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Abstract Head injury constitutes a ma.1or problem to the medical professi on and is a leading cause of death and disability partic ularl y in the you ng adults_ Head injury can be classified tem porall y into primary and secondary damage, while pathologically it is divided into diffuse and focal. Prim ary damage refers to damage sustained at the impact, whereas secondary damage refers to that additional damage sustained secondary to systemic and local insults including hypoxia, hypotensi on, hypercarbia, fever, seizures and sepsis. At the cellular level, severe trauma unleashes a myriad of complex events that contribute to secondary damage. First, there is anerobic glycolysis with lactic acidosis that disturbs cellular homeostasis and leads to cellular swelling, then there is the excitotoxity mediated via glutamate and aspartate acting on NMDA and AMPA receptors leading to influx of calcium intracellularly, then on reperfusion, there is the production of free radicals with membrane lipid peroxidation and the final destruction of the neurons _ Experimental and clini cal data suggest that the anti-oxidant tirilazad may be beneficial in impro\·ing the outcome via its effect on free radicals and lipid-peroxidation. Clinically, the anesthesiologist is an integral part of the traum a team, and in addition to provi ding anesthesia to the head injured patient, the anesthesiolo2-ist is needed to control airwav. initiate and control arti fi cial ven ti l ation _ organ ize the use of \’asoact i \’e agents and normal ize the vol um e status or the patient Head injury constitutes a ma.1or problem to the medical professi on and is a leading cause of death and disability partic ularl y in the you ng adults_ Head injury can be classified tem porall y into primary and secondary damage, while pathologically it is divided into diffuse and focal. Prim ary damage refers to damage sustained at the impact, whereas secondary damage refers to that additional damage sustained secondary to systemic and local insults including hypoxia, hypotensi on, hypercarbia, fever, seizures and sepsis. At the cellular level, severe trauma unleashes a myriad of complex events that contribute to secondary damage. First, there is anerobic glycolysis with lactic acidosis that disturbs cellular homeostasis and leads to cellular swelling, then there is the excitotoxity mediated via glutamate and aspartate acting on NMDA and AMPA receptors leading to influx of calcium intracellularly, then on reperfusion, there is the production of free radicals with membrane lipid peroxidation and the final destruction of the neurons _ Experimental and clini cal data suggest that the anti-oxidant tirilazad may be beneficial in impro\·ing the outcome via its effect on free radicals and lipid-peroxidation. Clinically, the anesthesiologist is an integral part of the traum a team, and in addition to provi ding anesthesia to the head injured patient, the anesthesiolo2-ist is needed to control airwav. initiate and control arti fi cial ven ti l ation _ organ ize the use of \’asoact i \’e agents and normal ize the vol um e status or the patient . The aim of this study was to highlight the anesthetist role in dealing with the severely head injured patients, the assessment of the arterio jugular venous oxygen difference as an important parameter in the management of the head injured patient and evaluation of the role of the free radical scavenger tirilazad mesylate in improving the outcome after severe head injury. This study was carried out on 80 patients who sustained isolated severe head injury and with a GCS score of 9-4. The patients were divided into 2 groups according to their arterio-jugular venous difference in 02 content (AVD02) into group I : patients with AVD02 > 7 vol. %. group II: patients with AVD02 :::; 7 vol. %. Each group was further subdivided into subgroups A and B; subgroups IA and IIA received tirilazad, while IB and IIB received placebo. For every patient. The following was done: • Assessment: Including history from a relative, clini cal examination and routine laboratory investigations together with an ECG, x. Ray cervical spine and CT-scan brai n . • Prima ry resuscita tion: Including securing the airway, fluid resuscitation and, mechanical venti lation when needed. Then retrograde jugular catheterization was performed and a sample is taken from the jugular bulb together with another taken simultaneously from the radial artery in order to estimate AVD02 and assign patients to groups I and II. Patients of both groups were then randomly assigned to subgroups A which received tirilazad mesylate 2 mg/ kg/ 8 hour for six days, and subgroups B which received placebo. • Anesthesia: General anesthesia was administered m cases who required neurosurgical interventions. Anesthesia was induced and maintained using propofol, intubation was facilitated by succinylcholine 1-2 mg/kg together with lidocaine to blunt the respm1se to intubation. Boluses of fentany were given as necessary. Muscle relaxation was maintained by pipecuroni um. • Measurments and monitoring A. Hemodynamic parameters - Continuous mean arterial blood pressure (MAP). - ECG. - Central venous pressure (CVP) B. Blood and alveolar gases - Arterial blood gases (ABGs) - Jugular bulb oxygen saturation and content - AVD02 - Capnography - Pu l se oxymetry . |