Acute Arterial Occlusion


Acute Arterial Occlusion

  1. Overview
    • differential diagnosis includes embolism, thrombosis, and trauma
    • emboli may originate from the heart or more proximal arteries
    • thrombosis may result from atherosclerosis, from an aneurysm, or from low flow states common in the ICU
    • traumatic injuries resulting in arterial occlusion include long bone fractures, penetrating trauma, and posterior knee dislocations

  2. Pathophysiology
    • acute arterial occlusion results in ischemia (ALI) of the tissues supplied by the involved arterial segment
    • embolus to a normal artery will result in the sudden onset of ALI since there will be an absence of collateral circulation
    • nerve is the most sensitive tissue to ischemia, and prolonged ischemia may result in foot drop or Volkmann’s contracture
    • tissue necrosis typically occurs after 6 to 12 hours of total ischemia

    Volkman's Contracture
    Volkman's Contracture

  3. Clinical Manifestations
    • most patients have one or more manifestations of the 6 P’s: pain, paresthesia, paralysis, pallor, pulselessness, and poikilothermia (coolness)
    • pain is the most common presenting symptom (75%)
    • paresthesia and paralysis result from ischemia of the sensory and motor nerve endings and are the most ominous findings - patients with these findings will develop gangrene if the underlying problem is not corrected
    • the level at which temperature and color changes occurs provides information regarding the level of the arterial occlusion: tissue ischemia usually develops one joint below the segment of occluded artery
    • the absence of pulses supports the diagnosis of acute arterial occlusion but does not prove it with certainty, since many patients will have chronically absent pulses
    • muscle turgor is also an important clinical finding: if the muscles are stiff and hard then the ischemic changes are irreversible, regardless of therapy

    1. Rutherford Classification of Acute Limb Ischemia
      • based on the neurologic and vascular examination of the affected limb
      • Class I patients need intervention with 24 – 48 hours
      • Class IIa patients need intervention within 24 hours
      • Class IIb patients need emergent intervention
      • Class III patients require amputation

    Rutherford Classification of Acute Arterial Occlusions
  4. Peripheral Arterial Emboli
    • most common cause of upper extremity acute limb ischemia
    • 2nd most common cause of lower extremity ALI, behind in situ thrombosis

    1. Sources
      1. Cardiac Emboli
        • heart accounts for 80% of cases
        • emboli lodge at arterial branch points, where the vessel diameter is greatly reduced
        • in the upper extremity, the most common affected sites are the brachial artery at the bifurcation of the radial and ulnar arteries, and the axillary artery at the takeoff of the deep brachial artery
        • in the lower extremity, the most common affected sites are the bifurcation of the common femoral artery, aortoiliac segments, and the popliteal artery
        • emboli result from atrial fibrillation, myocardial infarction, ventricular aneurysm, and valvular heart disease
        • an embolus may be the first manifestation of a serious cardiac disorder
        • a paradoxical embolus may develop from a deep venous thrombosis and pass through a patent foramen ovale
        • presence of normal pulses on the contralateral side is strongly indicative of an embolic source
        • EKG and echocardiography are used to search for the embolic source

      2. Noncardiac Sources
        • account for 15% to 20% of cases
        • fragments of ulcerated aortoiliac atherosclerotic plaques may become dislodged and travel downstream
        • since the fragments are tiny, they do not become lodged until they reach a small vessel
        • most common example is the ‘blue-toe’ syndrome (ischemia of the toes in the presence of palpable pedal pulses)
        • aortic and popliteal aneurysms may also be sources of peripheral emboli
        • plaque disruption can also occur as a result of endovascular interventions

        Blue Toe Syndrome
        Blue Toe Syndrome

    2. Diagnosis
      • history and physical exam is often sufficient to make a diagnosis of arterial embolus
      • in a class IIb limb, must avoid tests that delay definitive treatment
      • non-invasive tests such as ABI, pulse volume recording, Duplex ultrasound may confirm the site of occlusion
      • if the heart is not the source, CTA may identify an aortic aneurysm or ulcerative plaque
      • in patients with prolonged ischemia, CPK and urine myoglobin should be ordered

    3. Management
      1. Preoperative Management
        • once the diagnosis is made, the patient should be systemically heparinized
        • medical treatment of the underlying cardiac problem or arrythmia should be undertaken at the same time

      2. Embolectomy
        • embolectomy can be performed under a local anesthetic if the patient is too ill for a general anesthetic
        • in the lower extremity, the CFA is the access artery of choice for iliac, femoral, and popliteal emboli
        • the below knee popliteal artery can be used for tibial emboli
        • in the upper extremity, the distal brachial artery is accessed at its bifurcation
        • bilateral CFA access is used for an aortic saddle embolus
        • after proximal and distal control of the artery has been obtained, a transverse arteriotomy is performed
        • the embolus is removed by passing an embolectomy catheter proximally and distally to remove all propagated thrombus

