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Clinical features and diagnosis of acute lower extremity ischemia

Clinical features and diagnosis of acute lower extremity ischemia
Literature review current through: Jan 2024.
This topic last updated: Jun 22, 2022.

INTRODUCTION AND DEFINITIONS — Acute limb ischemia is defined as a quickly developing or sudden decrease in limb perfusion, usually producing new or worsening symptoms or signs, and often threatening limb viability [1]. Acute lower extremity ischemia is overwhelmingly related to arterial occlusion, though extensive venous occlusion can lead to extremity ischemia as well (ie, phlegmasia), but this is rare. This topic will focus on arterial occlusion. The incidence of acute peripheral arterial occlusion causing acute lower extremity ischemia is approximately 1.5 cases per 10,000 persons per year [2]. The clinical presentation depends upon the etiology and whether the patient has underlying peripheral artery disease. Patients who present later than two weeks after the onset of the acute event are considered to have chronic lower extremity ischemia [3-5].

The management of acute lower extremity ischemia remains a challenge for vascular specialists. Surgical or catheter-based thromboembolectomy and bypass grafting have been the mainstays of therapy for many years [6]. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients [7,8].

Despite these advances, the morbidity, mortality, and limb loss rates from acute lower extremity ischemia remain high [9]. Thus, regardless of the treatment modality used, early diagnosis and rapid initiation of therapy are essential to provide the best chance for limb salvage.

The etiologies, clinical features, and diagnosis of acute lower extremity ischemia will be reviewed here. The management of lower extremity embolic disease, peripheral artery disease, and other causes of acute limb ischemia (eg, aneurysmal disease) are reviewed separately. (See "Embolism to the lower extremities" and "Management of chronic limb-threatening ischemia" and "Management of asymptomatic abdominal aortic aneurysm" and "Popliteal artery aneurysm" and "Severe lower extremity injury in the adult patient".)

ETIOLOGIES — Acute lower extremity ischemia is overwhelmingly related to arterial occlusion, though extensive venous occlusion can lead to extremity ischemia as well (ie, phlegmasia), but this is rare. Venous occlusion is discussed briefly below and in separate topic reviews. (See 'Phlegmasia' below and "Overview of the treatment of proximal and distal lower extremity deep vein thrombosis (DVT)", section on 'Phlegmasia cerulea dolens'.)

Acute arterial occlusion is most commonly related to acute thrombosis of a diseased but previously patent, often atherosclerotic artery [10] but can also be due to acute thrombosis of a stent or graft, dissection of an artery, direct trauma to an artery, or the result of an embolus from a proximal source lodging into a more distal vessel (table 1).

Native arterial thrombosis — Acute thrombosis of a native lower extremity artery is most likely to occur at the site of a preexisting atherosclerotic plaque. Thrombosis can also occur at the location of an aneurysm, or at sites previously affected by dissection.

Atherosclerotic plaque — Thrombosis of a previously patent but stenotic artery is a well-known complication of atherosclerosis. Occlusion of atherosclerotic vessels may occur by two mechanisms:

Progressive atherosclerotic narrowing of the artery, with resultant low flow, stasis, and eventual thrombosis

Intraplaque hemorrhage and local hypercoagulability

The clinical manifestations of lower extremity ischemia resulting from arterial thrombosis in the face of underlying atherosclerosis are usually less dramatic in onset and less severe compared with those following an acute embolism or vascular thrombosis in individuals without atherosclerosis. This difference is primarily due to the collateral circulation that develops over time in patients with chronically narrowed vessels (figure 1). Collaterals are frequently so extensive that the patient notices no change or only a mild increase in his/her symptoms of chronic ischemia when an atherosclerotic vessel becomes occluded. (See 'Acute-on-chronic limb ischemia' below.)

Acute thrombosis of diseased iliac arteries can lead to occlusion of the distal aorta, with retrograde propagation, typically to the level of the renal arteries. In addition to limb ischemia, organ ischemia (gastrointestinal, renal) and paralysis or paresis from spinal cord ischemia can also occur [11]. Acute aortic occlusion due to saddle embolus can also occur but is much less common in modern case series.

