It is not commonly known that cerebral vasospasm may occur after surgical clipping of a UIA. Here we present the case of a patient developing DCI due to vasospasm after an uneventful surgical occlusion of an unruptured MCA aneurysm. Only a few cases of DCI after clipping of a UIA have been reported in the last few decades . Among these, the onset of symptoms varied considerably, ranging from 5 to 28 days after surgery. In contrast, vasospasm onset after SAH typically occurs within 14 days. Risk factors that are associated with DCI are unknown. It is assumed that temporal clipping and the application of two or more clips increase the risk for the development of vasospasm. In the present case, only one clip had been applied, and without the necessity of performing a temporary clipping.
Despite its high incidence, the precise pathophysiological mechanisms of vasospasm following SAH are still not fully understood. It is therefore not surprising that the pathophysiology of vasospasm following surgical treatment of UIA is also not understood. Some intriguing mechanisms are assumed to contribute. DeLong has proposed that erythrocytes’ breakdown products within the aneurysm sac may account for the development of vasospasm . That hypothesis was derived from the observation that resection, rather than the simple occlusion of the aneurysm, was related to a decreased incidence of vasospasm in patients suffering from SAH. A diffusion of blood breakdown products through the arterial wall is quite speculative. However, this slow process would account for the delay of occurrence of vasospasm. Another potential pathophysiological mechanism for vasospasm associated with an unruptured and untreated aneurysm has been reported by Friedman and colleagues . An unruptured aneurysm underwent symptomatic changes of size within a few days. It was assumed that the property to produce vasorelaxant lipoproteins was impaired in the adjacent endothelium. This hypothesis would support the mechanical theory, which proposes that instrumental manipulation involving the arterial endothelial layer (e.g., due to temporal clipping) at the major branches of the cerebral arteries may lead to impaired cerebrovascular reactivity . Contemporary theories presume that the source of vasospasm might be the cerebral arteries themselves. Particular attention has been directed at the adventitial network of nerves that is believed to initiate spasmogenic mechanisms rather than endothelial factors .
Because the incidence of vasospasm and DCI following the clipping of a UIA seems to be low and the pathophysiology is not fully understood, no treatment guidelines are available. However, in the present case, the treatment was derived from the guidelines for management of an SAH . For that reason, nimodipine was administered orally with a daily dosage of 360 mg. Transcranial ultrasonography was used to monitor the progression and regression of the vasospasm.
According to the few case reports available that are similar to the present case, most patients made a full recovery. Some patients, however, were reported to have had a poor outcome.
In our opinion, a probabilistic approach to clinical decision-making is always beneficial. If it looks like a duck, swims like a duck, and quacks like a duck, then it probably is a duck—but not always. Cerebral vasospasm is not the most common etiology in patients suffering a stroke, particularly in elderly patients with UIA. In the present case, all available diagnostic means were exploited to determine the cause of the stroke, including cerebral duplex ultrasonography and TFCA. In addition to the classic presentation of a spontaneous aneurysmal SAH, there are other factors that may contribute to the development of transient vessel narrowing. The similar clinical presentation of reversible cerebral vasoconstrictive syndrome (RCVS) is also associated with transient increased blood flow velocity, but without evidence of an SAH or an aneurysm. RCVS most commonly occurs because of vasoactive substances or during the postpartum period, but a cerebral venous sinus thrombosis or a traumatic brain injury may also cause increased cerebral blood flow velocity. In this case, typical angiographic signs of vasospasm and an exhaustive review of the medical history of the patient led to the proper diagnosis.
This patient with a surgically treated UIA developed vasospasm in the absence of an SAH. It is crucial to discern that the absence of a subarachnoid hemorrhage in patients with UIA does not preclude the presence of cerebral vasospasms. The incidence of vasospasm and DCI after a clipping of the UIA is completely unknown. There are probably several reasons for this lack. On the one hand, the clinical staff often does not know that DCI can arise after an uneventful clipping, and as a result, little attention is paid to this possibility. The latency of vasospasm onset for up to three weeks postoperative is another pitfall to consider. In one case, the report of onset of symptoms was 28 days after surgery . By that time, after an uneventful clipping of a UIA, most patients have usually been discharged as free of neurological symptoms. Thus, it may be difficult to recognize a causal relationship with such a time gap. On the other hand, the evolution of surgical techniques in the last decade has opened up the possibility of performing relatively low-risk surgeries in the elderly. Therefore, coinciding events such as an ischemic stroke are not unlikely.
To further stratify the risk of clinically relevant vasospasm in the management of UIA treatment, it may be beneficial to perform pre- and postoperative transcranial duplex sonography / TCD, especially considering the availability of the neuroprotective calcium channel blocker nimodipine. The resulting findings on the incidence of subclinical and clinical vasospasms after the clipping of a UIA would be of significance in the prevention of stroke.
In conclusion, cerebral vasospasm as a cause of ischemic stroke after uneventful surgery for a UIA seems to be a rare but possibly underestimated etiology that demands particular attention with respect to providing appropriate treatment. In future, it may be prudent to perform follow-up transcranial ultrasonography testing after the clipping of a UIA, especially considering the availability of potentially neuroprotective medications like nimodipine.