PMC3014759_01
Diagnosis of ruptured ID of the PCo-A. (a, b) Two SAH images detected at an interval of 9 hours show that the bleeding points in both episodes of hemorrhage were centered around the origin of the right posterior communicating artery and that the suprasellar cistern, sylvian cistern, ambient cistern, and tentorial margin were involved. Blood entry into the ventricles and the presence of ventriculomegaly were seen in (b). (c, d) Head CTA showed that a funnel-shaped expansion with a diameter of less than 3 mm occurred at the origin of the right posterior communicating artery and was in conjunction with the thin right posterior communicating artery at its apex (arrow). (e)-(g) The first DSA showed that a funnel-shaped expansion occurred at the origin of the right posterior artery and was in conjunction with the thin right posterior communicating artery at its apex, a finding similar to the results of CTA (arrow). (h) Reexamination by head CT after 20 days of conservative treatment demonstrated that SAH was absorbed and the size of ventricles was normal. (i) The second DSA examination after 20 days of conservative treatment revealed that the funnel-shaped expansion still existed at the origin of the right posterior communicating artery and was in conjunction with the thin posterior communicating artery at its apex, similar to the results obtained by CTA and the first DSA (arrow).
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A CT scan of the head revealed SAH mainly in the right suprasellar cistern with a Fisher grade of 3 (Figure 1(a)). A repeated head CT examination revealed rebleeding, acute hydrocephalus, hematocele at bilateral posterior horns of the lateral ventricle, and a Fisher grade of 4 (Figure 1(b)). In addition, no aneurysm was noted in angiography (arrow in Figures 1(c) and 1(d)). DSA and 3-D reconstruction were then performed, and these findings were similar to those seen in the CTA (arrow in Figures 1(e), 1(f), and 1(g)). A repeated head CT showed that SAH was reabsorbed, and the size of the ventricles became normal (Figure 1(h)). DSA was performed again and yielded the same result as the previous one (arrow in Figure 1(i)).
Endovascular coil embolization of ruptured ID of the PCo-A. (a) DSA before treatment showed that a funnel-shaped expansion with a diameter of 2 mm occurred at the origin of the right posterior communicating artery and was in conjunction with the posterior communicating artery at its apex. (b) Vertebral angiography showed that blood flew reversely from the posterior communicating artery into the internal carotid artery system after carotid artery compression. (c) A Neuroform3 stent was released in the internal carotid artery to cover the origin of the posterior communicating artery; an Echelon-10 microcatheter was used to release a Hydrocoil10 coil into the PCo-A ID through the stent mesh using a Transend300 microguidewire, but the coil was not detached. (d) A microcatheter was placed into ID of the PCo-A through the posterior vertebral artery and posterior communicating artery under the guidance of Roadmap. (e) Four Hydrocoil10 coils were released into ID of the PCo-A through anterior and posterior circulation. (f, g) No enhancement of ID of the PCo-A was noted after five coils had been filled into anterior and posterior circulation, and there was no contrast agent leakage. (h) Angiography of coils in anterior and posterior circulation after they were all detached, showing no enhancement of ID of the PCo-A and the posterior communicating artery.
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The result showed that blood flow reversed into the internal carotid artery through the posterior communicating artery (Figures 2(a) and 2(b)). HydroCoil 10 coil (2 mm x 2 cm, MicroVention, Aliso Viejo, Calif) was released into the ID of the PCo-A. However, the coil was not detached due to the unfavorable location (Figure 2(c)). The left femoral artery was punctured for introduction of a vascular sheath, and then an Echelon-10 microcatheter was placed into the PCo-A ID using a Transend-300 microguidewire via the posterior communicating artery (Figure 2(d)). Four HydroCoil 10 coils were sequentially released (2 mm x 2 cm, 2 mm x 2 cm, 2 mm x1 cm, 2 mm x 1 cm) to fill the ID of the PCo-A (Figure 2(e)). No enhancement of the ID of the PCo-A was shown in the angiography of anterior or posterior circulation, and leakage of the contrast agent did not occur (Figures 2(f) and 2(g)). The coil placed in the internal carotid artery was detached (Figure 2(h)).
Follow-up DSA. (a, b) The follow-up DSA did not show the recurrence of ID of the PCo-A.
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The follow-up DSA showed no signs of ID of the PCo-A (Figures 3(a) and 3(b)).