Aneurysm — Acute thrombosis of an aneurysm can lead to profound lower extremity ischemia, a clinical scenario that is most commonly associated with popliteal artery aneurysm. Distal embolization can also occur. For other peripheral aneurysm sites, ischemic complications are less common but have been reported. (See "Popliteal artery aneurysm", section on 'Acute ischemia' and "Femoral artery aneurysm", section on 'Clinical presentation' and "Iliac artery aneurysm", section on 'Aneurysm thrombosis and thromboembolism'.)

Dissection — Acute aortic or peripheral artery (eg, isolated iliac) dissection can result in acute malperfusion of extremities, as well as organs. Leg ischemia caused by acute aortic dissection is a marker of extensive dissection and is associated with greater patient morbidity and mortality. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Pulse deficit'.)

Hypercoagulability — Hypercoagulability (acquired, inherited) can lead to thrombosis of vascular grafts or stents, native vessels that are diseased (eg, atherosclerotic stenosis), physiologically impaired or constricted (eg, arteritides, ergotism), and even those that were previously normal, particularly in patients with low flow states [12]. Although many of these conditions more frequently affect the venous circulation, some are associated with arterial thrombosis as well. These include:

Malignancy (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults" and "Cancer-associated hypercoagulable state: Causes and mechanisms" and "Approach to the patient with retiform (angulated) purpura".)

Antiphospholipid antibodies (See "Clinical manifestations of antiphospholipid syndrome", section on 'Thrombotic events'.)

Hyperhomocysteinemia (See "Overview of homocysteine", section on 'Disease associations'.)

Heparin-induced thrombocytopenia (see "Clinical presentation and diagnosis of heparin-induced thrombocytopenia", section on 'Thrombosis')

Disseminated intravascular coagulation and other causes of purpura fulminans (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults" and "Cancer-associated hypercoagulable state: Causes and mechanisms" and "Approach to the patient with retiform (angulated) purpura".)

COVID-19 [13-15] (See "COVID-19: Hypercoagulability".)

Injury

Iatrogenic — Acute arterial occlusion at the arterial access site (eg, femoral) as a complication of a vascular or cardiac diagnostic or interventional procedure has become a more frequent cause of acute extremity ischemia. The incidence of arterial complications following interventional cardiac catheterization (including hematomas, arteriovenous fistulas, pseudoaneurysms, arterial occlusion, and cholesterol emboli) has been reported to range from 1.5 to 9 percent [16]. While the use of closure devices has reduced bleeding complications at the arterial access site, the incidence of arterial obstruction may be increased due to device malfunction. Thromboemboli can also develop at the sheath site or catheter tip, with embolization occurring during sheath removal. When access site complications occur following interventional catheterization procedures, immediate surgical consultation is warranted [17]. Intimal flaps and dissections are frequently the cause of the occlusion, and reintervention or operative repair of the vessel is often required. (See "Femoral artery pseudoaneurysm following percutaneous intervention" and "Acquired arteriovenous fistula of the lower extremity" and "Complications of diagnostic cardiac catheterization".)

Traumatic — Arterial injury due to extremity trauma (blunt or penetrating) can also lead to acute lower extremity ischemia from either direct arterial injury or from traumatic arterial dissection with subsequent thrombosis or thromboembolism. This can be especially prevalent in traumatic posterior knee dislocations. The diagnosis and management of arterial injury in association with severe extremity injury is discussed in detail elsewhere. (See "Severe lower extremity injury in the adult patient" and "Knee (tibiofemoral) dislocation and reduction".)

Thrombosis following intervention — Thrombosis can complicate open or endovascular revascularization.

Immediate failure of a bypass graft can result in acute ischemia, but late thrombosis of an autogenous bypass graft due to progressive intimal hyperplasia (over months), or progressive atherosclerosis (over years), rarely results in acute ischemia. For vein grafts, immediate graft thrombosis is typically related to retained valves or compression or narrowing at the anastomosis, but kinks or twisting of the vein graft can also occur. Prosthetic grafts can thrombose at any site along their length and are often associated with outflow artery thrombosis and more severe ischemia compared with late vein graft thrombosis. (See "Lower extremity surgical bypass techniques", section on 'Complications'.)

