- •Foreword
- •Preface
- •Glossary
- •1. Introduction
- •2. Historical Considerations
- •2.1 Arteriovenous Fistula and Pulsating Exophthalmos
- •2.2 Angiography
- •2.3 Therapeutic Measures
- •2.4 Embolization
- •References
- •3.1 Osseous Anatomy
- •3.1.1 Orbit
- •3.2 Anatomy of the Dura Mater and the Cranial Nerves
- •3.2.1 Autonomic Nervous System
- •3.3 Vascular Anatomy
- •3.3.1 Arterial Anatomy
- •3.3.1.1 Internal Carotid Artery
- •Meningohypophyseal Trunk (MHT)
- •Ophthalmic Artery
- •Ethmoidal Arteries
- •3.3.1.2 External Carotid Artery
- •3.3.1.2.1 Ascending Pharyngeal Artery
- •3.3.1.2.2 Internal Maxillary Artery
- •3.3.1.2.3 Middle Meningeal Artery
- •3.3.1.2.4 Accessory Meningeal Artery
- •3.3.2 Venous Anatomy
- •3.3.2.1.1 Embryology
- •3.3.2.1.2 Anatomy and Topography
- •Orbital Veins
- •Superior Ophthalmic Vein
- •Inferior Ophthalmic Vein
- •Central Retinal Vein (No Direct CS Tributary)
- •Uncal Vein, Uncinate Vein
- •Sphenoparietal sinus (Breschet), Sinus alae parvae, Sinus sphenoidales superior (Sir C. Bell)
- •Intercavernous Sinus, Sinus intercavernosus, Sinus circularis (Ridley), Sinus ellipticus, Sinus coronarius, Sinus clinoideus (Sir C. Bell), Sinus transversus sellae equinae (Haller)
- •Meningeal Veins
- •Veins of the Foramen Rotundum, Emissary Vein
- •Inferior Petrosal Sinus, Sinus petrosus profundus, Sinus petro-occipitalis superior (Trolard)
- •Venous Plexus of the Hypoglossal Canal, Anterior Condylar Vein
- •Posterior Condylar Vein
- •Lateral Condylar Vein
- •Inferior Petroclival Vein
- •Petro-occipital Sinus, Sinus petro-occipitalis inferior, petro-occipital vein (Padget)
- •Transverse Occipital Sinus (Doyen)
- •Basilar Plexus (Virchow)
- •Marginal Sinus
- •Foramen Ovale Plexus (Trigeminal Sinus), Sphenoid Emissary, “Rete” of the Foramen Ovale
- •Vein of the Sphenoid Foramen (Foramen Venosum, Foramen of Vesalius)
- •Foramen Lacerum Plexus
- •Pterygoid Plexus
- •3.3.2.4 Other Veins of Importance for the CS Drainage or for Transvenous Access to the CS
- •Facial Vein
- •Frontal Vein
- •Angular Vein
- •Middle Temporal Vein
- •Internal Jugular Vein
- •The External Jugular Vein
- •Vertebral Vein, Vertebral Artery Venous Plexus
- •Deep Cervical Vein
- •References
- •Introduction
- •4.1.1 Dural Arteriovenous Fistulas (DAVFs)
- •4.1.2 Cavernous Sinus Fistulas (CSFs)
- •References
- •Introduction
- •5.1 Etiology and Pathogenesis of Type A Fistulas
- •5.2 Etiology and Pathogenesis of Type B–D Fistulas
- •5.2.1 Pregnancy
- •5.2.2 Hormonal Factors
- •5.2.3 Thrombosis
- •5.2.4 Venous Hypertension
- •5.2.5 Trauma
- •5.2.6 Embolization
- •5.2.7 Congenital
- •5.2.8 Other Potential Factors
- •5.2.9 Various
- •5.3 Prevalence
- •5.3.1 Natural History
- •References
- •Introduction
- •6.1 Extraorbital Ocular Symptoms
- •6.1.1 Orbital Pain
- •6.2 Orbital Symptoms
- •6.2.1 Exophthalmos
- •6.2.2 Conjunctival Engorgement and Chemosis
- •6.2.2.1 Retinal Hemorrhage
- •6.2.3 Corneal Damage
- •6.2.4 Orbital Bruit
- •6.2.6 Secondary Glaucoma and Visual Loss
- •6.3 Other and Neurological Symptoms
- •References
- •7. Radiological Diagnosis of DCSFs
- •7.1 Non-invasive Imaging Techniques
- •7.1.2 Doppler and Carotid Duplex Sonography
- •7.2 Intra-arterial Digital Subtraction Angiography (DSA)
- •7.2.1 Introduction
- •7.2.2 Technique
- •7.2.3 Angiographic Protocol for DCSFs
- •7.2.4 Angiographic Anatomy of the Cavernous Sinus
- •7.2.5 Flat Detector Technology in Neuroangiography
- •7.2.6 Rotational Angiography and 3D-DSA
- •7.2.6.1 Dual Volume Technique (DVT)
- •7.2.6.2 Angiographic Computed Tomography (ACT), DynaCT (Siemens), C-arm Flat Detector CT (FD-CT), Flat Panel CT (FP-CT) or Cone Beam CT
- •7.2.6.3 Image Post-Processing
- •7.2.6.4 3D Studies of the Cavernous Sinus Region
- •References
- •8. Endovascular Treatment
- •8.1 Techniques of Transvenous Catheterization
