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Endovascular treatment of carotid blowout syndrome: who and how to treat
  1. A Patsalides1,2,
  2. J F Fraser1,2,
  3. M J Smith1,2,
  4. D Kraus3,
  5. Y P Gobin1,2,
  6. H A Riina1,2
  1. 1Division of Interventional Neuroradiology, Department of Neurological Surgery, New York Presbyterian Hospital, Weill Cornell Medical College, New York, New York, USA
  2. 2Division of Interventional Neuroradiology, Department of Radiology, New York Presbyterian Hospital, Weill Cornell Medical College, New York, New York, USA
  3. 3Head and Neck Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA
  1. Correspondence to A. Patsalides, Interventional Neuroradiology, Weill Medical College of Cornell University, 525 E. 68th Street, Box 99, New York, NY 10065, USA; atp9002{at}med.cornell.edu

Abstract

Carotid blowout syndrome (CBS) is a high-risk condition associated with significant morbidity and mortality that may result from invasion and destruction of the cervical carotid vasculature from head and neck squamous cell carcinoma. Endovascular approaches offer multiple modalities for treatment to prevent morbidity and death. In this paper we review our experience in addressing CBS and present an up-to-date algorithm of endovascular management.

16 lesions were identified in 8 patients treated with 9 procedures over the past year. Pseudoaneurysm and/or active extravasation were documented in at least one vessel in all 8 cases presenting with acute CBS. There were 13 pseudoaneurysms in external carotid artery (ECA) trunk (5), ECA branches (4), internal carotid artery (ICA) (1) and common carotid artery (CCA) (3). There were 3 additional ICA lesions due to tumor infiltration, resulting in ICA occlusion (2) and long segment stenosis (1).

Permanent vessel occlusion was performed in 11 lesions of the ECA trunk (4), ECA branches (4) and ICA (3). Stent-grafts were placed in 5 lesions in the CCA (3), ICA (1) and ECA trunk (1). Technical success and immediate hemostasis were achieved in all patients. There were no procedural deaths or immediate complications. With a median follow-up of 2 months (range, 1–13 months), three patients died: one from recurrent CBS, one from global brain ischemia after a cardiac arrest event unrelated to CBS and one from systemic disease. There was no other recurrence of bleeding or neurological complication.

Endovascular techniques offer an armamentarium to effectively address CBS, significantly affecting the care and outcome in this particular oncologic population. These techniques should be offered as early as possible in the context of a multidisciplinary approach.

  • Artery
  • larynx
  • malignant
  • intervention
  • stent

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Introduction

Weakening and rupture of the carotid artery and its branches is a well-recognized complication of head and neck cancer with a very high mortality. The clinical spectrum as a result of carotid artery rupture is referred to as ‘carotid blowout syndrome’ (CBS) and may present as acute transoral or transcervical hemorrhage, or as the potential threat of hemorrhage when there is asymptomatic exposure or invasion of the carotid artery.1 In a large series of patients with radical neck dissections to treat malignancy, CBS occurred in 4.3% of patients and was universally fatal.2 While not restricted to this type of pathology, patients with head and neck squamous cell carcinoma are especially vulnerable, since tissue removal can precipitate vessel wall weakening, while tumor progression and recurrence can invade and erode the vessel walls. Radiation is a major independent risk factor for the development of CBS and is associated with a sevenfold increase in the risk of CBS in patients with neck carcinoma.2 Furthermore, superimposed infections may infiltrate the vessel wall, and pharyngocutaneous fistulae can expose blood vessels to saliva from the oropharynx or to the external air, significantly increasing the potential for damage or erosion.

Historically, treatment consisted of emergency surgical ligation of the parent vessel to control bleeding and prevent repeat hemorrhage, with multiple series showing mortality rates of 9%–100% (median, 40%) and major neurological morbidity rates of 9%–84% (median, 60%).1 3 Surgical management of CBS is problematic because exploration and repair of a previously irradiated field, especially in patients with residual tumor, tissue necrosis, infection and prior neck dissection, has significant morbidity and mortality associated with it. Moreover, the complicated perioperative management due to hemodynamic instability, cerebral ischemia and coagulopathy from severe blood loss often precludes reconstructive surgery and carotid bypass.