Acute thrombosis of vascular stents can also lead to acute lower extremity ischemia, which can be a complication of aortic stent-grafts or peripheral arterial stents. (See "Complications of endovascular abdominal aortic repair" and "Endovascular techniques for lower extremity revascularization", section on 'Complications and management' and "Access-related complications of percutaneous access for diagnostic or interventional procedures".)

Embolism

Arterial embolism — The majority of arterial emboli that travel to the extremities originate in the heart, with the lower extremities affected more frequently than the upper extremities [18]. Thromboemboli typically lodge where there is an acute narrowing of the artery, such as an atherosclerotic plaque or a vessel branch point. The common femoral, common iliac, and popliteal artery bifurcations are frequent locations [19]. Improvements in anticoagulation therapy and advancements in the treatment of cardiac disease have reduced the proportion of acute limb ischemia events related to arterial embolism. (See "Embolism to the lower extremities" and "Embolism to the upper extremities".)

Potential sources of emboli from the heart include atrial thrombus formation due to atrial fibrillation, left ventricular thrombus formation following myocardial infarction or left ventricular dysfunction, and debris from prosthetic valves and infected cardiac valves (septic emboli). (See "Left ventricular thrombus after acute myocardial infarction" and "Echocardiography in detection of cardiac and aortic sources of systemic embolism".)

Arterial-to-arterial embolization of thrombus or plaque originating from aneurysms or atherosclerotic lesions is well described and accounts for approximately 20 percent of peripheral emboli. (See "Thromboembolism from aortic plaque" and "Clinical features and diagnosis of abdominal aortic aneurysm", section on 'Limb ischemia' and "Popliteal artery aneurysm", section on 'Acute ischemia'.)

Compared with thromboemboli, atheroemboli are less likely to produce symptoms of acute limb ischemia. Small vessel rather than large vessel occlusion is the usual cause of blue toe syndrome, which is usually due to embolic occlusion of digital arteries with atherothrombotic material from proximal arterial sources [20]. Blue toe syndrome is characterized by the sudden appearance of a cool, painful, cyanotic toe(s) or forefoot in the often perplexing presence of strong pedal pulses and a warm foot (picture 1). There may also be scattered areas of petechiae or cyanosis of the soles of the feet. Bilateral lower extremity involvement usually indicates an embolic source that is located above the aortic bifurcation. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)

Paradoxical embolism — Although more commonly associated with cryptogenic stroke, paradoxical emboli (venous thrombus that traverses a cardiac defect to access the arterial circulation) can also cause acute lower extremity ischemia [21-27]. One series found that 2 to 4 percent of embolic events over an eight-year period were due to paradoxical emboli; however, the source remained unknown in 20 percent of patients [27]. Patients with paradoxical emboli are typically younger compared with those who develop other forms of arterial thromboembolization (39 versus 68 years). Patients with paradoxical emboli may present with acute ischemia of an extremity, and they typically have little evidence of cardiac or peripheral artery disease. (See "Patent foramen ovale", section on 'Clinical manifestations'.)

Peripheral vasoconstriction/vasospasm — Conditions that cause vasospasm can lead to nonocclusive arterial ischemia. These include the Raynaud phenomenon, shock (eg, meningococcal sepsis, cardiogenic shock), and the administration of vasoactive drugs, which may have been given in a hospital setting to treat shock or self-administered (inadvertent arterial injection). If prolonged, arterial thrombosis may be superimposed.

Peripheral ischemia in patients who are treated with vasoactive drugs and for cardiogenic shock or sepsis is typically symmetrical and may affect the upper as well as lower extremities. Distal pulses are initially intact. (See "Clinical manifestations of meningococcal infection", section on 'Shock'.)

Self-administered injection affects the vascular distribution distal to the arterial injection site.

