الفهرس 
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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
.