As interventional neuroradiology techniques have evolved, we are able to treat this devastating syndrome with improved outcomes.3 Endovascular treatment has multiple merits compared with surgery in this setting: it requires less time, it avoids manipulation of previously irradiated neck with friable tissue, it can be performed without general anesthesia, it does not require temporary interruption of blood flow through the carotid artery except for balloon test occlusion (BTO) and it is suitable for palliative care. In this paper, we share our experience in treating patients with CBS and on the basis of our experience and published results we present an up-to-date algorithm of endovascular management coupled with selected case examples.

Categories of CBS

According to the clinical presentation and angiographic findings, CBS can be classified into one of three types, originally described by Chaloupka et al.1 Threatened carotid blowout includes those patients with exposed carotid artery or its branches without evidence of acute bleed. Although hemorrhage has not yet occurred, these findings suggest that it is inevitable if no action is taken. This category also includes patients with angiographic findings consistent with neoplastic invasion of the carotid arteries. The second category is called impending carotid blowout and includes those with acute transoral or transcervical hemorrhage that resolved either spontaneously or with simple packing or pressure. Impending CBS is typically caused by a pseudoaneurysm that leaks intermittently. Since a pseudoaneurysm has no structural integrity and support, complete rupture may occur at any time. The final category of CBS is called acute carotid blowout and includes those patients with acute, profuse and uncontrollable hemorrhage caused by active extravasation secondary to complete rupture of the affected carotid artery.

Types of endovascular treatment

There are essentially two endovascular treatment strategies that can be applied in patients with CBS: (1) Vessel occlusion or Deconstruction, and (2) Stent-graft placement or Reconstruction. The choice between the two approaches depends on clinical and anatomical factors such as clinical presentation, lesion location, the presence of adequate collateral circulation and the results of BTO when available.

Methods

CBS in our institution

Eight patients with head and neck cancer (six male and two female) with a median age of 66 years (range, 27–77 years) were referred to the interventional neuroradiology service for emergency diagnostic angiography and endovascular management of nine episodes of CBS. One patient was referred for two episodes of CBS. This represents the volume and types of cases presenting at our institution over the course of 1 year. All patients were treated with modified or radical neck dissection and radiation therapy for squamous cell carcinoma, except for one patient with an extensive skull angiosarcoma who was being treated with chemotherapy alone. CBS was classified into threatened, impending and acute. Diagnostic angiography followed by endovascular therapy was performed in all patients.

Diagnostic angiography

Many of these patients required either complex intubations or had a pre-existing tracheostomy. Angiography and treatment is performed with the patient alert and using only local anesthetic and moderate sedation, unless intubation is required for airway protection and/or cardiopulmonary support. This allows for a BTO to be performed if indicated based on the results of angiography. The angiograms are performed using the transfemoral approach and standard catheterization technique, without systemic anticoagulation. Angiograms of the common carotid artery (CCA), internal carotid artery (ICA) and external carotid artery (ECA) bilaterally were performed in all patients using standard neuroangiographic techniques. Particular assessment was made of arterial wall irregularity, luminal stenosis, pseudoaneurysm formation, arterial wall rupture and extravasation, and completeness of the circle of Willis. Angiogram of the vertebral arteries was performed when evaluation of collateral flow from the posterior to the anterior cerebral circulation was required. If bleeding occurred in the lower part of the neck, angiography of the subclavian, thyrocervical and costocervical arteries was also performed.