- •8.1.1 Inferior Petrosal Sinus Approach
- •8.1.2 Alternative Approaches to the Cavernous Sinus
- •8.1.3 Other Techniques
- •8.2 Embolic Agents
- •8.2.1 Polyvinyl Alcohol (PVA) and Embospheres
- •8.2.2 Stainless Steel Coils
- •8.2.5 Stents
- •8.3.1 Approaches (Benndorf et al. 2004)
- •8.3.2 Angiographic and Clinical Outcome
- •8.4 Discussion of Transvenous Occlusions
- •8.4.1 Approaches
- •8.4.1.1 IPS Approaches
- •8.4.1.6 Transfemoral Pterygoid Plexus Approach (PP Approach)
- •8.4.1.7 Transfemoral Cortical Vein Approach
- •8.4.1.10 Direct Puncture of the Foramen Ovale
- •8.4.2 Embolic Materials
- •8.4.2.1 Particles
- •8.4.2.2 Coils
- •HydroCoils (Hydrogel)
- •8.4.2.4 Ethylene-Vinyl Alcohol Copolymer (OnyxTM)
- •8.4.2.5 Stents and Covered Stents
- •8.4.3 Anatomic Results, Clinical Outcome and Complications of Transvenous Occlusions and Transarterial Embolizations
- •8.5 Conclusion
- •References
- •9. Alternative Treatment Options
- •9.1 Spontaneous Thrombosis
- •9.2 Manual Compression Therapy
- •9.4 Radiotherapy
- •9.5 Surgery
- •References
- •10. Hemodynamic Aspects of DCSFs
- •10.1 Introduction
- •10.2 Basic Hemodynamic Principles
- •10.3 Invasive Assessment of Hemodynamics
- •10.4 Flow Velocity and Pressure Measurements in Brain AVMs and DAVFs
- •10.5 Hemodynamics and Pathophysiology in CSFs
- •Comments
- •References
- •11. Summary
- •Subject Index
260 8 Endovascular Treatment
the other hand, evidence suggests that PTFE might reduce the rate of intimal hyperplasia (Redekop et al. 2001; Gercken et al. 2002). Fourth and not least, placing a covered stent may be effective in CSFs with solely ICA supply (Type B fistulas, see Case Illustration XI), while in Type C and D fistulas subsequent recruitment of ECA feeders may develop and the treatment remains ineffective.
Longer follow-ups and the development of softer stent grafts dedicated for neurovascular use will show whether or not covered stents play a role in the future armamentarium of endovascular treatment for DCSFs. The VIABAHNN Endoprosthesis from Gore (Gore & Associates, Inc., Arizona) has been FDA approved and may represent an alternative to the JoStent.
8.4.3
Anatomic Results, Clinical Outcome and Complications of Transvenous Occlusions and Transarterial Embolizations
Due to the paucity of early reports on transvenous treatment of DCSF, the validity of achieved results in anatomic and clinical cures as well as complications rates has been limited. Table 8.6 provides an overview of the results achieved by various groups and shows that more data have become available in recent years.
While most groups reported series of between 10–20 patients in the 1980s, the number of series studying more than 20 patients has increased. Thus, statements about efficacy and procedure released complications associated with TVO have become more valid.
In 1989, the first relevant series reporting transfemoral venous approaches was published by Halbach et al. (1989a) (n=13). The authors primarily used a transfemoral approach through the IPS, the SOV and the basilar plexus, achieving 90% angiographic cure and 77% clinical cure. They observed two complications; one patient developed a stroke after placement of a balloon, while another suffered from transient vision loss.
Yamashita et al. (1993) achieved complete angiographic cure in 14 of 16 (88%) cases, interpreting the failure in two cases with coils that were not optimally placed within the CS. This may have been caused by intracavernous trabeculae, thrombosis or unfavorable anatomy of the SOV. There were 12% transient and 6% permanent deficits.
Goldberg et al. (1996) presented the first larger series of SOV cannulation and achieved immediate improvement or clinical cure in 100% of their patients (n=10). They were unsuccessful in two additional patients and observed one case of severe intraorbital bleeding.
