Abstract
Carotid endarterectomy is an operation to prevent stroke in patients with symptomatic carotid stenosis. Hemodynamic control in these patients may be difficult to achieve and contribute to postoperative morbidity and mortality. Here we present a case in which over-aggressive blood pressure control in a patient experiencing significant intraoperative hypertension leads to subsequent hypotensive cerebral infarction. Intraoperative and postoperative blood pressure control is discussed, along with a suggested protocol for the management of blood pressure in the patient undergoing carotid surgery.
Keywords
arterial pressure, cardiovascular system responses, carotid endarterectomy, complications, hypertension, stroke prevention, surgery
Case Synopsis
An 82-year-old woman with a significant past medical history of hypertension and coronary artery disease undergoes carotid endarterectomy (CEA) under regional anesthesia. She experienced an episode of dysphasia and transient weakness affecting her left side 3 days previously. Investigations revealed an 80% stenosis of the right internal carotid artery. Her blood pressure is 180/95 mm Hg before surgery. Surgery proceeds uneventfully, although she remains hypertensive throughout. In the postanesthesia care unit postoperatively, the patient’s blood pressure is 200/100 mm Hg, and she becomes agitated and develops a frontal headache. Intravenous labetalol, 50 mg in divided doses, and intravenous hydralazine, 20 mg, are administered, causing her blood pressure to drop precipitously. Her conscious level deteriorates and she develops dysphasia and lateralizing signs suggestive of ischemic stroke. She undergoes computed tomography of the head, which reveals appearances consistent with cerebral infarction. Unfortunately her condition deteriorates and she dies the following day.
Problem Analysis
Definition
The aim of CEA is to decrease the subsequent risk of stroke in patients with significant carotid stenosis, but the benefits are only realized if perioperative morbidity and mortality are low. Patients undergoing CEA are at increased risk of complications because of cardiovascular comorbidities ( Box 41.1 ). Arterial pressure may be difficult to control, yet perioperative hemodynamic instability can directly or indirectly influence morbidity and mortality.
Hemodynamic instability
Hypertension
Hypotension
Myocardial infarction
Wound hematoma
Glossopharyngeal edema with airway compromise
Cranial nerve damage
Neurologic dysfunction
Acute graft thrombosis (may require reexploration)
Minor focal deficits
Watershed ischemia
Hyperperfusion syndrome leading to subarachnoid hemorrhage
CEA is unique in that one of the principal components of the physiologic control mechanisms of arterial pressure—the baroreceptors in the carotid sinus—are involved in the disease process itself, and may be affected by the surgical procedure, concurrent drug therapy, and the effects of anesthesia. Patients who have suffered recent transient ischemic attack (TIA) or stroke have altered baroreceptor sensitivity and are at increased risk of hemodynamic instability. Many patients presenting for CEA have essential hypertension, with others being diagnosed as hypertensive following their presenting TIA or stroke and have therefore recently been commenced on antihypertensive treatment. This latter phenomenon is made worse by the recent trend to operate on patients within days of their presenting neurologic event.
Thus blood pressure management during CEA involves “walking a tightrope” between two extremes. On the one hand, blood pressure must be maintained high enough to maintain cerebral perfusion, particularly during the carotid cross-clamp period when the ipsilateral cerebral cortex is relying on collateral flow around the circle of Willis. On the other hand, blood pressure must not be so high that hypertensive complications such as myocardial ischemia, hyperperfusion syndrome, or hemorrhagic stroke develop. This can be difficult to manage, which helps explain why perioperative stroke and mortality rate for CEA remain relatively high.
The choice of anesthesia for CEA does affect the intraoperative and postoperative hemodynamic profile. Patients undergoing CEA under regional anesthesia tend toward hypertension during the period of cross-clamping, and hypotension after restoration of cerebral blood flow and into the postoperative period. In contrast, the usual pattern under general anesthesia is of relative intraoperative hypotension and postoperative hypertension.
