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DOI: 10.1148/radiol.2332031213
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(Radiology 2004;233:376-384.)
© RSNA, 2004

Vascular and Interventional Radiology

Low-Flow Vascular Malformations: MR-guided Percutaneous Sclerotherapy in Qualitative and Quantitative Assessment of Therapy and Outcome1

Daniel T. Boll, MD, Elmar M. Merkle, MD and Jonathan S. Lewin, MD

1 From the Department of Radiology, University Hospitals of Cleveland, Case Western Reserve University, 11100 Euclid Ave, Cleveland, OH 44106-5056. From the 2003 RSNA scientific assembly. Received July 30, 2003; revision requested October 17; final revision received January 28, 2004; accepted March 16. Address correspondence to J.S.L. (e-mail: jlewin2@jhmi.edu).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
PURPOSE: To prospectively assess the therapeutic procedure and outcome of magnetic resonance (MR)-guided percutaneous sclerotherapy in patients with low-flow vascular malformations.

MATERIALS AND METHODS: Seventy-six percutaneous sclerotherapy treatments were performed by one radiologist with real-time MR guidance in 15 patients (six female patients; mean age, 54.4 years ± 11.1; nine male patients; mean age, 32.9 years ± 14.1) with vascular malformations in the head and neck (n = 64), spine (n = 5), and extremities (n = 7). Qualitative assessment was used to analyze (a) individual success of therapy, (b) occurrence of complications, (c) time required for minimally invasive MR-guided sclerotherapy in regression analysis, (d) ability of MR imaging to depict postinterventional perfusion changes within the vascular malformation with calculation of changes in contrast-to-noise ratios, and (e) detection of volume changes at follow-up examinations with volumetric analysis.

RESULTS: Percutaneous sclerotherapy was performed successfully and without complications by filling targeted vascular malformations with sclerosing agent. Induced vascular sclerosis was used to successfully treat individual predominant symptoms, such as hemorrhage, pain, cosmetic disfigurement, and functional impairment. Quantitative analysis focusing on the actual interventional length of time presented an acceleration over the 5-year time period, matching a cubic function in regression curve fit and taking 31 minutes 50 seconds ± 14 minutes. Induced vascular thrombosis was identified in all treated portions on postinterventional images by the statistically significant changes in contrast-to-noise ratio (P < .05) compared with preinterventional imaging. On follow-up images (ie, those obtained after 12 weeks ± 6), shrinkage was observed in targeted portions (67.2% ± 18.9).

CONCLUSION: MR imaging allows safe guidance and monitoring of minimally invasive sclerotherapy and permits verification of therapeutic success postinterventionally and during follow-up examinations.

Supplemental material: radiology.rsnajnls.org/cgi/content/full/2332031213/DC1.

© RSNA, 2004

Index terms: Angioma, soft tissues, 10.3141, 20.3141, 30.3141, 40.3141 • Magnetic resonance (MR), guidance, 20.129411, 91.129411, 92.129411, 93.129411 • Magnetic resonance (MR), vascular studies, 20.129411, 91.129411, 92.129411, 93.129411 • Sclerotherapy


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
Soft-tissue vascular anomalies are part of a spectrum of congenital malformations commonly found in children and adults (1). From a diagnostic and therapeutic perspective, an unambiguous classification scheme is crucial to differentiate between vascular tumors and malformations (2). Vascular tumors, such as hemangiomas, have endothelial hyperplasia with increased endothelial turnover at histologic analysis. During early childhood, these tumors undergo an initial proliferative phase, and they finally involute with age, which usually makes invasive treatment unnecessary (2–4). The opposite is true with vascular malformations, which histologically have sporadic and chromosomal-induced errors in endothelial development but demonstrate normal endothelial turnover and thin-walled dilated channels with sparse smooth-muscle cells and adventitial fibrosis (1,5). Vascular malformations remain stable or slowly grow over time and require therapy when pain, functional impairment, bleeding, airway obstruction, dental distorsion, or cosmetic disfigurement occurs (1,6). Furthermore, vascular malformations have various hemodynamic patterns that are of paramount importance in the choice of appropriate treatment: Whereas high-flow vascular anomalies, such as arteriovenous fistulas and arteriovenous malformations, are adequately addressed by means of transarterial embolization, low-flow malformations found to be solitary or combined in capillary, venous, or lymphatic vessels are successfully treated with sclerotherapy (7–9).