The Raynaud phenomenon typically presents with digital ischemia and can be distinguished from arterial thromboembolism by medical history and preserved proximal pulses. (See "Clinical manifestations and diagnosis of Raynaud phenomenon".)

CLINICAL PRESENTATIONS — Arterial occlusion results in a sudden cessation of blood supply and nutrients to the tissues in the distribution of the vessel, including skin, muscle, and nerves. The clinical presentation of acute arterial occlusion depends upon the time course of vessel occlusion; the location of the affected vessels, ranging from proximal large vessel occlusion resulting in ischemia of the entire extremity to distal small vessel occlusion resulting in digital ischemia; whether there is underlying vascular disease; and the ability to recruit collateral channels to provide flow around the occlusion (figure 1). Symptoms can develop over a period of hours to days and can range from new or worsening claudication to relatively sudden paralysis of the affected limb.

It is important to determine if the patient had symptoms of chronic ischemia prior to the acute event. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)

Acute-on-chronic limb ischemia — In patients with known peripheral artery occlusive disease or those who have undergone prior revascularization (eg, arterial repair, arterial bypass, arterial stent), symptoms of arterial occlusion can develop over a variable time period (hours to days). Suddenly increasing symptoms in a patient with a history of peripheral artery disease is indicative of arterial thrombosis.

Some patients with occlusion of an arterial bypass will experience symptoms similar to those prior to revascularization, while others will have symptoms that are worse, and potentially limb threatening, due to concomitant occlusion of vessels proximal or distal to the revascularized segment.

Acute limb ischemia — In patients with otherwise normal underlying vasculature who experience acute arterial occlusion, collateral blood vessels cannot be recruited quickly enough to circumvent the occluded artery, and the signs of acute ischemia most often develop rapidly. The sudden and dramatic development of ischemic symptoms in a previously asymptomatic patient is most consistent with an embolus. Patients with an extremity embolus can frequently pinpoint the exact time that symptoms began. The six Ps (pain, pallor, poikilothermia, pulselessness, paresthesia, paralysis) are the classic presentation of acute arterial occlusion in patients without underlying occlusive vascular disease. (See 'Six Ps' below.)

PHYSICAL EXAMINATION — A careful examination of both lower extremities is necessary to detect signs of ischemia. The level of arterial obstruction is usually one joint above the line of demarcation between the normal and ischemic tissue.

The neurologic examination should assess sensation and muscle strength. The quality and character of the peripheral pulses in the affected extremity, as well as the contralateral extremity, are evaluated and compared. The vascular examination should include palpation of all pulses, including the femoral, popliteal, dorsalis pedis, and posterior tibial pulses as well as the upper extremity pulses (ie, subclavian, axillary, brachial, radial, and ulnar). Since the quality of the pulse examination can vary, a handheld Doppler should be used to confirm the presence of distal pulses (eg, dorsalis pedis, posterior tibial Doppler signals). The operator should listen for arterial and venous signals (table 2). If Doppler signals are present, the ankle-brachial index (ABI) should be obtained. The manner of obtaining the ABI and interpretation is discussed separately. In general, the absence of any distal Doppler signals (arterial and venous) indicates severe ischemia. For the lower extremity, although the ABI may vary significantly depending upon the location of the thrombus or embolus, a value <0.4 is indicative of severe ischemia. (See "Noninvasive diagnosis of upper and lower extremity arterial disease", section on 'Ankle-brachial index'.)

Six Ps — The six Ps of acute ischemia include pain, pallor, poikilothermia, pulselessness, paresthesia, and paralysis.

Pain – Pain associated with acute arterial occlusion is usually located distally in the extremity, gradually increases in severity, and progresses proximally with increased duration of ischemia. Later, the pain may decrease in severity due to progressive ischemic sensory loss.

Skin perfusion – The skin of both the normal and affected extremity should be examined for temperature, color, and capillary refill. The skin of the ischemic extremity is typically cool (Poikilothermic) and Pale or mottled with delayed capillary filling. Blistering of the skin is an ominous sign of advanced ischemia. Both extremities should also be examined for signs of chronic ischemia such as atrophy of the skin, hair loss, and thickened nails. (See "Clinical features and diagnosis of lower extremity peripheral artery disease", section on 'Physical examination'.)

