high-velocity blunt trauma and penetrating trauma can lead to compartment syndrome. Clarify if the patient is on any antiplatelet or anticoagulant medications. In the non-trauma setting, the clinician should obtain a further history to evaluate for other possible etiologies including but not limited to toxicologic, iatrogenic, infectious, vascular, among others. The ability to gather history in children or patients with other injuries may be limited.

Compartment syndrome classically presents with pain out of proportion to the exam. He or she may describe it as deep, burning or aching or a fullness, swelling, or tense feeling. He or she may endorse pins and needle sensation, numbness, or tingling. The patient may report an inability to dorsiflex the leg or describe it as feeling “dead” or “weak.”

On exam, the provider should evaluate for any breaks in the skin, swelling, erythema, discoloration, or other signs of trauma. Palpation of the anterior compartment will reveal a swollen, tender muscle belly, typically at the middle and distal one-third of the leg. Pain is classically worsened with passive stretching of the affected muscles. In the case of anterior compartment syndrome, passive plantarflexion should worsen the patient's pain. The patient may have decreased sensation, especially to two-point discrimination. Vibration sense may also be diminished. He or she may have limited dorsiflexion, inversion and/or eversion. Both the dorsalis pedis and posterior tibial pulses should be documented.

Examining patients with symptoms concerning for chronic exertional compartment syndrome requires a unique approach. They will typically report pain that worsens with a specific activity and resolves with rest. These individuals can reliably predict when the symptoms will start and end. They are likely to have a normal exam at the time of evaluation. They should participate in an exercise challenge, for example, run on a treadmill or outside, and be re-evaluated after they become symptomatic. Once symptomatic, their exam should be abnormal; the clinician may observe swelling, muscle herniation, tenderness along the anterior compartment, pain with passive plantar flexion, and foot drop.

Evaluation

The history and physical examination should drive the evaluation and workup of a patient with suspected anterior tibial compartment syndrome, and the diagnosis is largely clinical. For example, evaluating for acute trauma, chronic exertional compartment syndrome, and snake envenomation all have a very different clinical context. Evaluation should be directed at the primary etiology of the patient’s symptoms. In patients with classic symptoms of compartment syndrome associated with a tibial fracture, further workup is often unnecessary. Lab work early in the course of the disease is likely to be within a normal distribution.

Measurement of intracompartmental pressure remains the gold standard for the diagnosis of compartment syndrome. Measurement is typically performed using a needle manometer. However other techniques that include slit catheter, microtip pressure, wick catheter, and microcapillary infusion are available. Ultrasound does not increase the diagnostic accuracy of needle placement.[6] Controversy exists about absolute cutoffs for acute compartment syndrome. In acute compartment syndrome, an absolute pressure greater than 30 mmHg or a systolic blood pressure minus compartment pressure measuring less than 30 degrees is worrisome.[7]

In chronic exertional compartment syndrome, compartment pressures are measured at rest. Then the patient exercises until symptomatic, and compartment pressures are measured again and compared to the baseline. The modified Pedowitz criteria are generally accepted for the diagnosis of CECS. Patients are considered positive with one or more of the following findings: (1) Pre-exercise pressure greater than or equal to 15 mmHg, (2) 1-minute post-exercise pressure greater than or equal to 30 mmHg, or (3) 5-minute post-exercise pressure greater than or equal to 25 mmHg.[8]

In general, imaging studies do not have a role in the diagnosis of compartment syndrome. They are likely to help exclude other causes of the patient's symptoms. Radiographs are the initial imaging study of choice in a patient with suspicion for anterior tibial pain.[9] Infrared spectroscopy and magnetic resonance imaging (MRI) may have a future role in diagnosing compartment syndrome; however, their role in current management is not established in the literature.

Treatment / Management

Definitive management of acute anterior leg compartment syndrome is a subcutaneous fasciotomy. Several techniques are described in the literature including single and double incision.[10] Care is taken to avoid the anterior tibial artery and deep peroneal nerve. The clinician should also direct management towards the primary etiology of the compartment syndrome. For example, in the setting of trauma, open reduction and internal fixation of the tibial fracture is the treatment of choice.(B2)

Treatment of CECS can initially be conservative. This includes activity modification including discontinuing the offending activities, nonsteroidal anti-inflammatory drugs (NSAIDs), stretching, foot orthotics, physical therapy, and an alternative exercise program for 6 to 12 weeks. In patients unwilling to modify their athletic activity or refractory to conservative management, fasciotomy is indicated. This can be successful in relieving symptoms in up to 90% of patients.

Differential Diagnosis

The differential diagnosis of anterior compartment syndrome is broad and includes infection (cellulitis, necrotizing fasciitis, osteomyelitis), neurologic (deep peroneal nerve entrapment), toxicology (snake envenomation), vascular (deep vein thrombosis, ischemic necrosis or gangrene, popliteal artery entrapment), trauma (vascular, nerve, muscle, or fascia soft tissue injuries, tibia or fibula fracture), musculoskeletal (chronic exertional compartment syndrome, stress fracture, medial tibial stress syndrome) and rhabdomyolysis.

Staging

There is currently no widely accepted staging criteria for acute or chronic compartment syndrome.

Prognosis

The prognosis for compartment syndrome depends on the etiology, diagnosis, and time from injury to intervention. If acute compartment syndrome is treated with fasciotomy within 6 hours, complete recovery of limb function is anticipated. After 6 hours of ischemia, necrosis occurs, and thus, 6 hours is the accepted upper limit of tissue viability. Fasciotomies of the anterior compartment tend to do better than those of the posterior compartment.

Late diagnosis of compartment syndrome leads to irreversible necrosis and subsequently permanent muscle and nerve damage. Patients may develop chronic pain and in the anterior compartment, deep peroneal nerve palsy, and foot drop. Volkmann’s contracture occurs with myonecrosis and the formation of new fibrous tissue leading to myotendinous adhesions. This results in a residual deformity and loss of function and can occur in up to 10% of patients with compartment syndrome. Calcific myonecrosis can occur.

In chronic exertional compartment syndrome, fasciotomy is associated with high levels of pain relief and patient satisfaction with successful outcomes reported between 80% and 100%.

Complications

Infection is a serious complication of compartment syndrome and fasciotomy. In one study, 11 out of 24 patients with surgical decompression developed infections. Infection can become chronic. Other complications include hematomas and seromas, peripheral nerve injury, and deep vein thrombosis.

The recurrence of symptoms ranges from 2% to 17% in published studies. This may be due to incomplete release of the fascial layers, failure to release all of the appropriate compartments, or fascial scarring. Thus, some patients may require revision.