Traumatic Brain Injury

Intracranial hypertension (IH) is currently managed in the intensive care unit with a combined medical – surgical approach. Progress in monitoring and in understanding pathophysiological mechanisms of IH could change current management in the intensive care unit, enabling targeted interventions that could ultimately improve outcomes. The prevention of secondary brain damage from raised intracranial pressure (ICP) is the central focus of neurologic intensive care. The primary goal of ICP management is to maintain ICP below 22 mmHg and cerebral pressure perfusion (CPP) above 60 mmHg. Optimization of oxygenation and cerebral blood flow (systolic blood pressure greater than 110 mm Hg) are essential. The use of positive end-expiratory pressure (PEEP) can increase intrathoracic pressure, thereby potentially increasing ICP by impeding venous drainage. Maintenance of euvolemia and strict monitoring of fluid balance are necessary. Several commonly described measures may be effective in reducing raised ICP such as keeping the patient’s head neutral and elevated at 15 to 30° as these optimize venous drainage. Proper muscle relaxation, adequate analgesia and sedation depth could further minimize elevation of ICP by reducing metabolic demand, ventilator asynchrony, venous congestion, and the sympathetic responses of hypertension and tachycardia. Fever increases brain metabolism and should be treated aggressively. Prophylactic antiepileptic medications should be considered only for traumatic brain injury. Dexamethasone and other steroids should not be used for treatment of IH, except in tumor patients. Hyperventilation should be limited to emergency management of life-threatening raised ICP until other methods of managing IH are available as it can acutely and reliably lower ICP and PaCO2. Hyperosmolar therapy is the principal medical management strategy for elevated ICP. Therapeutic strategies involve the use of mannitol or hypertonic saline. Mannitol is often considered the gold-standard therapy for medical management of IH but the preponderance of current evidence suggests that hypertonic saline could be. Failure of other conservative measures to control ICP should prompt consideration of the initiation of pentobarbital infusion. Aggressive strategies, like surgical decompression or hypothermia, carefully tested, have controversial effects on outcome. Decompressive craniectomy is indicated for massive ischemic stroke as it improved the survival rate and Glasgow outcome scale. Placement of an external ventricular drain should be considered in patients with moderately sized ventricles and signs and symptoms of raised ICP.

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The ability of the cerebral vascular bed to undergo constriction or dilation in response to various stimuli is termed vascular reactivity or cerebral autoregulation. When the stimulus is the change in cerebral perfusion pressure (CPP) the vascular response is termed cerebrovascular pressure reactivity. When the stimulus is the change in PaCO2 the vascular response is termed carbon dioxide reactivity. The transcranial Doppler (TCD) provides information about changes in flow velocities secondary to changes in CPP or PaCO2.

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