Pulses – Acute limb ischemia typically manifests with severely reduced pulses. Normal pulses in the contralateral extremity suggest the absence of chronic arterial occlusive disease and suggest that an embolus is the etiology of the acute ischemia. By contrast, reduced pulses in an asymptomatic contralateral extremity indicate the presence of underlying chronic disease and suggest acute thrombosis of an already diseased vessel as the most likely cause of the acute ischemia.

Neurologic examination – Subjective sensory deficits such as numbness or Paresthesias are signs of early nerve dysfunction secondary to ischemia. Major loss of sensory or motor function (Paralysis) is indicative of advanced ischemia. In the lower extremity, the anterior compartment (figure 2) of the leg is most sensitive to ischemia, and sensory deficits over the dorsum of the foot are often the earliest neurologic sign of acute vascular insufficiency.

DIAGNOSIS — A diagnosis of acute extremity ischemia can generally be made based upon the history and physical examination, including assessment of the ankle-brachial index bilaterally. The suspected cause and severity of ischemia determines whether or not to proceed with additional diagnostic testing. (See 'Clinical categories of ischemia' below and 'Vascular imaging' below.)

Clinical categories of ischemia — The following clinical categories of acute limb ischemia are commonly used (table 2) [3,28,29]. These categories are useful for helping guide decisions about additional vascular imaging and management. (See "Classification of acute and chronic lower extremity ischemia", section on 'Acute extremity ischemia'.)

Viable or marginally threatened Viable limbs are under no immediate threat of tissue loss. There is no sensory loss or muscle weakness, and both arterial and venous Doppler signals are audible. Marginally threatened limbs are salvageable if treated promptly. There is minimal pain (in the toes) or no sensory loss, no muscle weakness, arterial Doppler signals are often inaudible, and venous Doppler signals are audible. For patients with viable or marginally threatened limbs, there is usually sufficient time for vascular imaging to define the extent of disease. (See 'Vascular imaging' below.)

Immediately threatened – Immediately threatened limbs are salvageable with immediate revascularization. Sensory loss involves more than the toes and may be associated with rest pain. There is mild-to-moderate muscle weakness, arterial Doppler signals are usually inaudible, and venous Doppler signals are audible. (See "Embolism to the lower extremities", section on 'Immediately threatened extremity'.)

Irreversibly ischemic – Irreversibly ischemic limbs have major tissue loss or permanent nerve damage. Sensory loss is profound, muscle weakness is profound with paralysis and possible rigor, and arterial and venous Doppler signals are inaudible. Nonviable extremities require major amputation regardless of the therapy that is instituted. Vascular imaging is generally not immediately needed for limbs that are irreversibly damaged. Revascularization may be required to permit healing of the amputation or to allow amputation at a lower level. (See "Embolism to the lower extremities", section on 'Nonviable extremity'.)

Vascular imaging — The type of vascular imaging chosen weighs the availability of a specific imaging modality and the time required to perform and interpret the study against the urgency and possible methods of revascularization (eg, endovascular, open surgery) [2]. Patients with viable or marginally threatened limbs are usually candidates for urgent vascular imaging (typically computed tomographic [CT] angiography, or catheter-based arteriography) to evaluate arterial anatomy and to potentially institute thrombolytic therapy. However, patients with an immediately threatened extremity should preferentially undergo further evaluation and treatment in a surgical suite. (See 'Clinical categories of ischemia' above.)

Important factors that impact the timing and method of revascularization include the following:

Presumed etiology (embolus versus thrombus)

Lesion location and length

Duration of symptoms

Availability of autologous vein for bypass grafting

Suitability of the patient for surgery or intervention

These clinical and radiographic features help determine whether catheter-directed thrombolysis (with or without endovascular intervention) or surgical revascularization is the most appropriate initial treatment. When thrombolysis is more suitable, proceeding directly to catheter-based arteriography expedites treatment and minimizes overall intravenous contrast load. As an example, for occlusion of a distal vessel (eg, to the tibial artery) or one that is more difficult to expose, thrombolysis may be the best initial treatment.

