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- Explain how to identify patients at risk for acute lower extremity compartment syndrome (ALECS) and the importance of early diagnosis and treatment.
- Review anatomy and physiology of the lower extremity and relate it to the pathophysiology of ALECS.
- Summarize the treatment options for suspected ALECS.
- Describe modalities available for the treatment of post-fasciotomy wounds.
You are called to the room of a 63-year-old patient who is postop day 1 after arterial lysis and stent placement for the treatment of acute left lower extremity limb ischemia. The patient states that she noticed her leg starting to swell about 6 hours after surgery, and that she believes it has steadily worsened since then (Figure 1). She also reports that she is experiencing an extreme amount of pain in her lower leg, and this pain is unrelieved by narcotics.
Your physical examination reveals that the patient's left lower extremity is tense and edematous. It is warm, with brisk capillary refill and palpable posterior tibial and dorsalis pedis pulses. Upon further questioning, the patient also reports that she is experiencing numbness in the first and second web space.
What should you do now? After completing this continuing education activity, acute lower extremity compartment syndrome (ALECS) should be high on your list of differential diagnoses, enabling you to quickly respond to this limb-threatening and potentially life-threatening emergency.
Causes of ALECS
Vascular injury is a common cause of ALECS, but it is not the only one. Long bone fractures, burns, crush injury, bleeding into enclosed spaces, external compression of a limb, small embolic events, IV line infiltration and intramuscular injection have been implicated.1
Figure 1. Left lower extremity appearing tense and edematous. courtesy the author
The patient described above exemplifies many people with peripheral arterial disease in that she has poorly controlled hyperlipidemia, hypertension, diabetes mellitus and a history of cigarette smoking.2 These risk factors likely contributed to the development of the patient's chronic lower extremity arterial disease.
Two weeks prior, the patient's peripheral arterial disease had been treated with angioplasty and stent placement within the superficial femoral artery. As is the case with most patients who have newly placed stents, she was discharged on antiplatelet therapy consisting of clopidogrel and aspirin. When she presented to the hospital for assessment of acute lower extremity pain, the evaluating provider determined that the recently placed stent had occluded, resulting in acute limb ischemia.
The patient was emergently returned to the operating room, where blood flow was restored to the limb by catheter-directed thrombolytic therapy using a tissue plasminogen activator. The medication was infused overnight via an arterial sheath, and by the next day, the stent was reopened and symptoms of acute limb ischemia resolved.
So how does restoring blood flow to muscle that has been starved for oxygen lead to problems?
The muscles and other structures in the lower leg are encased by a relatively inflexible layer of fascia. Fascia divides the lower leg into four areas: the anterior, lateral, superficial posterior and deep posterior compartments.1 Under normal circumstances, fascia provides the muscles with support within these compartments, allowing them to function more efficiently. However, muscle injury (due to various causes; in this case ischemia-reperfusion injury) leads to swelling, the noncompliant fascia limits the amount of swelling that can be accommodated, leading to compartment syndrome.
Compartment syndrome is muscle injury that occurs at the capillary level. As tissue fluid from injury accumulates within a compartment, pressure within that compartment increases. When this pressure increases substantially, capillary blood flow diminishes, leading to tissue ischemia. Subsequently, the flow of lymph and venous blood decreases, causing further swelling. Sensory nerves are affected next, causing pain, numbness and tingling. Finally, arterial flow is compromised, causing worsening pain and impaired motor function (Figure 2).3
Acute compartment syndrome can occur wherever muscles and fascia are present: the hand, forearm, upper arm, abdomen, buttock, thigh and leg. The most common site is the leg (involving the anterior compartment); the second most common is the flexor compartment of the forearm.3
Figure 2. Cross section view of the four lower extremity compartments, divided by fascia: anterior, lateral, posterior and deep posterior.
