intracranial aneurysms

Patients with intracranial aneurysms present for surgery electively or emergently following SAH.

1. Preoperative evaluation of patients with SAH should include all components of a routine preoperative evaluation (see Chapter 1), with attention to known associated physiologic perturbations. These include the neurologic grade (Table 25.2), presence of vasospasm (and the hemodynamic parameters that have been effective in relieving clinical symptoms), degree of hydrocephalus, ICP elevation, and concurrent drug therapy such as calcium channel blockade with nimodipine, which may cause moderately lower systemic pressures intraoperatively. Electrocardiographic changes are common after SAH and include arrhythmias and fluctuating ST-segment, QT-interval, and T-wave changes. These are probably caused by subendocardial injury following the autonomic discharge that occurs in association with the initial SAH. Provided these are not associated with cardiac dysfunction, no modification of patient management is necessary although recent data suggest that a heart rate of either less than 60 or greater than 80 or the presence of nonspecific ST/T wave abnormalities are independently associated with increased mortality in SAH patients receiving aneurysm clipping. Cardiac biomarkers may be increased as well.
2. Current practice is to intervene early during the first 72 hours after SAH for patients with neurologic grades I to III, which decreases the risk of rebleeding and facilitates the hypertensive management of vasospasm.
3. Specific anesthetic considerations include the following:
   1. Avoidance of hypertension, which may increase the risk of aneurysm rupture, before aneurysm clipping. Prophylactic use of agents such as IV nicardipine, fentanyl, β-adrenergic blockers, lidocaine, or additional doses of barbiturates or propofol will often attenuate the blood pressure response to noxious stimulus such as laryngoscopy and intubation.
   2. Avoidance of hypotension to maintain adequate CPP in the recently insulted brain with resultant altered autoregulation and often marginally perfused areas of brain.
   3. Providing adequate brain relaxation to optimize surgical exposure. Rapid reductions in ICP may affect transmural pressure and increase the risk of aneurysm rupture. This should be done cautiously before dural opening.
   4. Induced hypertension may be requested during temporary clipping to improve collateral blood flow to regions that were perfused by the clipped arteries. Often, IV phenylephrine is used for this purpose. It is critical that hypertension be induced only after the temporary clip has been placed.
   5. Intraoperative aneurysm rupture can produce rapid and massive blood loss requiring large-bore IV access for volume resuscitation. Accurate estimation of blood loss is essential to guide volume repletion. Induced hypotension, adenosine planned arrest, or, occasionally, manual pressure on the ipsilateral carotid artery in the neck may be helpful during the desperate situation of a large and uncontrolled premature rupture.
   6. Mild hypothermia (34°C) has been traditionally used as a protective strategy for the brain during periods of cerebral ischemia. Data from the Intraoperative Hypothermia for Aneurysm Surgery Trial (IHAST), however, suggest that hypothermia does not improve either neurologic or neuropsychologic outcome in good-grade surgical SAH patients. Given the cardiac and infectious morbidity associated with hypothermia, it is now a matter of controversy whether hypothermia is the desired physiologic goal for aneurysm surgery.
   7. Once the permanent clips have been placed on the aneurysm, prevention of postoperative vasospasm becomes important. Blood pressure is increased moderately, and fluids are administered to achieve a mildly positive fluid balance.
   8. When appropriate, the anesthetic should be designed for a prompt emergence from anesthesia to enable an immediate neurologic examination to ensure that clip placement does not compromise the parent vessel.