Although noninvasive vascular imaging studies (eg, duplex ultrasonography, CT angiography, magnetic resonance [MR] angiography) may be reasonable for some patients with acute limb ischemia, catheter-based arteriography (digital subtraction arteriography) provides the most useful information. CT and MR angiography can reliably diagnose the location and severity of arterial stenosis or occlusion (image 1) with high sensitivity and specificity, but these modalities do not offer a treatment option (eg, thrombolysis, angioplasty).

In addition to demonstrating arterial anatomy, arteriography can usually distinguish between thrombosis and embolism.

Arterial thrombosis is usually seen as a sharp or tapered, but not rounded, cutoff on arteriography. Diffuse atherosclerosis with well-developed collateral circulation is generally present.

An embolus will often demonstrate a sharp cutoff with a rounded reverse meniscus sign. The embolus may also be visible as an intraluminal filling defect if the vessel is not completely occluded. Other findings that are most consistent with an embolus include the presence of otherwise normal vessels, the absence of collateral circulation, and the presence of multiple filling defects.

For patients with thrombosis of an atherosclerotic segment, or occlusion of a prior revascularization, vascular imaging studies should be compared with any previously performed studies (if available).

DIFFERENTIAL DIAGNOSIS — Acute limb ischemia due to intraluminal arterial obstruction needs to be differentiated from the following conditions that can cause acute limb pain and/or reduced extremity perfusion.

Chronic limb ischemia — Chronic limb-threatening ischemia is most often due to severe peripheral artery disease, but other etiologies include nonatherosclerotic vascular disease such as thromboangiitis obliterans, vasculitides, and connective tissue disorders. Chronic limb-threatening ischemia is distinguished from acute limb ischemia by a duration of symptoms that is longer than two weeks [3-5]. (See "Clinical features and diagnosis of lower extremity peripheral artery disease".)

Acute compartment syndrome — Acute extremity compartment syndrome, typically affecting the lower leg, can cause extrinsic compression of the arteries leading to ischemic symptoms and signs that can be difficult to distinguish from an intraluminal source of arterial obstruction. However, the pain of a compartment syndrome is more severe, more localized, and is likely to be elicited during palpation of the muscle or passive stretching. In addition, leg swelling is usually evident. It is important to note that patients with severe acute limb ischemia can have concomitant acute compartment syndrome. In addition, acute compartment syndrome frequently complicates reperfusion after resolution of the acute ischemic insult, resulting in recurrence of limb ischemia once the tissue pressure exceeds perfusion pressure. (See "Acute compartment syndrome of the extremities", section on 'Clinical features'.)

Phlegmasia — Extensive deep vein thrombosis with accompanying superficial vein thrombosis can lead to phlegmasia cerulea dolens, a condition in which venous pressure is increased to such an extent that extremity perfusion is impaired [12]. Lower extremity swelling and cyanosis distinguish this disorder from intraluminal arterial obstruction. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

Others — Limb pain from acute gout or neuropathy may mimic the pain of acute ischemia but is usually readily distinguished by normal pulses and normal or hyperemic skin, unless there is underlying peripheral artery disease. Other focal dermatologic conditions, particularly those that occur in the acral regions (eg, pernio (picture 2 and picture 3)), may mimic areas of ischemia but can usually be distinguished by a lack of typical risk factors for atherosclerosis or embolism and intact pulses, and either spontaneous resolution for idiopathic cases or resolution with appropriate diagnosis and treatment of the underlying condition. (See "Pernio (chilblains)", section on 'Associated disorders' and "Pernio (chilblains)", section on 'Differential diagnosis' and "Approach to the patient with retiform (angulated) purpura".)

Spontaneous hemorrhage/traumatic injury — Spontaneous hemorrhage or mild traumatic injury can cause pain and skin discoloration that can mimic acute or chronic ischemia. An antecedent injury or medication history of anticoagulation and typically intact pulses make the distinction. (See "Easy bruising".)

