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العنوان
Perioperative Management of
Traumatic Brain Injury
المؤلف
Ahmed ,Mohammed Abbas
هيئة الاعداد
باحث / Ahmed Mohammed Abbas
مشرف / Ahmed Abd El-Aala Al-Shawarby
مشرف / Khaled Ahmed Mostafa Salem
مشرف / Ibrahim Mamdouh Esmat
الموضوع
Anatomical and physiological considerations of the brain-
تاريخ النشر
2010
عدد الصفحات
209.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
التخدير و علاج الألم
تاريخ الإجازة
1/1/2010
مكان الإجازة
جامعة عين شمس - كلية الطب - Anesthesiology
الفهرس
Only 14 pages are availabe for public view

from 134

from 134

Abstract

Traumatic brain injury (TBI) is the result of an external mechanical force applied to the cranium and the intracranial contents, leading to temporary or permanent impairments, functional disability, or psychosocial maladjustment. TBI can manifest clinically from concussion to coma and death.
TBI is a major cause of morbidity and mortality in the world ranking and has emerged as the number one killer of young adults in Europe and the US .
TBI is commonly categorized by means of the Glasgow Coma Scale (GCS) as severe (GCS ≤ 8), moderate (GCS 9-13), and minor (GCS 14-15). Severe TBI accounts for approximately 10% of all cases, whereas moderate TBI accounts for another 10%; the remaining 80% are classified as minor.
Traumatic brain injuries can be divided into two major stages:
(1) Primary brain injuries that can occur at the time of impact include extradural and subdural hematomas, intracerebral contusions, and diffuse axonal injuries.
(2) Secondary injury can occur any time after the primary event, and potentially preventable causes include systemic hypotension, hypoxemia, hypercapnia, and hyperthermia.
Perioperative management of head-injured patients focuses on aggressive stabilization of the patient and avoidance of systemic and intracranial insults that cause secondary injury. Secondary brain injury may arise directly from activation of biochemical and inflammatory cascades, or indirectly following intracranial hypertension, reduced cerebral blood flow, vasospasm, hypoxemia, or increased cerebral metabolic rate. Secondary brain injury complicates the course of the majority of head-injured patients, adversely influencing outcome. These secondary insults are potentially preventable and treatable.
Pre-anesthetic Assessment and Stabilization
Pre-anesthetic assessment of the head-injured patient includes: airway (cervical spine), breathing (ventilation and oxygenation), circulatory status, associated injuries, neurological status (Glasgow Coma Scale), preexisting chronic illness, and circumstances of the injury (time of injury, duration of unconsciousness, associated alcohol or drug use).
Secondary insults complicate the course of more than 50% of head-injured patients. An outcome study using data from the Traumatic Coma Data Bank revealed that hypotension after head injury is associated with greater than 70% of patients experiencing significant morbidity and mortality. The combination of hypoxia and hypotension is significantly more detrimental (> 90% of patients with severe outcome or death). Hyperglycemia and hypoglycemia can be detrimental to neurosurgical patients, and studies suggest that blood glucose should be maintained in the range of 80-110 mg/dl to improve outcome.
Emergency Therapy: The first step is to secure an open airway and ensure adequate ventilation to prevent secondary injury from hypoxia and hypercarbia. When a cervical spine fracture has not been excluded by radiographic evaluation, cervical alignment with manual in-line stabilization (MILS) is recommended during emergent intubations. If facial fractures and soft tissue edema prevent direct visualization of the larynx, a fiberoptic intubation or intubation with other airway imaging devices may be attempted. In the presence of severe facial and/or laryngeal injuries, a cricothyrotomy may be required. Nasal intubations are avoided in the presence of a suspected basal skull fracture, severe facial fractures, and bleeding diathesis.
Following control of the airway in the head-injured patient, attention should focus on resuscitation of the cardiovascular system. A major concern during fluid resuscitation is the development of cerebral edema. Based on animal research, it appears that the best way to avoid cerebral edema during fluid resuscitation in the injured brain is to maintain normal serum osmolality and colloid oncotic pressure. Therefore, circulating blood volume should be restored to normovolemia with glucose-free isotonic crystalloids and colloid solutions. Glucose-containing solutions are avoided to enhance perioperative glycemic control. Hypertonic saline (HS) has been proposed as a more effective alternative to normal saline in the initial resuscitation of patients with hemorrhagic shock and TBI.
Control of increased ICP with mannitol, hypertonic saline or furosemide is indicated, and in some patients craniectomy is necessary. Hyperventilation, although effective in controlling ICP, may contribute to cerebral ischemia in head injury patients, and for this reason, it is a common recommendation to avoid hyperventilation unless necessary.
Intraoperative Management
Anesthetic Management: In some patients, severe intracranial hypertension precipitates reflex arterial hypertension and bradycardia (Cushing’s triad). A reduction in systemic blood pressure in these patients can further aggravate cerebral ischemia by reducing cerebral perfusion pressure (CPP = MAP - ICP). CPP should be maintained between 60-110 mm Hg. The choice of anesthetic agents depends on the condition of the patient. Anesthetic management is directed at avoidance of secondary brain injury. Intraoperative hypotension secondary to blood loss or precipitated by anesthetic drugs must be avoided by appropriate volume expansion. Maintenance of ventilation (PaCO2 > 30 mmHg) and oxygenation (PaO2 > 60 mmHg) is extremely important.
Brain Protection: Reducing the cerebral metabolic requirement for oxygen (CMRO2) is the mainstay of pharmacologic brain protection, and barbiturate administration is the only such intervention that has proven useful in humans. In addition to lowering CMR, barbiturates often reduce elevated ICP that is refractory to hyperventilation and mannitol. Experiments in non-human primates indicate that some of the protective effects of barbiturates during focal ischemia can be attributed to vasoconstriction in areas of healthy brain that shunts cerebral blood flow to injured areas.
A reduction of body temperature to 33 to 35° C may confer cerebral protection. When induction of hypothermia is elected, it is recommended that meticulous care is necessary to avoid adverse side effects such as hypotension, cardiac arrhythmias, coagulopathy, and infections. Rewarming should be carried out slowly. In this population, there is no doubt that hyperthermia associates strongly with poor outcome.
Post-operative Care/Critical Care
In the critical care unit, the main objectives are to optimize recovery from primary brain injury and prevent secondary injury. This requires provision of optimal systemic support for cerebral energy metabolism and adequate CPP, and normalizing of ICP for the injured brain. Prompt recognition and treatment of systemic complications that contribute to secondary injury are essential to head injury management.