Compartmental pressure is increased by conditions that cause increased compartment content or by external compression on the compartment itself, such as a cast or splint.3 An increase in pressure can also occur after a vascular ischemia-reperfusion injury, the most common vascular cause of ALECS. This occurs when muscle experiences an ischemic injury, usually from an acute arterial occlusion, as was the case in the clinical scenario described. Once blood flow is restored, intracompartmental pressure begins to build as the injured muscles swell.4
A dramatic venous outflow obstruction, such as phlegmasia cerulean dolens or harvesting deep veins of the thigh, can also cause ALECS.1
The final vascular cause of ALECS is hemorrhage, such as that resulting from postop hemorrhage after joint replacement surgery in a patient on anticoagulation therapy.3
Nonvascular causes of compartment syndrome include fracture, most often of the tibia or forearm.4 Injuries of this type cause bleeding within the compartment, which elevates compartment pressure.1
Crush injuries resulting from prolonged immobility due to intoxication, pinning of the victim or blunt trauma from assault can result in ALECS from direct compartment pressure and muscle ischemia.1
Iatrogenic causes of compartment syndrome include extravasation of large volumes of fluid within a muscle compartment as a result of pharmacotherapy and arterial or venous punctures in anticoagulated or coagulopathic patients.1
Signs of ALECS in the lower extremity include a swollen, tense extremity, palpable pedal pulses (pulses are not lost until late in the course of the syndrome) and impaired dorsiflexion of the great toe.4 Symptoms include pain that is out of proportion to the injury sustained and pain that occurs with passive movement of the muscles within the tense compartment.5 Finally, the patient experiences altered sensory and motor function distal to the compartment in question.4
Diagnosis can be made based on the clinical history. Presence of a collection of the 5 P's associated with ALECS - pain, pallor, paresthesia, paralysis and pulselessness - supports confident diagnosis of this condition without further workup.1 (Remember, pulse is lost late in the syndrome.) Knowledge of the etiology described previously, in addition to the patient's expression of pain and a tense/firm compartment on exam, is an urgent sign of possibile ALECS.
Severe pain at rest or with passive movement is a significant diagnostic clue.4 The earliest and most important symptom of ALECS is pain greater than expected for the injury.6 Pallor occurs as a result of increased capillary pressure and reduced blood flow to the capillary bed. The patient usually maintains palpable peripheral pulses, at least in the early stage of the condition.
When the anterior compartment of the lower leg is involved, early loss of sensation may develop in the web space between the first and second toes, since the deep peroneal nerve is affected by increased pressure.1 Pulselessness is a late and grave sign, because the pressure in the compartment or compartments is sufficient to overcome systolic blood pressure and reduce arterial blood flow to the limb.4 An additional late and grave sign is paralysis of the lower extremity, indicating probable prolonged nerve compression or irreversible muscle damage.4
Direct measurement of intracompartmental pressure (ICP) is possible using a measurement tool attached to a sterile needle inserted in the compartment.7 This can be helpful when assessing the unconscious or sedated patient who is unable to participate in the subjective component of a clinical exam. The Stryker Intra-Compartmental Pressure Monitor is an example of a commercial product used to measure compartment pressures. If such a device is not available, measurement can be obtained by using a needle attached to an arterial line monitor. A normal anterior compartment pressure is less than 10 mm Hg to 12 mm Hg.1 The most common pressure threshold cited to assist in diagnosing ALECS is 30 mm Hg to 45 mm Hg; an intracompartmental pressure of 30 mm Hg can cause irreversible changes after 6 to 8 hours.6
Additionally, a formula that takes into consideration the relationship between diastolic blood pressure and intracompartmental pressure can be used to determine the need for surgical intervention.8 Defined as absolute compartment pressure (delta P), the established threshold of 30 mm Hg or less between the diastolic blood pressure and the anterior leg compartment (delta P = DBP-ICP) warrants surgical treatment.6
Direct compartment pressure monitoring may be most useful in the evaluation of ALECS in the critically ill or unresponsive patient.6 However, direct measurement of compartment tissue pressures is not considered necessary to confirm diagnosis in most cases, and performing this test can waste precious time. As such, it should be reserved for cases in which the patient is unresponsive and when the diagnosis is in question.1
The first step in response to a diagnosis of ALECS is to institute a protocol of first aid to hypoxic cells (see table):3
Click to view larger graphic.
- Obtain an urgent surgical consult: Vascular, trauma, orthopedic and general surgeons can all perform fasciotomies. Know who to call in your particular institution.
- Maintain normal blood pressure: Avoid hypotension to ensure as much capillary perfusion pressure as possible.
- Remove bandages and casts if possible, to release any external pressure on the compartments.
- Immobilize the limb at heart level; some clinicians mistakenly believe that elevating the extremity will reduce edema and promote blood flow, but that will reduce capillary perfusion - the last thing you want to achieve.
- Provide oxygen to optimize oxygen saturation.
Figure 3. Medial fasciotomy incision, allowing access to the superficial and deep posterior compartments. courtesy the author
Figure 4. Left thigh fasciotomy, showing extensive muscle edema. Fasciotomy relieves pressure in compartments, relieving pressure on nerves and restoring capillary blood flow. Reprinted with permission from SAGE Publications.