COVID-19 dermatologic changes — Distinct from cases of arterial thrombosis that have been associated with COVID-19 related to alteration in coagulation (see 'Hypercoagulability' above), COVID-19 has been associated with a variety of dermatologic manifestations, including a viral exanthem, livedo reticularis, urticaria, petechial rashes, and acral pernio-like lesions [30]. The last of these are patches of erythematous-to-violaceous skin, which can affect the feet and toes ("COVID toes") (picture 4), hands/fingers, or other locations. The lesions may correspond to focal areas of vascular occlusion [31-35]. The mechanism is unknown but it does not appear to be related to macrovascular occlusive disease or embolism. Microscopic intravascular thrombi have been seen on biopsy of lesions in critically ill patients [36]. Some have speculated that the dermatologic lesions may be a clinical sign of systemic hypercoagulability. However, acral lesions have also been reported in asymptomatic individuals and those with a mild case of COVID-19. It remains unclear whether there is any causal relationship to COVID-19 or whether these represent idiopathic pernio, or possibly related to lifestyle changes associated with containment measures [37]. (See "Pernio (chilblains)" and "COVID-19: Hypercoagulability" and "COVID-19: Cutaneous manifestations and issues related to dermatologic care".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute extremity ischemia" and "Society guideline links: Extremity compartment syndrome" and "Society guideline links: Severe blunt or penetrating extremity trauma".)

SUMMARY AND RECOMMENDATIONS

Acute limb ischemia – Acute limb ischemia is a sudden decrease in limb perfusion that may threaten limb viability and is usually due to acute arterial occlusion; a venous etiology is rare. Acute arterial occlusion is most commonly related to acute thrombosis of a diseased but previously patent, often atherosclerotic artery but can also be due to acute thrombosis of a stent or graft, dissection of an artery, direct trauma to an artery, or the result of an embolus from a proximal source lodging into a more distal vessel (table 1). (See 'Introduction and definitions' above and 'Etiologies' above.)

Clinical presentation – The clinical presentation of acute arterial occlusion depends upon the time course of vessel occlusion, the location of the affected vessels, whether there is underlying vascular disease, and the ability to recruit collateral channels to provide flow around the occlusion. Subjective sensory deficits are signs of early nerve dysfunction, and major sensory or motor loss is indicative of advanced ischemia. The level of arterial obstruction is usually one joint above the line of demarcation between the normal and ischemic tissue. (See 'Clinical presentations' above and 'Physical examination' above.)

The classic physical signs of acute limb ischemia in a patient without underlying occlusive vascular disease are the six Ps (pain, pallor, pulselessness, poikilothermia, paresthesia, and paralysis).

For patients with known peripheral artery occlusive disease or those who have undergone prior revascularization (eg, arterial repair, arterial bypass, arterial stent), symptoms of arterial occlusion can develop over a variable time period (hours to days).

Classification of ischemia – A complete examination of the extremity is performed and should include documentation of the classification of ischemia (table 2) to assist in stratifying further diagnostic evaluation and treatment. (See 'Clinical categories of ischemia' above.)

Viable limbs are under no immediate threat of tissue loss.

Marginally threatened limbs are salvageable if treated promptly.

Immediately threatened limbs are salvageable with emergent revascularization.

Limbs with irreversible ischemia will require major amputation regardless of any therapy that is instituted.

Vascular imaging – Patients with viable or marginally threatened limbs are usually candidates for urgent vascular imaging (computed tomographic [CT] angiography, catheter-based arteriography) to evaluate arterial anatomy. When thrombolysis is suitable, proceeding directly to catheter-based arteriography expedites treatment and minimizes overall intravenous contrast load. Patients with an immediately threatened extremity treatment should preferentially undergo further evaluation and treatment in a surgical suite. (See 'Vascular imaging' above.)

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Emile R Mohler, III, MD (deceased), who contributed to an earlier version of this topic review. UpToDate also acknowledges Dr. Mohler's work as our Section Editor for Vascular Medicine.

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Topic 8213 Version 36.0

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