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Indications: Patients with parenchymal mass lesions and signs of progressive neurological deterioration referable to the lesion, medically refractory intracranial hypertension, or signs of mass effect on computed tomographic (CT) scan should be treated operatively. Patients with Glasgow Coma Scale (GCS) scores of 6 to 8 with frontal or temporal contusions greater than 20 cm3 in volume with midline shift of at least 5 mm and/or cisternal compression on CT scan, and patients with any lesion greater than 50 cm3 in volume should be treated operatively. Patients with parenchymal mass lesions who do not show evidence for neurological compromise, have controlled intracranial pressure (ICP), and no significant signs of mass effect on CT scan may be managed nonoperatively with intensive monitoring and serial imaging., Timing and Methods: Craniotomy with evacuation of mass lesion is recommended for those patients with focal lesions and the surgical indications listed above, under Indications. Bifrontal decompressive craniectomy within 48 hours of injury is a treatment option for patients with diffuse, medically refractory posttraumatic cerebral edema and resultant intracranial hypertension. Decompressive procedures, including subtemporal decompression, temporal lobectomy, and hemispheric decompressive craniectomy, are treatment options for patients with refractory intracranial hypertension and diffuse parenchymal injury with clinical and radiographic evidence for impending transtentorial herniation.

To date, despite very encouraging preclinical results, almost all phase II/III clinical neuroprotection trials in traumatic brain injury (TBI) have failed to show any consistent improvement in outcome for TBI patients. To understand the reasons behind such developments we need to review and evaluate the evolution of trial design as a result of our changing understanding of the pathophysiology of brain cell death and progress of translational research from the laboratory bench to the bedside. This paper attempts to critically appraise these neuroprotection trials, rationalize the paucity of effectiveness, review any recent developments in the field, and try to draw some conclusions on how to move forward.

Objective: Acute pupillary dilation in a head-injured patient is a neurological emergency. Pupil dilation is thought to be the result of uncal herniation causing mechanical compression of the IIIrd cranial nerve and subsequent brain stem compromise. However, not all patients with herniation have fixed and dilated pupils, and not all patients with nonreactive, enlarged pupils have uncal herniation. Therefore, we have tested an alternative hypothesis that a decrease in brain stem blood flow (BBF) is a more frequent cause of mydriasis and brain stem symptomatology after severe head injury. We determined the relation of BBF to outcome and pupillary response in patients with severe head injuries., Methods: One hundred sixty-two patients with a Glasgow Coma Scale score of 8 or less underwent stable xenon computed tomographic blood flow determination at the level of the superior colliculus, and this blood flow was correlated with pupillary features, intracranial pressure, computed tomographic scan pathology, and outcome., Results: A BBF of less than 40 ml/100 g/min was significantly associated with poor outcome (P < 0.009). In patients with bilaterally nonreactive pupils, the BBF was 30.5+/-16.8 ml/100 g/min, and in those with normally reactive pupils, the BBF was 43.8+/-18.7 ml/100 g/min (P < 0.001). Intracranial pressure and the presence of a brain stem lesion observed on the computed tomographic scan did not correlate with BBF, pupillary size, or reactivity. Unfavorable outcome at 12 months was directly related to age (P = 0.062) and inversely related to pupillary responsiveness (P = 0.0006), pupil size (P = 0.005), and BBF of less than 40 ml/100 g/min (P = 0.009)., Conclusion: These findings suggest that pupillary dilation is associated with decreased BBF and that ischemia, rather than mechanical compression of the IIIrd cranial nerve, is an important causal factor. More important, pupil dilation may be an indicator of ischemia of the brain stem. If cerebral blood flow and cerebral perfusion pressure can be rapidly restored in the patient with severe head injury who has dilated pupils, the prognosis may be good.

Forty consecutive patients who underwent craniotomy for traumatic hematoma after developing bilateral fixed dilated pupils were studied to determine the factors influencing quality of survival and to seek criteria for management. Clinical and computerized tomography (CT) data were correlated with outcome 1 year after craniotomy. The functional recovery (good outcome or moderate disability) rate was 25%, with a mortality rate of 43%. Patients with subdural hematoma had a higher mortality rate (64%) compared to patients with extradural hematoma (18%) (chi-square test, p > 0.05). Other factors associated with markedly increased morbidity and mortality were increasing age (> 20 years), a prolonged interval (> 3 hours) between loss of pupillary reactivity and craniotomy, compression of basal cisterns, and presence of subarachnoid hemorrhage on CT. There were no survivors among patients exhibiting any of the following features: surgery 6 hours or more after bilateral loss of pupillary reactivity; age greater than 65 years; or absent motor response. Apart from the latter group, the nature of motor response (before pharmacological paralysis and intubation) was not a reliable predictor of mortality. The results suggest that the presence of an acute subdural hematoma is the single most important predictor of negative outcome in patients with bilateral unresponsive pupils.

A traumatic cerebral contusion causes a zone of perifocal neuronal necrosis, the cause of which is not known; the surgical management of these lesions remains controversial. To determine the pathophysiological mechanisms responsible for brain damage after contusions, the authors performed cerebral blood flow (CBF) mapping studies and related these to change in local cerebral blood volume (CBV) and ultrastructure. In 11 severely head injured patients with contusion, CBF and CBV were measured in pericontusional areas using stable xenon-computerized tomography (CT). These studies demonstrated a profound reduction in perilesional CBF (mean 17.5 +/- 4 ml/100 g/min), which was always accompanied by a zone of edema defined by CT density measurements. Mean CBV in these regions was 2.3 +/- 0.4 ml/100 g, a reduction to approximately one-half the value of 4.8 ml/100 g found in the nonedematous regions, and to approximately 35% of the value of 6.0 ml/100 g found in normal volunteers. Ultrastructural analysis of the pericontusional tissue, taken at surgery in four patients with high intracranial pressure showed glial swelling with narrowing of the microvascular lumina due to massive podocytic process swelling. Additionally, some suggestion of vascular occlusion due to erythrocyte and leukocyte stasis was seen. These data support the conclusion that microvascular compromise by compression and/or occlusion is a major event associated with profound perilesional hypoperfusion, which is a uniform finding within edematous pericontusional tissue.

A detailed review of 100 consecutive head injury deaths in the Natal area was undertaken after forensic autopsies had been performed; neurohistological examination was carried out in 69 cases. It was found that one-third of deaths could have been prevented by medical treatment. Hypoxic and ischaemic brain damage was judged to be a contributing cause of death in 88% of all victims. Factors isolated as major causes of preventable death included: failure to prevent hypoxic brain damage by timeous endotracheal intubation and rapid resuscitation; major delays in referral from feeder hospitals; and failure to detect intracerebral haematomas and contusions which subsequently caused raised intracranial pressure. Recommendations for improving this situation are discussed, with particular reference to the situation in Natal.