Chapter 23: Carotid Revascularization and EC-IC Bypass

The patient's imaging and physical examination findings are highly suggestive of an ischemic stroke in the right frontal cortex secondary to thromboembolism from a right carotid stenotic atherosclerotic lesion (while this patient's MRA is highly suspicious for carotid stenosis as the cause of the ischemic stroke, an electrocardiogram [ECG] and transesophageal echocardiogram should be ordered to rule out cardiac causes as well). Since this patient is well outside the time window for intravenous thrombolysis, she should be started on acetylsalicylic acid (ASA) 325 mg tid for secondary prevention of stroke and should receive further diagnostics for her suspected carotid artery disease.

Extracranial, large-vessel stenosis should be evaluated by at least two of the following three noninvasive modalities to determine the extent and degree of stenosis: MRA, computed tomographic angiography (CTA), and carotid Doppler ultrasound. Carotid Doppler ultrasound is a quick, inexpensive, and portable modality that is easily performed at the bedside and assesses stenosis via focal measurements of flow velocity; however, the quality of the study is highly dependent on the physician/technician. MRA, which can be performed with or without contrast, does not expose patients to radiation and has demonstrated greater discriminatory power than ultrasound in assessing high-grade stenosis.¹ CTA, while an excellent modality for identifying carotid occlusion, has less discriminatory power in identifying high-grade stenosis.² If stenting is considered as a possible treatment modality, the patient can be evaluated with angiography, the gold standard for evaluating carotid disease, for possible intervention. However, it is a costly and an invasive procedure and is associated with risk of contrast nephropathy, especially in patients with underlying renal disease. This patient underwent carotid ultrasound, which demonstrated 80% to 90% stenosis of the right internal carotid artery (ICA) bifurcation, with confirmatory CTA showing severe atherosclerotic disease of the right carotid artery at the level of the bifurcation and a patent right ICA with 70% stenosis (Figure 23-2). Given this patient has symptomatic, high-grade stenosis 70% or greater present on at least two imaging modalities, neurosurgical intervention is indicated.³

Carotid atherosclerotic disease can be treated surgically with carotid endarterectomy (CEA) or with carotid angioplasty and stenting (CAS). The evidence from randomized clinical trials comparing CEA with best medical management in both symptomatic and asymptomatic patients is substantial. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) for surgical intervention found that CEA significantly reduced the risk of further stroke (17% at 2 years) and death (7% at 2 years) for patients with stenosis at or greater than 70%.³ The Asymptomatic Carotid Artery Stenosis Trial (ACAS) found that patients with greater than 60% stenosis had a 6% reduction in risk of stroke or death at 5 years.⁴ Since the results of these major trials, carotid stenting has surfaced as an alternative to surgery, especially in those patients who are poor surgical candidates.

The recent results from the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST)⁵ compared endovascular and surgical techniques in both symptomatic and asymptomatic patients and found comparable rates of the primary outcome measure of death, stroke, or myocardial infarction in the perioperative period and any ipsilateral stroke at 4 years, although perioperative stroke and myocardial infarction occurred more frequently in the stenting and CEA groups, respectively. However, the results of this trial should be interpreted with caution. The perioperative stroke but not myocardial infarction was associated with worse health status at 1 year in quality of life assessment, suggesting that the primary end point may have not been appropriately weighted to account for the greater morbidity rate associated with perioperative stroke and may have biased results in favor of stenting. Moreover, while rigorous credentialing of endovascular surgeons in this study is certainly a major strength of the design, such high standards may be possible only at highly specialized institutions. Hence, while carotid stenting is a suitable alternative in patients who are poor operative candidates, CEA remains the gold standard treatment for high-grade stenosis.

