50 Blood Blister–Like Aneurysms
Abstract
Blood blister–like aneurysms are rare aneurysms of the internal carotid artery. Unlike most cerebral aneurysms, they are true pseudoaneurysms lacking all three layers of the vessel wall. Additionally, they occur at nonbranching points along the internal carotid artery. Because of the thin-walled nature of these aneurysms, treatment is often fraught with peril. They have higher intraoperative rupture rates with attempted microsurgical clipping. Additionally, clip-wrapping of the aneurysm and parent artery occlusion with bypass have been employed. Coiling of blood blister aneurysms with or without stent assistance is also associated with higher complication rates due to the fragility of the aneurysm wall. More recently, flow diversion has been described as a viable endovascular treatment. However, flow diversion results in delayed occlusion during which time the aneurysm may be at risk for hemorrhage. Careful consideration of the treatment options within a multidisciplinary cerebrovascular treatment team is necessary to ensure the best outcomes in this very difficult subset of patients.
Introduction
Blood blister–like aneurysms (BBAs) are small sessile, thin-walled lesions without an identifiable neck located at nonbranching sites of the internal carotid artery (ICA). Also called blister or dorsal variant aneurysms, BBAs are treacherous lesions that can enlarge rapidly and rebleed frequently. They have a low prevalence, comprising 0.3 to 1% of intracranial aneurysms and 0.9 to 6.5% of aneurysms of the ICA, but have much higher morbidity and mortality than saccular aneurysms. In contrast to natural history data that suggest that small aneurysms have a minimal chance of rupture, most cases of BBAs are diagnosed in the setting of subarachnoid hemorrhage (SAH), and affected patients tend to be younger than those with ruptured saccular aneurysms.
Major controversies in decision making addressed in this chapter include:
Whether or not treatment is indicated.
Open vascular versus endovascular treatment for ruptured and unruptured BBAs aneurysms.
Timing of intervention.
Role of flow diverter in ruptured BBAs.
Whether to Treat
BBAs are frequently associated with SAH. They can have rapid growth rates and high rebleeding rates if they are not completely treated. Expeditious occlusion of the aneurysm via open surgical or endovascular technique is recommended ( 1 , 2 in algorithm ). The timing of intervention, however, is controversial depending on the technique chosen. If flow diversion is planned, the requirement for dual-antiplatelet medications raises concerns of hemorrhagic complications should the patient require another invasive procedure (e.g., ventriculoperitoneal shunt placement). Delay of treatment, however, exposes the patient to the risk of aneurysm rerupture ( 4 in algorithm ).
Treatment with flow modulation (i.e., trapping and bypassing the BBA) is potentially detrimental to cerebral hemodynamics in the setting of vasospasm and/or ischemia. In the acute phase of a SAH, patients may be afflicted by rapid fluctuations in blood pressure, elevated intracranial pressure, vessel reactivity, and hypoperfusion. Some neurosurgeons may prefer an alternative strategy to bypass if a patient has signs of vasospasm ( 4, 5, 6, 7 in algorithm ).
Anatomical Considerations
BBAs are most frequently located on the dorsal wall of the supraclinoid portion of the ICA, which is also known as the superior or anteromedial wall of the ICA. They have unique characteristics that differentiate them from regular saccular aneurysms. Although most saccular aneurysms arise within the angle formed by the parent artery and an arterial branch, BBAs typically arise directly from the parent vessel wall remote from an arterial branch. The predisposition for their formation on the dorsal wall of the ICA is not well understood. Although BBAs have been described on other vessels (i.e., anterior cerebral, middle cerebral, and basilar arteries), it is unclear whether they are the same disease.
Pathophysiology
BBAs are small, fragile, thin-walled, broad-based aneurysms without an identifiable neck; they lack an internal elastic lamina and a media layer. Histologically, BBAs resemble pseudoaneurysms with only thin adventitia, fibrous tissue, and a fibrin/platelet plug bolstering the wall. The pathogenesis remains controversial, with focal arterial dissections, arteriosclerotic ulceration, hemodynamic stress, and inflammation proposed as causative factors. The lesion can affect a significant part of the main vessel, which contributes to the high rates of morbidity and mortality. Occasionally, BBAs may appear on imaging as a saccular lesion, which may be due to organization of the blood clot adjacent to the wall defect. This saccular appearance is misleading because BBAs lack normal arterial structures in their walls.
Workup
Clinical Evaluation
The most common presentation of a BBA is SAH. Patients may present with altered mental status, headaches, cranial nerve palsy, seizures, hypertension, and neurological deficits. The presence of concomitant neurogenic cardiomyopathy, pulmonary edema, or hydrocephalus would influence treatment decision making.
