Anterior Communicating Artery Aneurysm: Rupture with SAH, Endovascular Occlusion with Bare Coils, Early Re-rupture, Poor Clinical Outcome

  • Muhammad AlMatterEmail author
  • Marta Aguilar Pérez
  • Hans Henkes
Living reference work entry


An 80-year-old female patient was referred with a spontaneous subarachnoid hemorrhage (SAH), graded as Hunt and Hess III, Fisher IV, with a thick clot along the course of the anterior cerebral artery (ACA). The SAH was due to a ruptured anterior communicating artery (AcomA) aneurysm. The irregularly contoured aneurysm was treated with coil occlusion with almost complete exclusion of the aneurysm from blood circulation. The presumed rupture site was identified and occluded with coils. However, the patient suffered an early re-hemorrhage 36 h after the coil treatment and deteriorated clinically. The site of the re-rupture was distinct from that of the first hemorrhage. The aneurysm was subsequently completely filled with further coils. The patient remained in a persistent vegetative state after the second hemorrhage and died three months after the endovascular treatment. Additional cases are also presented which illustrate early re-hemorrhage from the original rupture site. The rare event of an early re-hemorrhage after endovascular coil occlusion of a ruptured intracranial aneurysm is the main topic of this chapter.


AcomA aneurysm SAH Coil occlusion Early re-hemorrhage 


80-year-old, female, spontaneous SAH, Hunt and Hess III, Fisher IV

Diagnostic Imaging

The 80-year-old female patient with a previous history of arterial hypertension experienced a sudden, severe headache with mild left-sided hemiparesis. She was then admitted to the nearest neurology department where a noncontrast computer tomography (NCCT) of her head was performed which revealed a diffuse basal subarachnoid hemorrhage (SAH) with a thick clot in the frontal interhemispheric fissure and in the pericallosal sulcus and cingulate gyrus (Fig. 1).
Fig. 1

The initial cranial NCCT showing a thick basal SAH and blood in the interhemispheric fissure and in the pericallosal sulcus

The patient was then admitted to the angiography suite and a diagnostic 4-vessel catheter angiography was performed which revealed a bi-lobulated aneurysm of the AcomA with a fundus depth of 3 mm and a fundus width of 5 mm and with a neck diameter of 2.5 mm (Fig. 2).
Fig. 2

Selective injection of the left ICA showing the ruptured AcomA aneurysm in a lateral view (a) and in the working projection (b). The arrows indicate the presumed rupture site

Treatment Strategy

Due to the relatively good clinical condition and previously independent status of the patient, the decision was made to treat the aneurysm in order to prevent a second hemorrhage, despite the advanced age of the patient. As the neck-width to sac-width anatomy of the aneurysm was favorable, the neurovascular interdisciplinary team decided on endovascular coil occlusion.


Procedure #1, 10.05.2011: endovascular coil occlusion of a ruptured AcomA aneurysm

Anesthesia: general anesthesia; 1 × 5000 IU unfractionated heparin (Heparin-Natrium, B. Braun) IV, 1 × 1 g thiopental (Trapanal, Nycomed) IV

Premedication: none

Access: right common femoral artery, 1 × 8F sheath (Terumo); guide catheter: 1 × 8F SAAD left (Cordis); distal access catheter: 1 × FARGOMAX (Balt Extrusion); microcatheter: 1 × Echelon14 (Medtronic); microguidewire: 1 × Traxcess 0.014″ 200 cm (MicroVention)

Coils: 1 × Deltaplush10 2/6; 1 × Deltaplush10 2/4; 1 × Deltaplush10 2/3; 1 × Deltapaq10 1.5/2; 1 × Deltaplush10 1.5/2; 1 × Deltaplush10 1.5/1 (all Codman)

Course of treatment: The guiding catheter was navigated into the mid-segment of the left common carotid artery followed by selective catheterization of the left internal carotid artery using a distal access catheter; the microcatheter was then advanced into the aneurysmal sac over the 0.014″ microguidewire. The aneurysm was gradually filled using the aforementioned coils with minimal residual filling at the end of the procedure (Fig. 3).
Fig. 3