This patient has a number of cardiovascular risk factors and a possible history of angina, potentially placing her at high risk for surgery. However, carotid stenting may be difficult to accomplish safely and effectively in this patient for the following reasons. First, CTA demonstrates a significant amount of calcification at the bifurcation, which makes both the degree of stenosis and the anatomic margins difficult to evaluate. Second, the lesion of the location involves the bifurcation, which will complicate balloon positioning and inflation as well as stent deployment. Third, the proximal ICA has a tortuous appearance, which combined with the significant calcification creates a technically challenging situation for the endovascular surgeon and increases the risk of arterial trauma/dissection and thromboembolism. Hence, CEA is the best intervention for this patient, pending, of course, medical clearance by a cardiologist. She should also be continued on ASA up until surgery.⁶

Management during the postoperative period after endarterectomy should focus on blood pressure control and early detection and management of complications of endarterectomy. Table 23-1 lists rates of complications after CEA. In the postoperative period after endarterectomy, blood pressure may be especially labile during the first 24 hours owing to changes in flow and pressure at the carotid sinus. Such variation in blood pressure can result in undesirable stress on the myocardium, especially in patients with multiple cardiovascular risk factors and underlying coronary artery disease, hence the importance of an appropriate preoperative workup. Even in the absence of blood pressure instability, it is our routine to monitor patients with serial troponin assessments for the first 24 hours together with continuous ECG and an arterial line. In the absence of other concerns, we aim to keep the blood pressure about 10 points below the baseline mean arterial pressure (MAP) as long as the ECG and troponin levels are normal. The other reason to maintain blood pressure in this range is to guard against hyperperfusion syndrome. This generally occurs in patients with impaired autoregulation and very tight stenosis with poor collaterals. It may present with headache, mental status change, seizures, or, in the worst case, hemorrhage. Patients at high risk for hyperperfusion syndrome or with early signs can be evaluated with transcranial doppler (TCD), MR perfusion, or CT perfusion to aid in diagnosis and management. Avoiding postoperative hypertension may also prevent untoward disruption of the arteriotomy site, especially in the case of patched repairs, and may play a role in preventing expanding neck hematoma, which rarely requires reoperation. In those patients without contraindications (eg, asthma, chronic obstructive pulmonary disease [COPD]), intravenous β blockers are an excellent first-line approach, but calcium channel blockers may also be used. In contrast, relative hypotension is to be particularly avoided in patients with preexisting microangiopathy such as those with severe long-standing hypertension and/or diabetes mellitus. In terms of agents of choice, phenylephrine may be used as a first-line therapy for relative hypotension and nitroprusside or dopamine added as needed.

In addition to careful management of blood pressure, repeated focused neurologic examinations should be frequent following endarterectomy for early detection of cerebral ischemia/stroke in addition to other surgery-related complications. In particular, expected deficits in the distribution of the ICA operated on are of importance (loss of vision in ipsilateral eye, contralateral motor/sensory disturbances, speech disturbances if operated artery supplies dominant hemisphere). Signs of injury to cranial nerves encountered during surgery should also be monitored: deviation of tongue to ipsilateral side for hypoglossal nerve injury; hoarseness for recurrent laryngeal nerve; lip asymmetry from mandibular nerve injury. The operative site should be examined frequently for neck hematoma. Antiplatelet agents, usually aspirin 325 mg, should be resumed immediately the morning following surgery.¹⁴ Dipyridamole can also be given instead of aspirin, although the combination of medications has not proved beneficial in reducing the rate of restenosis after endarterectomy.¹⁵

This patient underwent an uneventful CEA on the right side without any obvious intraoperative EEG changes and confirmed patency of arteriotomy site by Doppler ultrasound just prior to skin closure. Upon emergence from anesthesia, however, the patient developed a new neurologic deficit consistent with the distribution of the right ICA. The differential diagnosis for this patient's new left hemiplegia includes thromboembolism from the endarterectomized surface to a distal vessel, ischemia from prolonged cross-clamping, or in situ thrombosis at the surgical site; rarely, hyperperfusion may be a cause of neurologic symptoms in the immediate postoperative period. In this patient, given the absence of concerning EEG changes throughout the operation, ischemia secondary to hypoperfusion from cross-clamping is unlikely. Postoperative thrombosis of the endarterectomy site is the most common cause of major postoperative transient ischemic attack (TIA)/stroke¹⁴ and should be emergently investigated using intraoperative angiography if readily available, although if suspicion is high for occlusion, reexploration should not be delayed. In addition, the patient should be given pressors (phenylephrine) to elevate blood pressure (preferably SBP in approximately 180-200 mm Hg range) as well as ample fluids to assist in the latter and to reduce blood viscosity. Heparinization and potentially long-term anticoagulation may be considered to prevent further thrombosis, although further studies are needed to evaluate the role of anticoagulation after postoperative thrombosis.

