Since they have been developed by Guglielmi et al. in the early 1990s [51], detachable coils have revolutionized the treatment of IC aneurysms. Most of these coils are made of platinum, and all of them are detachable. They are deployed inside the aneurysm via a microcatheter positioned in the sac and detached from a stainless-steel microguidewire by an electrical current (Fig. 6). The objective is to fill the aneurysm by means of decreasing size coils until total angiographic occlusion, while preserving the patency of the parent artery and other adjacent branches. Even if safe and efficient for the treatment of most IC aneurysms, large-necked aneurysms may be difficult to treat by regular coiling due to the risk of coil protrusion in the parent artery that may be responsible for thromboembolic complication.

The remodeling technique has been developed in the mid-1990s to overcome the limitation of the presence of a large neck for the endovascular treatment of IC aneurysms [52]. The principle of this technique consists in inflating temporarily a balloon in front of the aneurysm’s neck during the coil deployment. This balloon helps to constrain the positioning of the coil’s loops in the aneurysm’s sac during its delivery (Fig. 7). With this technique, almost all IC aneurysms are now eligible for endovascular treatment. Despite some controversies [53], there are no evidences that the balloon remodeling technique increases the thromboembolic complication rate [54, 55].

Parent artery occlusion is a potential therapeutic option for ruptured aneurysms, but can only be performed in case of sufficient collaterals, especially for large parent artery [26]. Moreover, the potential risks of delayed vasospasm that can lead to ischemic complications in patients with ruptured IC aneurysms may prevent from occluding a large vessel to preserve the circle of Willis.

Biological glue (n-butyl-cyanoacrylate [NBCA]) may be used in ruptured IC aneurysms for parent artery occlusion in dissecting aneurysms (e.g., posterior inferior cerebellar artery [PICA] dissecting aneurysm). The aim of this treatment is to perform a segmental occlusion by means of glue of the portion of the parent artery harboring the dissecting aneurysm [56]. The other main indication for the use of glue in aSAH is the presence of infectious IC aneurysms (aka mycotic aneurysms). As for dissecting IC aneurysms, the aim of the treatment is to obtain a segmental occlusion of the vessel harboring the aneurysm [57].

The use of intracranial stents is not recommended for the treatment of ruptured IC aneurysms at the acute phase. Indeed, these devices require a dual anti-aggregation platelet therapy that may be responsible for hemorrhagic complications. However, in some selected cases, IC stents may be used for the ruptured IC aneurysms. Indeed, in case of coil protrusion in the parent artery, the deployment of a stent in front of the aneurysm’s neck may be on option to avoid thromboembolic complication. This technique is called the “bailout technique” [58]. In case of uncoilable blood blister-like aneurysms, the use of flow diverter stents may be a valuable option, either at the acute phase or few days after the SAH (Fig. 8) [59].

Spontaneous rebleeding is the most severe complication in aSAH. Indeed, the clinical consequences of the rebleeding are frequently worse than the ones from the first bleeding [68]. The rebleeding is related to the lysis of the clot that stopped the first hemorrhage. The early rebleeding has been reported with a rate around 14 % [69] and is higher within the first 6 h [68]. This high rate of spontaneous rebleeding and the poor clinical consequences of such rebleeding are the rationale for an early treatment of ruptured IC aneurysms.

Hydrocephalus may be observed at the acute phase of the hemorrhage or can be delayed. The mechanisms that may lead to hydrocephalus are acute obstruction of the cerebrospinal fluid pathway by a clot and abnormal blood resorption due to the SAH. Hydrocephalus may occur in the following weeks after the SAH. It is related to a fibrosis of the subarachnoid spaces and an inflammatory proliferation of arachnoid villosities’ cells. Such delayed hydrocephalus is more frequent in patients in poor initial grade (WFNS). Clinically, consciousness disorders and psychiatric disorders may be observed. Communicant hydrocephalus may require a ventriculoatrial or ventriculoperitoneal shunting and can be temporarily treated by serial lumbar punctures [70].

Arterial vasospasm may occur few days after the hemorrhage (> day 3) until day 21. Its frequency and severity increase with the volume of blood in the subarachnoid space (see Fisher score; Table 3). Arterial vasospasm is seen on angiographic exams in about 70 % of the cases in aSAH. In 30 % of the cases, arterial vasospasm may lead to ischemic lesions [71]. Thus, vasospasm should be prevented by aggressive therapies and treated, when present, to prevent potential severe complications. The clear pathophysiology of arterial vasospasm related to aSAH remains unclear, some data suggesting an inflammatory vasculitis rather than a true vasospasm [72].

The “H therapy” is one of the first-line therapies in the armamentarium of the treatment of aSAH-related arterial vasospasm. This therapy associates hypertension while keeping normovolemia and normalized cardiac flow. Vasoconstrictor therapy with noradrenalin is administered in an intensive care unit, with continuous monitoring comprising, at least, an invasive measurement of the blood pressure. The “triple-H therapy” that associates hemodilution, hypervolemia, and arterial hypertension is no longer used to prevent arterial vasospasm because it did not prove its efficacy for the treatment of cerebral vasospasm. The use of a vasodilator with cerebral tropism like nimodipine is systematically performed during the first 3 weeks after the hemorrhage either per os or intravenously. Daily low doses of statins have proven their effectiveness in preventing cerebral vasospasm [73]. The diagnosis of vasospasm should be suspected in case of fever, disorders of consciousness, and motor or sensitive deficit or on ultrasonographic findings (accelerated mean velocities on arterial vessels). Such signs should incite to perform brain CT scan to rule out ischemic infarct, hydrocephalus, parenchymal hematoma, or rebleeding and a vascular imaging (CTA or DSA). On vascular imaging, arterial vasospasm typically appears as narrowing of the ICA termination, A1 and M1 segments (Fig. 10). Cortical defect may also be seen on capillary phase on DSA.