After atraumatic navigation of the microcatheter into the sac of the AcomA aneurysm, the aneurysm was gradually filled with six coils (ac, road map images). The final DSA run (d) shows a subtotal occlusion of the aneurysm sac with minimal filling at the upper lateral aneurysm pole (arrowhead), opposite the rupture site (arrow)

Duration: 1st–20th DSA run: 170 min; fluoroscopy time: 43 min

Complications: none

Postmedication: none

Clinical Course and Subsequent Treatments

Lumbar CSF drainage was inserted and the patient was then uneventfully extubated. The same evening, the clinical condition began to deteriorate and the patient became stuporous. The emergent NCCT examination showed mild dilatation of the lateral ventricles. The patient nevertheless deteriorated further. A repeated NCCT 36 h after the treatment showed a large hematoma at the level of the genu of the corpus callosum (Fig. 4).
Fig. 4

Due to a deteriorating level of consciousness, an NCCT was performed which showed a new hemorrhage into the anterior region of the corpus callosum, presumably due to a re-rupture of the AcomA aneurysm

An emergency cerebral angiography was performed and showed persistent filling of the lateral pole of the coiled AcomA aneurysm but no active hemorrhage and complete occlusion of the suspected rupture site (Fig. 5). The aneurysm remnant was felt to be untreatable at this stage due to the anticipated difficulty of the attempt to navigate a microcatheter into the still perfused aneurysm compartment and an increased risk of a second re-rupture during this procedure.
Fig. 5

Selective injection of the left ICA two days after the initial coil treatment. The rupture site is occluded (lateral view, arrow) (a). In the previous working projection, the aneurysm appears occluded during the early angiographic phase (b). The late angiographic phase demonstrates a persistent filling of the upper lateral compartment of the aneurysmal sac (arrowhead) (c), with contrast pooling into the venous phase (c). Five days later and seven days after the first coil procedure, the contrast medium pooling in the aneurysm dome has not changed (d)

A repeated angiography 13 days after the initial coil treatment showed loosening of the coil mass at the neck level of the aneurysm with increased filling of the sac. The decision was then taken to re-treat the early recurrence as the risk of a third hemorrhage was judged to be high due to the progressive reperfusion of the sac in the short term.

Procedure #2, 23.05.2011: endovascular re-treatment of progressive reperfusion of a re-ruptured AcomA aneurysm using coil occlusion

Anesthesia: general anesthesia; no further medication was administered

Premedication: none

Access: right common femoral artery, 1 × 6F sheath (Terumo); guide catheter: 1 × 6F Guider Softip (Boston); microcatheter: 1 × Headway-17 (MicroVention); microguidewire: 1 × Traxcess 0.014″ 200 cm (MicroVention)

Coils: 1 × MicroPlex10 Hypersoft 2/20 (MicroVention); 1 × Deltaplush10 1.5/10 (Codman)

Course of treatment: The guiding catheter was navigated into the left ICA; the microcatheter was then advanced into the sac remnant over the 0.014″ micro guidewire. The two coils were then subsequently placed into the aneurysm completely filling the aneurysm remnant (Fig. 6).
Fig. 6

Endovascular treatment of the aneurysmal remnant (arrowhead) (a) with complete coil occlusion (b) at the end of the procedure (c) and without contrast medium pooling during the late venous phase (d)

Duration: 1st–11th DSA run: 140 min; fluoroscopy time: 17 min

Complications: none

Postmedication: none

Clinical Outcome

The patient remained stuporous throughout the acute phase with non-localizing movements to painful stimuli. She was discharged into an intensive rehabilitation facility and died on August 8, 2011, from the sequelae of the aneurysm ruptures, about three months after the SAH and endovascular aneurysm treatment.

Follow-Up Examinations

There were no further follow-up examinations carried out.