This patient is on a heparin drip following perioperative occlusion of the endarterectomy site and had multiple episodes of sustained hypertension during the early postoperative period, increasing risk for bleeding from both the arteriotomy site and the associated soft tissues of the neck. The new-onset stridor and pulsatile neck mass are concerning for ruptured arteriotomy closure. The stridorous breathing suggests compression of the trachea, and the first priority should be establishing a safe airway. Awake, fiberoptic intubation should be attempted by anesthesia. If this cannot be accomplished, the wound may have to be opened and the clot evacuated. This should be done in the OR if time permits. Once the clot is cleared and the bleeding has been controlled, the patient should be intubated and prepped for formal exploration of the wound. Emergent tracheostomy should be a last resort in a patient on heparin with a deviated trachea as this could lead to complete loss of the airway, especially in inexperienced hands.

This patient is most likely suffering from cerebral hyperperfusion syndrome (CHS) after CEA. Clinical CHS, which characteristically occurs several days after endarterectomy, results from an increase in cerebral blood flow from baseline in an area of the brain that has lost its autoregulatory capacity after chronic hypoperfusion from high-grade carotid stenosis.¹⁶ This uncontrolled increase in cerebral blood flow leads to transudation of fluid into the brain parenchyma and cerebral edema formation. Reported rates after CEA range from 0.2% to 18.9%, depending on the clinical severity, and patients will typically present with headache, orbital pain, change in level of consciousness, and focal neurologic deficits. Rarely, CHS may lead to intracerebral hemorrhage (ICH). Hemorrhage is thought to be due to the existence of areas of ischemia secondary to perioperative emboli that in turn undergo hemorrhagic transformation when confronted with increases in cerebral blood flow. Patients typically present several days to weeks after surgery (peak incidence at postoperative day 6) with headache, focal neurologic signs, altered sensorium, and/or seizure. Patients with CHS complicated by ICH may additionally present with nausea and vomiting from rapid increase in intracranial pressure (ICP). Patients at greatest risk are those with advanced age, diabetes, high-grade stenosis, cerebrovascular atherosclerotic disease elsewhere, evidence of perioperative or intraoperative cerebral ischemia, sustained increases in cerebral blood flow as detected by TCD, uncontrolled hypertension in the postoperative period, and a preoperative decrease in cerebrovascular reactivity as detected by acetazolamide challenge.¹⁶

Patients experiencing headache without focal neurologic signs within the first week or 2 following surgery should undergo TCD; if a greater than 100% increase in perfusion is detected, patients should have aggressive blood pressure management, discontinuation of anticoagulants if they are on them (for atrial fibrillation), and possible administration of mannitol to reduce ICP and cerebral edema and antiepileptics for seizure prophylaxis.¹⁷ Patients with severe headache or those patients who have focal neurologic signs should undergo emergent CT scan to rule out ICH, which may require surgical evacuation in a minority of cases. Negative CT scan warrants MRI/MR perfusion for evaluation of infarct, as new neurologic deficits may reflect cerebral infarcts from embolic clots; new infarcts should be further investigated using carotid Doppler ultrasound to evaluate for thrombosis at the endarterectomy site and TCD for HITs (high-intensity transients). In addition to the above steps, this patient should be monitored in an ICU with an arterial line and should have strict blood pressure management, as this is the key to preventing the potentially devastating consequences of CHS.

The patient most likely has developed an ICH secondary to CHS. However, before any intervention, the patient should be assessed for ABCs (airway, breathing, circulation)! Ensure the airway is secure—This patient requires intubation as she is comatose and she cannot protect her airway. Once the patient's ABCs are secured, emergency CT scan is warranted to investigate the possibility of hemorrhage. While en route, if possible, intra-arterial and intravenous access should be promptly obtained, coagulation studies should be drawn, mannitol/hypertonic saline should be administered preemptively given the signs of increased ICP, and prophylactic antiepileptics should be administered.

