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Once intracranial hypertension is documented, prompt therapy must be initiated. Increases in pressure must be interpreted within the context of the clinical situation. While treating increased ICP it is important to expedite treatment of the underlying condition, which may also be therapeutic for the intracranial hypertension (i.e., evacuation of a hematoma, drainage of CSF in hydrocephalus, or antibiotics). The general approach to increased ICP includes the following maneuvers:
The head is elevated to 15 to 30 degrees and is kept in a midline position to enhance cerebral venous outflow and maximize cerebral perfusion pressure.
The airway is secured and oxygenation is maintained with PaO2 at 100 mm Hg or greater. Elevated airway pressures should be avoided if possible.
Mannitol reduces ICP by decreasing blood viscosity, transiently increasing CBF, and improving oxygen transport, which results in a decreased adenosine level. The drop in adenosine causes cerebral vasoconstriction in areas of the brain that have intact autoregulation.[197] CBF remains constant with a decrease in CBV and ICP. Administration of mannitol also reduces ICP by an osmotic effect, which takes 20 to 30 minutes to develop and is due to movement of water from the brain parenchyma into the circulation.[198] Mannitol should be administered in 0.25- to 1-g/kg intravenous boluses only when necessary to control ICP.
The use of 3% saline solution has been gaining in popularity recently. [199] Because sodium does not penetrate the blood-brain barrier quickly, hypertonic saline administration creates an osmolar gradient like mannitol does. It has additional theoretical beneficial effects, including enhancement of cardiac output, reduction of inflammation, restoration of normal cellular resting membrane potential and cell volume, and stimulation of release of atrial natriuretic peptide.
Neuromuscular paralysis may reduce ICP in patients with intracranial hypertension by reducing the increased intrathoracic and venous pressure associated with coughing, straining, or "bucking" the ventilator.
Fear, anxiety, and the response to painful stimuli (surgical procedures, intubation, neurologic examination) increase CBF and ICP. Although sedating unconscious patients may appear incongruous and can even obscure the neurologic examination, under some circumstances the benefits may outweigh the risk. Most intravenous sedatives, including benzodiazepines, butyrophenones, and barbiturates, are efficacious and frequently decrease CBF and ICP. Ketamine increases CBF and should be avoided. Opioids can be used if the patient has responses to painful stimuli and respirations are controlled.
Steroids are efficacious in decreasing the vasogenic edema surrounding a brain tumor and reducing eighth nerve swelling and associated hearing loss from bacterial meningitis.[200] [201] It has become increasingly clear that steroids play no role in the treatment of traumatic brain injury or global cerebral edema. Precautions to avoid gastric ulceration should be undertaken if steroids are administered.
Hyperthermia is to be avoided in all patients with brain injury. The cerebral metabolic rate is proportional to body temperature: it increases 5% to 7%/°C. Antipyretic agents (acetaminophen) and cooling devices should be used for temperatures higher than 37°C. By contrast, hypothermia reduces the cerebral metabolic rate. At 30°C, the cerebral metabolic rate is 50% of control values. [202] [203] Some evidence indicates that induction of hypothermia before a cerebral ischemic insult can permit prolonged periods of inadequate CBF, but no reliable evidence has shown that hypothermia induced after an insult improves neurologic outcomes. Theoretically, there may be a rationale for decreasing the metabolic rate with hypothermia of 30°C to 35°C. In practice, temperatures lower than 33°C are associated with a number of multisystem complications that may increase morbidity and mortality. Hypothermia should not be induced unless the patient is paralyzed and anesthetized to prevent shivering.
Poor neurologic outcome has been associated with hyperglycemia after head injury in adults and children.[204] [205] Several investigators have demonstrated in animal models that hyperglycemia in the setting of incomplete cerebral ischemia leads to enhanced anaerobic glycolysis and lactic acidosis.[206] [207] [208] The ensuing acidosis in at-risk tissue results in extension of the initial injury. When insulin is used to maintain normoglycemia during temporary cerebral ischemia in rats, fewer neurologic deficits are seen than in their hyperglycemic counterparts.[209] Blood glucose levels should be checked. Hypoglycemia should be avoided, but the routine administration of dextrose-containing intravenous solutions in the setting of head injury should also be avoided.
Seizures cause an increase in metabolic requirements that results in increases in CBF, CBV, and ICP. In a paralyzed patient, an EEG should be obtained to document any seizure activity, and all seizures should be aggressively treated with anticonvulsants.
Barbiturates induce the greatest reduction in CBF and cerebral metabolism.[210] Thiopental, 1 to 5 mg/kg as an intravenous bolus, acutely reduces ICP for 5 to 10 minutes. For a more prolonged effect, pentobarbital (Nembutal), 3 to 30 mg/kg as an intravenous loading bolus followed by a maintenance dose of 1 to 2 mg/kg/hr, is effective in reducing ICP. Blood levels of 20 to 40 mg/L are generally effective, although higher levels may be necessary to achieve burst suppression on EEG monitoring and lower ICP. In these doses, barbiturate metabolism and excretion may be altered, and levels must be monitored closely. Because myocardial depression and hypotension are significant complications of barbiturate therapy, cardiovascular function must be closely followed with specialized monitoring (e.g., Swan-Ganz catheter) if high levels of drugs (30 mg/L) are required or if cardiac decompensation is evident.[211] Although barbiturate administration decreases ICP, it has not been conclusively demonstrated that barbiturates improve survival or neurologic outcome.[212] [213] [214]
An intravenous bolus of 1 to 1.5 mg/kg may be helpful in minimizing ICP increases that occur with noxious airway stimulation (i.e., endotracheal suctioning).
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