Cerebral aneurysm is an acquired intracranial vascular disease. The rupture of the aneurysm is the most common cause of intracranial hemorrhage (hemorrhagic stroke) and associated with a high morbidity and mortality. Its etiology is still undefined， but hypertension is present in all patients. The prevalence is 2，000 per 100，000 (2%) in North America and patients in age of 40-60 years old. The incidence is higher in female than in male (1.6:1).

Clinical presentation

Unruptured aneurysm is asymptomatic and the diagnosed is made due to unrelated causes. When ruptured， the patient typically presents with a sudden onset of severe headache (“worst headache in my life”)， and usually does not respond to any pain treatments. Other symptoms and signs depend upon the involved brain area and the development of hydrocephalus. Hunt-Hess grading system (HHG) has been used to classify the severity (table 1). Patients in grade 0-II may have a favorable outcome after surgical clipping or coiling， while those in grade IV-V usually carry a high mortality risk or recover with severe disabling. Other abnormal findings include ST and T wave changes and arrhythmia shown on ECG (50%) and even elevated cardiac enzymes， which are likely due to increased central sympathetic output. The patients may develop hypovolemia due to fluid restriction， pharmacologic diuresis and supine position. Hyponatremia is the most common electrolyte disturbance and caused by the limitation of sodium replacement and inappropriate antidiuretic hormone (SIADH) secretion or cerebral salt wasting (CSW).

Clinical diagnosis

Any patient suspected to have a ruptured aneurysm should undergo an urgent non-contrast head computerized tomography (CT) scan. The presence of focally increased intensity in the subarachnoid space strongly suggests the diagnosis of subarachnoid hemorrhage (SAH). Other CT findings include a unilateral dilated ventricle， midline shift， and the clot accumulation in the skull base. The CT scan with positive findings is followed by an angiography of carotid and vertebral arteries to define the cause. Additionally， the angiography reveals the detailed anatomy of the aneurysm and， therefore， very helpful to the surgical clipping or coiling.

Clinical course

Any aneurysm of ≥1.0 cm is recommended for surgical clipping or coiling because of an increased probability of spontaneous rupture， while aneurysms of <7mm should be followed closely by periodical angiography. If ruptured， one third die immediately， the other third become severely disabled， and the remaining third with preserved neurological functions need an emergent intervention because of a high mortality associated with rebleeding (30-50%) or vasospasm (10-30%). The recent recommendations for ruptured aneurysm include early surgical clipping with removal of the clot and aggressive treatment of vasospasm， or coiling by endovascular approach. In addition， such an early intervention may decrease the cost (e.g.， shorter hospital stay).

Aneurysm clipping or coiling

Surgical clipping of the aneurismal sac is the “gold standard”. The advancement in microsurgery has increased the successful rates in clipping those anatomically challenging aneurysms. The endovascular approach of aneurysm coiling has been widely accepted. Studies suggest that coiling has a comparable outcome to surgical approach. It is also an invaluable alternative for those aneurysms in difficult anatomic locations (e.g.， basilar tip aneurysm) or for the patients who may not tolerate the surgery.

Anesthesia management

The goal is to maintain adequate cerebral perfusion and oxygen delivery， avoid increase transmural pressure (TMP = mean arterial pressure – intracranial pressure)， readily provide brain protection， and a rapid anesthesia emergence for neurologic assessment.

Pre-operative preparation: Knowing your patients， evaluating neurologic deficits， co-morbidity， medications， reviewing angiography， and discussing with surgeon the possibility of temporary clamp. The severity， acuteness， HHS， presence of intracranial hypertension as well as timing of the procedures will determine the anesthesia management.

Monitoring: besides standard monitors， an arterial catheter is routinely placed prior to induction. The core temperature is monitored using an esophageal probe. Central line， pulmonary catheter and TEE have their special indications but not routinely employed in my institution. Depending on institutions， special neurologic monitors may be applied， e.g.， electroencephalography (EEG)， somatosensory evoked potentials (SSEPs)， motor evoked potentials (MEPs)， and transcranial Doppler (TCD). However， there is no data to support such monitoring could improve the outcomes. Bispectral index (BIS) is useful for interpreting raw EEG during burst suppression.

Anesthetic techniques: there is no restriction in the choice of a specific anesthetic technique. Considering some special issues may help to formulate a special plan for a specific patient. CPP stands for the coronary and cerebral perfusion pressures. It is important to maintaining an adequate perfusion to the heart while avoiding over increase of TMP during induction. Propofol or thiopental combined with rocuronium and fentanyl (5-10 mcg/kg) is commonly used for induction. Anesthetic maintenance is by a volatile agent ≤1MAC (i.e.， isoflurane， sevoflurane， or desflurane) with opioids， or total intravenous infusion (TIVA) with a muscle relaxant (e.g.， vencuronium or cisatracurium). Keeping a steady anesthetic condition is especially important during neurologic monitoring. Intraoperative narcotic infusion has become popular (e.g.， sulfentanil 1-3 mcg/kg/hr or remifentanil 0.5-5 mcg/kg/hr) to blunt hemodynamic responses to noxious stimuli. Brain relaxation: a good brain condition is critical for surgical exposure. Maneuvers to lower ICP include hyperventilation to reduce PaCO2 to 25–30 mmHg， diuresis (mannitol 0.5-1.0 g/kg and furosemide 10-20 mg)， and positioning (a slight head elevation and avoidance neck over turn obstructing venous return). Seizure prevention: the exactly incidence of seizure is unknown but could be catastrophic if happens; intravenous (iv) delantin may be administered for prophylaxis. Blood pressure: the BP is increased (by 20% from baseline) prior to and during clipping to augment CPP. Phenylephrine is widely used and epinephrine is the drug of choice for those with poor left ventricular function. Controlled hypotension is no longer popular and only used under some extreme conditions. Brain protection/ burst suppression: when a temporary interruption of blood supply to a distal brain area is expected to exceed 12-15 minutes， a focal brain protection is mandatory. This is achieved by iv sodium thiopental and guided by burst suppression in raw EEG monitoring during the period of interruption. Fluids and intravascular volume: most patients are volume depleted due to NPO， fluid restriction and use of diuretics， and therefore， susceptible to hypotension. The recommendation for fluid management is to maintain normovolemia with isotonic saline solution. Anesthesia emergence: patients in HHG 0-II are aimed for a smooth extubation in operating room for neurologic assessment， while those with poor neurologic score are likely remain intubated and transported to intensive care unit (ICU) directly. Postoperative care: all patients are admitted into ICU postoperatively for the close monitor and prompt treatment of potential complications， e.g.， rebleeding， ischemic cardiac events， SIADH， CSW， or diabetes insipidus. Daily TCD is mandatory for early detection of cerebral vasospasm.

Special issues

1. Hydrocephalus: 15-20% of patients would develop a communicating or obstructive hydrocephalus. It may require an emergent drainage (cerebra