Endovascular treatment

Deconstructive management

The indications for deconstructive management and vessel occlusion in our institution are the following: (a) lesions involving the trunk of the ECA or its branches, and (b) patients with CCA or ICA lesions in whom a BTO demonstrated that the vessel can be occluded without significant risk of brain ischemia. A BTO is performed in a hemodynamically stable, cooperative and alert patient in whom the angiogram suggests that the CBS is caused by lesions of the CCA or ICA. The BTO in our institution is performed in the following way: After baseline neurological examination, a guide catheter is positioned into the CCA or ICA. A microcatheter with a non-detachable balloon at its distal end is coaxially advanced through the guide catheter into the abnormal artery, just proximal to the lesion. After measuring a baseline activated clotting time and administering a bolus of intravenous heparin (70 IU/kg), the balloon is carefully inflated and vessel occlusion is confirmed with angiography through the guide catheter. The neurological examination is repeated every 3–5 min for a total test time of 20–30 min, after which the balloon is deflated. If the patient tolerates the test and neurological exam remains unchanged during the test, permanent occlusion of the CCA or ICA can be considered. If on the other hand, the patient experiences new neurological symptoms, the BTO is terminated immediately to avoid irreversible brain ischemia and vessel occlusion is avoided. In unstable, sedated or intubated patients in whom occlusion of the CCA or the ICA is the only option, for example, because of tortuous vessels that do not allow delivery of a stent-graft, a modified BTO can be performed with temporary occlusion of the abnormal vessel and diagnostic angiogram of the contralateral carotid artery and the posterior circulation. If the circle of Willis is complete and there is adequate collateral flow, then the patient is at low risk for brain ischemia. While not as sensitive as a clinical assessment, this radiographic test reassures deconstructive approaches in cases where a reconstructive approach is not an option; in the case of acute CBS, the risk of vessel deconstruction must be compared with the associated high mortality of the natural history of the disease. For lesions of the ECA trunk and its branches, a BTO is not indicated because the risk of brain ischemia is negligible.

The embolic materials used depend upon the target vessel. For occlusion of the ECA trunk we typically use a combination of detachable coils and liquid embolization materials. The procedure is performed with a guide catheter placed in the proximal segment of the diseased vessel and a microcatheter advanced coaxially to the diseased segment. The vessel occlusion is performed by placement of coils, followed by injection of liquid embolic material. The coils act as a nidus for entrapment of the liquid material. Ideally, the embolization material should cover the proximal and distal ends of the abnormal segment; this allows for exclusion of the aneurysm from the arterial circulation and avoids possible collateral refill (cross occlusion). For ICA occlusion, the embolization material should be placed in the petrous or even cavernous portion of the ICA, allowing for the ophthalmic artery to remain patent via collateral supply. Thus, retrograde flow via the ostium of the ophthalmic artery will supply the distal ICA and its branches, and the space with stagnant blood from the distal aspect of the occluded segment and the ostium of the ophthalmic artery (‘dead space’) is decreased, minimizing the risk of thrombosis in the carotid stump and the risk of thromboembolic stroke. It is important to note that liquid embolic material is typically not used for ICA or CCA occlusion because of the risk of migration into the brain, unless there is pre-existing occlusion. An alternative modality for large vessel occlusion is a self-expandable occlusion device (Amplatzer vascular plug; AGA Medical Corporation, Plymouth, Minnesota, USA) delivered through a guide catheter. For occlusion of small vessels such as distal ECA branches, we may use particles or liquid embolic material injected through a microcatheter. After vessel occlusion, absolute flow arrest and complete resolution of extravasation must be verified angiographically not only immediately after the procedure, but also at an interval (at least 15 min) to ensure no revascularization or flow around the implanted occlusive devices.

