3 Acute Ischemic Stroke: Acute Internal Carotid Artery Occlusion and Tandem Lesions
Abstract
Internal carotid artery (ICA) occlusion has a mortality of more than 50%. Tissue plasminogen activator has minimal to no beneficial effect. Intracranial ICA terminus occlusions have the worst functional outcome and are usually secondary to cardiac embolism. Extracranial ICA occlusion can be caused by atherosclerosis, dissection, and rarely by cardiac embolism; most cases are associated with sudden occlusion of a previously preexisting ICA stenosis or plaque rupture. Tandem occlusions (extracranial ICA occlusion and intracranial ICA or middle cerebral artery [MCA] occlusion) involve the complexity of different stroke mechanisms and endovascular treatment is challenging. Computed tomography angiography of the neck and head is the best imaging study to diagnose ICA occlusion. Endovascular management strategy varies depending on the site of occlusion. Treatment includes mechanical thrombectomy with or without intracranial or extracranial carotid artery stenting (CAS). After an ICA occlusion is confirmed with cerebral angiography, the extracranial occlusion/stenosis is usually resolved first with aspiration thrombectomy or CAS. Once the extracranial ICA has been revascularized, better visualization of the intracranial ICA or MCA occlusion is possible. Intracranial mechanical thrombectomy is performed with direct aspiration using a large bore catheter or with a stent retriever. Balloon guide catheters are frequently used in ICA occlusions allowing endovascular mechanical thrombectomies and CAS to be performed under flow arrest to decrease the risk of iatrogenic intracranial thrombus embolism. Other potential risks include injury to the ICA resulting in dissection and/or occlusion. Extracranial–intracranial bypass is usually not indicated in the acute ICA occlusion management, but it can be considered once patient is stable and adequate revascularization was not achieved by endovascular means.
Introduction
Acute ischemic stroke (AIS) caused by intracranial internal carotid artery (ICA) occlusion has a dismal natural history, with neurological morbidity and mortality rates of 70 and 55%, respectively. Recanalization rates after intravenous (IV) tissue plasminogen activator (tPA) in patients with intracranial ICA are exceptionally poor (4.4–12.5%). Recanalization rates after intra-arterial (IA) therapy in patients with extra- and/or intracranial ICA occlusion are 62 to 63%. Extracranial ICA occlusion has a better prognosis than intracranial ICA occlusion due to collateral supply from the external carotid artery (ECA) and the circle of Willis.
Major controversies in decision making addressed in this chapter include:
Should acute symptomatic ICA occlusion be treated medically, endovascularly, or with both therapies?
Whether the benefit of improved recanalization associated with therapy is outweighed by time delays and complications, such as embolization of thrombotic material into more distal territories.
The precedence of endovascular recanalization—which one should be considered first, extracranial or intracranial occlusive lesion?
The role of open cerebrovascular techniques in the management of ICA occlusion.
Whether to Treat
In individuals with extracranial ICA occlusion and poor collateral circulation or simultaneous intracranial ICA occlusion, the treatment goal is to achieve rapid and complete recanalization of the artery ( 1 and 2 in algorithm ). For patients with tandem lesions, revascularization of both lesions is warranted to achieve a good outcome. The natural history of patients with acute symptomatic ICA occlusion is poor. Historically, due to the poor prognosis, many clinicians used to hesitate, wondering if outcome could be improved with therapy. A Dutch study, the Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands (MR CLEAN), changed that misperception; in fact, of all the cohorts in that trial, the group most likely to benefit from revascularization was the group with cervical and intracranial occlusion presenting with AIS. Unfortunately, the Food and Drug Administration did not allow patients who presented with tandem cervical and intracranial ICA occlusion in U.S.-based trials (e.g., Solitaire With the Intention For Thrombectomy as PRIMary Endovascular treatment [SWIFT PRIME], Assess the Penumbra System in the Treatment of Acute Stroke [THERAPY], and Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion with Emphasis on Minimizing CT to Recanalization Times [ESCAPE]) because of concern about safety of acute extracranial ICA angioplasty and/or stenting. Patients with complete recanalization of the occluded ICA have the best chance of regaining independence. There was a major concern that aggressive endovascular therapy resulted in symptomatic intracranial hemorrhage (ICH) and decreased survival. However, MR CLEAN demonstrated that the rate of symptomatic ICH is similar in patients treated with IV tPA (medical therapy) alone or with endovascular therapy ( 1 , 2 in algorithm ).
