Control of hypertension following carotid endarterectomy

The role of carotid endarterectomy in the treatment of extracranial carotid artery disease has been well established. Postoperative hypertension is a significant prognostic factor and is associated with an increased incidence of both transient and permanent neurologic deficits. We studied 110 patients undergoing unilateral carotid endarterectomy to review the efficacy of the drug combination of hydralazine and propranolol to treat postoperative hypertension. All patients receiving hydralazine and propranolol had their blood pressure controlled postoperatively, and no patients developed hypotension, myocardial infarction, or postoperative neurologic deficits. There were no mortalities in the study group. We conclude that propranolol-hydralazine therapy is a safe and effective means to control hypertension associated with carotid endarterectomy.     

Incidence of cranial nerve dysfunction following carotid endarterectomy

An analysis of postoperative injuries to the recurrent laryngeal, hypoglossal, marginal mandibular, and superior laryngeal nerves was undertaken in 517 patients who underwent 535 carotid endarterectomies between April 1978 and March 1981 at The Cleveland Clinic Foundation. A review of the literature is presented followed by the results of this analysis and a discussion of the findings. Suggestions for decreasing or avoiding such injuries are made. Conclusions are drawn to help the otolaryngologist identify the endarterectomized patient with an impaired upper aerodigestive tract.     

Hypertension following carotid endarterectomy.

Seventy-nine patients undergoing staged bilateral carotid endarterectomy were studied to determine the relationship of perioperative hypertension to postoperative neurologic deficits. Six of the eight neurologic deficits following 158 endarterectomies (5%) occurred after the first operation, all being temporary. Comparison of the mean blood pressures in patients with and without postoperative strokes revealed no statistically significant differences. Patients on antihypertensive medications were at a significantly higher risk of developing postoperative strokes. A trend towards higher blood pressure was noted following the second endarterectomy, particularly when they were staged more than 60 days apart. Based on our findings, a cautious approach is warranted in the treatment of postendarterectomy hypertension.     

Nicardipine versus nitroprusside for breakthrough hypertension following carotid endarterectomy

STUDY OBJECTIVE: To evaluate the effectiveness of nicardipine and nitroprusside for breakthrough hypertension following carotid endarterectomy. DESIGN: Prospective, randomized, double-blind, controlled effectiveness trial. SETTING: University-based surgical intensive care unit. PATIENTS: 60 ASA physical status I, II, III, and IV patients experiencing breakthrough hypertension at the time of admission to the intensive care unit (ICU). INTERVENTIONS: Patients received either nicardipine (n = 29) and placebo or nitroprusside (n = 31) and placebo for up to 6 hours postoperatively. Loading doses of nicardipine were provided, but placebo was used as a load for patients randomized to nitroprusside. MEASUREMENTS AND MAIN RESULTS: Rapidity and variability of blood pressure (BP) control were assessed. During the first 10 minutes, 83% of nicardipine patients compared to 23% of nitroprusside-treated patients, achieved BP control (p < 0.01). Following initial control, 12 nicardipine- and 24 nitroprusside-treated patients required additional titration of their infusions to maintain blood pressure within the targeted range (p < 0.05). No patient suffered a stroke, myocardial infarction, or was returned to the operating room (OR) for bleeding. CONCLUSIONS: Nicardipine administration produced more rapid BP control, most likely related to the administration of a loading dose. In addition to more rapid control, nicardipine-treated patients had less variability in BP and required significantly fewer additional interventions. Although no patient suffered a major event during this study, this study was not powered sufficiently to assess safety.     

Intracerebral haemorrhage following carotid endarterectomy.

OBJECTIVES: To determine risk factors for the development of hyperperfusion and intra-cerebral haemorrhage following carotid endarterectomy and formulate potential protocols for prevention. METHODS: MEDLINE database search of the English language literature (1966-2002) was performed using the words 'cerebral haemorrhage', 'intracranial haemorrhage' and 'carotid endarterectomy'. Other articles were cross-referenced by hand. RESULTS: There are no data from randomised trials confirming the significance of any single risk factor. The evidence suggests that the following may have a role: pre-operative hypertension, recent ipsilateral non-haemorrhagic stroke, previous ischaemic cerebral infarction, surgery for a > 90% ipsilateral internal carotid artery (ICA) stenosis, impaired cerebrovascular reserve, intra-operative haemodynamic or embolic ischaemia, post-operative hypertension, an ipsilateral increase of > or =175% in peak middle cerebral artery velocity (MCAV) and/or a > or =100% increase in pulsatility index. CONCLUSIONS: A critical ICA stenosis with impaired cerebrovascular reserve resulting in maximal intracerebral vasodilatation and post-operative hyperperfusion (impaired autoregulation) appear to be central to the development of ICH. Appropriate pre-operative screening and post-operative monitoring in high risk patients might identify those who would benefit from manipulation of the haemodynamic events that appear to promote ICH.     

