Treatment of Lower-extremity Compartment Syndromes



Treatment of Lower-extremity Compartment Syndromes


W. D. Turnipseed



Compartment syndrome develops when pressure within a closed myofascial space increases to a point that tissue perfusion is impaired; this results in neuromuscular compromise. Compartment syndromes may be classified as acute or chronic. Both conditions impair normal limb function but are quite different in etiology and natural history. Although there is general awareness of the problem, the diagnosis is often delayed or missed altogether because the clinical presentation may be subtle and easily confused with other musculoskeletal complaints. Surgical treatment is the only reliable means of preventing morbidity, which can range from claudication to amputation. Failure to correctly diagnosis extremity compartment syndromes is a failed opportunity to treat and cure.


Acute Compartment Syndrome

Normal compartment pressures in the lower extremity are less than 15 mmHg. When pressure exceeds 25 mmHg, venous drainage from closed myofascial spaces is impaired. When pressures exceed 30 mmHg, there is complete venous collapse, and this sets into play a malignant physiologic cascade of events that results in muscle edema and increasing compartmental pressures. Arterial perfusion is compromised when compartment pressures come within 30 mm of diastolic pressure. When pressures exceed 60 mmHg, neuromuscular ischemia predictably occurs.

The acute compartment syndrome usually results from a sentinel clinical event. Blunt or penetrating injuries, long bone fractures, delayed treatment of sudden arterial occlusions resulting from trauma or embolism, severe soft tissue crush injury, extrinsic muscle compression, thermal burns, or accidental extravasation of caustic chemicals into subcutaneous tissues can trigger a spectrum of events that, left unchecked, will result in permanent neuromuscular injury, disability, and possible amputation. One of the earliest descriptions of acute compartment syndrome was made by Richard Von Volkmann in 1881. He correlated the development of permanent flexion contractures of the hand with use of rigid casting and the treatment of supracondylar humoral fractures in adolescents. Bardenheuer in 1911 was the first to propose and successfully employ fasciotomy in the treatment of this condition. The diagnosis of acute compartment syndrome may require diligent clinical surveillance. This condition should be suspected when progressive motor or sensory limb dysfunction is associated with provocative trauma. The most common early presentation is swelling and edema of compartment muscles, and this is followed by disproportionate muscle pain aggravated by passive extension and subsequently by impaired capillary refilling and the loss of peripheral arterial pulses. Clinical diagnosis of acute compartment syndrome may be quite difficult to confirm, particularly in the comatose or confused patient, and it may require compartment pressure measurements for confirmation. Compartment pressures can be measured with a Wick catheter, the Whiteside needle method, or by use of a variety of more contemporary computerized hand-held transducers. There is no absolute compartment pressure associated with the clinical development of compartment syndrome. This is particularly true in patients who present in hypovolemic shock. These patients may have multiple injuries that divert the clinician’s attention from an evolving crisis in the extremity. For this reason serial evaluations are necessary. Clinical impressions can be fortified by performing repeat compartment pressures and/or by hand-held Doppler assessment of peripheral venous flow. The loss of phasic flow is the first Doppler change that occurs when pressures exceed 25 mmHg, and loss of flow augmentation correlates with pressures exceeding 30 mmHg. If tense muscle swelling occurs in conjunction with these physiologic changes, surgical intervention is indicated. In general it is safer to err on the side of commission and to perform compartment release when clinical signs and symptoms are present. Early decompressive fasciotomy will frequently avert ischemic complications and prevent permanent disability and/or amputation.

