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العنوان
Implementation of therapeutic hypothermia to
improve patient’s outcome after traumatic brain
injury & cardiac arrest in Intensive Care Units /
المؤلف
El-Sharkawy,Moustafa Gaber Mohamed.
هيئة الاعداد
باحث / Moustafa Gaber Mohamed El-Sharkawy
مشرف / Amir Ibraheem salah
مشرف / Sherif Samir wahba
مشرف / Dina Salah El din Mahmoud
تاريخ النشر
2015
عدد الصفحات
150p.;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
العناية المركزة والطب العناية المركزة
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة عين شمس - كلية الطب - طب الرعاية الحرجة
الفهرس
Only 14 pages are availabe for public view

Abstract

Traumatic brain injury and cardiac arrest remain a major cause of death
and severe disability throughout the world. The definition of TBI has not been
consistent and tends to vary according to specialties and circumstances. The
Centers for Disease Control and Prevention (CDC) defines TBI as
“craniocerebral trauma associated with neurological or neuropsychological
abnormalities, skull fracture, intracranial lesions or death”.
Several treatment modalities have been studied to improve outcome
after TBI and CA, from those modern modalities therapeutic hypothermia. TH
has been used in various clinical conditions and now is a popular technique in
most ICUs worldwide.
Ischemia has a key role in all forms of brain injury and preventing
ischemic (or secondary) injury is at the core of all neuroprotective strategies. A
complex cascade of processes ensues at the cellular level after a period of
ischemia beginning from minutes to hours after injury and continuing for up to
72 hours or longer. Thus, there may be a window of opportunity of several
hours, or even days, during which injury can be mitigated by treatments such
as hypothermia.
It was presumed that the protective effects of hypothermia were due to
a slowing of cerebral metabolism leading to reduced glucose and oxygen
consumption. This assumption is not completely incorrect: cerebral metabolism
decreases by 6% to 10% for each 1°C reduction in body temperature during
cooling. In addition to reduction in cerebral metabolism, several mechanisms
explaining the protective effects of therapeutic hypothermia include; inhibition
of caspase enzyme activation, prevention of mitochondrial dysfunction,
decrease of excitatory neurotransmitters, inhibition of coagulation cascade,
Summary 
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attenuation of the imbalance between vasoconstrictors and vasodilators and
increase in the speed of metabolic recovery.
The aim of the work was to evaluate the use of therapeutic hypothermia
as a primary neuroprotective strategy in patients with severe traumatic brain
injury and to study the safety of therapeutic hypothermia as a therapeutic
intervention post cardiac arrest.