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.