Quinones et al. (1997) achieved a 92% occlusion rate in 12 successfully catheterized patients and a clinical recovery in all but two patients (83%). The authors observed two delayed complications. One patient developed a palpebral silk granuloma, another transient contralateral cavernous sinus syndrome (6th nerve palsy). With the exception of two additional cases (Case 11 and 12), the aforementioned represents the same series as the one published by Goldberg et al. (1996) 1 year earlier. It should be noted, however, that the 82-year-old female who suffered from severe intraorbital hemorrhage after attempted transorbital deep puncture was not included in their results, and has not been mentioned in the second report of this group (Quinones et al. 1997). Identifiable on the angiographic images [Figs. 6 and 3, respectively, in Leibovitch et al. (2006)], this patient was recently presented by Leibovitch et al. (2006) as an 86-year-old female in more detail with an apparently more complicated post-craniotomy course suffering from permanent left hemiplegia and vision loss. Such an unfortunate outcome after TVO of a DCSF is rather unusual and will presumably remain an exception, if less invasive routes and means are considered first.
Roy and Raymond (1997) reported on 24 patients with DAVFs; 12 with DCSFs. Nine were treated using transvenous occlusions only; 89% demonstrated complete anatomic occlusion. In this series, transient CN deficits occurred relatively frequently (50%), and in one patient permanent sixth nerve palsy was seen (8%). The authors explained these complications with local thrombosis inside the CS that led to CN irritations, and considered mechanical pressure less likely the reason, since the symptoms were irreversible.
Oishi et al. (1999) reported results and complications that may occur when employing different venous approaches. They achieved complete angiographic cure in 89% of cases with a relatively high complication rate of 32%. These complications consisted of transient 6th nerve palsies (n=3), dissections of the IPS (n=1), blepharoptosis (n=2), as well as permanent dysesthesia of the forehead (n=1) due to upper lid incision for the SOV approach. The authors were able to reduce this complication rate with
8.4 Discussion of Transvenous Occlusions |
261 |
gained experience and more frequent use of the IPS approach.
Gobin et al. (2000) reported angiographic cure in 24 of 26 patients (92%) and a complete clinical cure in 25 patients (96%). The authors observed two complications (7%): one transient 6th nerve palsy (4%) and one case of visual loss due to thrombosed central retinal vein (4%).
Cheng et al. (2003) treated 27 patients with TVO achieving complete angiographic obliteration 89% (30% immediate) and clinical cure in 96%. Two patients presented with recurrent symptoms and underwent a second procedure. The authors observed transient 6th nerve palsy in three patients (11%), which occurred with delay in two, suggesting progressive thrombosis and inflammation inside the CS, as discussed by others (Roy and Raymond 1997).
Meyers et al. (2002) recently reiterated the UCSF experience in 135 patients followed over a period of 15 years. The majority (76%) of patients undergoing EVT were treated by transvenous approach, achieving angiographic and clinical cure rates of 90%. Eight patients (6%) experienced symptomatic complications, including infarction (n=1), visual deterioration (n=2), diabetes insipidus (n=1) and orbital ecchymosis (n=1), but it remains unclear if these occurred during TVO or TAE. The overall procedurerelated permanent morbidity was 2.3%; however, the authors do not specify whether it was related to TVO or TAE. Angiographic follow-up was obtained in 54%; one third of the patients required more than one intervention.
More recently, Theaudin et al. (2007) reported on 27 consecutive patients undergoing transvenous occlusions (n=16) or transarterial embolizations (n=4). Complete occlusion was achieved in 14/16 patients (88%) with early-improved symptoms in 12 (75%). One patient (6%) developed a temporal lobe hemorrhage immediately following transvenous occlusion in a fistula with cortical venous drainage, possibly due to blockage of the fistula drainage by placement of the guiding catheter into the IPS. The patient fully recovered without permanent deficit when seen at 1 year follow-up.
Yu et al. (2007) reported a series of 61 patients undergoing 64 successful TVO procedures and achieved anatomical cure in 95%. In 38 patients the fistula was occluded immediately after the procedure, in 20 a mild residual fistula was documented and completely occluded in FU exams (3–16 months). Three patients showed persistent symptoms and underwent repeat TVO, while 16 patients showed cure within 2 weeks,
22 after 3 months. There were two patients with transient 6th nerve palsy. Using catheterization of the SOV either via the facial or the middle temporal veins the authors were successful in 11/11 cases. It is interesting to note that the authors’ technical success rate increased from 71.6% to 86.5% after adapting this transfacial SOV approach. Furthermore, it is worth mentioning that in 7/8 patients with residual symptoms the IPS was used as initial route.
Kim et al. (2006) achieved an immediate 75% occlusion rate (complete or nearly complete) with cure or improvement of symptoms in 91% of patients. A total of 11 complications (20%) were observed, including six cranial nerve palsies, three venous perforations and two patients who developed brainstem congestion. Although this rate is relatively high, most of the adverse events were transient or clinically silent. These authors discuss in detail potential mechanisms and possible management strategies (Kim et al. 2006):
First, transient CN palsies seen in six cases (10.7%) were likely due to overpacking of the cavernous sinus or extensive thrombosis within the CS. This was also observed by us in one case after coil packing the left and right CS with a total of 16 GDCs-10, and two GDCs-18-VortX. The patient presented with exophthalmos and chemosis and developed a new diplopia due to 6th nerve palsy the day after treatment. She was heparinized for 3 days and treated with corticosteroids for 1 week. The patient recovered completely within 8 weeks. A follow-up arteriogram after 6 months confirmed complete occlusion of the fistula. It can be assumed that the relatively stiff VortX-18 coil may have caused nerve compression.