Anatomical Considerations
For endovascular procedures, anatomical relevance starts with arterial access. Transfemoral access is most commonly used for stroke interventions. Other alternatives include transradial or transbrachial access (especially for the posterior circulation) and even direct carotid artery access in cases of a type III arch, extreme tortuosity, or ostial stenosis of the common carotid artery (CCA). A computed tomography angiography (CTA) of the aortic arch extending up to the vertex (therefore including the entire intracranial circulation) should be obtained and evaluated before the procedure to assess for difficult anatomy and assist with planning. A heavily calcified cervical ICA (seen on CTA) suggests extracranial ICA occlusion with possible intracranial occlusion. An intracranial ICA bifurcation occlusion could have the radiographic appearance of an extracranial ICA occlusion. Here, a four-dimensional (4D) CTA can be very useful to distinguish an intracranial from an extracranial occlusion. This noninvasive study reciprocates a diagnostic angiogram revealing the extension of contrast material intracranially during the venous phase for pure intracranial ICA occlusions. Alternatively, contrast material can be noted to head downward from the circle of Willis toward the occluded carotid artery during extracranial occlusion. This is a key distinction because if there is complete extracranial occlusion, it is likely that stent-assisted revascularization and a loading dose of dual-antiplatelet therapy are needed emergently en route to the interventional suite; although if the lesion is solely intracranial, one can forgo the additional anticoagulation therapy.
Once endovascular access into the CCA has been established, the anatomy and site(s) of occlusion should be assessed. The following anatomical characteristics should be addressed:
Flame-shaped occlusion at the cervical ICA bifurcation indicating possible dissection or intracranial ICA terminus occlusion (▶ Fig. 3.1 ).
Collateral flow from the ECA into the intracranial ICA, most commonly through an anastomosis or anastomoses with the ophthalmic artery.
Presence of retrograde filling of the ICA to the level of the skull base. This is a good marker for the absence of thrombus in the petrocavernous segment.
Contralateral ICA and vertebral artery injections to evaluate collateral flow through the anterior and posterior communicating arteries are typically not recommended if the patient has a high National Institutes of Health Stroke Scale (NIHSS) score and CT or magnetic resonance (MR) perfusion imaging suggests salvageable penumbra. This is because the presence of collaterals may erroneously suggest adequacy, when the clinical picture suggests otherwise. Conversely, a low NIHSS score may be explained by excellent intracranial collaterals, which obviates the need for revascularization and subsequent exposure of the patient to distal and more consequential embolization.
Pathophysiology/Classification
Intracranial Internal Carotid Artery Occlusion
The outcome depends on the site of vessel occlusion. Occlusion of the ICA terminus has the worst functional outcome. Most of these cases are caused by cardiogenic embolism; however, other etiologies, such as atherosclerosis and dissection, should be considered. Functional ICA terminus occlusions are prone to impaired collateral circulation because they cut off the circle of Willis.
Extracranial Internal Carotid Artery Occlusion
Various mechanisms have been proposed to cause extracranial ICA occlusion, including atherosclerosis, dissection, and in rare cases cardiac embolism. Most cases of extracranial ICA occlusion are associated with sudden occlusion of a previously preexistent ICA stenosis, plaque rupture with hemorrhage, or cardioembolic thrombus on a preexistent ICA stenosis.
Tandem Lesions
Some cases of ICA terminus occlusion are due to cervical ICA plaque rupture and secondary artery-to-artery large embolus with resultant tandem occlusion of the extracranial ICA and intracranial ICA terminus. In these cases, total blockage of anterograde ICA flow and the major collateral pathways of the circle of Willis results in a severe perfusion deficit and acute dense neurological symptoms. Tandem occlusions involve the complexity of different stroke mechanisms. Some patients have clinical symptoms caused by a focal thrombus at the site of the intracranial occlusion. Other patients have symptoms caused by an entire hemispheric ischemia due to cervical occlusion. Treatment strategies are challenging because of the coexistence of hard, though fragile, ruptured plaque and the secondary very large thrombus extending from the cervical ICA up to the ICA terminus (▶ Fig. 3.2 ).
Workup
Clinical Evaluation
The NIHSS score is the standard bedside clinical evaluation for patients with stroke. It measures multiple functions, such as level of consciousness, speech, motor and sensory function, vision, neglect, and extinction. Patients with an NIHSS score of ≥6 should be considered for endovascular stroke revascularization associated with large vessel occlusion (LVO) ( 3 in algorithm ). Endovascular mechanical thrombectomy could be indicated even with an NIHSS score of less than 6 if the neurological deficit is severe (e.g., severe aphasia) or perfusion imaging suggests severe hemodynamic susceptibility (see below) and is likely to result in long-term morbidity ( 1 , 2 in algorithm ).
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
