The perioperative anesthetic management of carotid body tumor resection includes a comprehensive preoperative airway assessment, optimization of patient comorbidities, and identification of symptoms pointing to secreting tumors. The goals of intraoperative hemodynamic management are to maintain normal baseline hemodynamics, avoiding extreme swings in blood pressure and heart rate. Whether regional or general anesthesia is used, the goals of perioperative management are to preserve stable hemodynamics and maintain end-organ perfusion, to prepare for resuscitation of acute major blood loss, to utilize monitoring modalities to identify, avoid, and manage cerebral ischemia, and to provide a smooth controlled emergence. Internal carotid artery clamping, reconstruction or sacrifice may be required for large grade III tumors or when the internal carotid artery is inadvertently injured. In the postoperative period, complications should be anticipated, diagnosed, and promptly managed. Patients undergoing bilateral carotid tumor surgery should be continuously monitored in an intensive care environment postoperatively.

This chapter explains the mechanisms leading to neuronal cell death and the most important neuroprotective strategies. Cerebral ischaemia and/or hypoxia may occur as a consequence of shock, respiratory failure, vascular stenosis or occlusion, vasospasm, neurotrauma or cardiac arrest. Ischaemic or traumatic challenges affect both inadequate delivery of oxygen and glucose, and impairment of mitochondrial function, leading to inadequate production of ATP. Two different types of cell death may occur following brain injury: necrosis and apoptosis. New therapeutic targets could be designed to obtain a correct modulation of the immune system and to reduce cerebral damage after brain injury. The proposed mechanisms of anaesthetic protection include reduction of cerebral metabolism and intracranial pressure (ICP), and suppression of seizures and sympathetic discharge. Hypoxia and ischaemia are recognized as important driving forces of erythropoietin expression in the brain, suggesting that erythropoietin is part of a self-regulating physiological protection mechanism to prevent neuronal injury.