The endovascular treatment of ruptured cerebral aneurysms has been proven to be safe and effective since its introduction in the early 1990s, an assertion which has been supported by clinical trials in the early twenty-first century (Byrne et al. 1999; Molyneux 2002; Viñuela et al. 2008). The high rates of recanalization, especially after treatment of ruptured aneurysms in the acute phase, were recognized early on but the rates of re-hemorrhage, and the rates of procedural complications associated with retreatments are low (Molyneux et al. 2005; Raymond et al. 2003; Renowden et al. 2008).

A variety of pathomechanisms have to be considered as potentially responsible for aneurysm re-rupture. Ultra-early pretreatment re-rupture of aneurysms is a possibility, and if there is no CT imaging done immediately prior to the endovascular treatment, it can be impossible to determine whether a new hemorrhage has happened before, during, or after the coiling procedure.

In the early days of endovascular coil treatment, there were no small, soft coils available, making the endovascular treatment of ruptured aneurysms with a fundus diameter below 3 mm sometimes a real challenge, not infrequently resulting in only partial aneurysm occlusion (Fig. 7).
Fig. 7

Early re-hemorrhage after partial coil occlusion of a small, ruptured anterior choroidal artery (AChoA) aneurysm. The 37-year-old woman was referred in November 1995 after a spontaneous SAH (Hunt and Hess III, Fisher IV). The DSA showed a small aneurysm on the right ICA at the AchoA origin (a). Due to the small size of this aneurysm, it was only possible to insert a single 2/20 mm standard GD coil (b). There was persistent perfusion of the aneurysm sac remnant (c). Three days after the endovascular partial coil occlusion, the patient suddenly complained of a severe headache and became stuporous. The CT examination showed a new hemorrhage adjacent to the right ICA and from there into the temporal pole (d). The patient was managed conservatively. Her final clinical outcome was equivalent to GOS III

Partial occlusion of ruptured aneurysms was also recognized early on as a risk factor for re-hemorrhage in the acute phase. The wall of a recently ruptured aneurysm tends to be weak. Treatment through coil occlusion may be feasible; however, the pliable aneurysm wall may give way to coil compaction, enlargement of the aneurysm sac, and aneurysm reperfusion (Fig. 8). Partial coil occlusion might also modify the intrasaccular blood circulation with redirection of the blood flow to a part of the aneurysm wall different from the primary rupture site, triggering a re-rupture from there. It may help to understand the pathomechanisms behind individual cases of early aneurysm re-rupture if it is determined whether the re-hemorrhage originated from the original rupture site or from a different place.
Fig. 8

This 52-year-old female patient experienced a sudden headache and was admitted to the nearest neurology department. The neurological examination was within normal limits, except for nuchal rigidity. The lumbar puncture revealed blood-stained cerebrospinal fluid (CSF). The subsequently performed NCCT (a) revealed a right-sided SAH, mainly in the Sylvian fissure and in the suprasellar cistern. The cerebral angiography (b, c) confirmed an aneurysm at the right MCA-bifurcation. The small “wart” on the aneurysm dome was the suspected rupture site. The aneurysm was then treated with stent-assisted coiling with apparently sufficient occlusion (d). On the fifth postprocedural day, the patient experienced a severe headache with a progressive loss of consciousness. The NCCT showed a large parenchymal hematoma (e), and the DSA demonstrated an early reperfusion of the aneurysmal sac and active extravasation (arrow) of contrast medium (f, g). The aneurysm was rapidly occluded with further coils (h). The hematoma was then evacuated via a decompressive craniectomy. DSA two days later confirmed the complete occlusion of the aneurysm (i). The further course was complicated by cerebral vasospasm and subsequent ischemia, and the patient remained in a vegetative state throughout the acute phase. Despite her poor clinical condition at discharge, the patient regained some functionality after intensive rehabilitation and was eventually ambulatory with assistance. In this case, the re-hemorrhage originated from the initial rupture site

The Cerebral Aneurysm Re-rupture After Treatment (CARAT) study reported a 2.2% risk of non-procedural re-rupture in the first year following surgical and endovascular treatment of 706 and 295 patients, respectively. The study demonstrated a significant correlation between the degree of occlusion and the risk of re-rupture (with a cumulative risk of 17.6% for occlusion of less than 70% compared to 1.1% and 2.9% for complete and 91–99% occlusion, respectively). The risk of re-rupture was higher after coil occlusion but did not differ significantly after adjustment for degree of aneurysm occlusion (Johnston et al. 2008).

