C Cerebral aneurysm
1. Introduction
Cerebral aneurysms are abnormal, localized dilations of the intracranial arteries. They are classified as berry or saccular, mycotic, traumatic, fusiform, neoplastic, or atherosclerotic. Rupture of a saccular aneurysm is a leading cause of subarachnoid hemorrhage (SAH).
Approximately 5 million people in North America have cerebral aneurysms, with approximately 30,000 new cases of SAH occurring annually. The peak age for rupture of a cerebral aneurysm is 55 to 60 years. Aneurysmal ruptures are more common in women, occurring in three women for every two men.
More than one-third of patients with SAH die or develop significant and lasting neurologic disabilities before they receive any treatment. A small bleed occurs in approximately 50% of patients and is often tragically ignored or misdiagnosed. Even in patients who receive prompt care, only half remain functional survivors; the other half of patients die or develop serious neurologic deficits.
Aneurysms may arise at any point in the circle of Willis. The most common locations of aneurysms are shown in the following table. Most aneurysms are broad based and located in the middle cerebral system. Traumatic aneurysms develop as a result of direct trauma to an artery with injury to the wall.
Mirror aneurysms of the internal carotid system are common, and other combinations of locations occur (see table below). The site of the bleeding aneurysm is best located by computed tomography (CT) studies, evidence of vasospasm in the immediate vicinity, and lobulation of the aneurysm wall on angiographic studies.
Location and Occurrence of Cerebral Aneurysms
| Location | Occurrence (%) |
| Internal carotid | 38 |
| Anterior cerebral system | 36 |
| Anterior communicating junction | 30 |
| Internal carotid at posterior communicating junction | 25 |
| Middle cerebral system | 21 |
| Vertebrobasilar system | 5 |
From Frost AEM: Management of neurosurgical anesthesia: aneurysms. Curr Rev Clin Anesth 1991; 11:125-132.
b) Diagnosis of subarachnoid hemorrhage: Subarachnoid hemorrhage produces an abrupt intense headache in 85% of patients, and transient loss of consciousness may be seen in up to 45% of patients. Nausea and vomiting, photophobia, fever, meningismus, and focal neurologic deficits are common. The severity of an SAH can be graded clinically with the use of classifications listed in the table on pg. 372. Although surgical mortality rates vary somewhat among institutions, patients with a neurologic grade I SAH generally undergo surgical clipping with a low mortality rate (less than 5%), but grade V patients generally do not survive.
Hunt’s Classification of Patients with Intracranial Aneurysms According to Surgical Risk
| Grade | Perioperative Criterion | Mortality Rate (%) |
| I | Asymptomatic or minimal headache and slight nuchal rigidity | 0-5 |
| II | Moderate to severe headache, nuchal rigidity, no neurologic deficit, possible cranial nerve palsy | 2-10 |
| III | Drowsiness, confusion, or mild focal deficit | 10-15 |
| IV | Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity and vegetative disturbances | 60-70 |
| V | Deep coma, decerebrate rigidity, moribund appearance | 70-100 |
From Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28:14.
c) General considerations
Hypertension often accompanies acute SAH and is postulated to develop secondary to autonomic hyperactivity, which may increase transmural pressure in the aneurysmal sac. Transmural pressure is defined as the differential pressure between mean arterial pressure (MAP) and intracranial pressure (ICP) and represents the stress applied to the aneurysm’s wall.
Increases in blood pressure directly increase the transmural pressure and the likelihood of bleeding; conversely, reductions in blood pressure reduce transmural pressure. Caution should be exercised when purposefully reducing transmural pressure because cerebral autoregulation may be impaired after SAH, and a reduction in blood pressure may induce or aggravate cerebral ischemia, particularly if vasospasm is present. To balance these opposing concerns, many neurosurgeons attempt to maintain systolic blood pressure between 120 and 150 mmHg before clipping the aneurysm.
Electrocardiographic (ECG) changes are common after SAH and have been reported to occur in 50% to 80% of patients. The most common changes involve the T wave or the ST segment, but other changes such as the presence of a U wave, QTc-interval prolongation, and dysrhythmias may be present. Whether such changes in the ECG represent myocardial injury has long been debated. In the majority of patients, these changes do not appear to be associated with adverse neurologic or cardiac outcomes.
Rebleeding from a previously ruptured aneurysm is a life-threatening complication. The incidence of rebleeding is approximately 50% in the first days after SAH, and rebleeding is associated with an 80% mortality rate. The chance of rebleeding from an unsecured aneurysm declines over time, and by 6 months, the risk stabilizes at approximately 3% per year. Approaches used to decrease the risk of rebleeding include early surgical clipping, the use of antifibrinolytic agents, and blood pressure control.
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