Vascular sclerotherapy, which is the injection of aqueous or oleic solutions into abnormally dilated vessels, successively causes thrombosis, fibrosis, stenosis, and scarring of the treated vessels by irritating and damaging the endothelial lining. This percutaneous treatment is usually performed with fluoroscopic guidance, whereas cross-sectional imaging is used for preinterventional planning and postinterventional control (1) to limit complications resulting from extravasation of the sclerosing agent into the regional soft tissue or draining veins. Reported complications include skin necrosis, neuropathy, muscle atrophy and contracture, deep vein thrombosis, pulmonary embolus, disseminated intravascular coagulation, and cardiopulmonary collapse (10,11).

Magnetic resonance (MR) imaging has proved useful in the delineation of the extent and spatial relationships of soft-tissue vascular anomalies (12). Furthermore, over the past several years, there has been a substantial increase in interest in interventional MR imaging as a minimally invasive treatment modality because of its excellent soft-tissue contrast, good spatial and temporal resolution, and multiplanar section selection for guidance of needle insertion and monitoring of drug application (13,14). Pilot studies have proved the technical feasibility and safety of using MR imaging for malformation characterization, target localization, guidance, and monitoring of percutaneous sclerotherapy, as well as for postinterventional control (15). We hypothesized that MR-guided sclerotherapy could be used to successfully treat predominant symptoms in patients with congenital low-flow vascular malformations in a safe and efficient manner and could allow further quantitative verification of therapeutic success after intervention and during follow-up examinations. Thus, the purpose of our prospective study was to assess the therapeutic procedure and outcome of MR-guided percutaneous sclerotherapy in patients with low-flow vascular malformations.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
Patients
Over the 5-year period from August 1997 to June 2003, a total of 15 patients—six females and nine males—were referred to the radiology division of our institution for MR evaluation and subsequent MR-guided treatment of low-flow vascular malformations outside the central nervous system. The female patients ranged in age from 7 to 80 years, with a mean age of 54.4 years ± 11.1. The male patients ranged in age from 16 to 62 years, with a mean age of 32.9 years ± 14.1. The overall patient group ranged in age from 7 to 80 years, with a mean age of 48.8 years ± 15.2. Of the fifteen patients with low-flow vascular malformations who were examined and treated, 10 malformations were localized in the head and neck—these malformations were particularly distributed within the masticator, parapharyngeal, parotid, and carotid spaces and the face. Two vascular malformations were located in the paraspinal region, and three were found in the extremities—in particular, the elbow, knee, and foot. Individual clinical symptoms and the corresponding sites of vascular malformations are described in Table 1.


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  		TABLE 1. Symptoms of Low-Flow Vascular Malformations in Various Anatomic Locations

 
Seventy-six MR-guided sclerotherapy procedures were performed; 64 were performed in the head and neck, five in the spine, and seven in the extremities. All procedures were performed after written informed consent was obtained, and the protocol was approved by our institutional review board for human investigation.

MR-guided Sclerotherapy
All imaging for lesion characterization, target localization, guidance, and monitoring of sclerotherapy and postinterventional follow-up was performed with a 0.2-T C-arm imaging system (Magnetom Open; Siemens, Erlangen, Germany) supplemented with an MR-compatible high-resolution monitor, basic MR operating controls, and MR-compatible surgical lighting, pulse oximetry, and blood pressure monitoring. All initial and subsequent MR-guided sclerotherapy was performed by the same interventional radiologist (J.S.L.), who had 10 years of experience in vascular procedures, the past 2 years of which included MR-guided vascular interventions.

For initial lesion characterization, turbo spin-echo (SE) T2-weighted MR imaging (repetition time msec/echo time msec, 4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) and T1-weighted MR imaging (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) were used (Fig 1a, 1b). Low-flow patterns of vascular malformations were individually assessed by detecting an absence of flow-void artifacts on T2-weighted fast SE images.



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  		Figure 1a. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 


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  		Figure 1b. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 


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  		Figure 1c. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 


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  		Figure 1d. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 


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  		Figure 1e. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 


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  		Figure 1f. MR images obtained in a 31-year-old man with congenital vascular malformation in bilateral masticator and parotid spaces after right-sided surgery. (a) Preinterventional transverse T1-weighted SE image (532/15; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows implanted surgical clip (*) within right masticator space and surrounding vascular malformation (arrows). (b) Coronal T2-weighted fast SE image (4914/102; 19 sections acquired; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows surgical clip (*) and surrounding vascular malformation in the craniocaudal extension (arrows). (c, d) Localization of target malformation (arrows) with water-filled syringe (arrowhead in c) and subsequent MR-guided needle (arrowhead in d) placement with fast imaging with steady-state procession interventional imaging sequences (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 182 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft. (e) MR-monitored injection of contrast agent-tagged sclerosing agent (arrow) via MR-compatible needle (arrowhead) with the same interventional imaging sequences used to obtain images c and d. (f) Transverse T1-weighted SE image (532/15; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 4 minutes 36 seconds) shows the vascular malformation (arrows) in the right masticator space filled with contrast-tagged sclerosing agent.