Stenosis following carotid endarterectomy

Carotid endarterectomy is well established in the treatment of selected cases of atherosclerosis of the carotid bifurcation but the incidence of restenosis is unknown. During a four year period 80 endarterectomies of the internal carotid artery were performed in 73 patients. Post-operatively we studied our patients prospectively by means of Doppler ultrasound in combination with real time spectral analysis and where indicated digital venous angiography to determine the incidence of restenosis. We report a 12.5% incidence of stenosis following carotid endarterectomy with a 1% incidence of symptomatic restenosis. We therefore question the role of carotid endarterectomy in the treatment of asymptomatic carotid stenosis.     

Recurrent carotid artery stenosis following endarterectomy.

Spectral analysis was used to examine 257 carotid arteries in 227 patients who had undergone carotid endarterectomy at 1, 3, 6, and 12 months after surgery and annually thereafter. Routine intraoperative completion angiography ensured that the operations were technically satisfactory. Postoperative restenoses were identified in 38 patients (15%). In 23 arteries (9%), the restenosis exceeded a 50% diameter reduction while in 15 arteries (6%) the stenosis was less than 50% of the diameter. Restenosis developed in 24/96 women (25%) and 14/161 men (9%). Twenty-nine (70%) stenotic lesions occurred within 12 months. In three patients early lesions regressed. Reoperation with patch angio-plasty was required in six patients. When the 219 carotid arteries that remained widely patent were compared to the 38 that restenosed , no differences were noted for age, diabetes mellitus, hypertension, smoking, or degree of preoperative stenosis. Early stenotic lesions appear to be due to myointimal hyperplasia, which is probably platelet mediated. The predominant female sex distribution may be explained by differences in platelet responsiveness in men and women.     

Long-term effect of carotid endarterectomy on carotid sinus baroreceptor function and blood pressure control

In order to assess whether carotid endarterectomy had any long-term hypotensive effect, by altering the function of the carotid sinus baroreceptors, blood pressure and carotid sinus baroreceptor function were recorded in 25 patients undergoing carotid endarterectomy. No overall change in blood pressure was recorded 6 months after surgery. Sinus function was shown to decrease in 2 (8 per cent), to remain unchanged in 15 (60 per cent) and to increase in 8 (32 per cent) patients 6 months postoperatively. There was no relationship between changes in sinus function and changes in blood pressure over the 6 months period. Thus, carotid endarterectomy has no long-term hypotensive effect.     

Motor speech deficit following carotid endarterectomy.

Stroke as a complication of carotid endarterectomy has been extensively reviewed. Considerably less attention has been directed to local injuries of the cranial nerves and their branches. Verta, Hertzer, Imparato, DeWeese, and Matsumoto have reported experience with these injuries. DeWeese found a 9.7% rate of cranial nerve injury, while in Hertzer's series, 15% of patients had nerve dysfunction in the early postendarterectomy period. In 1980, Liapis in a preliminary report found that when postoperative examination was supplemented by detailed evaluation by speech pathologists, the incidence of early abnormalities reached 27%. The purpose of this study was to expand upon Liapis' early observation and to clarify the contribution of the speech pathologists in identifying cranial nerve dysfunctions, specifically those resulting in motor speech abnormalities, following carotid endarterectomy.     

Arterial hypertension after carotid endarterectomy

Arterial hypertension as a consequence of carotid endarterectomy is a relatively frequent event and potentially dangerous because of the development of central postoperative neurological deficiency. The main pathogenetic theories are reviewed, with reference to hypotensive phenomena and preventive action also. Stress is laid on the importance of recognising potential risk factors, such as the use of anaesthetics which interfere with cerebral flow self-regulation mechanisms, diabetes and atherosclerosis.     

Effect of lignocaine injection in carotid sinus on baroreceptor sensitivity during carotid endarterectomy

OBJECTIVES: This study was undertaken to test the hypothesis that there is a neural basis for baroreceptor deterioration during carotid endarterectomy (CEA), by investigating intraoperative hemodynamic changes induced by intraluminal carotid stretch stimulation, before and after application of local anesthetic to the adventitial layer of the carotid sinus region. METHODS: This was a prospective study of 20 patients undergoing elective CEA. During CEA, before removal of the atheroma, intraluminal stretch simulation of the carotid baroreceptors (rub test) was performed before and after injection of 1% lignocaine into adventitial tissue of the artery in the region of the carotid sinus. Continuous measurements of mean arterial blood pressure (MAP), electrocardiographic r-r intervals (R-R), heart rate, cardiac vagal tone, and carotid sinus baroreflex were recorded to determine alterations in baroreceptor function. RESULTS: Rub test before injection of lignocaine was associated with a decrease in MAP and heart rate and an increase in R-R, cardiac vagal tone, and carotid baroreflex response, indicating a functioning baroreflex. After lignocaine injection and repetition of the rub test, no significant change was seen in MAP, heart rate, R-R, cardiac vagal tone, or carotid baroreflex response, indicating a nonfunctioning baroreflex. Comparing the peak responses to the rub test stimulus before and after lignocaine injection showed significant differences for all variables (P <.05), with carotid baroreflex response and heart rate being highly significant (P <.0005). CONCLUSIONS: The baroreflex response to intraluminal stretch stimulation of the carotid sinus area is operational in patients undergoing CEA, and this response is abolished by infiltration of local anesthetic into the periadventitial tissue around the carotid sinus.     

