Quadruple Spontaneous Cervical Artery Dissection Following Aneurysm Embolization: A Rare Posttreatment Complication

Discussion

The frequency of saccular intracranial aneurysms in patients with sCAD was estimated at 5.5%,⁸ higher than that of the general population, supporting the evidence for an underlying vasculopathy.^1,8,9 Especially in the article of Mazighi et al,⁹ 7 cases of sCAD were reported in the course of ruptured saccular intracranial aneurysms, implying a common predisposing factor for both diseases, but more important, a higher frequency of sCAD in the course of aneurysmal SAH is supported, due to SAH-induced intense sympathetic stimulation. Female sex, migraine, and minor trauma, as in our patient, are mentioned as risk or triggering factors of sCAD.^1–5 Moreover, when carotid artery dissection occurs, in 15%–29% of cases, it is bilateral or associated with VA dissection.⁵ Clinical vasospasm after aneurysmal SAH resulting in stroke or death occurs in 15%–20% of patients. The development of a new focal deficit in patients with SAH that cannot be explained by hydrocephalus or rebleeding is the first objective sign of vasospasm.¹⁰ Control CTA in our patient revealed another reason for neurologic deterioration in aneurysmal SAH, not previously reported.

Multiple sCADs in this patient as a periprocedural complication were ruled out because there was no intervention in any cervical vessel except the right ICA. The patient was extubated the same day without any neurologic sequelae. Her deterioration 4 days later corresponded to the median delay of the onset of neurologic deficits after sCAD. However, it is not easy to define “minor trauma” or its impact on multiple sCADs.^11,12 Mild mechanical stress plays a role as a possible triggering factor in the pathogenesis of the disease.¹² In our case, head extension during embolization to achieve a safe working projection for coiling appears to be the only plausible cause of multiple sCADs.

There is no standard treatment protocol or guidelines for treatment of sCAD. There are only recommendations and no evidence to support the routine use of anticoagulants or antiplatelet drugs or the superiority of each for the treatment of extracranial carotid dissection.¹³ Moreover, the prognosis of the disease seems to be benign,⁵ and spontaneous resolution is observed in >80% of patients within 3 months.^1,6 Endovascular procedures are mainly reserved for traumatic dissections.¹⁴ Because stroke is the main manifestation and its recurrence rate is approximately 2%–4% in this disease,¹⁵ it is reasonable to administer anticoagulation or/and antithrombotic treatment. In our case, having secured the SAH source, we used anticoagulation therapy to prevent further ischemia, which could also progress in the course of post-SAH vasospasm.

In conclusion, we draw attention to details such as head position during embolization and propose a meticulous examination of neck vasculature in patients with SAH who deteriorate, to rule out another possible cause of deterioration frequent mostly in younger patients.