Complication Of Carotid Endarterectomy Research Articles

Airway Management in Patients Who Develop Neck Hematomas After Carotid Endarterectomy

Progressive airway compromise from neck hematoma and edema is a feared complication of carotid endarterectomy (CEA). Despite this, the relationship of airway management technique to patient outcome has not been systematically studied in this population. We report the rate of successful airway management using various techniques in post-CEA patients. A 10-year retrospective analysis was conducted to identify patients requiring airway management for neck exploration within 72 hours after CEA at Mayo Clinic, Rochester, MN. Three thousand two hundred twenty-five patients underwent CEA over a 10-year period at our institution. Forty-four (1.4%) required neck exploration for hematoma, and 42 of these required airway management immediately before neck exploration surgery. (The tracheal tube had not been removed after CEA in the remaining 2 patients.) The average interval between the completion of CEA and return to the operating room for hematoma evacuation was 6.0 +/- 6.0 hours (mean +/- SD; range, <1-32 hours). Fiberoptic airway management, performed before the induction of anesthesia, was successful in 15 of 20 patients (75%) and, in patients in whom fiberoptic tracheal intubation failed, direct laryngoscopy (DL) was successful in all 5 (3 before and 2 after the induction of general anesthesia). In the remaining 22 patients, DL was used as the initial management technique without a trial of fiberoptic intubation. DL was successful in 5 of 7 patients (71%) when performed before induction of general anesthesia and was successful in 13 of 15 patients (87%) when performed after induction of general anesthesia. Hematoma decompression facilitated DL in 3 of 4 failures of DL; tracheostomy was performed in the remaining patient. An arterial site of bleeding was subsequently identified in 36% of patients in whom no difficulty was encountered during laryngoscopy for hematoma evacuation versus 6% in whom difficulty was noted (P = 0.03). In 36 of 44 patients (82%), the tracheal tube was removed within 24 hours of surgery for neck exploration. No adverse events related to airway management were noted. There were no deaths at 2 weeks after hematoma evacuation. Multiple techniques resulted in successful airway control both before and after the induction of general anesthesia. Tracheal intubation was accomplished with both fiberoptic visualization and DL. In instances of poor direct visualization of the glottis, decompression of the airway by opening of the surgical incision may facilitate intubation of the trachea.

Deglutition Syncope: A Manifestation of Vagal Hyperactivity Following Carotid Endarterectomy

Background: Transient hypotension and bradycardia after carotid endarterectomy (CEA) is related to increased baroreceptor activity at the carotid bifurcation. These symptoms, mediated by afferent impulses through the nerve of Hering, result from increased vagal activity. We report a case of deglutition syncope after CEA. Case report: A 61-year-old man presented with left amaurosis fugax and bilateral >80% internal carotid artery stenoses. His surgical history was significant for a right CEA 12 years previously. After an uneventful left CEA, he was hemodynamically stable and without neurologic deficits. On the first postoperative day, the patient experienced crushing chest pain, bradycardia, hypotension, and bilateral vision loss as he began to eat breakfast. Results of an electrocardiogram, computed tomography (CT) scan with pulmonary embolism protocol, cardiac isoenzyme analysis, and echocardiogram were normal. His blood pressure, chest pain, and vision loss responded initially to the administration of pressors. During the next day, similar symptoms developed each time he attempted to eat. With initiation of anticholinergic medication, he was able to eat without symptoms. Results of a barium swallow were normal. The patient's symptoms resolved, and the anticholinergic medication was discontinued. The patient underwent an uneventful right CEA 3 months later. He was hemodynamically and neurologically stable during the procedure and postoperatively. The morning after the CEA, diaphoresis, hypotension, and tachycardia again developed when he began eating breakfast. Anticholinergic medications were again initiated and all symptoms resolved ≤48 hours. Results: The patient has been seen in follow-up. He has had no further episodes of deglutition syncope or other neurologic symptoms. His CEA are widely patent. Conclusions: Increased vagal tone after CEA, mediated by hypersensitivity of the baroreceptors of the carotid sinus, is well described. The nerve of Hering, an afferent branch of the glossopharyngeal nerve, synapses with efferent fibers of the vagus nerve in the nucleus tractus solitarius within the medulla. The glossopharyngeal nerve also transmits afferent impulses from the esophagus. We hypothesize that after CEA, our patient had a transient increase in afferent activity to the nucleus tractus solitarius related to changes of the carotid baroreceptor. With additional glossopharyngeal afferent activity associated with swallowing, deglutition syncope developed. Deglutition syncope is considered an unusual manifestation of vasovagal episodes and usually has been reported in association with esophageal, cardiac, and thoracic aortic abnormalities. To our knowledge, this patient is the first case of deglutition syncope reported after CEA. Because deglutition syndrome can be associated with esophageal abnormalities, a barium swallow should be evaluated. Clinicians should be aware of and know how to address this rare complication of CEA.