Second, venous perforations during IPS catheterizations were seen in 5.4% (three cases), none of which resulted in clinical sequelae due to immediate recognition and coil embolization. Extravasation during IPS catheterization occurred in one of our patients; however, it remained clinically silent. Rupture of an IPS may not cause serious clinical complications as most perforations occur when a catheter is advanced through a thrombosed or occluded IPS with minimal or no AV shunt flow.
Finally, venous congestion in association with DCSFs has been reported by a number of authors (Iwasaki et al. 2006; Kai et al. 2004; Uchino et al. 1997; Teng et al. 1991). Kim et al. (2006) demonstrated a rate in 3.6%, attributed to rerouted venous drainage after coil packing within the CS.
262 8 Endovascular Treatment
Such rerouting of venous drainage towards the posterior fossa following TVO of DCSFs has not been observed in the material studied. In all cases with preexisting cortical or leptomeningeal drainage, it was possible to disconnect the communication between the CS and the efferent venous drainage at the beginning of the procedure.
However, venous rerouting after TVO of a direct high-flow CCF using coils without achieving complete occlusion has occurred and resulted in an intracranial hemorrhage several hours after the procedure.
In summary, the results achieved by the various groups (Tables 8.6 and 8.7) show anatomic cure rates ranging from 52%–100%, depending on whether or not immediate complete or near complete (subtotal) obliteration of the AV shunt is considered the endpoint. Similarly, the rate of clinical cure ranges from 63%–100%, with the majority of groups achieving more than 80%–90%. This is higher than what was accomplished in the early era of EVT and lies above results obtainable using transarterial embolizations (Goldberg et al. 1996; Halbach et al. 1987; Sonier et al. 1995), thus reflecting the experience gained
Table 8.6. Anatomic and clinical results of TVO in DCSFs reported in the literature (600 patients)
Author |
N |
Approach |
Result DSA |
Partial |
None |
Result |
Improved |
None |
||
|
|
|
(complete cure) |
|
|
(clinical cure) |
|
|
||
Teng et al. (1988) |
5 |
SOV |
4 |
(80%) |
1 |
- |
5 |
(100%) |
- |
- |
Halbach et al. (1989) |
13 |
IPS |
9d (90%) |
1 |
- |
10e (76%) |
3 |
- |
||
Yamashita et al. (1993) |
16 |
IPS |
14 (88%) |
- |
2 |
14 (88%) |
1 |
1 |
||
Miller et al. (1995) |
10 |
SOV |
9 |
(90%) |
- |
1r |
10 (100%) |
- |
- |
|
Roy and Raymond (1997) |
9 |
IPS; - |
8 |
(89%) |
- |
1 |
8 |
(89%) |
1 |
- |
Quinones et al. (1997) |
12a |
SOV |
11s (92%) |
1 |
- |
10 (83%) |
- |
2 |
||
Oishi et al. (1999) |
19 |
IPS, SOV |
17 (89%) |
2 |
- |
17 (89%) |
2 |
- |
||
Gobin et al. (2000) |
26 |
IPS, SOV, PP |
24 |
(92%) |
2 |
- |
25 |
(96%) |
2 |
- |
Annesley-Williams |
11 |
IPS, SOV |
7f (64%) |
5g |
- |
8 |
(73%) |
3 |
- |
|
et al. (2001) |
|
|
|
|
|
|
5j |
|
|
|
Meyers et al. (2002) |
101t |
IPS, SOV |
121/135 (90%)o |
- |
- |
90% |
- |
4% |
||
Biondi et al. (2003) |
7 |
FV, SOV |
6 |
(100) q |
- |
- |
4 |
(67%) |
2 |
- |
Cheng et al. (2003) |
27 |
IPS, SOV, CV |
24 |
(89%) |
- |
- |
26 |
(96%) |
- |
- |
Klisch et al. (2003) |
11 |
IPS, SOV, FV |
-h |
|
- |
- |
8 |
(72%) |
3 |
- |
Benndorf et al. (2004) |
45 |
IPS, SOV, |
42 |
(93%) |
- |
- |
41(91%) |
- |
- |
|
|
|
SPS, SV, FrV |
|
[100%]i |
|
|
|
|
|
|
Wakhloo et al. (2005) |
14 |
IPS, SOV |
12 |
(86%) |
2 (100%)m |
- |
14 (100%) |
- |
- |
|
Kim et al. (2006) |
56 |
IPS, FV, SOV |
29 |
(52%) |
13 (75%)n |
14 |
42 |
(46)k |
- |
- |
|
|
|
|
|
|
|
(91%) |
|
|
|
Kirsch et al. (2006) |
141u |
IPS, SOV |
114 (81%)u |
18 (13%) |
6 (4%) |
94%l |
- |
5% |
||
Yu et al. (2007) |
61b |
IPS, SOV, FV, |
58 |
(95%) |
20 (33%) |
3 (5%) |
58 |
|
22 x |
3 |
|
|
MTV |
38p |
|
|
16w |
|
|
||
Theaudin et al. 2007 |
16c |
IPS, SPS, SOV |
14 (88%) |
- |
- |
10 (63%) |
6 |
|
||
IPS = inferior petrosal sinus, SPS = superior petrosal sinus, SOV = superior ophthalmic vein, PP = pterygoid plexus, FrV = frontal vein, FV = facial vein, CV = clival venous plexus
– no angiographic result or FU reported