Imaging
Because of their small size, BBAs are frequently missed on computed tomography or catheter angiography. Meticulous technique and a high index of suspicion are needed in many cases. High-resolution magnetic resonance vessel wall imaging that can detect intramural hematoma on the dorsal surface of the vessel may be useful in some cases. In cases in which a BBA is missed on initial angiography, a questionable bulge may be identified retrospectively. Multiple angiographic projections are often needed to accurately visualize the lesion. BBAs often demonstrate rapid enlargement on short-term follow-up angiography.
It is imperative to identify the collateral flow to the involved hemisphere in case of compromise during treatment or emergent sacrifice for intractable hemorrhage. If bypass, aneurysm trapping, or ICA sacrifice is planned, cerebral angiography using the Matas and/or Allcock maneuvers may help delineate the extent of collateral flow through the anterior and posterior communicating (PCOM) arteries, respectively. Additionally, an endovascular balloon test occlusion (BTO) can be performed. However, in the setting of high-grade SAH, the results of a BTO may not be reliable for patients with a decreased level of consciousness and/or neurological deficits. It is important to note that results of the BTO may not predict the patient′s tolerance in the setting of vasospasm.
Differential Diagnosis
BBAs may be mistaken for saccular aneurysms of the ophthalmic, anterior choroidal, or PCOM arteries. In the setting of SAH without an obvious source, meticulous angiography should be performed to look for a BBA as they have a tendency to enlarge rapidly and rebleed. Multiple interval angiograms may be required to visualize a BBA.
Treatment
Choice of Treatment
The optimal treatment for BBAs is controversial. Because of the fragility of the aneurysm wall, their small size, and their ill-defined necks, BBAs are challenging to treat by either open surgical or endovascular techniques. There is a high risk of intraoperative and postoperative rupture and high rates of morbidity and mortality regardless of whether the treatment is surgical or endovascular. Direct surgical clipping and primary coil embolization must be approached with great trepidation. Because of these inherent risks, a variety of alternative open surgical and endovascular treatment strategies have been described, but evidence guiding decision making remains ill defined. The presence of an intracerebral hematoma may favor an open surgical approach because endovascular treatment using flow diversion would require dual-antiplatelet medications, which may be risky after a recent craniotomy.
Cerebrovascular Management—Operative Nuances
Among the open surgical techniques described for treatment of BBAs are direct clipping, parallel clipping of the parent vessel, clip reconstruction of the parent vessel, clip-wrapping, trapping with bypass, and parent vessel sacrifice ( 3 in algorithm ).
Direct clipping of the neck of a BBA is considered risky because of the fragility of the vessel wall, which can easily rupture or avulse. Parallel clipping of the normal ICA wall to exclude the BBA has been described. The clip is placed beyond the diseased segment onto the normal carotid wall in a parallel configuration, thereby purposefully narrowing the parent artery. A major concern of parallel clipping is that if the clip does not engage the wall of the parent artery, the aneurysm may rupture or avulse from the parent artery. Additionally, clipping in this fashion may cause a stenosis. If the ICA is narrowed too severely, the restriction in blood flow may lead to a stroke. Flow restriction should especially be avoided in patients with a SAH who are at risk for vasospasm.
Parent vessel reconstruction using clips or clip-wrapping materials has been described. The BBA can be wrapped in a muslin gauze or Gore-Tex sling, which is then clipped to reinforce the vessel (▶ Fig. 50.1 ). A portion of the normal vessel can be included in the wrapping material, which is then secured tightly with a clip, thereby inducing a mild circumferential narrowing. Clip reconstruction of the parent artery, however, is generally not effective at completely occluding the aneurysm and may not prevent future rebleeding events and/or growth of the BBA. This technique may also injure perforating arteries and small branch vessels. Slits can be made in the wrapping material to accommodate branch vessels. Some surgeons consider clip-wrapping to be a temporizing measure for the acute subarachnoid period and not a definitive treatment; delayed endovascular treatment can be performed when the patient is at less risk for complications. Others, however, consider clip-wrapping to be a definitive treatment ( 3, 5, 7, 8 in algorithm ).
Considering the uncertainty regarding the durability of these techniques, some have proposed aneurysm trapping with bypass as a definitive treatment for unclippable aneurysms. Poor outcomes have been reported in patients who underwent ICA sacrifice without revascularization. Bypass techniques may include a superficial temporal artery–to–middle cerebral artery (STA–MCA) anastomosis or high-flow technique using a radial artery interposition graft from the external carotid artery to the middle cerebral artery. A high-flow technique may better augment cerebral perfusion compared with STA–MCA bypass, which may be advantageous in patients at risk for vasospasm ( 6 in algorithm ).
Bypass operations are technically challenging and are usually performed in the acute setting. If performed after ischemia, they may have deleterious results from hyperperfusion and hemorrhage. Additionally, some patients may not even tolerate temporary clamping of the ICA for the anastomosis if a high-flow bypass is performed.
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