Intracranial Internal Carotid Artery Aneurysms

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CHAPTER 367 Intracranial Internal Carotid Artery Aneurysms

Saccular aneurysms of the internal carotid artery (ICA) trunk and posterior communicating segment represent about 30% to 50% of all intracranial aneurysms. Although in the past these aneurysms were considered relatively easier to approach surgically than other aneurysms, currently most of them are amenable to endovascular coil embolization, which has proved to be less risky in selected cases.1 Consequently, the remaining aneurysms referred for surgical treatment are no longer straightforward cases, are generally large or giant, and incorporate a major artery into their neck. These aneurysms may have a complex anatomy and relationship to surrounding neurovascular structures in the subarachnoid space; thus, an intimate understanding of the relationship of the aneurysm to these structures is necessary and can be achieved by careful assessment using multislice computed tomographic angiography (CTA), three-dimensional CTA,2 and if necessary, four-vessel cerebral angiography.

In this chapter, we discuss aneurysms arising from the posterior communicating artery, anterior choroidal artery, ICA bifurcation, and ICA trunk; the anatomy relative to their specific locations; current diagnostic evaluation methods; general surgical management and techniques; and pitfalls. The blood blister–like aneurysms and their management are also briefly described.

Diagnostic Evaluation

In the setting of subarachnoid hemorrhage (SAH), computed tomography (CT) scan of the brain is the investigation of choice to detect blood in the subarachnoid space. It is extremely sensitive for detecting subarachnoid blood in the acute phase. It also gives an idea about the possible location of the aneurysm, which may be helpful in determining the aneurysm that has likely ruptured in a patient with multiple intracranial aneurysms. CTA, three-dimensional CTA, and magnetic resonance angiography (MRA) have shown reliable results in detecting aneurysms equal to or grater than 2 to 3 mm in diameter.24 Digital subtraction angiography (DSA) remains the “gold standard” when the CTA findings are negative or doubtful and when dynamic studies need to be undertaken. It is superior to other diagnostic modalities in determining certain characteristics of the aneurysm, although the current CTA technology can better detect some features such as intra-aneurysmal calcification and atherosclerotic changes in the parent vessel as well as the relationship with the bony structures intracranially. The possibility of sacrificing the posterior communicating artery during clipping of the aneurysm, which is extremely dangerous in patients with fetal origin of posterior cerebral artery, could be evaluated using dynamic DSA. DSA also demonstrates some of the perforating arteries in and around the aneurysm and the parent vessel. The location of the proximal neck of the aneurysm and the projection of the angiographic pictures are extremely important in deciding the surgical strategy and the need for additional bone removal. It is now routine practice to manage intracranial aneurysms based on CTA5 results, and DSA is requested only in specific situations, such as very large or giant aneurysms or the need for dynamic studies and carotid test occlusion.

Operative Management

Preoperative Care

Based on the presentation of the patient, preoperative preparations vary. Patients with SAH are first checked for airway, breathing, and circulation, and are then assessed neurologically to determine SAH clinical grade using the World Federation of Neurological Surgeons (WFNS) grading system.6 The four major issues to be addressed before planning a strategy to obliterate the aneurysm are rebleeding, hydrocephalus, electrolyte abnormalities, and vasospasm. Rebleeding can be as high as 6% in the first 48 hours and may be associated with devastating results. Hydrocephalus may occur as early as a few hours after the hemorrhage, and when shown on a CT scan of a patient with a poor-grade SAH or a patient whose condition has deteriorated, an external ventricular drain will help return most of these patients back to a better grade. Serum electrolyte disturbance is also seen after SAH and must be corrected before deciding on management plans. Vasospasm starts and peaks at day 3 through day 14 and kills or severely disables about 14% of patients.7

The current practice suggests treatment of favorable-grade aneurysms within the first 24 to 48 hours after the SAH. Poor-grade patients (WFNS grade V and some WFNS grade IV patients) are allowed to recover in the intensive care unit with optimization of their electrolytes and antiseizure medications and an external ventricular drain if they have hydrocephalus, and they are only treated if they show improvement in SAH grade. If they are not suitable candidates for endovascular coiling, surgical clipping is performed. A calcium channel blocker (e.g., nimodipine) is administered orally in a dose of 60 mg every 4 hours, and the patient is kept euvolemic to slightly hypervolemic if his or her cardiac status allows that. Hypertension is controlled with the use of β blockers or calcium channel blockers, especially preoperatively, and is allowed to rise slightly postoperatively.