 
Target localization was achieved by moving a water-filled syringe over the skin above the vascular malformation, while rapidly and continuously imaging the tip of the syringe until the desired puncture site was identified by using a fast imaging with steady-state precession, or FISP, gradient-echo sequence (17.8/8.1; flip angle, 90°; number of sections acquired, three; section thickness, 5 mm; matrix, 128 x 256; field of view, 250 x 250 mm; number of signals acquired, one; acquisition time, 9 seconds) oriented along the needle shaft (Fig 1c).

The same gradient-echo sequence was used for guidance of MR-compatible 22-gauge needle (E-Z-Em, Westbury, NY) advancement after subcutaneous infiltration of 1% lidocaine for local anesthesia (Fig 1d). After final needle placement within the low-flow vascular malformation, the position was confirmed with a T1-weighted SE sequence (500/24; number of sections acquired, three; section thickness, 4 mm; matrix, 250 x 256; field of view, 250 x 250 mm; number of signals acquired, three; acquisition time, 1 minute 19 seconds). Blood was subsequently aspirated to reconfirm venous low-flow perfusion patterns within the vascular malformation.

To allow monitoring of sclerotherapy with MR imaging, the sclerosing agent, ethanolamine oleate (Ethamolin; Questcor Pharmaceuticals, Union City, Calif) (50-mg/mL concentration) was mixed with 2 µmol of the contrast agent gadopentate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) (0.5-mol/L concentration) per milliliter of sclerosing agent, which is a concentration that is typically used for MR arthrography (16). Percutaneous sclerotherapy was performed with rapid and continuous imaging by using the fast imaging with steady-state procession sequence while slowly injecting 2–6 mL of the tagged sclerosing agent until various-sized targeted portions of the malformation were completely filled (Fig 1e; Movie 1 radiology.rsnajnls.org/cgi/content/full/2332031213/DC1).

For postinterventional imaging, the T1-weighted SE sequence of the malformation characterization protocol was used (Fig 1f, Movie 2 radiology.rsnajnls.org/cgi/content/full/2332031213/DC1). Patients were followed up with clinical examinations and MR imaging for 12 weeks ± 2.4 (95% confidence interval: 7.3, 16.7) after treatment by using the malformation characterization protocol. Owing to the size of vascular malformations, further treatments were performed until all initial clinical symptoms were addressed successfully.

Qualitative Assessment of Therapeutic Outcome
Patients with vascular malformations presented with a wide variety of individual clinical symptoms (Table 1). Prior to every subsequent treatment after the initial MR-guided sclerotherapy session, individual patient interviews were conducted, and clinical examination by the performing radiologist (J.S.L.) was performed to address therapeutic progress. Principal attention was focused on the most relevant and disturbing symptoms, such as decrease of hemorrhaging and pain, as well as on improvement of function. Furthermore, any occurrence of complications—such as skin necrosis, neuropathy, muscle atrophy and contracture, deep venous thrombosis, or cardiopulmonary problems—was evaluated. Immediately after every sclerotherapy session, patient interviews were conducted to evaluate individual sensations of experienced discomfort or pain during MR-guided sclerotherapy. All results were documented, and further sclerotherapeutic stages were decided on the basis of improvement of the most relevant and disturbing symptoms. An increase in pain after sclerotherapy in addition to marked acute swelling of the treated portion of the low-flow vascular malformation were not considered to be complications (17).

Quantitative Assessment of Therapy and Outcome
Quantitative analysis of therapy and outcome was performed by one radiologist (D.T.B.) in a three-fold manner. The length of time for the entire MR-guided sclerotherapy treatment was evaluated with differentiation into the preinterventional imaging phase, duration of the actual interventional procedure, and postinterventional imaging phase. The preinterventional imaging phase included initial image acquisition and interpretation focusing on anatomic morphology and underlying perfusion patterns and localization of the target lesion. The interventional procedure phase consisted of MR-guidance and MR-monitoring phases for needle placement and drug application, respectively. The postinterventional imaging phase consisted of image acquisition and interpretation, focused on the distribution and possible extravasation of sclerosing agent.

