Prevention of Back Bleeding During Carotid Endarterectomy: Analysis of Clamping Techniques.

OBJECTIVE: Complete control of back bleeding during carotid endarterectomy (CEA) is important. We investigated the causes of back bleeding during CEA and techniques for the control of bleeding. METHODS: A retrospective review was performed of 214 CEA procedures. We assessed the results of routine preoperative examinations, instruments used for arterial clamping (vessel loop and crude or bulldog clamps), and severity of carotid artery stenosis and arterial wall calcification. The study end point was incomplete control of back bleeding before arteriotomy. Factors associated with back bleeding were identified by univariate analysis. The culprit artery and intraoperative technique used in patients with back bleeding were also determined. RESULTS: Transient back bleeding occurred in 19 CEA procedures (8.9%). Back bleeding was from the ascending pharyngeal artery in 9 cases, common carotid artery in 8 cases, and external carotid artery in 2 cases. Univariate analysis identified the following factors as being related to incomplete control of back bleeding: moderate carotid artery stenosis (20 mm thick) and use of bulldog clamps. CONCLUSIONS: Transient back bleeding during CEA was uncommon, with the risk factors being severe carotid calcification and moderate carotid stenosis. Transient back bleeding was managed by clamping an undetected ascending pharyngeal artery or by additional clamping of the common carotid or external carotid artery. The vessel loop and crude were superior to the bulldog clamp for clamping the carotid artery.

Vagus nerve neuromonitoring during carotid endarterectomy.

To determine the causes and site(s) of nerve injury and to identify potential predictors of vocal fold paralysis (VFP) after carotid endarterectomy (CEA) by application of intraoperative neuromonitoring (IONM). A total of 68 CEA patients were enrolled in this study. A 3-step IONM procedure was designed to obtain vocal fold EMG data at V1 (just after identification of the vagus nerve [VN]), V2 (just before arteriotomy), and V3 (just before wound closure). We also performed IONM before/after hemostasis near the VN using bipolar forceps and before/after dissection of the VN. All patients underwent laryngoscopy to assess postoperative VFP. One patient showed loss of EMG signals between V2 and V3 and developed VFP that persisted for 11 months. The other 62 patients had no loss of EMG signals, but 2 patients had confirmed VFP for 1 month after CEA. There were no changes of EMG signal before and after VN dissection or hemostasis with bipolar forceps near the VN.

Carotid atherosclerosis and arterial peripheral pulse wave velocity in cerebral thrombosis.

Stiffening and thickening of the arterial walls are two important components of atherosclerosis. A better understanding of the relationship between stiffening and thickening of the large arteries might lead to optimal strategies for the prevention of cerebrovascular disease. However, there have been few investigations of the correlation between carotid artery wall thickening and arterial stiffness. In this study, we investigated the relationship between arterial stiffness (assessed by the ankle-brachial pulse wave velocity) and carotid plaque (detected by high-resolution real-time B-mode ultrasonography) in patients with cerebral thrombosis. The subjects were 109 patients with cerebral thrombosis aged 40-80 years. Fifty-six subjects had carotid plaque (27 had low-grade plaques (plaque score<7.0) and 29 had high-grade plaques (plaque score >or=7.0)) and 53 subjects did not have plaques. High pulse wave velocity was found to be significantly associated with existence of carotid plaque (p<0.001), but was not associated with the severity of the plaque (p=0.14) in multivariate logistic regression models. This study shows that the pulse wave velocity is associated with the existence of carotid atherosclerosis, but not with the severity of carotid atherosclerosis, in patients with cerebral thrombosis.