In addition to the above measures, the patient has a coagulopathy that should be promptly corrected. Patients with therapeutic INRs (2 to 3 in most cases) should be treated with 2 to 3 units of fresh-frozen plasma, although this patient's supratherapeutic levels warrant 6 units.¹⁴ Prothrombin complex concentrates may also be used for reversal of warfarin-induced anticoagulation. The patient may also benefit from external ventricular drainage to relieve increased ICP from hematoma compression and ventricular hemorrhage. Surgical hematoma evacuation may be useful in patients who have lobar or cerebellar hemorrhages, but such efforts in basal ganglia hemorrhage have been proved futile.¹⁸ In cases that ventriculostomy is not effective in reducing regional ICP, hemicraniectomy can be considered without clot evacuation, but the data on its effectiveness are only anecdotal. Blood pressure (BP) should be monitored through a dedicated arterial line; while the most appropriate target for blood pressure after ICH is controversial, a target of 140/90 mm Hg is reasonable, although hypotension should be avoided to maintain adequate cerebral perfusion. Slightly higher BP may be allowed for chronic hypertensives. Normoglycemia¹⁹ and normothermia²⁰ are also appropriate goals in this patient. See Chapter 2 for further details regarding management of ICH.

Tight blood pressure control is crucial in this patient, preferably with systolic BP in the range of 130 to 160 mm Hg in the early postoperative period. Hypertension may cause bleeding both from the anastomotic site, the open dural edges, or hemorrhage in reperfused areas, while hypotension may result in cerebral hypoperfusion and/or graft occlusion. The patient's BP should be monitored in the NICU with an arterial line, and short-acting pressors or vasodilators should be given as needed for BP control. Adequate intravenous fluids will also protect against hypotension. Frequent neurologic checks are necessary to monitor for new ischemic events, either from embolism or graft occlusion. Perioperative seizures can occur in this population as well, and perioperative antiepileptic drugs (AEDs) are generally felt to be of value. Frequent TCDs may be used to monitor graft patency, although some centers advocate MRA or CTA on the first postoperative day to evaluate the graft. Any new neurologic signs should be promptly investigated with CTA/CT or MRI/angiography, with the latter being more sensitive. Patients are generally operated on aspirin 81 mg daily without perioperative discontinuation. Perioperative dexamethasone is generally not indicated.

The new onset of neurologic symptoms referable to the left hemisphere in this patient may represent ischemia secondary to either (1) occlusion of the graft, (2) thromboembolism from the right carotid artery, (3) hyperperfusion, or (4) subdural hematoma.

Graft patency may become compromised secondary to hypotensive episodes, inadequate IV hydration, surgical technique, quality of donor and recipient vessels, or excessively tight head dressing impairing flow through the donor vessel. TCDs may be used to quickly assess graft patency. If patency of the graft is in question, intravenous dextran may be administered to inhibit platelet function,²¹ or a return to the operating room for graft revision may be necessary. CT should be ordered to rule out ICH due to hyperperfusion or epidural/subdural hematoma from graft/dural leakage. In these cases, surgical decompression and/or hematoma evacuation may be warranted and underscores the importance of prompt investigation of neurologic deterioration. It should be noted, however, that epidural hematoma formation secondary to oozing can be prevented intraoperatively using 50% protamine for heparin reversal or completely avoiding the use of heparin.²² Arterial blowout at the anastomosis site may also occur leading to epidural or subdural hematoma, although this is quite rare with superficial temporal artery/middle cerebral artery (STA-MCA) bypass as this is a low-flow conduit.²² Any patient with a hemorrhagic complication should have coagulation labs drawn and reversal of any underlying coagulopathy. MRI will be useful in identifying the presence of new infarcts, although intravenous tissue plasminogen activator (tPA) in these patients would be contraindicated given the close proximity of surgery. Additionally, seizure may be the cause of neurologic deficits in patients who are not placed on antiepileptic treatments.