Carotid Artery Stenting Versus Carotid Endarterectomy: Systematic Review and Meta‐Analysis

The aim of this study was to evaluate and investigate the complications of carotid endarterectomy (CEA) and carotid artery stenting (CAS) by performing a meta-analysis based on prospective randomized controlled trials (RCTs). We performed a search of multiple electronic databases for RCTs containing patients with carotid stenosis who underwent CAS or CEA, focusing on studies published during 1995-2008. Eight trials with 2942 patients (1462 with CEA, 1480 with CAS) were analyzed. The pooled relative risk (RR) after CEA for stroke/death 30 days or 1 year was similar to that for CAS. Thirty-day RR = 0.69, 95% confidence interval (CI) = 0.45-1.07, p = 0.10. One-year RR = 0.88, 95% CI = 0.43-1.79, p = 0.72. The rates of death, disabling stroke, and nondisabling stroke at 30 days did not differ significantly between CEA and CAS in the subgroup analysis. Compared with CEA, the relative risk of disabling stroke/death within 30 days was not significantly less for CAS with embolic protection devices (EPDs). The relative risk of myocardial infarction within 30 days, myocardial infarction within 1 year, and cervical/peripheral nerve injury within 30 days were significantly higher after CEA; the relative risk of bradycardia/hypotension within 30 days and the 1-year restenosis rate were significantly higher after CAS. CAS is equal to CEA with regard to the incidence of stroke/death. These procedures may be considered complementary rather than competing modes of therapy, each of which can be optimized with careful patient selection. CAS with an EPD may be appropriate in certain patients, and in general CAS should be considered cautiously in symptomatic patients.

Atherosclerotic Peripheral Vascular Disease Symposium II

Carotid artery disease is a major cause of ischemic stroke, the risk of which is directly related to the severity of stenosis and presence of symptoms.1,2 Stroke is the third leading cause of death in the United States, with approximately three quarters of a million strokes per year. Stroke is the leading cause of functional impairment, with more than 20% of survivors requiring institutional care and up to one third having a permanent disability.3 More worrisome, however, is the fact that as the population ages, the number of patients having strokes appears to be increasing.4 The pathophysiology of stroke may be broadly classified as hemorrhagic, embolic, or ischemic. The majority of strokes are caused by embolic events due to atheroemboli from the carotid artery, the ascending aorta, and arch vessels or cardiac thromboembolism from the left atrium or ventricle. It is estimated that carotid artery stenosis is responsible for 15% to 20% of all strokes.5 As percutaneous treatment options expand, there is uncertainty about appropriate therapy for carotid disease. This document will focus on 3 current controversies: (1) carotid artery revascularization in asymptomatic patients, (2) carotid artery stenting (CAS) in patients who are considered to be at increased surgical risk for carotid endarterectomy (CEA), and (3) the current role for CAS in patients at average surgical risk. ### Prevalence and Natural History The prevalence of asymptomatic extracranial carotid stenosis (≥50%) in persons >65 years of age is estimated to be between 5% and 10%, whereas ≤1% of patients are estimated to have a severe narrowing (>80%).6 In asymptomatic patients with ≥50% carotid artery stenoses, the annual risk of stroke is between 1% and 4.3%.2,7 Long-term (10- to 15-year) cohort studies in asymptomatic patients with moderate to severe carotid stenosis demonstrate an ipsilateral stroke rate between 0.9% and 1.1% per …

Carotid angioplasty and stenting in octogenarians: Is it safe?

