Fusiform and giant saccular aneurysm treatment - SLICE Next Frontiers 2023 - Jacky GOUDA

Fusiform and Giant Saccular aneurysms (A time bomb in the brain)

We all know that treatment of Fusiform and Giant Saccular aneurysms is very challenging. But we need first to know What is meant by a Giant Aneurysm?

Giant cerebral aneurysms, defined by a diameter above 25 mm, are often discovered through their mass effect or hemorrhage. [1] They represent approximately 5% of intracranial aneurysms [2].Two thirds of giant aneurysms are implanted on the anterior circulation, and 1/3 on the posterior circulation. [3].

Let’s talk about the natural history of Giant Aneurysms….

Three types of pathological event feature in the natural history of giant aneurysms: spontaneous thrombosis, progressive growth responsible for mass effect and rupture[1].

Giant aneurysms are classified as follows: Saccular, Fusiform, and serpentine.

Saccular that has an individualized neck comes from the progressive growth of small aneurysms most often on branching sites due to endothelial injury by the blood flow. Fusiform originates from the expansion of the entire circumference of the arterial wall. It can occur as a consequence of atherosclerosis or non-atherosclerotic diseases of the conjunctive tissue, such as Ehlers-Danlos syndrome or elastic pseudoxanthoma. Serpentine was initially described as a giant aneurysm partially thrombosed with serpentine channels coursing through regions of the thrombus [4].

What’s the Classification for Cerebral fusiform aneurysms?

(Mizutani classification):[6]

Type 1: Classic dissecting aneurysm: characterized by acute widespread disruption of the IEL without intimal thickening. Patients with Type 1 aneurysms had an ominous clinical course, and many presented with sudden subarachnoid hemorrhage with frequent rebleeding.

Type 2: segmental ectasias: They had an extended and/or fragmented IEL with intimal thickening. Weakness of the arterial wall caused by the damaged IEL was assumed to be compensated by the intimal thickening. The patients with Type 2 aneurysms had a placid clinical course.

Type 3: dolichoectatic dissecting aneurysms: They are characterized by fragmentation of the IEL, multiple dissections of thickened intima, and organized thrombus in the lumen. Most of them were symptomatic and progressively enlarged over time.

Type 4: saccular aneurysms arising from arterial trunk: They arose in areas with minimally disrupted IEL without intimal thickening, and there was a risk of rupture.

What is the clinical presentation of Fusiform and Giant Saccular aneurysms?

You need to know that sometimes the presentation can be mysterious like the case in this session that was presented with only psychiatric symptoms. So, if you don’t consider it, unfortunately you are going to miss it.

1. Pseudo tumoral syndrome: The mass effect syndrome gives nearly all the symptoms with a gradual neurologic deterioration. It exists in 50–75% of the cases in all reported series. [2]

2. Optic tract and hypothalamic compression: occurs with giant paraclinoid [7], and from ACOM aneurysms [8]. Visual symptoms are an asymmetric chiasmatic syndrome, associating a bitemporal quadrantanopia or hemianopia, seldom a scotoma and a decrease of visual acuity leading to blindness [9]. A hypothalamic compression is rarely observed, revealed by a hypopituitarism or a diabetes insipidus[10].The giant aneurysm of the anterior communicating system may exceptionally cause a frontal syndrome or olfactive disorders.

3. Hemispheric compression: The inferior compression of the hemisphere comes from giant aneurysms of the middle cerebral artery [11] and of the division of the internal carotid artery. This syndrome is associated with hemiparesis, visual dysfunction, or seizures through the irritation of the medial part of the frontal lobe (generalized or uncinate).

4. Posterior fossa syndrome: it can compress the inferior cranial nerves (IX, X, XI) with impairment of swallowing, intracranial hypertension syndrome (hydrocephalus), brainstem dysfunction with alternate or cerebellar syndrome [12]. Other cranial nerves VII, VIII with vertigo may be affected.

5. Subarachnoid hemorrhage: In a study of re-bleeding in initially untreated patients with giant aneurysms, 28% had a second hemorrhage. Moreover, the re-bleeding of giant aneurysms does not look more frequent than that in smaller aneurysms [13].

6. Brain ischemia: it can occur in 5% of the patients [5]. The mechanism is either embolic migration of fibrous deposits promoted by the turbulent intrasaccular flow, either an extensive thrombosis of the parent artery which is stretched and compressed by the giant aneurysm mass [14]; in some cases, intraluminal thrombus can reduce the size of the parent artery.

-Other symptoms may exist, such as headaches, ischemic stroke, or seizures. Whatever the topography, headaches alone or in association to other symptoms are often encountered. [1]

What are the strategies for treatment suggested by the faculty after a stunning discussion?

Treatment of Fusiform, giant saccular and irregular aneurysms is very challenging and strategy for treatment is tailored on a case-by-case basis, but we will mention options for treatment and some useful tips and tricks to put in consideration as you manage such complex cases.

For fusiform and Giant saccular aneurysm:

• Clip ligation at the distal end of the fusiform aneurysm combined with high flow bypass.