Steroids are not used in the perioperative management of patients with SAH unless they were on replacement therapy for other reasons, in which case they take a stress dose of hydrocortisone 100 mg twice daily. Anticonvulsants are used in patients who develop seizure after SAH. Broad-spectrum antibiotics are given just before the operation to reduce the risk for wound infection and are continued for 3 postoperative doses. Patients with unruptured aneurysms are admitted on the same day of surgery after a preoperative assessment by the neurosurgeon and the neuroanesthetist and are discharged from the hospital 2 to 4 days after a CTA or angiogram if they are well enough and have not had a complication.

Postoperative Care

The major concerns in the patient with aneurysmal SAH after treatment of a ruptured aneurysm are vasospasm, hydrocephalus, electrolyte imbalance, seizures, brain swelling, postoperative stroke, and rebleeding from a residual portion of the aneurysm. The patient is kept in the intensive care unit in a euvolemic to slightly hypervolemic state with central venous pressure kept at 8 to 12 cm H2O. The blood pressure is allowed to rise to the patient’s high normal without the use of inotropes or vasopressors unless the patient shows clinical evidence of vasospasm. The serum sodium level is kept at 135 to 148 mmol/L. Patients with SAH-induced seizure are maintained on phenytoin (Dilantin) postoperatively for 6 months to 1 year. CT and CTA of the head are done only if the patient’s condition deteriorates or on postoperative day 2 as a baseline examination to check the quality of aneurysm clipping and evaluate the size of the major vessels in the circle of Willis in patients with SAH. Symptomatic hydrocephalus documented on CT scan is treated initially with external ventricular drainage (EVD) and then with ventriculoperitoneal shunt insertion if there is persistent symptomatic hydrocephalus. When there is significant residual clot inside the ventricles, EVD or repetitive lumbar puncture is used, and after the CSF is cleared, a permanent shunt is inserted. Routine DSA is done on postoperative day 7 to 10 to ensure complete obliteration of the aneurysm unless the patient shows clinical evidence of vasospasm, in which case an angiogram is done, possibly with balloon angioplasty or intra-arterial papaverine injection, or both. If clipping is incomplete, surgical, endovascular, and follow-up options are discussed for treating the residual aneurysm.

Specific Aneurysm Location

Posterior Communicating Artery Aneurysms

Anatomy

The communicating segment of the ICA (C7 segment)8 begins just below the posterior communicating artery and ends at the bifurcation. Two major arterial branches—the posterior communicating artery and the anterior choroidal artery—arise from this segment. The posterior communicating artery arises from the posteromedial surface of the ICA and courses medially and inferiorly, through the membrane of Liliequist, above and medial to the oculomotor nerve, to join the posterior cerebral artery at the junction of the P1 and P2 segments of the latter. Multiple perforators arise from the posterior communicating artery and are named the anterior thalamic perforators. These can be stuck to the aneurysm and should not be clipped with the aneurysm. In about 20% of patients, the P1 segment of the posterior cerebral artery is hypoplastic, and the posterior cerebral artery arises directly from the posterior communicating artery.9 This is called fetal origin of posterior cerebral artery, and in these patients, the posterior communicating artery cannot be sacrificed, and the aneurysm must be clipped in a way to guarantee patency of the parent vessel.