Figure 5. Left lower extremity medial fasciotomy incision utilizing delayed primary closure with vacuum-assisted therapy. courtesy the author
Figure 6. Left lower extremity lateral fasciotomy incision after split-thickness skin grafting. courtesy the author courtesy the author
Fasciotomy is an emergency surgical intervention for patients who develop ALECS as a result of critical ischemia to muscle and nerves of the lower extremities. Patients with vascular ischemic-reperfusion injuries,9
crush injuries or burns, as well as surgical orthopedic patients who have undergone internal or external fixation of fractures and those who have experienced prolonged external pressure from casts or tight-fitting bandages, are all at risk for this syndrome.4
If ALECS is not detected and treated within hours, a patient may develop irreversible muscle and nerve damage, joint contracture or gangrene and may even require amputation.4
Once a patient has been examined by the surgical team and the diagnosis is confirmed, he or she will be taken emergently to the operating room. Under general anesthesia, a fasciotomy will be performed. Single- and double-incision techniques have been described for decompression of the four compartments of the lower extremity, but most vascular surgeons now favor the double-incision technique because it is less tedious and it presents less potential for nerve injury.1
Two 5-inch to 7-inch incisions are made on the calf (Figure 3). The lateral incision provides access to the lateral and anterior compartments, and the medial incision allows access to the superficial and deep posterior compartments.10 When the fascia is opened, swollen edematous muscle protrudes through the incisions, relieving pressure on nerves and restoring blood flow to capillary tissue (Figure 4). Muscle viability can then be assessed by its pink color, contraction when stimulated, and blood flow when cut.
Fasciotomy may solve ALECS, but it creates wounds that may cause short- or long-term morbidity.1 Fasciotomy wounds sometimes remain open, covered only with moist gauze, for the first 24 to 48 hours after surgery.1 This allows for inspection of muscle viability and evaluation of the need for debridement. Upon re-evaluation, delayed primary closure (such as vacuum-assisted compression therapy; Figure 5) and eventually split thickness skin grafting (Figure 6) may be performed after the swelling subsides.
Fasciotomy predisposes a patient to future problems: altered sensation at the margins of the wound, disfiguring appearance, neurologic deficits and chronic venous insufficiency.6
The overall complication rate associated with ALECS increases dramatically if treatment is delayed more than 12 hours (54%) compared with early fasciotomy (4.5%).1 Almost half of patients with delayed treatment require amputation, and 92% have significant neuropathy.1 Delay to fasciotomy of more than 36 hours almost always results in amputation due to infection and muscle necrosis.3
In the upper extremity, Volkmann's contracture is a classic complication of missed diagnosis or incomplete decompression.1 Ischemic muscle and nerve are fibrosed, leaving the compartment firm, contracted and largely nonfunctional. The only treatment is contracture and joint capsule release.1
The patient in this case left the hospital with vacuum-assisted compression therapy applied to the fasciotomy wound and returned 3 weeks later for skin grafting. She returned to full functional status and avoided neurologic deficits, wound complication or significant cosmetic deformity. Due to some minor venous insufficiency, the patient now wears prescription-strength compression stockings. This insufficiency may worsen in the future. Due to the astute diagnostic and treatment skills of her healthcare provider, serious complications were avoided.
- Modrall JG. Compartment Syndrome. In: Cronenwett JL, Johnston KW, eds. Rutherford's Vascular Surgery. 7th ed. Philadelphia, PA: Saunders Elsevier; 2010: 2412-2421.
- Raffetto JD, et al. Differences in risk factors for lower extremity arterial occlusive disease. J Am Coll Surg. 2005;201(6):918-924.
- Weinmann M. Compartment syndrome. Emerg Med Serv. 2003;32(9):36.
- Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg. 1996;4(4):209-218.
- Johnston-Walker E, Hardcastle J. Neurovascular assessment in the critically ill patient. Nurs Crit Care. 2011;16(4):170-177.
- Percical TJ, et al. Compartment syndrome in the setting of vascular injury. Perspect Vasc Surg Endovasc Ther. 2011;23(2):119-124.
- Kosir R, et al. Acute lower extremity compartment syndrome screening (ALECS) in critically ill trauma patients. J Trauma. 2007;63(2):268-275.
- Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010;92(2):361-367.
- Ashok NB, Moore EE. Extremity Vascular Injuries. In: Harken AH, Moore EE, eds. Abernathy's Surgical Secrets. 6th ed. Philadelphia, PA: Mosby Elsevier; 2009: 158-164.
- Simon B. Fasciotomy. In: Scott-Conner CEH, Dawson DL, eds. Operative Anatomy. 3rd ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2009: 262-267.
Shawn Mangan Pierce is an adult nurse practitioner who works in the Department of Vascular and Endovascular Surgery at Thomas Jefferson University Hospital in Philadelphia. She has completed a disclosure statement and reports no relationships related to this article.