The depiction of intravascular perfusion changes induced by MR-guided sclerotherapy—such as thrombosis, fibrosis, and scarring—was based on calculation of the contrast-to-noise ratio (CNR): CNR = (SIi – SIe)/SDN on T2-weighted image datasets (18), where SIi represents intravascular signal intensity, SIe represents extravascular signal intensity, and SDN represents the standard deviation of noise level. The background signal intensity and the intra- and extravascular muscular signal intensities were measured on corresponding images that depicted the low-flow vascular malformation before treatment and during follow-up examinations. Additionally, the signal intensities of neighboring and still perfused portions of the vascular malformation imaged during the follow-up examinations were determined. These signal intensities were compared with preinterventional perfused regions and postinterventional sclerosed portions of the vascular malformation to ensure analysis validity. Fixed regions of interest were placed on the same homogeneous structures in artifact-free zones throughout all courses of treatment. Regions of interest for background signal intensity with an area of 500 mm2 were placed vertically above the treated anatomic regions. Regions of interest for intra- and extravascular signal intensities with areas of 50 mm2 were positioned within the vascular malformation and on adjacent soft-tissue structures, respectively. For signal intensity measurements on each frame, three separate regions of interest from different areas were evaluated, and the results were averaged.

The semiautomatic vessel wall definition of targeted portions of the low-flow vascular malformations and the subsequent automatic geometric assumption to calculate the volume of the dilated vascular channels were accomplished by using commercially available software (SurfDriver; University of Hawaii, Kailua, Hawaii) to process T1-weighted preinterventional image datasets. Segmentation and volume assumption were performed before treatment and at consecutive follow-up examinations.

Statistical Analysis
Statistical analysis was performed for the quantitative analysis results by assessing length of time for sclerotherapeutic intervention, signal intensity measurements for depiction of intravascular perfusion changes, and volumetric evaluation of treated vascular malformations over time. For all evaluated parameters, mean values with corresponding standard deviations and ranges were calculated. All quantitative analysis results were correlated with patient age and sex as independent factors; all statistical analysis was performed by using SPSS version 11.5 (SPSS, Chicago, Ill).

The mean preinterventional, interventional, and postinterventional lengths of time were evaluated with regression statistics over the 5-year observation period. Curve estimation regression produced regression parameters for different curve estimation regression models. Initially, the preinterventional, interventional, and postinterventional lengths of time were visualized in three scatterplots in relation to the 5-year observation period. If the plotted data were not linearly related, different curve estimation regression models—such as quadratic, cubic, logarithmic, or exponential models—were used to identify the specific type of regression and the regression parameters, such as the regression coefficient, slope, and significance level.

Statistical analysis of the signal intensity measurements for depiction of intravascular changes in perfusion after sclerotherapy was performed by directly comparing the pre- and postintervention contrast-to-noise ratios with results of the Student two-tailed t test for data sets with unequal variance. A P value of less than .05 was considered to indicate a statistically significant difference. Measurement validity was analogously assessed by successively comparing the pre- and postinterventional contrast-to-noise values with the contrast intensities of the control group.

The volume change of the treated vascular malformations over time was evaluated by calculating the percentage volume decrease differentiated into the initial treatment results and the first and second subsequent treatment effects.

Statistical analysis of the signal intensity measurements for depiction of intravascular changes in perfusion after sclerotherapy, volume change of the treated vascular malformations over time, and length of time for sclerotherapeutic interventions were correlated with patient age and sex as independent factors by performing a multivariate general linear model analysis with Bonferroni post hoc comparisons. Analogously, a significance level of less than .05 was considered to indicate a statistically significant difference.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 
Qualitative Assessment of Therapeutic Outcome
For all of our patients with low-flow vascular malformations in the head and neck, bleeding into the oral cavity and cosmetic disfigurement were the most relevant and disturbing symptoms. Oral bleeding was successfully addressed with MR-guided sclerotherapy in all patients, and all patients subjectively recognized an improvement in cosmetic appearance, especially a decrease in facial swelling and skin discoloration (Fig 2).



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  		Figure 2a. Images obtained in a 34-year-old man with congenital vascular malformation in the right upper lip. (a) Initial preinterventional photograph shows extension of initial skin discoloration (arrow) and cosmetic disfigurement (* = 43 mm, arrowhead = 25 mm). (b) Preinterventional transverse T2-weighted MR fast SE image (4914/102; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the cavernous anterior portion (arrow) and the lateral portion (arrowhead) of the vascular malformation with high signal intensity and without apparent flow voids. (c) Photograph obtained 6 weeks after intervention shows decrease in size (* = 34 mm, arrowhead = 20 mm) in the low-flow vascular malformation and partial regaining of physiologic lip vermilion (arrow). (d) Follow-up transverse T2-weighted MR fast SE image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows intravascular thrombus (*) within the larger portion of the vascular malformation (arrow) and complete thrombosis of smaller portion (arrowhead) with substantial overall shrinkage.