a successfully catheterized out of 13, b technical success out of 71, c patients undergoing TVO out of 27,
d out of 10 seen for angiographic FU and occluded, |
e out of all 13 patients, f one bilateral fistula, |
g not specified if immediate or long term occlusion, |
h group mixed with direct CCFs, TCCD or MRPA for FU, |
i all patients seen for angiographic FU showed complete occlusion, j immediately improved, k FU available,
l 55% of the patients seen for long term FU, m after 6mos FU, n complete and nearly complete occlusion together (n=42), o not specified for TVO or TAE, angiographic FU obtained in 54%, p immediately occluded,
q out of 6 patients with technical success, r required TAE for complete occlusion,
s 3 patients seen for angiographic FU, t undergoing TVO out of 135, u TVO failed in 3, TAE performed in 32 patients , v FU in 4 patients pending, w =cured in 2 weeks, x cured after 3 months
|
|
|
8.4 Discussion of Transvenous Occlusions |
263 |
||
Table 8.7. Reported procedure-related complications during TVO in the literature |
|
|
|
|||
Author |
N |
Approach |
Complications |
Rate |
|
|
Halbach et al. (1989) |
13 |
IPS |
S (1), VL (1) |
15% [8%] |
|
|
Yamashita et al. (1993) |
16 |
IPS |
VI (2), III (1), W (3), VP (1) |
44% |
[0] |
|
Miller et al. 1995 |
10 |
SOV |
VI (1) |
10% [10%] |
|
|
Roy and Raymond (1997) |
9i |
IPS ;- |
VI (1) |
66% |
[11%] |
|
|
|
|
VI (5) |
|
|
|
Quinones et al. (1997) |
12 |
SOV |
VI (1) |
8% |
[0] |
|
Oishi et al. (1999) |
19 |
IPS,SOV |
VI (3), D (1), BP (2), VP (1)e |
32% [16%] |
|
|
Gobin et al. (2000) |
26 |
IPS,SOV,PP |
VI (1), TCRV (1) |
8% |
[4%] |
|
Annesley-Williams et al. 2001 |
11 |
IPS, SOV |
W (2) |
18% [0] |
|
|
Meyers et al. (2002) |
101 |
IPS |
S (1) |
|
[1%]d |
|
|
|
|
VL (2) |
5% |
|
|
|
|
|
OE (1) |
|
|
|
|
|
|
VP (1) |
|
|
|
Cheng et al. (2003) |
27 |
IPS, SOV,CV |
VI (3) |
15% [0] |
|
|
|
|
|
MND (1) |
|
|
|
Klisch et al. (2003) |
11 |
IPS, SOV,FV |
S (1)a |
9% |
[0] |
|
|
|
|
SAH (1)a |
|
|
|
Benndorf et al. (2004) |
45 |
IPS,SOV, |
VI (1) |
9% |
[0] |
|
|
|
SPS,SV,FrV |
W (2) |
|
|
|
|
|
|
VP (1)b |
|
|
|
Wakhloo et al. (2005) |
14 |
IPS,SOV, |
VP (1) |
14% [0] |
|
|
|
|
|
VI (1)f |
|
|
|
Kim et al. (2006) |
56 |
IPS,FV,SOV |
CN (5) |
20% |
[2%] |
|
|
|
|
VI (1)c |
|
|
|
|
|
|
VP (3)b |
|
|
|
|
|
|
BC (2) |
|
|
|
Kirsch et al. (2006) |
141 |
IPS, SOV |
W (4) |
13% [0] |
|
|
|
|
|
VP (5)b |
|
|
|
|
|
|
AE (5) |
|
|
|
|
|
|
RH (2) |
|
|
|
|
|
|
PE (2)g |
|
|
|
Leibovitch et al. (2007) |
25 |
SOV |
IOB (2)j |
12% [4%] |
|
|
|
|
|
S (1)h, VL (1)h |
|
|
|
Yu et al. (2007) |
61 |
SOV, FV |
VI (2) |
3% |
[0] |
|
Theaudin et al. (2007) |
16 |
IPS, SPS, SOV |
ICH (1) |
6% |
[0] |
|
IPS = inferior petrosal sinus, SPS = superior petrosal sinus, SOV = superior ophthalmic vein, PP = pterygoid plexus, FrV = frontal vein, FV = facial vein, CV = clival venous plexus
S = stroke, VI = permanent 6th CN deficit (VI = transient), B = bleeding, BP = blepharoptosis, D = dysesthesia, TCRV = thrombosis of the central retinal vein, W/W = permanent/transient ophthalmological worsening, CN = cranial nerve palsy (CN = transient), VP = venous perforation, BC = brainstem congestion,
ICH = intracranial hemorrhage, IOB = intraorbital bleeding, OE = orbital ecchymosis, VL = vision loss, AE = 5 arterial emboli detected by MRI, RH = retinal hemorrhage, MND = minor neurological deficit, PE = pulmonary embolism, TIA = transient ischemic attack
*[ ]= rate of procedure related permanent morbidity, [?] = not reported
Retroperitoneal hematomas, femoral artery pseudoaneurysms or deep venous thrombosis are not considered
a same patient, b clinically silent, c mild residue after 42 months FU in one of six patients,
d not specified if caused by TVO or TAE, e dissected dura caused transient 6th CN palsy, f 2 patients with NBCA migration into SOV and ICA without sequelae, g causing non-life threatening dyspnoe, h same patient as reported by Goldberg et al., i undergoing TVO only out of 12 with DCSF, j unremarkable recovery in one case; stroke and vision loss in another
264 8 Endovascular Treatment
and the skill level in utilizing transvenous occlusion techniques.