Early re-hemorrhage after coil occlusion is a rare event with an estimated incidence of just over 1% (Cho et al. 2012; Sluzewski and van Rooij 2005).

A study of 431 patients who had been treated with coil occlusion for ruptured aneurysms reported early re-hemorrhage in 6 (1.4%) cases with 100% mortality. A small ruptured aneurysm and the presence of an adjacent hematoma were independent risk factors (Sluzewski and van Rooij 2005). In a study of 1167 consecutive cases of ruptured aneurysms treated with coil embolization, early re-hemorrhage occurred in 13 patients (1.1%) within two weeks and was associated with a high mortality and morbidity rate. The authors recognized incomplete occlusion, antiplatelet and anticoagulation medication, and the presence of parenchymal hemorrhage as possible risk factors of ultra-early re-rupture after coil treatment (Cho et al. 2012).

A retrospective review of all patients treated at our institution between 2007 and 2016 for aSAH revealed three patients with early re-hemorrhage after endovascular coil occlusion of 470 consecutive patients (0.64%). In the first case (Figs. 1, 2, 3, 4, 5, and 6), the aneurysm was incompletely occluded at the end of the procedure. In the second case, the re-hemorrhage was associated with early recanalization of the aneurysm sac after coil occlusion (Fig. 8). In the third case, the circumstances of re-hemorrhage remain elusive (Fig. 9).
Fig. 9

This image series illustrates the clinical course of a 59-year-old female patient, who was admitted due to an acute confusional state. The initial CT (a) showed a diffuse basal SAH with a thick clot in the left Sylvian fissure. The CTA revealed an aneurysm on the left ICA at the level of the ICA bifurcation (b). The patient’s consciousness rapidly deteriorated and she was then intubated and referred to us for further treatment. The DSA confirmed a 9.5 × 8.5 mm AChoA aneurysm with a daughter sac measuring about 5 mm at the posterior-superior aspect of the main aneurysm (c). The aneurysm sac was filled with coils (d) leading to a disruption of the blood circulation in the aneurysm with contrast medium stasis in the daughter sac (e). The immediate postprocedural CT and CT on the following day showed minor redistribution of the SAH and unchanged clot thickness in the left Sylvian fissure (f). On the second postinterventional day, bright blood was observed draining through the external ventricular drainage. The emergent CT (g) showed a massive re-hemorrhage into the Sylvian fissure with enlargement of the preexisting hematoma. The DSA, however, showed no active extravasation from the aneurysm (h). The daughter sac, meanwhile, was completely occluded. The remainder of the acute course was unremarkable, and the patient was only moderately disabled at discharge. The most recent follow-up DSA (i) was performed 10 years after the hemorrhage and showed persistent complete occlusion of the coiled AChoA aneurysm. The patient recovered without a focal neurological deficit. At the last follow-up visit, she reported that she had never returned to her previous job, suffers from complex epileptic seizures, which started two years after the SAH, and has impaired memory and poor cognitive functions

In this case the mechanism underlying the re-hemorrhage two days after the coil occlusion of the aneurysm remains undefined. Vasospasm as a potential cause of ischemia with secondary hemorrhage into an infarcted brain parenchyma was never confirmed during the acute-phase follow-up. Compromise of the venous drainage by the initial hematoma triggering a second hemorrhage is only a speculative explanation.



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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Muhammad AlMatter
    • 1
    Email author
  • Marta Aguilar Pérez
    • 1
  • Hans Henkes
    • 1
  1. 1.Neuroradiologische Klinik, NeurozentrumKlinikum StuttgartStuttgartGermany

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