Acute Lower Limb Ischemia

How to Cite This Chapter: Szalay D, Frołow M, Leśniak W, Bodzoń W. Acute Lower Limb Ischemia. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.2.27.2. Accessed October 04, 2024.
Last Updated: December 9, 2021
Last Reviewed: December 9, 2021
Chapter Information

Definition, Etiology, PathogenesisTop

Acute lower limb ischemia refers to any sudden deterioration of limb perfusion that carries a risk of amputation.

Causes:

1) Embolism of cardiac origin (80% of cases; most often associated with atrial fibrillation) or originating from the aorta or large arteries (from aneurysms or atherosclerotic plaques). It usually leads to occlusion at branch points, such as the aortic bifurcation/proximal common iliac artery, common femoral artery bifurcating into superficial femoral and profunda arteries, and distal popliteal artery/proximal tibial arteries.

2) Thrombosis:

a) Primary thrombosis (usually a complication of atherosclerotic stenosis or aneurysm).

b) Thrombosis at the site of previous revascularization (bypass, endarterectomy, stent).

c) Thrombosis due to hypercoagulable states.

3) Arterial trauma or dissection (including iatrogenic trauma from catheters and arterial punctures).

4) Compartment syndrome.

Clinical Features and Natural HistoryTop

Manifestations: Arterial occlusion, which initially manifests as lack of pulse and pale cold skin. The subsequent timeline can vary depending on etiology and preexisting disease; times presented here serve only as approximation: after 15 minutes, pain in the limb develops. After 2 hours, hypoesthesia and paresthesia are present. After 6 hours, mottled cyanosis and anesthesia occur. After 8 hours, motor paralysis and muscle rigidity develop. After 10 hours, the patient develops blisters, local hemostasis disturbances, and necrosis. The dynamics and severity of symptoms depend on the location and extent of occlusion. Arterial thrombosis usually has a less dynamic course than arterial embolism. Preexisting chronic limb ischemia reduces the dynamics and severity of symptoms because of the previously developed collateral circulation.

Clinical classification: Table 1.

DiagnosisTop

Diagnosis should be established on the basis of clinical manifestations by the physician who examines the patient first and who should immediately refer the patient to a specialist vascular surgery center. Arterial duplex ultrasonography is used to reveal the absence of blood flow in limb arteries and to locate the occlusion (this is particularly helpful in the assessment of patency of bypass grafts). Computed tomography (CT) arteriography reveals the site of occlusion, provides information on the etiology of acute ischemia, and enables planning for revascularization. Conventional (catheter) arteriography can be both diagnostic and allow for immediate intervention if the underlying pathology is amenable to endovascular treatment.

TreatmentTop

Invasive Treatment

1. Indications: Surgery or endovascular treatment in patients with acute lower limb ischemia are potentially limb-saving procedures to which no contraindications exist. Urgently refer the patient to a surgical center.

2. Preoperative management:

1) As early as possible administer unfractionated heparin (UFH) 5000 to 10,000 IU followed by a continuous IV infusion (dosage: see Table 2 in Deep Vein Thrombosis).

2) Analgesics (opioid analgesics).

3) Protect the limb against heat loss, pain, and potential trauma.

3. Methods:

1) Surgery: Prompt revascularization surgery is indicated in patients with Rutherford stage IIb and early stage III ischemia (see Table 1 in Lower Extremity Peripheral Artery Disease). Most often this involves thromboembolectomy, which should be performed within 6 to 8 hours of the onset of symptoms of ischemia. An arterial repair, stent, or bypass may be required in addition to or instead of thromboembolectomy, particularly if there is preexisting arterial occlusive disease or dissection.

2) Endovascular treatment: Intra-arterial thrombolysis administered via a catheter with the catheter tip placed (embedded) in the thrombus; this involves a continuous infusion of low-dose streptokinase and alteplase. Thrombolytic therapy may be considered in patients with no contraindications and recent (<14 days) thrombosis or embolism. It may be the method of choice in patients with Rutherford stage I and IIa ischemia (where there is time to allow for thrombolysis to work) and may eliminate the need for or reduce the extent of surgical treatment. Any deterioration in perfusion during thrombolysis indicates a need to stop the infusion and perform immediate surgery. After restoring arterial patency, percutaneous angioplasty or reconstructive surgery may be performed to ensure sustained patency. Percutaneous aspiration thrombectomy or percutaneous mechanical thrombectomy may also be performed in place of or together with thrombolysis.

After thrombolysis, use an anticoagulant (see Anticoagulant Treatment) for ≥3 months (or lifelong in patients with thromboembolism associated with atrial fibrillation or a prosthetic valve).

TablesTop

Table 3.19-4. Clinical classification and treatment of acute limb ischemia (based on the Rutherford classification)

Grade/category

Prognosis

Clinical features

Treatment

Sensory loss

Motor deficit

I. Viable

Not immediately threatened

None

None

Thrombolysis or surgery

II. Threatened

– IIa. Marginally

Salvageable if promptly treated

None or minimal (toes)

None

Thrombolysis or surgery

– IIb. Immediately

Salvageable if promptly revascularized

More than toes

Mild or moderate

Surgery, may be combined with thrombolysis

III. Irreversible

Inevitable high-level amputation or permanent nerve damage

Profound, anesthetic

Profound, paralysis (rigor)

Primary amputation in the case of prolonged ischemic time with low likelihood of improvement and high risk of revascularization; early (6-8 h) embolectomy or thrombectomy may be considered to determine the extent of reversibility or to improve the level of amputation

Adapted from J Vasc Surg. 1997;26(3):517-38 and Eur Heart J. 2011;32(22):2851-906.

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