The only acceptable treatment for acute compartment syndrome is open fasciotomy and/or fasciectomy. There is no place for limited subcutaneous fasciotomy in these patients, because skin and subcutaneous tissue have limited ability to stretch. Several techniques for compartment release have been described. The double incision technique first described by Mubarek is the most widely used procedure and is performed using linear incisions made on the anterior lateral surface of the lower leg halfway between the anterior border of the tibial and lateral border of the fibula. Fasciotomy and/or fasciectomy can be used to release the anterior and lateral compartments through this approach. A medial incision is made just posterior to the tibia at the medial calf and is used to relieve both
the superficial and deep posterior compartments. It is necessary to take down the medial tibial attachments of the soleus to completely relieve the distal deep posterior compartment muscles. Alternative methods of lower-extremity surgical decompression include fibulectomy fasciotomy and the lateral four compartment fasciotomy without the use of fibulectomy. Fibulectomy was originally proposed by Kelly and Whiteside in 1967. This technique is not widely employed unless the fibula has been fractured. The fibula itself has no weight-bearing function in the adult and exists primarily as a strut for musculoligamentous attachment, maintaining stability of the ankle joint and preventing a valgus deformity. If four-compartment infrageniculate decompression is necessary, excision of the fractured fibula can be carried out with little additional morbidity. Fibulectomy fasciotomy is a good technique, but reservations about its routine use are hard to dispute. It is probably most appropriate when crush injuries are associated with multiple lower long bone fractures, as the fibula plays no significant part in functional orthopedic repair of these injuries. As an alternative to fibulectomy, complete myofascial decompression can be performed by making a lateral skin incision over the fibula extending from the neck to approximately 4 cm above the lateral malleolus. This incision is carried down to the overlying lateral compartment fascia, which is opened its entire length, and the anterior fascia is exposed by retracting the skin and using a separate parallel fasciotomy to release the anterior compartment. Skin and subcutaneous tissue overlying the posterior superficial compartment are retracted and the fascia incised along the length of the gastrocnemius and soleus muscles. Attachments of the soleus muscle to the fibula are divided so that the deep posterior compartment can be released. This technique is effective and assures complete decompression of each compartment without the functional consequences of fibulectomy, and it can be performed with one incision.

The incisions used for acute compartment lower-extremity release procedures will to some extent be dictated by orthopedic and vascular injuries that need to be treated. When possible, incisions should be positioned so as to allow appropriate myocutaneous coverage of orthopedic and vascular repairs. As a technical note, this author prefers the use of fasciectomy instead of fasciotomy, because there is a lower incidence of scar-down recurrence, a more complete compartment release, particularly in the anterior and lateral compartments, and, when necessary, skin grafts can be applied earlier to exposed, well-perfused muscle. As a rule of thumb, decompression surgery in the lower extremity is recommended when arterial and venous injuries occur simultaneously or when restoration of circulation to an ischemic limb has been delayed more than 6 hours.

Acute compartment syndrome is much less likely to develop in the thigh muscles than in the calf muscles, because they are much larger in volume and blend anatomically with muscles of the hip and buttocks. Acute compartment syndromes of the thigh are usually the result of crush injuries or high-velocity vehicular accidents. These patients frequently have ipsilateral femoral fractures and multiple associated injuries to the head, thorax, and abdomen. A proximal acute compartment syndrome in the lower extremity associated with massive soft tissue trauma may result in the development of myoglobinuria and even renal failure. The thigh has three myofascial compartments (anterior, medial, and posterior). The anterior thigh compartment contains the quadriceps muscle along with the femoral neurovascular structures. Passive flexion of the knee with the hip in full extension will cause symptoms of pain and decreased sensation in the medial thigh. The posterior compartment contains the hamstring muscles and sciatic nerve. Compartment symptoms in this distribution can be elicited by passive extension of knee with the hip in full flexion. The medial compartment contains the adductor muscles and the cutaneous branch of the obturator nerve. The anterior and posterior compartments are most commonly associated with acute thigh injury resulting from femoral fractures, coagulopathies with intramuscular hemorrhage, and/or crush injuries. Surgical release of both the anterior and posterior compartments can be achieved using a single laterally placed incision.

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Jun 16, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Treatment of Lower-extremity Compartment Syndromes

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