New horizons (Baltimore, Md.)
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Mannitol has replaced other diuretics as the agent of first choice for control of raised intracranial pressure (ICP) after brain injury. Mannitol should be given as a bolus intravenous infusion, over 10 to 30 mins, in doses ranging from 0.25 to 1.0 g/kg body weight. It may be given when high ICP is suspected, prior to computed tomography scanning, e.g., in patients who develop a fixed, dilated pupil or neurologic deterioration. ⋯ A Foley catheter should always be inserted when mannitol is used. Serum osmolality should be measured frequently after mannitol and maintained < 320 mOsm to avoid renal failure. Its beneficial effects and the rationale for its use are also reviewed.
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Following severe head injury, derangements of the cerebral vasculature and cerebral blood flow (CBF) often occur, rendering the brain at risk of secondary ischemia. Therefore, monitoring of CBF in head-injured patients is considered useful for understanding the pathophysiology and effects of therapy, although such monitoring has not yet become part of routine patient management in most centers. In this article, we review the current research on CBF in head injury. ⋯ Disturbances of cerebrovascular CO2 reactivity and autoregulation appear to be less frequent than previously assumed. However, when present, such derangements do have consequences for therapy, in particular the management of blood pressure and cerebral perfusion pressure. Potential implications for patient management are discussed.
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Monitoring and management of intracranial pressure (ICP) are fundamental to modern neurotraumatology. Although never formally proven to independently improve outcome in prospective, randomized, placebo-controlled trials, there is such a predominance of indirect support for this modality that most neurotrauma protocols are impossible with-out its inclusion and ethical considerations virtually preclude placebo-controlled trials of its efficacy. In addition to the question of improving outcome, ICP monitoring is also useful in guiding the use of potentially harmful treatment modalities such as hyperventilation, mannitol, and barbiturates, and also provides important prognostic data. ⋯ Cerebral autoregulation generally remains at least partially preserved after severe head injury, although the CPP value at which it is activated appears to be shifted upward. Therefore, maintaining adequate CBF appears to require using an elevated minimal CPP threshold when treating the injured brain. A generally accepted value of 70 mm Hg is suggested.
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The management of brain swelling that frequently occurs following severe traumatic brain injury (TBI) presents a difficult challenge for physicians treating these patients. A traditional cornerstone for the treatment of post-traumatic brain swelling has been prophylactic hyperventilation to reach PaCO2 levels of 25 to 28 torr. While there are anecdotal reports of improvement in intracranial pressure (ICP) and neurologic functioning following institution of this therapy, the only prospective, randomized trial of its use has found worse outcomes in those treated with prophylactic hyperventilation therapy for 5 days. ⋯ In some cases, TBI also causes an increase in cerebral vascular responsivity to hypocapnia, increasing the drop in regional CBF that occurs with hyperventilation. Thus, there is a well defined physiologic basis for expecting hyperventilation to cause worsened clinical outcomes following TBI. While this therapy clearly is indicated for the management of acute neurologic deterioration or intracranial hypertension refractory to all other forms of medical therapy, hyperventilation is no longer recommended as a first-line therapy for intracranial hypertension or as prophylactic therapy following severe TBI.
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In patients requiring ICP monitoring, a ventricular catheter connected to an external strain gauge transducer or catheter-tip pressure transducer device is the most accurate and reliable method of monitoring ICP, and enables therapeutic CSF drainage. Clinically significant infections or hemorrhage associated with ICP devices causing patient morbidity are rare and should not deter the decision to monitor ICP. ⋯ These devices are advantageous when ventricular ICP is not obtained or if there is obstruction in the fluid coupling. Subarachnoid or subdural fluid-coupled devices and epidural ICP devices are currently less accurate.