Use of intraoperative duplex ultrasonography for identification and patch repair of kinking stenosis after carotid endarterectomy: a single-surgeon retrospective experience.

OBJECTIVE: To provide an incidence and descriptive evaluation of kinking of the internal carotid artery (ICA) after carotid endarterectomy (CEA) in a consecutive CEA series that included the use of intraoperative duplex ultrasonography (IDUS) monitoring and to determine the effect of kink patch repair on long-term postoperative ICA restenosis. METHODS: The electronic medical records and IDUS recordings of all CEA cases performed over a 10-year period (March 2000 to October 2010) by a single neurosurgeon were retrospectively reviewed to assess cases of kinking after CEA. RESULTS: IDUS assisted in the identification of 27 of 285 cases (9.5%) of kinking after CEA. Kinked vessels with hemodynamically significant peak systolic velocities of ≥ 120 cm/second on IDUS (11 of 285 cases; 3.9%) were repaired using a synthetic patch. During follow-up, there were no neurologic symptoms, stroke, or death related to a cerebrovascular accident associated with kinking. The total incidence of postoperative stroke in this CEA series was 3 of 285 cases (1.1%). CONCLUSIONS: ICA kinking stenosis after CEA was a common finding in this CEA series. Because of their unique anatomic and hemodynamic properties, the identification and assessment of kinks after CEA required the use of IDUS monitoring. A selective patch closure method for kinked vessels with peak systolic velocities of ≥ 120 cm/second identified by IDUS was effective in resolving hemodynamically significant stenosis and minimizing long-term postoperative restenosis.

Physiological glucose is critical for optimized neuronal viability and AMPK responsiveness in vitro.

Understanding the mechanisms that govern neuronal responses to oxidative and metabolic stress is essential for therapeutic intervention. In vitro modeling is an important approach for these studies, as the metabolic environment influences neuronal responses. Surprisingly, most neuronal culture methods employ conditions that are non-physiological, especially with regards to glucose concentrations, which often exceed 20mM. This concentration is a significant departure from physiological glucose levels, and even several-fold greater than that seen during severe hyperglycemia. The goal of this study was to establish a physiological neuronal culture system that will facilitate the study of neuronal energy metabolism and responses to metabolic stress. We demonstrate that the metabolic environment during preparation, plating, and maintenance of cultures affects neuronal viability and the response of neuronal pathways to changes in energy balance.