How is increased ICP treated?

How is increased ICP treated?

Treatment of increased ICP may begin by changing the patient’s position. Recent studies have shown that a change to the reverse Trendelenburg position in anesthetized patients will rapidly reduce ICP. Head elevation promotes drainage of venous blood from the brain and is surpris-ingly effective at reducing brain bulk. Obstruction of this venous outflow (e.g., by improperly placed tape around the neck, improper positioning of the patient, positive end-expiratory pressure (PEEP), etc.) is often an overlooked cause of increased brain volume. Hyperventilation is the most common means of acutely reducing ICP. Acutely lowering ICP via hyperventilation (PaCO₂ reduction) is another method frequently employed in the intubated patient. Hyperventilation is simple to perform and results in rapid and dramatic decreases in ICP. Until recently it was implemented in all patients suspected of having raised ICP, but neuronal ischemia caused by hyperventilation has now been demonstrated in humans. Alteration of PaCO₂ within the range of approximately 20–80 mmHg causes parallel changes in CBF.

The two other intracranial compartments, CSF and brain parenchyma, are also amenable to volume reduction. CSF withdrawal can take place through a ventriculostomy, and its production reduced by acetazolamide, a carbonic anhydrase inhibitor. Brain edema may respond to osmotic or loop diuretics, such as mannitol and furosemide respec-tively. The resulting diuresis reduces intravascular volume and cerebral blood volume. Mannitol’s onset of action is approximately 30 minutes and its effect is accelerated by furosemide. Use of osmotic agents requires a globally intact BBB with only minimal areas of disruption.

Struggling or coughing against a tracheal tube should be prevented and is best accomplished via administration of sedative agents such as benzodiazepines, barbiturates, propo-fol and opioids, as well as muscle relaxants. Prevention of hypertension, tachycardia and straining results in lowering of CMRO₂ and CBF.