Reconstructive management

Indications for reconstructive management with stent-grafts (covered stents) at our institution include patients with CCA or ICA lesions at risk for brain ischemia after carotid occlusion. This category includes patients who have one or more of the following: (a) failed the BTO, (b) have incomplete circle of Willis on angiogram, (c) have contralateral severe carotid stenosis or occlusion and (d) their condition precludes BTO or contralateral carotid angiogram. Any stent placed in the carotid artery serves as a nidus for platelet aggregation and formation of thrombus, and stent-grafts in general are more thrombogenic than bare metal stents. Thus, antiplatelet medication is required to prevent stent thrombosis and thromboembolism. In elective cases the patients are typically premedicated with antiplatelet medication for at least 1 day prior to the placement of the stent, but in patients with impending and acute CBS the risk of exacerbating the hemorrhage and the need to intervene as quickly as possible preclude any premedication. In our practice, patients referred for threatened CBS (based on cross-sectional imaging findings) are typically premedicated with oral aspirin (325 mg daily) and oral clopidogrel (75 mg daily) for at least 1 day prior to the procedure. Patients with impending or acute CBS treated on an emergency basis are administered aspirin orally (325 mg) or by suppository (300 mg) immediately after placement of the stent. During all stent placement procedures, we administer 70 IU/kg heparin to achieve an activated clotting time 2–3× baseline. An appropriately sized stent-graft is advanced through a guide catheter placed through the femoral artery into the CCA, and deployed under fluoroscopic guidance into the CCA, ICA or carotid bifurcation, depending on the location of the lesion. For lesions adjacent to the carotid bifurcation, the ECA trunk is occluded before deployment of the stent to prevent rebleeding from reconstitution of the aneurysm through retrograde filling of the ECA branches. The procedure is completed when the lesion is completely covered with the stent-graft showing apposition to the arterial wall. Complete resolution of extravasation must be verified angiographically immediately after the procedure and at least 15 min later. After hemostasis is achieved and hemorrhage is excluded, aspirin (325 mg) and clopidogrel (75 mg) by mouth are added for the next 30 days.

Follow-up and outcome evaluation

Following endovascular therapy, all patients are admitted to the intensive care unit for hemodynamic and neurologic monitoring. Discharged patients are seen in the outpatient clinic, initially at 4-weekly and then at 3-monthly intervals. For patients treated with stent placement, aspirin and clopidogrel are continued for 30 days, after which clopidogrel is discontinued; patients remain on aspirin life-long. Follow-up angiograms are only performed when there is evidence for recurrent CBS or new neurological symptoms related to the procedure. Technical success of the endovascular treatment, immediate hemostasis, procedural and post-procedural complications, need for additional endovascular treatment, recurrence of CBS and survival time (from the time of initial CBS to death) are used as outcome measures.

Results

Nine diagnostic and therapeutic procedures were performed in eight patients referred to our service for evaluation and management of CBS over the course of 1 year. There were eight episodes of acute CBS and one episode of threatened CBS. One patient presented with acute CBS twice. Sixteen vascular lesions were identified on angiography. The presence of pseudoaneurysm and/or active extravasation was documented in at least one vessel in all eight cases presenting with acute CBS. There was no episode in which angiography failed to identify at least one lesion associated with the CBS, and five out of nine episodes were attributed to involvement of more than one vessel.

Thirteen focal pseudoaneurysms were identified: 5 in ECA trunk, 4 in ECA branches (3 lingual arteries, 1 facial artery), 3 in the CCA and 1 in the proximal ICA. There were three additional ICA lesions: in one patient with acute CBS and ECA pseudoaneurysm, both cervical ICAs were invaded by tumor with the presence of occlusive tumor-thrombus in the vessel lumen. In another patient with threatened CBS, angiography showed long-segment invasion of the cervical ICA resulting in severe irregular stenosis without evidence of focal pseudoaneurysm.

Permanent vessel occlusion was performed in 11 procedures: 4 for pseudoaneurysms of ECA branches (figure 1), 4 for pseudoaneurysms of the ECA trunk (figure 2), and 3 for ICA lesions. In the patient with tumor-thrombus in the ICA bilaterally, both ICAs were completely occluded to prevent rebleed and/or massive distal thromboembolism (figure 2). A BTO was not performed because the patient was already intubated but good collateral flow from the ECA branches and the posterior circulation was evident on the diagnostic angiogram. The patient with long-segment ICA stenosis tolerated the BTO and the ICA was subsequently occluded (figure 3). Stent-grafts were placed in 5 procedures: 3 to treat pseudoaneurysms in the CCA, 1 to treat a pseudoaneurysm of the ECA trunk (figure 4) and 1 to treat a pseudoaneurysm in the proximal ICA (figure 5).