Elderly patients have a higher risk of complications in carotid endarterectomy. The aim of the study was to evaluate whether carotid artery stenting (CAS) performed in octogenarians also increases the procedure related risk. 870 patients (male 626) mean age 70.9 +/- 9.3 years underwent 930 CAS for de novo lesions (n = 851) restenoses (n = 54) post radiation (n = 14) inflammatory arteritis (n = 9) post trauma aneurysms (n = 2). Indications for treatment: symptomatic carotid stenosis > or = 70% (n = 577) or asymptomatic stenosis > or = 80%. Patients were separated into two age groups: <80 years (749 patients, 806 CAS) and >80 years (121 patients, 124 CAS). 187 CAS performed without protection (N.P-) 6 patients >80 years, 743 with protection (NP+) (occlusion balloon: 334, filters: 404, reversal flow: 6) 118 patients >80 years. Data analysis included neurological complications, death and myocardial infarction (MI) rate at 30 days, anatomical particularities. Technical points will be described depending on the age of the patient. Technical success 804/806 in patients <80 years, 123/124 in patients >80 years (NS). 30 days outcomes: in the patient group <80 years we observed 9 TIA (1.1%) 3 without NP (1.7%) 6 with NP (0.9%), 5 minor strokes (0.6%) 2 without NP (1.1%) 3 with NP (0.5%), 3 major strokes: 2 without NP (1.1%) 1 with NP (0.2%), 5 deaths (0.6%) 2 without NP (1.1%) 3 with NP (0.5%). Death/stroke/MI: 14 (1.8%) 6 without NP (3.3%), 8 with NP (1.3%). In the group >80 years, we observed 2 TIA (1.7%) 1 without NP 1 with NP (0.92%) 1 minor stroke without NP (17%) no major stroke, no death. Death/stroke/MI 1 without NP (17%). CAS can be performed in elderly patients without higher risk than in younger patients. But good indications, a meticulous technique, protection devices are mandatory and some technical points must be pointed out to avoid neurological complications and failures.

Endogenous endophthalmitis following ipsilateral carotid endarterectomy

We report a case involving a 75-year-old lady who presented to our department of ophthalmology complaining of a 1 day history of ocular pain and reduced vision in the right eye, associated with rigors and diarrhoea. This patient, who had undergone a right carotid endarterectomy (CEA) 4 days previously, was subsequently confirmed to have developed endogenous endophthalmitis. To our knowledge, endogenous endopthalmitis has not previously been described as a postoperative complication of CEA, and should be considered in patients presenting with ocular complaints after this type of surgery.

Œdème cérébral vasogénique par syndrome de reperfusion post-endartérectomie carotidienne

Reperfusion (or hyperperfusion) syndrome may be a possible complication of carotid artery endarterectomy or angioplasty. We report the case of a 54-year-old man who underwent a right carotid endarterectomy for an asymptomatic carotid stenosis and developed reperfusion syndrome a few days after surgery. The symptoms were marked by a prolonged partial epileptic status and then left hemiplegia lasting several days. Brain MRI with Diffusion sequences was normal, whereas there was a right frontoparietal hypersignal in FLAIR sequences, suggesting the presence of brain vasogenic oedema. Clinical and neuroradiological outcomes were good, confirming the relative good prognosis attributed to vasogenic brain oedema in previous similar publications. This condition may be misdiagnosed as cytotoxic brain oedema, another possible complication of carotid endarterectomy, whose management and prognosis are different. When a focal neurological deficit or epileptic seizures follow carotid artery endarterectomy, it is important to consider reperfusion syndrome. MRI (with FLAIR and Diffusion sequences) will show a vasogenic brain oedema, with a better prognosis than what can be expected with cytotoxic oedema.

Platelet Mapping and Desmopressin Reversal of Platelet Inhibition During Emergency Carotid Endarterectomy

POSTOPERATIVE BLEEDING WITH cervical hematoma is a possible complication of carotid endarterectomy (CEA). Its incidence is about 5%, with 99% of the events occurring within 8 hours of the operation. 1 Sheehan M.K. Baker W.H. Littooy F.N. et al. Timing of postcarotid complications: A guide to safe discharge planning. J Vasc Surg. 2001; 34: 13-16 Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar

Síndrome de hiperperfusão (pós-operatória) após três semanas da endarterectomia de carótida

Cerebral hyperperfusion syndrome is a recognized complication of carotid endarterectomy. Various studies have documented an incidence of 0.3 to 1.2%. It occurs in the setting of sudden reperfusion of a chronically hypoperfused hemisphere. We present here a case of a 48-year-old lady who developed cerebral hyperperfusion syndrome three weeks after undergoing a carotid endarterectomy for high-grade carotid artery stenosis.