When examining anatomic (angiographic) results, one should consider the following confounding aspects. First, criteria used for determining angiographic endpoints may vary. Second, in some series, TAE is used prior to or in combination with TVO, skewing results (Cheng et al. 2003; Oishi et al. 1999; Wakhloo et al. 2005; Kim et al. 2006; Goldberg et al. 1996; Quinones et al. 1997; Kirsch et al. 2006). Third, in several series, complete occlusion was achieved after multiple “multi-channel” approaches were used, either in the same or sequential sessions (Benndorf et al. 2004; Klisch et al. 2003; Cheng et al. 1999; Yu et al. 2009). This was emphasized by Klisch et al. (2003) who studied 31 DAVFs including 11 DCSFs, whereby some were managed by either several transvenous occlusion steps or by a combination of EVT with surgical techniques.
The complication rate of TVO, as documented by some groups, appears relatively high (31%) (Oishi et al. 1999). However, one should note that serious complications, such as stroke or intraorbital/ intracranial hemorrhage, seldom occur (Halbach et al. 1988; Theaudin et al. 2007). Furthermore, many complications have been reported as anecdotal cases (Table 8.8) versus larger series, underlining the fact that with increasing experience and skills, their rate can be reduced considerably. This becomes clear when looking at overall transient and permanent complication rates reported in relevant studies (Table 8.9), revealing that the overall rate of transient and permanent complications is in fact very low (11.6% and 1.8%, respectively).
The perforation of the IPS, to date the most frequent complication (2.1%), often remains clinically silent and can be effectively managed with endovascular techniques (Benndorf et al. 2004; Kim et al. 2006).
The majority of CN deficits consist of 6th nerve palsies (overall 4.1%), most of which are transient. The abducens nerve may be more exposed to mechanical pressure caused by overpacking of the CS as the only true intracavernous nerve. Another explanation of this predilection could be its embedment into the wall of the IPS that is mostly used as venous approach.
The relatively low rate of CN deficits in our series (2%) could be related to the more frequent use of soft coils (GDC Soft coils) that may create less mechanical pressure to neuronal structures. CN deficits due to overpacking may likely further de-
crease with increasing use of softer platinum coils (or HydroCoilsTM) and liquid embolic agents. A permanent CN is rarely seen (0.5%) and has not been observed in our group, despite using aggressive techniques such as deep puncture of the SOV, craniotomy and puncture of the Sylvian vein. Permanent neurological deficits due to stroke during or after TVO occurred in 0.5% of patients and are below the rate reported by TAE series in 75 patients (5.3%) (Vinuela et al. 1984; Halbach et al. 1987; Picard et al. 1987; Kupersmith et al. 1988). The reported complication rates also vary due to the fact that some investigators include femoral or retroperitoneal hematomas, femoral vein thromboses and pulmonary embolisms (Meyers et al. 2002; Klisch et al. 2003; Kirsch et al. 2006). Furthermore, one of the largest series to date reporting on 101/135 treated patients using TVO does not spec-
Table 8.8. Reported anecdotal complications during TVO of DCSFs
Author |
Event |
Tress et al. |
Intraorbital hemorrhage |
(1983) |
|
Halbach et al. |
Diabetes insipidus after CS |
(1991a) |
catheterization (n=1)b |
Halbach et al. |
Cerebellar hemorrhage after IPS (n=1)b |
(1991b) |
|
Golnik et al. |
Angle-closure glaucoma after TVO |
(1991) |
|
Fukami et al. |
Central retinal vein occlusion after |
(1996) |
TAE/TVO |
Araki et al. |
Intracerebral extravasation during |
(1997) |
TVO |
Devoto et al. |
Acute exophthalmos during TVO |
(1997) |
|
Gupta et al. |
Severe vision loss and neovascular |
(1997) |
glaucoma |
Gioulekas et al. |
Intraorbital bleeding during SOV |
(1997) |
cannulationa |
Aihara et al. |
Deterioration of ocular motor |
(1999) |
dysfunction after TVO |
Wladis et al. |
Intraorbital hemorrhage and vision |
(2007) |
loss during TVO |
Hayashi et al. |
Intraorbital bleeding during SOV |