Figure 1

Patient with squamous cell carcinoma of the tongue and larynx presented with acute carotid blowout syndrome. Catheter angiography revealed a pseudoaneurysm of the lingual artery (A, arrow), which was selectively embolized with contour polyvinyl alcohol embolization particles (Boston Scientific, Freemont, California, USA) via a microcatheter placed in the lingual artery. The pseudoaneurysm was completely occluded (B).

Figure 2

Patient with angiosarcoma, presented with acute carotid blowout syndrome. Catheter angiography showed bilateral internal carotid artery (ICA) occlusion from tumor-thrombus (A,B, straight arrows) and right external carotid artery (ECA) pseudoaneurysm (A, circle). Cerebral perfusion was provided by the vertebrobasilar system alone via patent posterior communicating arteries bilaterally (not shown). The patient was treated by embolization of the ICA bilaterally (C, arrows) to prevent rebleed or distal migration of thrombus from ICA recanalization, and by embolization of the right ECA pseudoaneurysm (C, circle), using a combination of coils and N-butyl cyanoacrylate (Trufill NBCA; Cordis Neurovascular, Miami, Florida, USA).

Figure 3

Patient with squamous cell carcinoma of the tongue presented with threatened carotid blowout syndrome (internal carotid artery (ICA) infiltration evident on neck CT, not shown). Catheter angiography showed irregular narrowing of the cervical segment of the right ICA (A, arrow). A balloon test occlusion (BTO) was performed (B, arrow), which showed good collateral flow from the left ICA, as well as the posterior circulation and the right external carotid artery, via anastomotic branches with the ophthalmic artery (not shown). The patient remained neurologically intact during the BTO. The right ICA was then occluded (C) using coils in the cavernous ICA below the ophthalmic artery (straight arrow) and an Amplatzer vascular plug (AGA Medical Corporation) at the proximal ICA (block arrow). The ophthalmic artery and distal ICA are reconstituted via retrograde flow from external carotid artery branches (C, arrowhead).

Figure 4

Patient with squamous cell carcinoma of the oral floor presented with acute carotid blowout syndrome and angiographic findings of pseudoaneurysm in the external carotid artery trunk (A, arrow). The aneurysm was treated with placement of a 3 mm×12 mm Jostent Graftmaster covered stent (Abbott Vascular, Redwood City, California, USA) across the abnormal arterial wall (B, arrow) with no residual extravasation on the post-stent angiogram (C).

Figure 5

Patient with squamous cell carcinoma of the larynx presented with acute carotid blowout syndrome (CBS) and findings of a carotid bifurcation and proximal internal carotid artery pseudoaneurysm (A, arrows). A 7 mm×38 mm Atrium iCast balloon expandable covered stent (Atrium Medical Corporation) was used to treat the pseudoaneurysm (B, arrow), and a 6 mm Amplatzer vascular plug (AGA Medical Corporation, Hudson, New Hampshire, USA) (B, block arrow) was used to occlude the origin of the external carotid artery (ECA) in order to prevent reconstitution of the pseudoaneurysm and rebleed. This patient was previously treated with a covered stent for a common carotid pseudoaneurysm, also presenting with acute CBS (not shown).

Technical success was 100% and immediate hemostasis was achieved in all patients. There was no procedural death and no immediate complications. Clinical follow-up ranged from 1 to 13 months (median, 2 months). Three patients died during the follow-up period. One patient treated with CCA stent for acute CBS died 2 months after treatment from recurrent CBS at an outside hospital; this was the only patient with recurrent CBS. The patient with tumor invasion and occlusion of the ICA bilaterally developed global cerebral ischemia after cardiac arrest and died in hospice also 2 months after treatment for CBS; this was the sole neurological complication in our series. The third patient died 11 months after treatment for acute CBS with ECA trunk stent; his death was attributed to disease progression.