無症候性頸動脈狭窄に対する内膜剥離術（ＣＥＡ）―ＣＥＡの妥当性について―

Reduction of complications of carotid endarterectomy (CEA) for carotid artery stenosis is essential for keeping the superiority of CEA over the medical treatment. Therefore, we must recognize the specific features of the asymptomatic carotid artery stenosis (AS-ICAS) to avoid operative complications. Of 290 CEAs performed on patients with carotid artery stenosis, 109 CEAs were done for the AS-ICAS. Our indications of CEA for AS-ICAS were stenosis over 60%, hypoechoic or heterogeneous echogenesity and ulceration detected by B-mode ultrasonography and progression of the stenosis. We routinely use the T-shaped shunt tube and intraoperative monitoring such as somatosensory evoked potential (SEP). To obtain specific features of AS-ICAS, we analyzed cerebral blood flow, intraoperative monitoring and frequencies of associated systemic diseases in the patients with AS-ICAS. Perioperative mortality and morbidity of CEA for the patients with AS-ICAS were 0 and 1.8%, respectively. Cerebral blood flow of the territory of the middle cerebral artery (rCBF) and cerebrovascular reactivity (rCVR) were not lower than those on the contralateral side. Compared with those of symptomatic carotid artery stenosis (S-ICAS), there was no significant difference in rCBF or rCVR, although rCVR of S-ICAS was relatively lower than that of AS-ICAS. There was no significant difference in the intraoperative monitoring between AS-ICAS and S-ICAS. Hyperperfusion after CEA of AS-ICAS occurred in 2.0% which was not significantly lower than the 6.5% of S-ICAS. Specific features of CEA for AS-ICAS were not obtained from this study. According to the mortality and morbidity of our CEAs, CEA for AS-ICAS was acceptable.

Predicting Medical and Surgical Complications of Carotid Endarterectomy

Several generic cardiac risk assessment tools predict perioperative cardiac complications, but their ability to predict a broader range of medical, neurologic, and surgical complications is unknown. A multicenter retrospective observational cohort study of 1998 patients undergoing carotid endarterectomy (CEA). Complications within 30 days of surgery were assessed by medical record review, including death or nonfatal stroke and cardiac, noncardiac medical, minor neurologic, and wound complications. Logistic regression and receiver operating characteristic curve analyses assessed the predictive abilities of the Goldman, Detsky, Revised Cardiac Risk, and American Society of Anesthesiologists indexes and of 2 CEA-specific risk models (the Halm and Tu scores). Death or stroke occurred in 3.2% of patients, cardiac complications in 4.0%, noncardiac medical complications in 3.2%, minor neurologic complications in 6.9%, and wound complications in 6.0%. All risk models (except the Tu score) significantly predicted cardiac complications equally well (P<.05). All 6 risk models were equivalent in predicting noncardiac medical complications. Only the Revised Cardiac Risk Index and the 2 CEA-specific risk models (Halm and Tu scores) predicted death or stroke and minor neurologic and wound complications. The Halm score was superior in predicting death or stroke compared with the Tu score and the Revised Cardiac Risk Index (area under the receiver operating characteristic curve, 0.72 vs 0.62 and 0.61, respectively; P<.05). Patients with cardiac, noncardiac medical, minor neurologic, or wound complications had 3- to 16-fold increased odds of death or stroke. The Halm score CEA-specific risk model and the generic Revised Cardiac Risk Index predicted a broad range of medical, neurologic, and surgical complications following CEA.

Hemodynamic instability after extracranial carotid stenting

Hemodynamic instability (hypertension, hypotension and bradycardia) is a well-known complication of carotid endarterectomy. Carotid angioplasty and stenting (CAS) is becoming a valuable alternative treatment for patients with severe carotid stenosis and increased surgical risk. CAS implies instrumentation of the carotid bulb, so baroceptor dysfunction may provoke hemodynamic instability. The aim of this work was to calculate the incidence of this complication and to detect factors to predict it. Medical records and angiograms of 51 consecutive patients submitted to CAS for severe atherosclerotic stenosis (40 cases) or postsurgical restenosis (11 cases) were retrospectively reviewed in order to detect the occurrence of intra- and post-procedural hypertension (systolic blood pressure >160 mmHg), hypotension (systolic blood pressure <90 mmHg) and bradycardia (heart rate <60 beats/min). The relationship between clinical, procedural and angiographic factors and the occurrence of hemodynamic instability was assessed with univariate and multivariate analysis (logistic regression). Transient mild systolic post-procedural hypertension occurred in five cases (10%); preprocedural hypertension, asymptomatic stenosis and ipsilateral post-surgical restenosis predicted this. Hypotension with bradycardia also occurred in five cases (10%), one with neurological sequelae. Transient periprocedural bradycardia occurred in 19 cases (37%). Severe bradycardia without hypotension arose in one case only. Factors predicting post-procedural hypotension included the presence of a fibrous plaque and the ratio between the pre- and post-stenting diameter of the internal carotid artery. Peri-procedural bradycardia predicted post-procedural bradycardia. None of these factors were confirmed by multivariate analysis as a significant prognostic predictor. Mild systolic hypertension may occur after CAS, but is resolved by medical treatment. Prolonged hypotension and bradycardia may also arise and this can be dangerous because it may cause neurological deterioration due to hypoperfusion. These complications cannot be predicted by clinical, procedural, and angiographic factors.

