الفهرس 
Introduction & Aim of work.Only 14 pages are availabe for public view
 |  | from | 146 |  |  |
| | | from | 146 | | |
Abstract
The human body is not a static entity, but is .n a constant state of flux. Tissues are synthesized and b: oken r down con~inuously, processes which need energy. In the critically 111 patient there is a variety of factors 1 ~ich prevent the individual from meeting his energy requireD nts.
These include anorexia; possible associated gast’rointes1 Lnal disease; increase or altered requirements; and al’ ered vitalization. The imbalance between reduced intake and IUgmented or altered requirement results in effects whic~ are similar to those of starvation Ihdications for parenteral nutr i tion include ; :ute hypercata/?olism (multiple trauma; burns; septicaer La); pyloric stenosis; pancreatitis; cardiac surgery; gastl lintestlnal cutaneous fistulae; inflammatory bowel dise lse; cancer surgery cahexia
The choice of appropriate intravenous ,nutrient I Ilutions clearly depends on knowledge of changes in the sub strate endocrine relationships that take place during the perioperative period. These changes are influenced by I :arvation, trauma, anesthesia, and excess glucose adain!! :ration.T.P.N. may be tak.,en in the form of peripheral inti lvenous nutrition in patients with limited protein cal Iric requirement but for hyper catabolic and hypermetabolic pa- 69 tlents and patlents recelvlng long term T.P.N. cer :ral access becomes necessary. Nutrltlonal assessment of patlents depends on a detalled h1story, lncludlng dletary hlstory. Physlcal exa lnatlon and the use of certaln variables, for example an hropomatry of arm, serum prealbumln and retlnal blndlng sy tem. The object of nutrltional assessment ls to detect and ategorlze patlents wlth dlfferent types and degrees of m lnutrltlon and related these to the r1sk of morbidlt~ and moral1ty. careful monltoring is requlred after the infusi n is begun to evaluate the progress of the nutritional s1 ltuS. Sheldon.1ft al., (1983), designed a monitoring protocc. for, . T.P.N. Slgns of success are positive nitrogen ba: ance, weight gain, response of serum protein and delayed hyp, raensltivlty. skin testlng becoming normal, this is an early lndex of the r.etilrn to normal following adequate nutri lonal repletion. Complications of T.P.N. may be grouped into three categories technical, metabolic and septic. The most ,0lRlllon
compllcations of T.P.N.• are related to catheter pla :ement throug~ a crowded thoraclc inlet, pneumothorax ls th most COlRlllobnut air embolism is the most serious.Traumatic brain injury (TBI) is defined as functionally significant disruption of brain function manifested as immediately apparent cognitive or physical impairments that result from blunt or penetrating trauma or rapid acceleration or deceleration forces .This definition excludes lacerations or contusions or the face eye or scalp and fractures of facial bones alone. Additionally, injury to brain resulting from brain trauma, hypoxic-ischemia (anoxic) inflammatory toxic or metabolic encephalopathies, primary ischemic or hemorrhagic strokes seizure disorders, intracranial surgery and cerebral neoplasm also are outside the definition of TBI (163).TBI has dramatic impact on the nation‘s health it accounts for 15-20%of deaths in people aged 3-35 ys old and is responsible for 1% of all adult deaths. Approximately 1.4 million people in the UK suffer a head injury every year resulting in nearly 150000 hospital admissions of these approximately 3500 patients require admission to ICU. In addition to the high mortality approximately 60% of survivors have significant ongoing deficits including cognitive competency major activity leisure and recreation. This has a devastating financial emotional and social impact on survivors left with lifelong disability (165).
The principal mechanisms of TBI are classified as (a) focal brain damage due to contact injury types resulting in contusions laceration and intracranial haemorrhage, (b) diffuse brain damage due to acceleration/deceleration injury, types resulting in diffuse axonal injury or brain swelling (184).Outcome from head injury is determined by two substantially different mechanisms/stages (a) the primary insult (primary damage - mechanical damage) occurring at the moment of impact. In treatment terms this type of injury is exclusively sensitive to preventive but not therapeutic measures. (b) The secondary insult (secondary damage delayed non - mechanical damage) represents consecutive pathological processes initiated at the moment of injury with delayed clinical presentation. Cerebral ischemia and intracranial hypertension refer to secondary insult and in treatment terms this type of injury is sensitive to therapeutic intervention. The key of management is to deal with these patients as emergencies. This relies on early recognition of those patients with potential intracranial injuries, immediate correction of factors leading to secondary injuries, rapid diagnosis of intracranial pathology, computerized tomography and magnetic resonance imaging and then immediate delivery to the definitive management (177).Aim of work
Understanding the pathophysiology after traumatic brain injury for adequate and oriented treatment.
Evaluating the importance of monitoring the injured brain to enable the detection of harmful physiological events before they cause irreversible damage to the brain.
To discuss the problem of traumatic brain injury and its assessment, resuscitation and intensive care management.