The typical posterior communicating artery aneurysm arises just distal to the origin of the artery from the wall of the ICA and hence is classified as an ICA aneurysm. It projects posteriorly, laterally, and slightly inferiorly and may pinch the oculomotor nerve as it enters the dural fold of cavernous sinus, and hence the third nerve palsy, with an acutely expanded posterior communicating aneurysm. It does not usually point medially and so does not bleed into the sella because its pushed out by the curve of the internal carotid laterally. However, some posterior communicating artery aneurysms arise just proximal to the posterior communicating artery origin and might have a slightly less lateral or even medial projection.10

Presentation

Aneurysms of this segment of the ICA are the most common type of ICA aneurysms, representing about 50%,11 and are more common in females. They usually cause symptoms when smaller than 10 mm in patients with SAH, with a lateral suprasellar and ambient cistern pattern, intraparenchymal hemorrhage into the uncus of the temporal lobe, intraventricular hemorrhage into the temporal horn, or hemorrhage into the subdural space, or they could expand and compress the third cranial nerve, causing painful non–pupil-sparing oculomotor nerve palsy. SAH could also irritate the dura and cause retro-orbital pain,12 The environmental conflict of this location has been suggested as a risk factor for rupture of these aneurysms with smaller size.13 The International Study of Unruptured Intracranial Aneurysms (ISUIA) has shown a likelihood of rupture for this location, similar to that associated with posterior circulation aneurysms.14

Operative Technique

Under general anesthesia and endotracheal intubation, the patient is positioned in the supine position, the head is secured in the point fixation, the ipsilateral shoulder is raised using a gel roll, and the patient is strapped to the table to allow intraoperative rotation of the operating table. The head is then slightly extended and tilted to the opposite side, The neck is slightly flexed to allow proper venous drainage. This allows the brain to fall away from the base of the skull, minimizing retraction on the brain. A curvilinear shape half an inch wide is shaved, and the skin is then prepared and draped along the line. The skin incision is made starting at the ipsilateral zygoma and curving forward and medially to the forehead at midline, and the skin flap is reflected forward leaving the pericranium on the bone. The pericranium is then reflected as a vascularized flap based frontally. The interfascial dissection of the temporalis muscle is performed to preserve the frontal branch of the facial nerve, and the muscle is reflected inferoposteriorly, leaving a cuff of fascia superiorly to suture it to at closure. The “keyhole” region behind the frontozygomatic junction is exposed.

The large bur of the drill is used to make a bur hole in the posterior temporal region under the muscle, and the dura is stripped away from the bone to allow placement of the foot plate epidurally. The drill is used to carry out the craniotomy, and the keyhole region is drilled down to the internal sphenoid ridge. The dura is then separated from the sphenoid wing medially, and the wing is either drilled or rongeured to enter the lateral exposure of the superior orbital fissure. The frontal inner table is then beveled with the drill. If the frontal air sinus is opened, it is exenterated and packed with the muscle piece and covered with the vascularized pericranial flap and fibrin adhesive at the end of the procedure. The dura at the edge of the craniotomy is then tacked up to the bone through tangential holes. A curvilinear incision is made in the dura, and the dural flap is reflected anteriorly. If the brain is still full despite mannitol and hyperventilation to PCO2 of 25 to 30 mmol/L, especially if the patient has hydrocephalus, a catheter is passed into the frontal horn of the lateral ventricle 2.5 cm above the base of the frontal lobe and 2.5 cm anterior to the sylvian fissure.15 Wide splitting of the fissure should be performed for all aneurysms in the anterior circulation to minimize brain retraction. The aneurysm can be exposed without brain retractors because the surgeon can use microsurgical bipolar forceps and the microsuction simultaneously to keep the fissure open and work around the aneurysm. The use of retractors is recommended for ruptured aneurysms and when the splitting of the fissure is completed.

During the splitting of the fissure, gentle frontal lobe retraction by microsuction or retractor allows proper visualization of the proximal end of the fissure, the optic nerve, and the proximal ICA. The optic and carotid cisterns are then opened. The optic nerve is then separated from the undersurface of the frontal lobe using sharp dissection to allow the frontal lobe to fall away with minimal retraction.

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