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connection between the initial GCS score and outcome only if the alternative of survival or death is considered; the quality of survival bore no relation to the initial status when evaluated merely on the basis of the GCS score. References 1. Becker DP , Miller JD , Ward JD , et al : The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg 47 : 491 – 502 , 1977 Becker DP, Miller JD, Ward JD, et al: The outcome from severe head injury with early diagnosis and intensive management

I n 1977, we reported on the outcome of 160 patients treated for severe head injury using a uniform and intensive management protocol. 1 There appeared to be a reduction in mortality without an increase in severe morbidity compared with results reported from some other centers. 11, 17, 18, 21 A management regimen of immediate diagnosis and surgical decompression of mass lesions, artificial ventilation, and intracranial pressure (ICP) monitoring was strongly advocated. 1, 15 The relationship between several neurological and physiological variables and

T he reported incidence of hospital-acquired bacterial pneumonia in critically ill trauma patients varies from as low as 4% to as high as 87%, 24 , 31 with fatality rates varying from 6% to 59%. 10 , 12 Clinical studies have identified the risk factors for pneumonia; they are severe head injury, 27 flail chest managed by endotracheal intubation and mechanical ventilation, 31 length of stay in the critical care setting, 9 immobilization of the trauma patient in a conventional bed, 26 hypotension, 8 and misuse of pharmacotherapy. 1 We undertook this

T he efficacy of corticosteroid administration in the management of the edema associated with primary and metastatic brain tumors is well established. 4, 12, 24, 26 The results of studies to investigate the effects of corticosteroids on experimental brain injury are, however, contradictory. 5, 16, 20, 21, 25, 28, 29, 31, 35 Similarly, the usefulness of corticosteroids in the management of severe head injury in humans remains controversial. Sparacio, et al., 32 Gobiet, et al., 13 Faupel, et al., 9 and Ransohoff 30 believe that corticosteroids are

presented large series of head injuries managed according to protocols calling for ICP monitoring and medical management of raised ICP. 2–5, 10, 11, 13 Two facts have become apparent in this field: 1) levels of ICP between 20 and 30 mm Hg (if uncontrolled) are associated with extremely high and unacceptable mortality rates; and 2) ICP monitoring and aggressive medical management of elevated ICP may improve the morbidity and mortality rates of patients with severe head injury. Bowers and Marshall 3 have demonstrated a difference in the mortality rates of patients with

O utcome after severe head injury is determined by both primary and secondary injury. Despite experimental evidence of considerably more complex mechanisms, clinicians focus mainly on cerebral ischemia as the central mechanism leading to secondary brain damage. Prevention and early treatment of high intracranial pressure (ICP), low cerebral perfusion pressure (CPP), hypercapnia, hypoxia, and vasospasm are thought to reduce the incidence of secondary insults and to improve outcome after severe head injury. 1, 2, 6, 8, 12–14 The S-100B protein is a small 21-kD

I n 1961, Galicich and French 6 documented the beneficial effect of steroids in the management of cerebral edema due to primary and metastatic brain tumors. Subsequently, this effect has been confirmed by other investigators, and steroids are now a universal part of the treatment of intracranial neoplasms. 14, 15 However, the efficacy of steroid therapy in the management of patients with severe head injury remains controversial. The results of both experimental and clinical investigations have been contradictory. Studies can be found that support the

areas of abnormal brain tissue, 4, 14, 18 it may be questioned if the bimodel method of calculation is justified in abnormal brain tissue. In the study presented here we have used the bicompartmental model in the calculation of flow conditions in a group of patients with severe head injuries, although we knew from initial-slope flow-index calculation, 4 that very low flow, abnormally high flow, as well as tissue peaks were common in these patients. Material and methods have been described in previous papers. 4, 6 Only a summary will be given here. Clinical

A dult respiratory distress syndrome has been reported in approximately 20% of patients with severe head injury. 4 An even greater percentage of patients with severe head injury, perhaps as high as 50%, have increased extravascular fluid accumulation in the lungs. 12 The development of ARDS complicates the treatment of head-injured patients ( Fig. 1 ), because many therapies that are protective for lungs afflicted with ARDS can raise ICP or decrease CPP. Fluid restriction, diuretic medications, and pulmonary vasodilating agents, as well as PEEP and

medication (vecuronium bromide) during the entire period of cooling (mean 45 hours). During the first 5 days after injury, brain temperatures in the normothermia group were maintained at 37° to 38°C with the use of external cooling or warming blankets as necessary. All patients in the normothermia group also received neuromuscular paralytic medication for a minimum of 24 hours after injury. General Critical Care The focus of our critical care for all patients with severe head injury is to maintain cerebral perfusion pressure above 70 mm Hg. We attempted to