Recognition
Perfusion of the brain is at risk throughout carotid surgery. Before internal carotid artery cross-clamping, perfusion of the ipsilateral cerebral cortex through a narrow carotid stenosis may be dependent on maintenance of a relatively high blood pressure. During cross-clamping, perfusion of the ipsilateral cerebral cortex is reduced and reliant on collateral flow around the circle of Willis. Once the cross-clamp is released after removal of the stenosis, perfusion of both sides may be affected by fluctuations in arterial pressure. The cerebral vasculature is also affected by the type of anesthesia used. Cerebral autoregulation and baroreceptor function are both affected considerably more by general anesthesia compared with regional anesthetic techniques. Arterial carbon dioxide levels also have significant influence on cerebral vasodilation and vasoconstriction.
Close arterial pressure control is therefore vital throughout the operation, coupled with some method of assessing cerebral perfusion while the carotid is cross-clamped. The choice of which monitoring technique to use may be affected by the surgeon’s decision whether or not to use a carotid shunt (a method of bypassing the carotid cross-clamp and thereby maintain ipsilateral perfusion during carotid cross-clamping). Whereas some surgeons elect to place a shunt in all patients, others never use a shunt, relying instead on speed of surgery to minimize cerebral ischemia. However, a third group of vascular surgeons use intraoperative monitors of cerebral perfusion and ischemia to guide them as to whether to place a shunt. Shunting is not without risk; vessel wall disruption, dislodgment of atheromatous plaque with thromboembolism, shunt kinking, or air embolism can all occur, as well as brisk arterial hemorrhage if the shunt is accidentally dislodged.
Methods used to assess the need for a shunt include: neurologic assessment of awake patients (under local or regional anesthesia, such as cervical plexus block); transcranial Doppler; electroencephalogram (EEG), somatosensory evoked potentials (SEPs); measurement of distal cerebral artery stump pressures (i.e., pressure created by backflow from the contralateral carotid artery across the circle of Willis); or direct measurement of cerebral blood flow with xenon ( Table 41.1 ). The sensitivity of any technique for detecting perioperative ischemia is limited, because most strokes occur postoperatively and are likely caused by thromboembolic phenomena.
| Regional Anesthesia | |
| Central nervous system examination of the awake patient | The “gold standard.” Assessment of contralateral grip strength, speech, and cerebration at regular intervals during the cross-clamp period. |
| General Anesthesia | |
| Electroencephalogram (EEG) | EEG represents cortical electrical activity, which decreases with cerebral ischemia. Disadvantages of EEG monitoring include the inability to monitor deep brain structures, the presence of false-negative findings due to preexisting or fluctuating neurologic deficits, and the influence of general anesthesia on EEG patterns. |
| Somatosensory evoked potentials (SEPs) | SEPs can monitor deeper brain structures. SEPs are a result of electrical impulses that originate peripherally and travel through first- and second-order neurons to synapse in the brainstem. Subsequently, these impulses are transmitted to the somatosensory cortex. As with EEG monitoring, false-negatives may result if anesthetics produce SEP changes that mimic cerebral hypoxia. |
| Internal carotid artery stump pressure | Now largely historical. The presence of a palpable pulse or a mean stump pressure greater than 60 mm Hg suggests sufficient backflow to prevent ischemia. |
| Xenon-133 washout | Intravenous or intracarotid administration of radioactive xenon or krypton. This method is specialized, expensive, and largely a research tool. |
| Transcranial Doppler ultrasonography (TCD) | TCD measures the velocity of blood flow in the middle cerebral artery. It can be used to detect acute thrombotic occlusion or embolization during or after carotid surgery, or to identify patients at risk for developing a postoperative hyperperfusion syndrome. |
| Near-infrared spectroscopy (rSO 2 ) | Noninvasive assessment of cortical oxygen saturation using a sensor on the forehead. A decrease in rSO 2 of <20% from preclamp to early cross-clamp value has a high negative predictive value. However, it has a high false-positive rate. |
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