Airway obstruction following carotid endarterectomy

Upper airway obstruction after carotid endarterectomy is a rare but potentially fatal complication of carotid endarterectomy. Upper airway obstruction is also a well recognized complication after neck surgery involving the thyroid gland and cervical spine. The airway obstruction usually develops slowly over a few hours and the onset is unpredictable. We report a patient who developed upper airway obstruction 16 hours following carotid endarterectomy. She required re-intubation in the intensive care unit (ICU). Fibreoptic assessment demonstrated severe supraglottic and glottic oedema. Tracheostomy was performed on day 2 postoperatively. Serial fibreoptic assessment of the upper airway showed gradual resolution of glottic edema and decanulation was successful on day 43.     

Cerebral hyperperfusion following carotid endarterectomy

Serial measurements of cerebral blood flow (CBF) were performed in 56 patients before and one to four times after uncomplicated carotid endarterectomy. The findings were related to the ratio between internal carotid artery (ICA) and common carotid artery (CCA) mean pressures. Within the 1st postoperative day CBF increased by a median of 37% in the ipsilateral and 33% in the contralateral hemisphere. Later recordings showed a gradual return of CBF toward the preoperative level. Sixteen patients with an ICA/CCA pressure ratio below 0.7 showed a significantly more pronounced and longer-lasting flow increase than did 40 patients with a ratio above this level. On Day 1, the median CBF increase in the ipsilateral hemisphere was 61% and 24% in the two groups, respectively (p less than 0.01). A significant improvement in side-to-side asymmetry, resulting from a higher gain in the ipsilateral hemisphere, occurred in the low pressure ratio group, while the hemispheric asymmetry on average was unchanged in the high pressure ratio group. This relative hyperemia was most pronounced 2 to 4 days following reconstruction. The marked hyperemia, absolute as well as relative, in patients with a low ICA/CCA pressure ratio suggests a temporary impairment of autoregulation. Special care should be taken to avoid postoperative hypertension in such patients, who typically have preoperative hypoperfusion, to avoid the occurrence of cerebral edema or hemorrhage.     

Massive intracerebral hemorrhage following carotid endarterectomy

To our knowledge, a particularly lethal complication of carotid endarterectomy, intracerebral hemorrhage, has not been given due consideration in the literature concerning carotid surgery. In the Atlanta area, massive intracranial hemorrhage developed in ten patients following routine carotid endarterectomies performed during a recent ten-year period. All ten of the patients in this series died despite a variety of therapeutic interventions. Risk factors may include the following: extreme arterial stenosis with resultant postoperative hyperperfusion, involvement of multiple extracranial cerebral vessels, postoperative systemic hypertension, and administration of anticoagulant or antiplatelet medications. Unfortunately, identification of the subset of patients potentially at risk for this complication is difficult, and, to date, therapy has been generally ineffective.     

Noninvasive carotid artery evaluation following endarterectomy

There has been recent interest in carotid restenosis following endarterectomy. To evaluate the significance of this complication, 2549 consecutive patients who were evaluated for suspected carotid artery occlusive disease by carotid phonoangiography, ocular plethysmography, and B-mode scanning techniques over a 21-month period were reviewed. Within this group a total of 155 patients had previously undergone a carotid endarterectomy. Of these, only four patients manifested clinically significant restenosis. In the majority of patients the carotid bifurcation was free of significant disease. The “carotid shelf” that represents the superior aspect of residual intimal plaque following endarterectomy could be clearly identified in the early postoperative period; however, it later blended to become less distinct. In a few instances, however, the amount of residual plaque at the lower extent of the endarterectomy was very prominent and remained so during follow-up studies, suggesting the possibility that this might represent a focus for future thrombosis. We conclude that noninvasive testing as used herein is an accurate method of assessing the carotid artery following endarterectomy. The accuracy of these techniques has been of such high degree that 16 carefully selected patients have subsequently undergone carotid endarterectomy without preoperative angiography. (J VASC SURG 1984;1:403-8.)