Occlusion of the Internal Carotid Artery

Clinical Presentation:

The daughter, a healthcare worker, witnessed her elderly mother become paralyzed on the right side and unable to speak. It was clear she was having a stroke with right hemiplegia, aphasia, and altered mental status. She called 911. EMS responded immediately bringing her to the hospital for the treatment of a possible acute stroke.

Neurological examination at the hospital found an NIHSS of 23. Head CT/CTA showed complete occlusion of the left internal carotid artery (ICA) Approximately 160ml of hypo-perfused brain tissue, with approximately half being “core” and presumably not salvageable, and half being “penumbra”, presumably salvageable were identified on CT brain perfusion parametric maps of rCBF (relative cerebral blood flow) and TTP (time to peak) (Figures 1,2,3). CTA collaterals were absent in the left hemisphere, portending a grave prognosis and high probability of advanced irreversibly infarcted brain tissue.

Two weeks prior, she had experienced a right occipital stroke that had resolved to a small residual visual field cut. Placed on anticoagulation initially, she developed a hemorrhagic conversion. Her anticoagulation was stopped, and she was placed on ASA alone for stroke prevention. (Figure 1).

Figure 1. Non-contrast head CT scan. Left dense MCA-sign is seen (arrow). Subacute hemorrhagic conversion of a right occipital stroke from two weeks prior is shown as a high-density area with mass effect effacing the right occipital horn (*).

Figure 2. CTA of head and neck. AP coronal view shows the left internal carotid artery occluded in the neck (yellow circle), filled with moderately high attenuation clot. Intra-cranially, no vessels of the left MCA territory are seen (dotted circle; left). Axial head CTA through the suprasellar carotid and MCA region shows occlusion of the left MCA. No MCA vessels are seen in the Left hemisphere (dotted circle; right).

Figure 3. Head CT perfusion. A large area of 88ml with reduced CBF <30% is seen, identified as core (red, top). This is presumed to be tissue that is destined to die inspite of successful revascularization. A large area of 70ml of mismatch (= TMax – rCBF), identified as penumbra, that is expected to salvaged by revascularization.

Clinical Management and Treatment:

There was a frank and difficult conversation regarding the poor expected clinical outcome, even with successful revascularization due to the advanced presentation in this patient. However, the family, with significant healthcare experience, wished clot extraction to be attempted, recognizing the poor prognosis despite the intervention.

The endovascular procedure was performed under general anesthesia, necessitated due to developing airway protection concerns and diminished level of consciousness. Initial angiogram confirmed total occlusion of the left ICA from the common carotid artery to beyond the ophthalmic artery into the left ICA intracranial bifurcation and the proximal segments of both the anterior cerebral artery (ACA-A1) and middle cerebral artery (MCA-M1) (Figure 4). After successful endovascular extraction of the extensive thrombus, the ICA, ACA, and MCA were completely revascularized with restoration of brain perfusion to the left cerebral hemisphere (Figure 5).

Figure 4. Lateral (left) and AP (right) left common carotid artery angiogram, pre-treatment. The only filling vessels are the branches of the external carotid artery and the stump of the left internal carotid artery.

Figure 5. Lateral (left) and AP (right) left carotid artery angiogram post-treatment. Filling of all vessels of the anterior circulation, including the internal carotid and middle and anterior cerebral arteries.

Figure 6. Head CT immediately post-recanalization procedure shows enhancement and early edema of the left MCA ischemic territory, and of the previous right occipital stroke (left). Head CT 48 hours post-ictus shows edema with marked mass effect and pending trans-falcine and tentorial herniation (right).

Despite successful revascularization, over the next few days, she continued to deteriorate functionally, developing rapid progression of her infarct and marked cerebral edema (Figure 6). The family made the difficult decision to place her “on comfort care”.  She soon passed from her ischemic injuries.

Discussion:

Carotid artery occlusions from clot traveling from the heart have an extremely poor prognosis. The clot usually occludes from the common carotid artery in the neck to the internal carotid artery (ICA) bifurcation in the head (Figure 7). Additionally, a blizzard of clot, often has traveled to other critical vascular territories including the coronaries, kidneys, liver, and bowel. This large multi-system clot burden is universally lethal.

Figure 7. Thrombus/clot from a cardiac source. Mechanism of a cardiac embolus.

Extraction of large volumes of clot within the ICA can be performed with good angiographic results. However, the risk of dislodging emboli into previously not involved cerebral territories is significant. Extensive thrombosis of the ICA may also extend into its ACA and MCA branches occluding the collateral perfusion pathways, and often resulting in rapid progression of ischemia to infarct, often well visualized on CT Perfusion (large matched deficits) and CTA (absence of hemispheric collaterals). Despite excellent angiographic results, the likelihood of a good functional outcome is dismal.

Although clot traveling from the heart accounts for most intra-cranial large vessel occlusions (MCA, basilar artery), thankfully, such massive clots are uncommon causes of carotid artery occlusions. Most ICA occlusions are from the progression of atherosclerosis, torn vessels, or dissections.

Carotid occlusions from atherosclerosis occur because of progressive narrowing or intramural plaque hemorrhage and expansion. Fortunately, statins have demonstrated the ability to stabilize plaques which are associated with a decrease in the frequency of such events. Often, carotid occlusions present as pressure-dependent watershed ischemia, and can otherwise be asymptomatic when chronic and hemodynamic compensation is sufficient (preservation of collaterals from the Circle of Willis, i.e. anterior or posterior communicating arteries). Revascularization is seldom considered in well compensated patients, unless they present with clinical instability or demonstrate high risk perfusion profiles for clinical progression (diminished CBF secondary to limited collaterals).

Torn or dissected ICA occlusions usually present with neck pain and is believed to cause hemodynamic and/or embolic stroke. With impending or complete occlusion, anticoagulation or antiplatelet has been very effective in preventing recurrent embolic events, allowing these dissections to naturally heal over time. Acute revascularization is considered, if there is an associated distal intracranial clot, or hemodynamic acute ischemic compromise with clinical progression. Recanalization is often successful, but not without technical challenges, often including rapid anti-platelet loading, aggressive GP2b/3a inhibition, and emergent stenting of high-grade dissections.

Fibro-Muscular Dysplasia (FMD) is a relatively common cause of bilateral ICA narrowing, but an uncommon cause for complete occlusion. It rarely requires revascularization treatment, but when required, it can be treated effectively with relatively low risk, with either medical therapy or percutaneous angioplasty in rare cases.

Conclusions:

In summary, large vessel occlusions (LVO’s) present in many different locations, from a variety of different pathologies (atherosclerotic disease, dissections, cardioembolic). The prognosis and functional responsiveness to successful revascularization therapy, especially in the carotid artery, varies widely depending on the extent of the occlusion, the volume of clot burden, and the perfusion and physiologic/metabolic profile of the affected brain tissue. Despite revolutionary advances in acute stroke neurointerventional therapy, novel strategies to slow down ischemic progression and resuscitate brain tissue are still needed to save patients from death or disability.

References

• Internal Carotid Artery Occlusion: clinical and therapeutic implications. V U Fritz, C L Voll, L J Levien. Nov1985 Stroke. 1985;16:940–944
• Management and Prognosis of Acute Extra-Cranial Internal Carotid Occlusion. Lukas Mayer, Astrid Grams, Christian F Freyschlag, Maria Gummerer, Michael Knoflac. Ann Transl Med. 2020 Oct;8(19):1268.