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Acute Limb Arterial Ischemia

Although acute limb ischemia is a relatively rare condition, it is a true medical emergency requiring prompt diagnosis and management to prevent limb loss.

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References

Acute limb ischemia (ALI) is an emergent medical condition that is characterized by a precipitous decrease in limb perfusion that threatens the viability of the affected limb, and symptoms that have been present for 14 days or less.1-5 The incidence of lower extremity ALI in the US is nine to 16 cases per 100,000 persons per year, and one to three cases per 100,000 persons per year for upper extremity ALI.3 Symptoms suggestive of this condition classically include pain in the effected limb at rest, loss of sensation, impaired motor function, and cyanosis/pallor. Irreparable damage can occur in as quickly as 4 to 6 hours with complete arterial occlusion. A majority of ALI is caused by thrombosis, with the remainder of cases caused by embolism, 85% and 15% respectively.1-6 If not addressed promptly, this condition carries a high degree of morbidity (ie, limb loss) and mortality. Immediate initiation of anticoagulation therapy and vascular surgery consultation are mainstays of ED management. Time-to-treatment is a predictor of success and is an area where the emergency physician (EP) can make a significant difference in patient outcomes.7 Although vascular interruption via traumatic mechanism is not addressed in this review, it should remain a consideration in relation to the historical features of each case.

Presentation

Traditionally, symptoms of ALI can be remembered as the “six Ps”: pain, pallor, paresthesia, paralysis, pulselessness, and poikilothermia. Note that ALI represents a spectrum of disease, and the presenting features depend heavily on the level and degree of obstruction. Pain, however, is most frequently the first presenting symptom of patients with ALI.1-6 Pain will occur in muscle groups distal to the occlusion. Obstruction of the aortoiliac region might produce pain in the buttocks, thigh, and hip, whereas occlusion of the femoral artery may produce pain in the calf. Single-level disease will often produce claudication, but multilevel disease may present as a nonhealing ulcer or with focal gangrene. The differential diagnosis of ALI includes direct arterial injury, vasospasm, compartment syndrome, chronic peripheral artery disease, stroke, spinal cord injury, vasculitis, muscular trauma, and radiculopathy.3,5

Etiology

As stated previously, ALI is a result of either thrombotic or embolic phenomena that either partially or completely occludes a vessel such that adequate perfusion is no longer achieved. Consequently, there is a decrease in the metabolism of the tissue supplied in those territories, which can rapidly progress to necrosis. Thrombosis is the most common cause of ALI, accounting for approximately 85%.2,3Typically, thrombosis presents in the setting of pre-existing peripheral artery disease (PAD).8 As PAD worsens, damage to the arterial endothelium triggers platelet activation, and accumulation in a manner conceptually similar to thrombosis in myocardial infarction.9 Hypercoagulable states increase the risk of thrombi development.10 Symptoms of thrombosis are often more insidious in onset when compared to embolism, and signs/symptoms of prior claudication are almost always present. Consequently, there is a greater chance that collateral circulation has developed over time.2,6,11,12

By contrast, ALI caused by embolism is more acute in onset, and is often more emergent due to complete occlusion without chance of collateral vessel development.1,3,6,12 See Table 1 for differences in risk factors and presentation between thrombotic and embolic occlusion.

Table 1. Differentiation Between Embolic and Thrombotic Arterial Ischemia

Patients with known risk factors for embolic phenomena should raise clinical suspicion for this etiology. Therefore, an investigation of embolic risk factors should be initiated in all patients in whom ALI secondary to embolism is suspected. Risk factors include atrial fibrillation, impaired myocardial contractility, prosthetic heart valves, endocarditis, prior arterial injury, and other exogenous devices, such as stents.3,5,1

Historical Features

Information should be obtained systematically in all presentations and should include time of symptom onset, duration, severity, and location; however, special attention should be paid to the evolution of symptoms over time. One historical pearl that should raise suspicion of embolism vs thrombus is a patient history with a specific time of symptom onset. Specific questioning about history of claudication, including description of typical symptoms, is critical. A full list of other medical comorbidities should be obtained. This may reveal risk factors for thrombotic and embolic disease.1,3-5 This also may alter available treatment options.7,8,12,13 At presentation, the EP should obtain a list of the patient’s current medications, and special attention should be given to prothrombotic medications and medications that may interact with anticoagulants.

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