Intraoperative Recognition and Treatment of Cerebral Ischemia During Carotid Endarterectomy

John Blebea

Neurologic complications during the performance of carotid endarterectomy (CEA) are most commonly caused by embolization from the area of the carotid bifurcation or a result of hypoperfusion from inadequate collateral blood flow during carotid clamping. The recognition of intraoperative cerebral ischemia during surgery depends on the type of anesthetic protocol used: regional anesthesia with the patient awake or general anesthesia with or without cerebral perfusion monitoring. These are important variables both in terms of when cerebral ischemia is diagnosed and in evaluating its severity, clinical importance, and subsequently the most appropriate treatment options.

Regional Anesthesia

Optimal regional anesthesia makes the patient insensate to the pain and discomfort of the surgical dissection, comfortable through the use of intravenous anxiolytics, but awake enough so that neurologic function can be effectively monitored. This means that the patient is sufficiently responsive to verbal stimuli to be able to demonstrate upper and lower extremity motor function through toe and foot flexion as well as squeezing an audible toy or manometric device held in the contralateral hand. These simple techniques are sufficient to demonstrate cognition and major motor function. More qualitative in nature, but also important, is being able to evaluate higher cerebral function, which can reflect the adequacy of perfusion as opposed to a focal embolic event. This can be assessed by avoiding oversedation so that the surgeon can carry on a conversation with the patient. Having become acquainted with the patient before surgery, the surgeon is in the best position to evaluate any confusion or significant changes in the patient’s level of consciousness. This is particularly important in the elderly, whose baseline function might already be impaired, or in those who have previously suffered a stroke.

It is evident that an anesthesiologist experienced in this technique is a critical member of the operative team. However, not all patients are appropriate candidates for regional anesthesia. This includes those who have difficulties communicating as a result of language barriers or prior stroke, are claustrophobic, are noncooperative, or are overly anxious. On the other hand, regional anesthesia has advantages for those with cardiopulmonary disease when general anesthesia and intubation may be associated with higher morbidity and mortality.

The greatest advantage of regional anesthesia during CEA is the immediate diagnosis of cerebral ischemia and an appreciation of its clinical significance. Unlike the indirect methods necessarily used during procedures under general anesthesia, regional anesthesia allows an immediate diagnosis, recognition of the most likely etiology, and initiation of treatment. After heparinization, the internal carotid artery (ICA) is test clamped, and the external (ECA) or common (CCA) carotid arteries are also clamped to prevent collateral flow that would not exist during CEA, and the patient is neurologically monitored. If any changes are noted, intraluminal shunting is instituted.

From the context of the neurologic event during the procedure (clamping/unclamping) and the type of neurologic deficit (focal motor dysfunction), one can reasonably conclude whether an embolic event has taken place. On the other hand, if the patient develops aphasia, confusion, or loss of consciousness within a minute or two following test clamping, or in the later setting of relative systemic hypotension, then a low-perfusion state is the most likely cause and should be treated with shunting or alleviation of the hypotension.

With awake CEA, a neurologic event noted during an intervention is most commonly addressed with further diagnostic modalities. In more unusual circumstances, such as when presumed hypoperfusion is not relieved through the placement of a shunt, or when a change in neurologic status occurs near the end of the procedure after vessel closure and reperfusion has taken place for more than 5 minutes, additional diagnostic studies need to be performed to investigate the cause of such changes. This most often employs the use of a hand-held Doppler probe, duplex ultrasound, or intraoperative angiography.

General Anesthesia

With general anesthesia, only indirect methods for the intraoperative diagnosis of cerebral ischemia are available. Interventions are based on generally accepted guidelines, although there are few absolute thresholds to predict the probability and severity of neurologic dysfunction if nothing is done. These monitoring methods can be broadly characterized into those used to diagnose hypoperfusion, embolization, and overall clinical neurologic status. They include stump pressure measurements, electroencephalography, evoked potentials, and cerebral oximetry. These topics are described elsewhere in this text.Although not specifically meant to evaluate cerebral ischemia, completion studies after closure of CEA can reveal flow has stopped owing to in situ thrombosis or can reveal low flow secondary to a dissection or high-grade stenosis, a nonocclusive thrombus that could embolize, a large frond, or other technical defects that can be a source for later embolization. Although not all vascular surgeons perform completion studies, these studies are recommended to ensure optimal technical success in this highly scrutinized procedure. The simplest completion study is a hand-held continuous Doppler probe. This will detect the rare in situ thrombosis at the CEA site and, in experienced hands, provide a qualitative appreciation of increased velocities indicating a high-grade stenosis.

In circumstances where distal embolization is suspected, digital subtraction angiography should be performed. If the CEA is not yet completed, or the endarterectomy site has been reopened, a short 6-Fr vascular sheath over a flexible-tip J wire is introduced into the internal carotid artery. This allows both diagnostic angiography and any potential endovascular interventions. If the surgical site has been closed and the surgeon has excluded any thrombus or technical issues at the endarterectomy site with duplex ultrasound, the vascular sheath can be introduced in the more proximal undiseased common carotid artery.

The final method of evaluation of cerebral ischemia is the clinical evaluation when the patient awakens from general anesthesia in the operating room. Abnormal responsiveness or speech and motor dysfunction are usually obvious. However, depending only on clinical evaluation is suboptimal. The examination may be hampered by the variable amount of remnant sedation and an acceptance of less optimal patient responses in order to move the patient out of the operating room. It is also impossible at that time to differentiate between neurologic deficits induced by embolization or hypoperfusion. Finally, intervention now almost always requires that the patient be reintubated and the surgical site reopened. This is attended with increased morbidity.

When a neurologic deficit is first detected upon awakening, the patency of the endarterectomy site and internal carotid artery must first be ascertained. This can be done immediately with duplex ultrasound. Identification of any technical defects or the presence of clot mandate exploration of the surgical site. If visualization is impaired owing to the presence of air among the tissues, the presence of an overlying drain, or a prosthetic patch, angiography can be performed in the operating room. In many cases, surgical reexploration may be faster and more expeditious. If nonsurgical methods clearly demonstrate no abnormalities, the event is likely embolic, and reoperation would not be of clinical benefit.

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