• Reconstructive technique: either Antegrade or Retrograde in a telescoping way then jail the microcatheter inside the sac for coiling.

• (Double flow divertor): place a long flow divertor to cover the whole length of the aneurysm and then put another short FD in a row with the first one to ensure thrombosis of the aneurysm.

• Intrasaccular FD: ex; WEB, Contour or Nautilus.

• Y-stenting: in case of Saccular aneurysms at a bifurcation site.

• For giant irregular saccular aneurysm: Balloon assisted, stent assisted coiling or simple coiling by placement of 2 microcatheters one in the daughter sac and the other in the Aneurysm itself are also options to consider.

• In cases of Giant irregular Saccular aneurysm with a daughter sac 🡪 you may first consider coiling of the daughter sac and then placing a web inside the aneurysm or placing a contour device🡪 to decrease the risk of bleeding from the daughter sac.

What are the tips and tricks suggested by the faculty?

• knowing the vascular anatomy of the Aneurysm is crucial especially for the perforators that may come out of the aneurysm.

• when a flow divertor comes in contact with perforators that are not coming out of the aneurysmal sac, the chance of them to be occluded is very low.

• If there are branches that come out of the sac 🡪 you should check for collaterals (Functional anatomic test) For example: if there are 2 divisions come out of the sac-🡪 place a proximal balloon 🡪 then place a microcatheter in each division to check which one has better collaterals🡪then inflate the balloon🡪inject contrast in both branches. if there is antegrade flow and stagnation occurs 🡪 this means that this branch has no collaterals, and you cannot sacrifice this branch.

• If there is a retrograde flow in this branch🡪 this means that this branch has good collateral flow and so you can sacrifice this branch by putting the flow divertor inside the sac.

• In case there is another feeder of the fusiform aneurysm ex: A1 segment in the mentioned case, it is crucial to know if there is a functioning ACOM as if it is present, coiling the A1 segment could be considered to prevent further growing of the aneurysm.

• Don’t oversize the Flow divertor in length or in diameter 🡪 this can lead to difficult opening.

• Try not to cover the ophthalmic artery origin and if you have to do so, you have to inform the patient before the procedure about the possible risks and complications that may occur.

• Always remember: the simpler, the shorter the duration, the more reproducible your procedure is, the better the outcome, and the fewer complications that occur.

References:

1. Lonjon, M., et al., Epidemiology, genetic, natural history and clinical presentation of giant cerebral aneurysms. Neurochirurgie, 2015. 61(6): p. 361-5.

2. Choi, I.S. and C. David, Giant intracranial aneurysms: development, clinical presentation and treatment. Eur J Radiol, 2003. 46(3): p. 178-94.

3. Lubicz, B., et al., Giant vertebrobasilar aneurysms: endovascular treatment and long-term follow-up. Neurosurgery, 2004. 55(2): p. 316-23; discussion 323-6.

4. Roos, Y.B., et al., Genome-wide linkage in a large Dutch consanguineous family maps a locus for intracranial aneurysms to chromosome 2p13.Stroke, 2004. 35(10): p. 2276-81.

5. Christiano, L.D., et al., Giant serpentine aneurysms. Neurosurg Focus, 2009. 26(5): p. E5.

6. Mizutani, T., et al., Proposed classification of nonatherosclerotic cerebral fusiform and dissecting aneurysms. Neurosurgery, 1999. 45(2): p. 253- 9; discussion 259-60.

7. Figueiredo, E.G., et al., Surgical nuances of giant paraclinoid aneurysms. Neurosurg Rev, 2010. 33(1): p. 27-36.

8. Lownie, S.P., et al., Clinical presentation and management of giant anterior communicating artery region aneurysms. J Neurosurg, 2000. 92(2): p. 267-77.

9. van Rooij, W.J. and M. Sluzewski, Unruptured large and giant carotid artery aneurysms presenting with cranial nerve palsy: comparison of clinical recovery after selective aneurysm coiling and therapeutic carotid artery occlusion. AJNR Am J Neuroradiol, 2008. 29(5): p. 997-1002.

10. [Round table. Giant aneurysms]. Neurochirurgie, 1980. 26(5): p. 309-31.

11. Shi, Z.S., et al., Management of giant middle cerebral artery aneurysms with incorporated branches: partial endovascular coiling or combined extracranial-intracranial bypass--a team approach. Neurosurgery, 2009. 65(6 Suppl): p. 121-9; discussion 129-31.

12. Nagahiro, S., et al., Thrombosed growing giant aneurysms of the vertebral artery: growth mechanism and management. J Neurosurg, 1995.82(5): p. 796-801.

13. Piepgras, D.G., V.G. Khurana, and J.P. Whisnant, Ruptured giant intracranial aneurysms. Part II. A retrospective analysis of timing and outcome of surgical treatment. J Neurosurg, 1998. 88(3): p. 430-5.

14. Sugita, M., et al., Giant middle cerebral artery aneurysm with parent artery occlusion--case report. Neurol Med Chir (Tokyo), 1991. 31(1): p. 37- 40