Discussion

Over the last decade, endovascular management of CBS has emerged as the treatment of choice for this devastating complication of head and neck cancer and has essentially replaced surgical ligation of the carotid artery. The high morbidity and mortality associated with surgery in patients with CBS might be explained from the inherent limitations of the surgical approach in an unfavorable surgical field, the added risks of general anesthesia and the lack of diagnostic angiography pinpointing the type and precise location of vascular injury. The angiographic findings in patients with CBS are heterogeneous, with the majority of lesions identified in the CCA and carotid bifurcation, cervical ICA, ECA trunk and distal ECA branches.1 4 5 In a series of patients with CBS and history of nasopharyngeal cancer treated with radiation therapy alone, the majority of pseudoaneurysms occurred in the petrous segment of the ICA, which suggests that the location of the lesion might be associated with the underlying risk factors.6 Such variability in pathological findings necessitates a complete angiographic evaluation with (super) selective catheterizations and multiple views in order to identify the lesion(s) and plan for appropriate treatment. In our series most patients had more than one lesion, which emphasizes the importance of meticulous and thorough angiography.

The initial endovascular technique used to treat CBS was permanent balloon occlusion of the injured carotid artery, and it resulted in significant improvement of the outcome after carotid artery rupture. Citardi et al3 reported on a series of 12 patients treated by endovascular occlusion of the affected vessel with detachable balloons; hemostasis was achieved in all patients without major neurological complications. Along the same lines, in a series of 18 patients with CBS treated with vessel occlusion, Chaloupka et al,1 reported 89% survival with two recurrent hemorrhages, one of which was fatal. Delayed transient ischemia was seen in 15% of patients treated with permanent occlusion of the ICA, but there was no major neurological morbidity. It is important to note that BTO identifies patients at risk of immediate ischemia from occlusion; the sensitivity of BTO in identifying patients at risk of delayed brain ischemia due to hemodynamic insufficiency or thromboembolism is significantly more controversial. Depending upon the methods used, despite “adequate” BTO, the rate of delayed ischemia after vessel occlusion may be as high as 20%.1 7 The one patient who experienced stroke in our series presented with acute CBS, with tumor-thrombus occluding the ICA lumen bilaterally. At the time of procedure the patient had good collateral flow from the vertebrobasilar circulation, but cerebral perfusion was pressure dependent, and the stroke occurred after cardiac arrest and hypotension. Our decision to treat this patient with tumor infiltration of bilateral ICA was not based on BTO results but on the notion that both the ICAs were already occluded from tumor-thrombus and partial recanalization would result in recurrent CBS and/or migration of thrombus distally in the intracranial branches. As a palliative measure instituted for this patient with extensively invasive oncologic disease, this procedure averted mortality without immediate ischemic complication.