Post-carotid endarterectomy cerebral hyperperfusion syndrome

Cerebral hyperperfusion syndrome, a serious complication of carotid endarterectomy, is easily missed when the patient presents as a medical emergency.

Intracerebral Hemorrhage after Carotid Revascularization Procedures

Carotid revascularization procedures for the prevention of acute ischemic stroke have a low but definite risk of intracerebral hemorrhage (ICH). After carotid endarterectomy (CEA) the risk is less than 1%, and accumulating data on the newer carotid angioplasty and stenting (CAS) procedure suggest a similar risk. A probably more common and underdiagnosed complication of CEA and CAS is the so-called “hyperperfusion” syndrome. A post-revascularization increase in cerebral blood flow (CBF) in the ipsilateral hemisphere is thought to underlie the pathophysiology of the syndrome. The increased unilateral hemispheric CBF leads to vasogenic edema due to re-perfusion of maximally dilated capillaries which have lost their autoregulatory capacity as a result of chronic ischemia. The clinical features of severe post-procedural hypertension followed by headache, focal neurological deficits, and seizures has an imaging correlate of unilateral hemispheric vasogenic edema in the absence of MRI features of infarction. In the absence of associated ICH, the symptoms often improve over a period of days after aggressive control of hypertension. The key to the prevention of the hyperperfusion syndrome and post-carotid revascularization ICH is close monitoring of peri-procedural blood pressure, and aggressive treatment of hypertension.

Hyperperfusion Syndrome after Carotid Endarterectomy

The hyperperfusion syndrome is a rare delayed postoperative complication of carotid endarterectomy (CEA) characterized by headache and seizure, with or without intracranial edema or hemorrhage. Between January 1996 and December 2003, 1,602 CEAs were performed. Six patients (0.4%) developed symptoms of hyperperfusion within 2 weeks of surgery. All patients had critical stenoses, five > or =90% and one 80-90%, with poor backbleeding from the distal internal carotid artery noted at operation in all cases. Five patients were asymptomatic prior to operation; one had a hemispheric transient ischemic attack. Three patients had severe contralateral internal carotid disease (two occlusions and one severe stenosis). Two patients developed severe, self-limiting headache that prolonged hospitalization. Three patients had ipsilateral intracranial bleeding, two occurring after an uneventful postoperative course. After initial discharge from the hospital, severe intracranial hemorrhage caused death in two patients. One patient experienced focal seizures 1 week after discharge. Hypertension did not appear to be related to the symptoms in any case. During the study period, the hyperperfusion syndrome caused three of five perioperative strokes (60%) and two of seven deaths (29%) in the entire endarterectomy population. Although rare, the hyperperfusion syndrome accounts for a significant percentage of the neurological morbidity and mortality following CEA.

Acute Airway Obstruction Complicating Unilateral Carotid Endarterectomy

Injury to the vagus nerve or any of its branches is a recognised complication of carotid endarterectomy (CEA) under both local and general anaesthesia. Although in most cases this type of injury is transient, cases of permanent nerve injury have been reported. Despite this, the pre-operative assessment of vocal cord (VC) function in patients undergoing CEA is not undertaken routinely in clinical practice. We report a case, which we believe is of value in identifying patients undergoing CEA, where preoperative assessment of VC function is important, and provides an additional useful tool for risk benefit analysis.

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.