(2008) |
cannulation (n=2) |
|
|
a Same case as Tress et al. (1983)
bBoth cases reported in a large series of EVT (1200 cases) with a total of15 arterial and venous perforations
8.4 Discussion of Transvenous Occlusions |
265 |
Table 8.9. Overall complication rate in larger TVO series (from Table 8.7, total of 613 patients)
Complications |
Transient |
Permanent |
||
Cranial nerve deficit |
25 |
(4.1%) |
3 |
(0.5%) |
Venous perforation (IPS) |
13 |
(2.1%) |
- |
|
Stroke |
- |
|
3 |
(0.5%) |
Blepharoptosis |
- |
|
2 |
(0.3%) |
Worsening of ophthalmic |
11 (1.8%) |
- |
|
|
symptoms |
|
|
|
|
Visual loss |
4 |
(0.7%) |
1 |
(0.2%) |
Intraorbital bleeding |
2 |
(0.3%) |
- |
|
Subarachnoid hemorrhage |
1 |
(0.2%) |
- |
|
Intracranial hemorrhage |
1 |
(0.2%) |
- |
|
Transient ischemic attack |
1 |
(0.2%) |
- |
|
Orbital ecchymosis |
1 |
(0.2%) |
- |
|
Brainstem congestion |
2 |
(0.2%) |
- |
|
Thrombosis of the |
- |
|
1 (0.2%) |
|
central retinal vein CRVa |
|
|
|
|
Minor neurological deficit |
1 |
(0.2%) |
- |
|
Pulmonary embolism |
2 |
(0.3%) |
- |
|
Retinal hemorrhage |
2 |
(0.3%) |
- |
|
Arterial emboli |
5 |
(0.8%) |
- |
|
Dysesthesia |
- |
|
1 |
(0.2%) |
TOTAL |
71 |
(11.6%) |
11 (2.0%) |
|
a Untreated patient
ify whether the observed permanent neurological deficits were related to TVO or TEA (Meyers et al. 2002).
The discussion of transvenous embolizations must consider angiographic and clinical results of TAE, representing the traditional way of treating arteriovenous shunting lesions (Vinuela et al. 1984; Picard et al. 1987; Fermand 1982; Barrow et al. 1985). One of the first series was reported by Vinuela et al. (1984), describing 10 patients with Type D fistulas, of which seven were occluded by embolizing the ECA feeders using PVA particles or IBCA. Cure was documented in five patients (50%) after 5 months. One patient developed hemiplegia and aphasia due to reflux of IBCA through the FRA into the ICA and MCA. Another experienced acute deterioration of his vision. Barrow et al. (1985) achieved good results in three of five patients (60%) treated by embolizing the ECA supply. Grossman et al. (1985) reported complete resolution of symptoms after particulate embolization in five of seven patients.
Picard et al. (1987) communicated results in a group of 32 patients; 25 (78%) underwent superselective embolization, achieving complete clinical and anatomical cure in 18 (72%) and demonstrated clinical cure without anatomic cure in six (24%). One patient (4%) suffered from stroke due to IBCA migration into the cerebral circulation and died after 3 months.
Halbach et al. (1987) achieved clinical cure in 77% and an improvement in 18% (n=22) patients treated between 1978 and 1986 by TAE of ECA branches using IBCA. One permanent deficit (4.5%) was seen in a patient who developed a stroke due to clot formation in the guiding catheter, as well as transient deficits in three cases (13%). The group later reported (Halbach et al. 1992) a complete cure rate of 78%, improvement in 20%, and a complication rate of 4%.
In the earlier series published by Debrun et al. (1988), who treated 25 patients with either PVA or Histoacryl, complete occlusion was reported in 48%. In two cases (8%), enlargement of ECA feeders occurred; additional TVO had to be performed in two others (8%), and one patient (4%) required surgical exposure of the SOV. Sonier et al. (1995) reported a 61% success rate by particulate embolization of IMA branches. In two cases (25%), TAE had to be repeated to achieve a complete occlusion, and transient facial edema was observed in another.
Kupersmith et al. (1988) reported the successful embolization of ECA branches in 88% of their patients using PVA and IBCA with two recanalizations (12%) and four complications (25%), including hemiparesis and hemianopia, permanent 12th nerve palsy and persisting visual field defect.
Vinuela et al. (1997) reiterated their experience based on 74 patients, reporting complete cure in 31% and positive clinical response in 85%. The morbidity was 3.2%; in two patients untoward glue migration into the intracranial circulation occurred, leading to hemiparesis and aphasia in one.