Such ischemic risks after deconstructive techniques provided an indication for stenting as an alternative strategy for the management of CBS, preserving patency and flow in the carotid artery in patients at high risk of brain ischemia. Lesley et al8 reported on 12 patients with CBS (10 with head and neck carcinoma and two with post-traumatic CBS) who were deemed high-risk for cerebral ischemia and were treated with a variety of stents (mostly bare metal stents). Immediate hemostasis was achieved in all patients with one episode of transient brain ischemia (8%), but no procedure-related death or stroke. Although stent placement has major advantages such as reinforcement of the mechanical integrity of the carotid wall and patency of the carotid artery, several limitations became evident. Reports of stent placement in a contaminated field suggested that there is increased risk of stent occlusion and recurrent bleeding. Chang et al9 reported on a series of eight patients with CBS from head and neck cancer treated with placement of self-expandable stent-grafts. Antiplatelet medications were administered during and after treatment in all patients. While technical success and immediate hemostasis was achieved in all patients, initial complications included acute thromboembolism in three patients, resulting in one stroke. Delayed complications included carotid thrombosis in three patients and brain abscess formation in one patient, likely secondary to stent infection. The results of this study highlight two difficulties in balancing risks and benefits of stent placement in this patient population. First, the increased risk of infection in patients with open wounds or pharyngocutaneous fistulae must be considered. Second, the risk of bleeding from residual tumor or sites of radiation necrosis must be weighed against the need for an antiplatelet regimen to prevent in-stent thrombosis. Although previous authors5 9 used self-expandable stent-grafts for carotid reconstruction, we prefer to use balloon-expandable stent-grafts because they generally have higher radial force, which allows for better apposition against the arterial wall that is critical for a good result. In addition, the drawback of less flexibility and increased mechanical stress to the vascular wall compared with the self-expandable stents is offset by delivery systems of smaller diameter. In our series, four stent-grafts were placed in three patients. There was no complication of in-stent thrombosis, which might be attributed to the type of stent used or early administration of two antiplatelet agents after hemostasis is achieved. Whereas other authors9 used glycoprotein IIb/IIa receptor inhibitors during the procedure in addition to heparin, aspirin and clopidogrel, our regimen of immediate application of aspirin after the stent deployment followed by institution of aspirin and clopidogrel upon confirmation of postoperative protection from exsanguinations was sufficient to prevent stent thrombosis in our series.

Recurrent CBS after endovascular treatment is an important concern with variable incidence, as high as 50%.4 5 10 In our series there was one (12%) recurrence in a patient treated with CCA stent and facial artery occlusion for acute CBS. The patient was admitted at a remote hospital and died from uncontrollable hemorrhage. The different rates of recurrent CBS probably reflect progression of malignancy and duration of follow-up and mean survival time rather than type of treatment.

In a recent paper, Chang et al4 compared the outcomes of the reconstructive (n=11) versus deconstructive (n=13) endovascular treatment for patients with CBS attributed to the CCA, ICA and ECA trunk that could be treated by either approach. Patients with lesions in ECA branches only eligible for deconstruction were excluded from the comparison. Technical success and hemostasis was achieved in all patients. Initial complications were seen in 4/11 patients (thromboembolism in three and dissection in one) in the reconstructive group and 1/13 patients in the deconstructive group (stroke). Delayed complications were seen in 1/11 patient (septic thrombosis of the stent with multiple brain abscesses) in the reconstructive group and 1/13 patients in the deconstructive group (brain abscess). The stent was patent in 9/11 patients with follow-up imaging in 3 months and 3/6 patients with follow-up imaging in 6 months. Rebleeding was seen in 5/11 patients in the reconstructive group and 3/13 patients in the deconstructive group. Mean survival was approximately 12 months in both groups. The authors concluded that there is no significant difference in outcome between the two methods and that outcome is mostly related to CBS severity at presentation. Representing the largest published series specifically addressing this disease, these results demonstrate the difficulties but also the success of endovascular treatment of this highly mortal disease process. While larger series with better controls would be necessary to accurately compare deconstructive and reconstructive techniques and outcomes, the two techniques together provide the interventional neuroradiologist, in consultation with the otolaryngologist, with an armamentarium to address a previously virtually uncontrollable often-emergent pathology.

Conclusion

Using a systematic approach based on lesion location and risk for stroke, every vascular lesion causing CBS can be expeditiously and effectively treated by endovascular means. Our results corroborate the findings of other studies that CBS can be treated with endovascular reconstruction or deconstruction in the acute phase with great efficacy, low and acceptable risks, suitable for palliative care. Thus, endovascular treatment should be offered as early as possible in the context of a multidisciplinary approach to CBS.

References

Footnotes

  • Competing interests None.

  • Provenance and peer review Not commissioned; not externally peer reviewed.