Intravenously Administered Abciximab in the Management of Early Cerebral Ischemia after Carotid Endarterectomy: Case Report

Cerebral ischemia is the most worrisome perioperative complication of carotid endarterectomy (CEA). The stroke rate occurring with CEA is estimated to range from 2.3 to 6.3%. Numerous treatment options are available to the neurosurgeon in this scenario, although no "gold standard" exists. A 61-year-old woman presented with acute left arm weakness 40 minutes after an uneventful CEA for symptomatic carotid stenosis. Emergent angiography demonstrated vascular irregularities in a "moth-eaten" pattern along the arteriotomy closure, suggestive of platelet-fibrin aggregates ("white clot"). Abciximab was immediately administered intravenously in the angiography suite, with subsequent improvement of the visualized vascular irregularities on a second angiogram performed 12 minutes after infusion and complete resolution of the presumed platelet-fibrin aggregates on a third angiogram performed the next day. The patient had no further episodes of cerebral ischemia. She was discharged home on the fifth postoperative day with improving left arm weakness, which had completely resolved by her 2-month follow-up visit. To our knowledge, this is the first reported case of abciximab administered intravenously in the setting of acute thromboembolic brain ischemia after CEA. For the unique situation in which an acute thrombus, or white clot, is thought to be the cause of cerebral ischemia, we believe that abciximab may offer an effective and potentially safer alternative than fibrinolytics and may be a more appropriate drug to use from a physiological perspective.

Carotid Artery Stenting:The Need for Randomised Trials

Endovascular treatment for carotid artery stenosis avoids some of the complications of carotid endarterectomy, but has not been widely accepted. Concerns about the risks and benefits of endovascular treatment led to the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS). There was no difference in major outcome events between endovascular treatment and carotid endarterectomy, but the rate of procedural stroke or death was higher than desirable. There was no difference either in the rate of stroke during follow-up, but the confidence intervals were very wide and severe ipsilateral carotid stenosis was more frequent 1 year after endovascular treatment than after carotid surgery. Two other randomised trials of carotid stenting were stopped early after poor outcomes in stented patients. These early trials used techniques which have now been superseded, but the results emphasise the need to improve the safety of endovascular treatment. Recent advances designed to improve safety include new designs of stents and delivery systems, and devices designed to protect the brain from embolisation during stenting. However, there is little convincing evidence that these new devices reduce the rate of stroke. Moreover, a systematic review of the existing randomised trial data concluded that there the current evidence does not support a shift away from recommending carotid endarterectomy as the standard treatment for carotid stenosis. There is therefore a clear need for further randomised trials of carotid stenting. Three of the ongoing trials, EVA-3S, SPACE and ICSS (CAVATAS-2), have prospectively agreed to combine individual patient data after completion of follow-up. This meta-analysis will provide results similar to a mega-trial and should also allow informative subgroup analyses. The co-operation between the trials in agreeing to perform this meta-analysis is a major advance in trial design. The result should determine whether carotid stenting truly rivals carotid endarterectomy as the treatment of choice for carotid stenosis.

Gender-specific risk of perioperative complications in carotid endarterectomy patients with contralateral carotid artery stenosis or occlusion.

Carotid endarterectomy (CEA) has been shown to be effective in stroke prevention in selected patients. Some studies, however, identified gender as an independent risk factor for perioperative CEA complications demonstrating an increased rate of perioperative stroke or death in women. Furthermore, contralateral internal carotid artery (ICA) occlusion has been associated with higher rates of perioperative CEA complications. Therefore, we sought to analyse the gender-specific risk of perioperative CEA complications between patients with or without contralateral ICA stenosis or occlusion. We retrospectively analysed 212 consecutive CEA patients (male = 156, Female = 56) for their gender-specific, perioperative risk of stroke, transient ischemic attack (TIA), restenosis and cardiac complications in the presence (62%) or absence (38%) of a contralateral ICA stenosis/occlusion. In women but not in men, risk of perioperative ischemic events (stroke, TIA) or re-stenosis (p = 0.036) and combined perioperative complications (ischemic events, re-stenosis or cardiac complications; 38.2 % vs. 9.1%; p = 0.028) was significantly increased in the presence of a contralateral ICA stenosis or occlusion. Furthermore, in the presence of a contralateral ICA stenosis/occlusion the number of perioperative ischemic events (p = 0.008) and combined perioperative complications (38.2 % vs. 14.3%; p = 0.006) was significantly higher in female than in male patients. Our study suggests that women with contralateral ICA stenosis or occlusion may have a significantly higher risk for perioperative CEA complications than other subgroups of CEA patients. This risk increase seems to be gender-specific and, if confirmed in larger prospective studies, may influence ICA stenosis therapy in the presence of a contralateral ICA stenosis/occlusion in female patients.