Cerebral Aneurysm

Grade the bleed - Hunt and Hess grade and GCS tell you where the patient sits. Intubate for GCS 8 or less, hypoxia or hypoventilation, hemodynamic instability, or when deep sedation or general anesthesia is needed for imaging.

Blood pressure before the aneurysm is secured - Keep systolic under 160 mm Hg and MAP under 110 mm Hg. Nicardipine, clevidipine, esmolol, and labetalol are the usual agents. Nitroprusside is avoided because it raises cerebral blood volume and ICP. Do not overcorrect into hypotension.

Nimodipine - 60 mg orally or by NG tube every 4 hours, started within 48 hours of the bleed and continued for 21 days. It improves outcomes and is standard of care.

Preinduction arterial line - Put it in before induction in most patients, and certainly with cardiac dysfunction, elevated troponin, or hemodynamic instability. Deferring until after induction is reasonable only in low rupture-risk patients.

Induction - The goal is no hypertensive response to laryngoscopy, because that is a rebleed. Adequate depth first, short-acting opioid or an antihypertensive alongside the induction drugs. Treat post-induction hypotension aggressively with vasopressors, and avoid both hypo- and hypercarbia during mask ventilation. Succinylcholine is fine if you need an RSI.

Intraoperative targets - SBP under 160 mm Hg, MAP under 110 mm Hg, CPP above 60-70 mm Hg. Pin placement, positioning, and surgical stimulation are the critical moments. Normalize pressure once the aneurysm is secured.

Access and blood - Large-bore peripheral access is mandatory; blood loss can be high with intraoperative rupture. A central line is usually unnecessary unless postoperative pressors or inotropes are anticipated.

Temporary clipping - Raise systolic pressure 10-20% to push collateral flow, keep the clip on under about 10 minutes, use burst suppression to drop CMRO2, and lean on IONM to catch ischemia.

Intraoperative rupture - Adenosine 0.3-0.5 mg/kg produces roughly a minute of moderate hypotension and flow arrest so the surgeon can find and control the bleed. Expect transient arrhythmias on recovery, and avoid it in coronary artery disease, conduction abnormalities, and reactive airways.

Brain relaxation - Depth of anesthesia and analgesia, head-up positioning for venous drainage, PaCO2 of 30-35 mm Hg, mannitol, furosemide, or hypertonic saline, and CSF drainage through an EVD. Brief hyperventilation below 30 mm Hg only if the other maneuvers fail.

Glucose and temperature - Hyperglycemia worsens neurologic outcomes; check periodically and hold glucose between 80 and 180 mg/dL. Avoid hyperthermia. Intraoperative hypothermia for neuroprotection is not recommended.

Monitoring - Arterial line for pressure and serial gases, glucose, and electrolytes. SSEP and MEP for early ischemia, EEG when burst suppression is planned for temporary clipping, and ICP and CPP if an EVD is in place.

Endovascular coiling - Same hemodynamic goals. IONM and brain relaxation are not needed, but absolute immobility during coil deployment is, which is why general anesthesia is usually chosen over MAC. Heparin is commonly given and may need reversal.

Emergence - No coughing, straining, or hypertension. IV lidocaine 1-1.5 mg/kg blunts airway reflexes; remifentanil or dexmedetomidine can run through emergence. Skip nitrous oxide given pneumocephalus and PONV risk. Treat hypertension with labetalol, esmolol, nicardipine, clevidipine, diltiazem, or hydralazine, with caution on beta blockade in stress-induced cardiomyopathy.

When not to extubate - Discuss with neurosurgery for preoperative intubation, low preoperative GCS, cases running 8-10 hours, posterior circulation or posterior fossa work, or expected cerebral edema. Still wean the anesthetic for a neuro exam, and get a head CT if extubation cannot happen within an hour.

Sodium after SAH - Hyponatremia hits up to 30%, usually cerebral salt wasting (hyponatremia, volume contraction, urine sodium above 50 mmol/L) rather than SIADH — treat with isotonic or hypertonic fluid to normovolemia and normonatremia, not fluid restriction. Later hypernatremia is often iatrogenic from hyperosmolar therapy, or central diabetes insipidus at 12-48 hours postop: urine output above 250 mL/hour for 2 hours with sodium above 140 and dilute urine, treated with DDAVP 1-2 mcg and volume.

Cardiac complications - Stress-induced cardiomyopathy and arrhythmias are common after SAH. Baseline ECG, troponin, and echocardiography define the ventricle you are working with, and inotropes, vasopressors, and antiarrhythmics may be needed.

Watch for the delayed complications - Rebleeding in the first 24 hours, hydrocephalus in 20-30% needing CSF diversion, and cerebral vasospasm between days 3 and 14 causing delayed cerebral ischemia.

Cerebral aneurysms are dilations at weak points along the intracranial arterial circulation. About 90% are saccular (berry) aneurysms with a thin or absent tunica media and a fragmented or absent internal elastic lamina, and roughly 85% sit in the anterior circulation at bifurcations along the circle of Willis. Formation is multifactorial — hemodynamic stress on the internal elastic lamina, structural fatigue from turbulent flow, and T-cell and macrophage-mediated inflammatory remodeling of the wall.

Prevalence is roughly 3.2%, and risk rises with age, hypertension, smoking, alcohol, and atherosclerosis, as well as with polycystic kidney disease, Ehlers-Danlos syndrome, fibromuscular dysplasia, and coarctation. Rupture causes subarachnoid hemorrhage with about 20% mortality, 30-40% morbidity, and a 4-14% rebleed rate in the first 24 hours. The perioperative problem is simple: a wall that cannot tolerate a pressure surge until it is clipped or coiled.