Postoperative Considerations

Most transient and permanent neurologic complications after carotid endarterectomy are explained by intraoperative embolization, hypoperfusion during carotid clamping, and embolization or thrombosis from the endarterectomy site. Other important, but less common, factors include intracerebral hemorrhage and cerebral hyperperfusion. It is generally accepted that most neurologic complications are related to surgical technique. Thromboembolic rather than hemodynamic factors appear to be the major mechanism of perioperative neurologic complications,^{[563] [643] [657]} and most perioperative neurologic deficits occur in the postoperative period.^{[563] [643] [668] [669] [670]} Hemodynamic factors may account for up to 21% of perioperative strokes.^[657]

2105

Hypertension is common in the postoperative period after carotid endarterectomy.^{[583] [676] [677]} Not surprisingly, patients with poorly controlled preoperative hypertension often have severe hypertension postoperatively. The causes are not well understood, but surgical denervation of the carotid sinus baroreceptors is likely contributory.^{[678] [679]} Regional anesthesia is associated with less hypertension.^[680] Other causes of postoperative hypertension, such as hypoxemia, hypercarbia, bladder distention, and pain, should be excluded or treated. Because neurologic and cardiac complications may be associated with postoperative hypertension,^{[583] [676] [681] [682] [683] [684]} blood pressure should be aggressively controlled near preoperative values after surgery. Short-acting drugs are safest and most effective. Patients with persistent hypertension are ultimately converted to longer-acting intravenous or oral agents before discharge from the intensive care unit.

Postoperative cerebral hyperperfusion syndrome is an abrupt increase in blood flow with loss of autoregulation in the surgically reperfused brain manifesting as headache, seizure, focal neurologic signs, brain edema, and possibly intracerebral hemorrhage.^[682] Unfortunately, little is actually known about the cause and management of this syndrome. Typically, this syndrome does not occur until several days after carotid endarterectomy.^[685] Patients with severe postoperative hypertension and severe preoperative internal carotid artery stenosis are believed to be at increased risk for developing this syndrome.^{[682] [683] [686]} However, more recent data do not corroborate this common belief and suggest that recent contralateral carotid endarterectomy may be predictive of cerebral hyperperfusion.^[685]

Postoperative hypotension occurs almost as frequently as hypertension after carotid endarterectomy.^{[687] [688]} Carotid sinus baroreceptor hypersensitivity or reactivation likely plays an important role. Postoperative hypotension may be more common after regional anesthesia.^{[627] [681] [687] [688] [689]} To avoid cerebral and myocardial ischemia, hypotension should be corrected promptly. Cardiac output is frequently normal or elevated and systemic vascular resistance reduced in hypotensive patients after carotid endarterectomy.^[687] Intensive surveillance for evidence of myocardial and cerebral ischemia and judicious use of fluids and vasopressors are recommended for postoperative hypotension. In most cases, hypotension resolves over a period of 12 to 24 hours.

Cranial and cervical nerve dysfunction after carotid endarterectomy is well documented in the literature.^{[690] [691] [692] [693] [694] [695] [696]} Although most injuries are transient, permanent injuries can lead to significant disability. ^[690] Patients should be examined for injury to the recurrent laryngeal, superior laryngeal, hypoglossal, and marginal mandibular nerves shortly after extubation. Unilateral recurrent laryngeal nerve injury may result in ipsilateral true vocal cord paralysis in the paramedian position. Although most patients have hoarseness and an impaired cough mechanism, the injury is usually well tolerated. However, bilateral recurrent laryngeal nerve injury and resultant bilateral vocal cord paralysis can result in life-threatening upper airway obstruction. This situation must be anticipated in patients who have undergone previous contralateral carotid endarterectomy or neck surgery.

Carotid body denervation may occur after carotid endarterectomy as a result of surgical manipulation. Although rarely of clinical significance, unilateral loss of carotid body function may result in impaired ventilatory response to mild hypoxema.^[697] Bilateral carotid endarterectomy is associated with loss of normal ventilatory and arterial pressure responses to acute hypoxia and increased resting partial pressure of arterial carbon dioxide. ^[698] In this situation, the central chemoreceptors are the primary sensors to maintain ventilation, and serious respiratory depression may result from opioid administration.^[699] Fortunately, most patients require little more than acetaminophen or ketorolac for postoperative pain.

Wound hematoma probably occurs more frequently than is reported in the literature. In the North American Symptomatic Carotic Endarterectomy Trial, ^[540] 5.5% of patients had wound hematomas. Most cases are the result of venous oozing and require little more than external compression for 5 to 10 minutes. Expanding hematomas require prompt evaluation at the bedside and immediate evacuation if airway compromise is evident. Aggressive postoperative blood pressure control may help to reduce the incidence of hematoma.

I believe that all patients should be monitored in an intensive care setting for at least 8 to 12 hours after carotid endarterectomy because most events requiring intervention occur within this time frame.^{[700] [701] [702] [703]} Although some clinicians believe that intensive care monitoring is not routinely required, a significant number of patients do require intensive monitoring and active intervention.^{[700] [704]}