Before operation or stenting, the existence of the carotid lesion and its extent must be determined. CTA and MRA have emerged as a surrogate procedures to the previously used catheter based imaging (Fig. 33-19). Severe stenosis is also indirectly reflected in filling of the distal branches of the external carotid artery before the branches of the middle cerebral artery are opacified—a reversal of the usual pattern. Increasingly, the diagnosis of carotid stenosis is being initially made by less invasive methods, but with ultrasonography there is some difficulty in quantifying severe stenosis and in separating it from complete carotid artery occlusion.
Endarterectomy, in a small number of cases may be followed by a new hemiplegia or aphasia that becomes evident in the hours after the procedure, usually by the time the patient arrives in the recovery room. In these cases, surgeons prefer to return the patient to the operating room and open the artery, as discussed earlier on. An intimal flap at the distal end of the endarterectomy and varying amounts of fresh clot proximal to it are usually encountered; but after removal and repair of the vessel, the effects of the stroke, if one has occurred, are not usually improved. The postoperative care of carotid endarterectomy focuses on reversing reflex hypotension that is induced by exposing the carotid wall to high perfusion pressure. This phenomenon can be reduced by infiltrating the carotid sinus with anesthetic prior to the operation. An uncommon but rather striking hyperperfusion syndrome develops several days to a week after carotid endarterectomy. The features are headache, focal deficits, seizures, brain edema, or cerebral hemorrhage. These are thought to reflect autoregulatory failure of the cerebral vasculature in the face of abrupt restoration of normal blood pressure and perfusion. After a long period of autoregulatory compensation for a stenotic carotid artery, then a normal cerebral perfusion pressure may result in endothelial incompetence with leakage of water across the blood–brain barrier. Unilateral severe headache is the most common symptom and may be the only manifestation. On occasion, cerebral edema is so massive as to lead to death (Breen et al). Treatment is by control of hypertension; it is unclear whether antiepileptic medications are required if there has been a seizure as a component of the syndrome. We mention here that an identical syndrome of focal cerebral deficits and brain edema, perhaps with the exception of seizures, has been seen, rarely and with no explanation spontaneously, in migraineurs (not those who have had endarterectomy), including two patients under our care.
For intracranial internal carotid occlusion that extends into the siphon and distally, a transcranial (superficial temporal–middle cerebral) and has caused a stroke, anastomosis had been employed in the past. Although this operation is technically feasible, its therapeutic value has been questioned by the multicenter study of The EC/IC Bypass Study Group (1985), who found that it did not produce a reduction in TIAs, strokes, or deaths. That study was criticized for having a skewed patient selection and several smaller and uncontrolled trials have suggested that the procedure may benefit some patients. A later trial (SAMMPRIS reported by Chimowitz and colleagues, 2011) indicated worse outcomes with intracranial stenting compared to medical management. There may, nevertheless, be particular circumstances that justify its use; for example, when there are ongoing TIAs in relation to upright posture or with episodes of mild hypotension.
Bypass procedures and their derivatives such as temporal-pial synangiosis may be useful in reestablishing flow to a hemisphere when there has been progressive intracranial carotid stenosis. Testament to the success of the bypass procedure is the regression of symptoms and of the network of collateral vessels in moyamoya disease (see further on).