Liu et al. (2001) communicated the only larger series (n=55) in patients who were followed prospectively. In a subgroup of 41 patients (75%), TAE was performed using PVA (150–250 μm) and Histoacryl, injected into the distal ECA branches. The involved ICA branches were not approached. A 70.9% complete clinical cure rate was achieved, with improved symptoms in 14.5%. The authors do not specify whether these results were any different in the embolized (41 patients), or the non-embolized group (14 patients). Further, in 24 of these patients (58.5%), a transient worsening was observed that might be
266 8 Endovascular Treatment
considered a transient adverse event, or even a complication (Benndorf et al. 2004; Meyers et al. 2002). In four patients (9.7%) there was no improvement, while four demonstrated aggravation of symptoms (9.7%). It is not reported whether procedure related transient or permanent neurological deficits were seen. The authors suggest the use of TAE to convert Type D into Type B fistulas and to shorten the time to complete cure with “conservative management”. This treatment strategy appears questionable, however, since no evidence exists to date demonstrating that changing a Type D into a Type B fistula improves the overall prognosis of a DCSF.
Furthermore, it is important to note that in some TVO series, patients initially underwent inefficient TAE. Goldberg et al. (1996) performed PVA embolization of the ECA feeders prior to the SOV approach. Although the patients benefited clinically from the treatment due to reduction of the AV shunt, or even transient occlusion of the fistula, all demonstrated recanalization at angiographic followup and underwent subsequent TVO. Theaudin et al. (2007) recently reported a success rate of only 25% (1/5 patients) in patients undergoing TAE with 300–500 μm, followed by 500–700 μm until flow in the internal maxillary artery stopped. It is emphasized that none of these patients became completely asymptomatic, although clinical improvement was seen. A relatively large particle size (>300 μm) is recommended by some operators for ECA embolizations to avoid cranial nerve damage (Halbach et al. 1992), while others suggest 100–300 μm (Vinuela et al. 1997). Larger particles will more likely produce an occlusion proximal to the fistula site, triggering recruitment of collaterals and recanalization. It must be borne in mind that the dural branches feeding a DCSF may also be involved in the normal blood supply of CN (4th, 5th, 6th, 7th, 9th, 10th, 11th, 12th) (Halbach et al. 1992). As eluded to in Chap. 2, detailed knowledge of arterial anatomy in the CS area, ECA-ICA collaterals and anatomic variants is essential for performing TAE effectively and safely.
Gregoire et al. (2002) recently published the interesting case of a 60-year-old female presenting with diplopia and gait disturbance 3 days after arterial embolization due to cerebellar dysfunction caused by reversible pontine venous congestion. It demonstrates that the thrombotic process within the CS, triggered by particle embolization, may also be unpredictable. Paradoxical worsening caused by SOV thrombosis may occur following TAE (Sergott et al. 1987), and has been
documented in a significant number (61.5 %) of patients (Liu et al. 2001).
Aside from passage of PVA particles or liquid embolic agents into the brain circulation via ECA-ICA anastomoses, a major risk associated with transarterial injections of embolic agents is reflux of the embolic agent from cavernous ICA branches. Due to their size (normal diameter approximately 0.3 mm), they can be difficult or impossible to catheterize, even when enlarged and supplying an AV shunt. Even when possible, due to tortuousities, only their most proximal segments are usually accessible, making safe and effective injection of particles or liquid adhesives difficult to control (Gobin et al. 2000; Picard et al. 1987; Phatouros et al. 1999; Halbach et al. 1989b). The TMH give rise to the inferior hypophysial artery, thus injection of embolic agents may cause malfunction of the pituitary gland resulting in diabetes insipidus, as was observed in one case after injection of 50% dextrose and pure alcohol mixture (Phatouros et al. 1999).
The occlusion of dural ICA branches using GDCs has been suggested (Vinuela et al. 1997) as a safer alternative to particles or liquid adhesives and may be effective in selected cases, but may be followed by recanalization.
Although liquid adhesives have been largely replaced by PVA particles and microspheres for TAE, their use can be a feasible option under certain conditions. Liu et al. (2000b) injected 10%–15% mixtures of NBCA with lipiodol and tungsten into ECA branches, achieving complete resolution of symptoms after 1 month without definite neurological complication. If anatomy of the arterial supply is favorable, complete cure may be achieved by injecting even small amounts via an enlarged ILT or MHT. This technique, however, is not without risk and requires an experienced operator (Illustrative Case VII). Another elegant alternate solution for “difficult-to-treat” cases is demonstrated in Illustrative Case IX, where an occlusion balloon, inflated across the ipsilateral TMH supply, allows for controlled injection of Onyx™ via a single pedicle from AMA (indirect flow control), resulting in complete obliteration of the fistula (Gal et al. 2008).
Gandhi et al. (2009) recently communicated a case of a Type D fistula that was successfully managed by TAE via the distal IMA using Onyx-18 in a single injection. The patient showed significant immediate improvement, but developed a novel 6th nerve palsy that resolved over 12 weeks. The figures of this case show an extensive Onyx cast not only