          • Embolectomy
        • additional incisions may be required to remove thrombus from distal vessels
        • a completion arteriogram should be performed to check the completeness of the embolectomy
        • fasciotomies may be necessary if compartment syndrome is anticipated
        • anticoagulation should be continued in the postoperative period
        • overall mortality is > 25%, largely due to the underlying cardiac disease

      3. Endovascular Techniques
        1. Thrombolysis
          • catheter-directed thrombolysis can be beneficial in Class I and Class IIa ALI, or in patients with a medically high operative risk
          • can dissolve clot in small vessels not amenable to open embolectomy
          • treatment of choice, if time permits, of emboli associated with popliteal aneurysms
          • downsides of thrombolysis are the longer time period required for reperfusion and the risk of bleeding complications
          • absolute contraindications include stroke/TIA within 2 months and GI bleeding within 10 days
          • in general, thrombolysis works better for in situ thrombosis than for emboli

          Bilateral Lower Limb Emboli
          Bilateral Lower Limb Emboli (A + B) Cleared by Thrombolysis (C - F)

      4. Postoperative Management
        1. Reperfusion Syndrome
          • release of free oxygen radicals that further injure ischemic tissue
          • hyperkalemia, metabolic acidosis, myoglobinuria, and acute renal failure may develop
          • hydration and urine alkalinization with bicarbonate are the mainstays of treatment

        2. Compartment Syndrome
          • may develop during reperfusion
          • incidence correlates with the length and severity of ischemia
          • clinical diagnosis, but measuring compartment pressures may help in some cases
          • during fasciotomy, all compartments must be released, and the skin opened over its entire length

        3. Anticoagulation
          • patients with cardiogenic embolism will require lifelong anticoagulation as the risk of recurrent embolism is ~ 30%

        4. Additional Procedures
          • noncardiogenic sources of emboli need to be addressed as long as the risk is acceptable
          • aortic aneurysms and aortoiliac plaques can often be managed with endovascular techniques

  5. Acute Arterial Thrombosis
    1. Etiology
      1. Atherosclerosis
        • most commonly occurs at a site of stenosis caused by atherosclerosis
        • thrombosis is initiated by plaque disruption and exposure of the thrombotic core
        • thrombosis may also occur secondary to inadequate cardiac output

      2. Hypercoagulable States
        • antithrombin-III deficiency, protein C and S deficiency, lupus, thrombocytosis
        • should be suspected when the patient lacks the usual risk factors for atherosclerosis

      3. Repetitive Trauma
        • subclavian artery thrombosis resulting from the first rib or an accessory cervical rib compressing the subclavian artery

        Thoracic Outlet Syndrome
    2. Presentation
      • clinical findings may be the same as those observed in acute embolus, and the same classification system is used to guide the urgency of management
      • since most patients have longstanding PAD, collateralization may make the presentation less acute than in acute embolus
      • a previous history of symptomatic peripheral vascular disease is suggestive of a thrombotic cause
      • physical findings of chronic arterial insufficiency also suggest a thrombotic cause (skin and nail changes, absence of distal pulses in the uninvolved extremity)

    3. Imaging
      • Duplex ultrasound is quick and noninvasive
      • arteriography is diagnostic and allows for therapy with catheter-directed thrombolysis

    4. Management
      1. Surgical Revascularization
        • mandatory for Class IIb ALI
        • surgical bypass, graft revision, endovascular techniques are all valid approaches

      2. Catheter-Directed Thrombolysis
        • may be used instead of or in addition to standard operative techniques
        • indications include acute thrombosis (<14 days) of a native artery or bypass graft in Class I or Class IIa patients
        • randomized trials do not show any significant differences in mortality or amputation rates between patients treated with thrombolysis or surgery
        • currently used lytic agents include urokinase and recombinant tissue plasminogen activator, which work by converting plasminogen to plasmin, which in turn degrades fibrin

      3. Mechanical Thrombolysis
        • adjunct to catheter-directed thrombolysis
        • suction thrombectomy, rotational/infusion devices, ultrasound are all finding use in acute arterial thrombosis







References

  1. Sabiston, 20th ed., pgs 1777 - 1779
  2. Schwartz, 10th ed., pgs 885 - 890
  3. Cameron, 13th ed., pgs 1013 - 1022
  4. UpToDate. Clinical Features and Diagnosis of Acute Lower Extremity Ischemia. Marc E. Mitchell, MD, Jeffrey P. Carpenter, MD. Sep 11, 2020. Pgs 1 - 25