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العنوان
CEREBRAL PROTECTION IN INTENSIVE CARE UNITS/
المؤلف
Mammon,Mohamed Sayed
هيئة الاعداد
باحث / محمد سيد مأمون
مشرف / رؤوف رمزى جادالله
مشرف / أيمن أحمد عبد اللطيف
مشرف / داليا محمود أحمد الفاوى
الموضوع
INTENSIVE CARE UNITS
تاريخ النشر
2015
عدد الصفحات
113.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
التخدير و علاج الألم
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة عين شمس - كلية الطب - Intensive Care
الفهرس
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Abstract

T
he brain lies in the cranial cavity, consists of cerebrum, brain stem and cerebellum continuous with the spinal cord through the foramen magnum. It is surrounded by three meninges, the dura mater, the arachnoid mater and the pia mater; these are continuous with the corresponding meninges of the spinal cord.
Blood supply to brain is carried by two internal carotid arteries and two vertebral arteries that anastomose at base of brain to form circle of Willis; that is another natural protection to brain.
In normal range of arterial pressure, cerebral blood flow is regulated by local intrinsic mechanism called autoregulation. This mechanism help to ensure a constant rate of blood flow despite changes in systemic blood pressure. This regulation is achieved by metabolic and myogenic mechanisms.
An interruption of blood flow to brain for more than ten seconds causes loss of consciousness and interruption of flow for few minutes generally results in irreversible brain damage. Within a few minutes of cerebral ischemia, the core of brain tissue subsequently undergoes necrotic cell death.
Tissue injury begins with an inflammatory reaction, which is a common response of the cerebral parenchyma to various forms of insult. This requires the infiltration of leukocytes, both polymorphonuclear, leukocytes and monocytes, which are the cellular mediators of subsequent microvessel obstruction, edema formation, cellular necrosis, and tissue infarction.
Key principles in neurocritical care, regardless of the pathology or procedure, include the prevention of secondary insults to the brain, ischemic or otherwise, and the maintenance of cerebral blood flow. Traditionally, these goals have been achieved through monitoring of intracranial pressure (ICP) and maintenance of an appropriate cerebral perfusion pressure (CPP). Intraparenchymal bolts for measuring ICP are inserted in patients with a neurologic exam that is difficult to follow, typically equivalent to a Glasgow Coma Scale of 8 or less. Standard thresholds for intervention are an ICP greater than 20 mm Hg or a CPP less than 60 mm Hg, although care should be tailored on an individual basis. Hemodynamic monitoring in the care of the critically ill neuroscience patient provides information that assists the clinician in minimizing secondary neuronal injury.
Neuroprotection can be defined as the protection of cell bodies and neuronal and glial processes by strategies that impede the development of irreversible ischemic injury by effects on the cellular processes involved. Neuroprotection can be achieved using pharmaceutical or physiological therapies that directly inhibit the biochemical, metabolic, and cellular consequences of ischemic injury.
Physiological therapies including; therapeutic hypothermia for 12-24 hours, normoglycemic state, optimal blood pressure and non pharmacological methods to reduce elevated ICP.
Pharmaceutical therapies including anesthetics neuroprotective drugs, calcium antagonists, N-methyl-D-aspartate receptor antagonist, hyperosmolar therapy, stains, oxygen free radical inhibitors and hormonal therapy.