 


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  		Figure 2b. Images obtained in a 34-year-old man with congenital vascular malformation in the right upper lip. (a) Initial preinterventional photograph shows extension of initial skin discoloration (arrow) and cosmetic disfigurement (* = 43 mm, arrowhead = 25 mm). (b) Preinterventional transverse T2-weighted MR fast SE image (4914/102; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the cavernous anterior portion (arrow) and the lateral portion (arrowhead) of the vascular malformation with high signal intensity and without apparent flow voids. (c) Photograph obtained 6 weeks after intervention shows decrease in size (* = 34 mm, arrowhead = 20 mm) in the low-flow vascular malformation and partial regaining of physiologic lip vermilion (arrow). (d) Follow-up transverse T2-weighted MR fast SE image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows intravascular thrombus (*) within the larger portion of the vascular malformation (arrow) and complete thrombosis of smaller portion (arrowhead) with substantial overall shrinkage.

 


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  		Figure 2c. Images obtained in a 34-year-old man with congenital vascular malformation in the right upper lip. (a) Initial preinterventional photograph shows extension of initial skin discoloration (arrow) and cosmetic disfigurement (* = 43 mm, arrowhead = 25 mm). (b) Preinterventional transverse T2-weighted MR fast SE image (4914/102; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the cavernous anterior portion (arrow) and the lateral portion (arrowhead) of the vascular malformation with high signal intensity and without apparent flow voids. (c) Photograph obtained 6 weeks after intervention shows decrease in size (* = 34 mm, arrowhead = 20 mm) in the low-flow vascular malformation and partial regaining of physiologic lip vermilion (arrow). (d) Follow-up transverse T2-weighted MR fast SE image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows intravascular thrombus (*) within the larger portion of the vascular malformation (arrow) and complete thrombosis of smaller portion (arrowhead) with substantial overall shrinkage.

 


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  		Figure 2d. Images obtained in a 34-year-old man with congenital vascular malformation in the right upper lip. (a) Initial preinterventional photograph shows extension of initial skin discoloration (arrow) and cosmetic disfigurement (* = 43 mm, arrowhead = 25 mm). (b) Preinterventional transverse T2-weighted MR fast SE image (4914/102; number of sections acquired, 19; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the cavernous anterior portion (arrow) and the lateral portion (arrowhead) of the vascular malformation with high signal intensity and without apparent flow voids. (c) Photograph obtained 6 weeks after intervention shows decrease in size (* = 34 mm, arrowhead = 20 mm) in the low-flow vascular malformation and partial regaining of physiologic lip vermilion (arrow). (d) Follow-up transverse T2-weighted MR fast SE image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows intravascular thrombus (*) within the larger portion of the vascular malformation (arrow) and complete thrombosis of smaller portion (arrowhead) with substantial overall shrinkage.

 
In two patients, vascular malformations surrounding teeth that were in need of dental therapy were successfully treated, thereby allowing subsequent dental care.

One patient with buccal swelling due to an underlying vascular malformation that resulted in chewing dysfunction and speech problems was successfully treated with MR-guided therapy, thereby decreasing the size of the abnormal vessels. This shrinkage led to a subjectively recognized improvement in speech clarity and mastication.

One patient with extensive bilateral distribution of low-flow vascular malformations within the masticator, parapharyngeal, parotid, and carotid spaces initially presented with additional buccal numbness. Although this was successfully treated, the complex relationships of the various portions of the vascular malformations led to constantly changing patterns of perfusion. In this patient, MR-guided sclerotherapy was successful in the treatment of predominant symptoms; however, the constantly changing appearance of vascular malformations resulted in an ongoing repetition of treatment sessions every 3 months (Fig 3).



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  		Figure 3a. Images obtained in a 57-year-old woman with extensive bilateral distribution of low-flow vascular malformations within the masticator, parapharyngeal, parotid, and carotid spaces. (a) Preinterventional transverse T2-weighted fast SE MR image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the targeted portion of the vascular malformation (arrow) within the right masticator space, leading to facial disfigurement and fatty and atrophic changes within right masseter muscle. (b) Early follow-up MR image obtained with the same transverse T2-weighted fast SE sequence 5 weeks after MR-guided sclerotherapy showed intravascular thrombus formation (arrow) and decrease in size of perfused vascular malformation; however, the incomplete sclerosed vascular malformation shows the tendency to compensate for the loss of perfused portions by an increase of perfusion in neighboring veins (arrowheads). (c) Late follow-up MR image obtained analogously with the same transverse T2-weighted fast SE sequence 11 weeks after MR-guided sclerotherapy showed further shrinkage (arrow) of the treated portion and decrease in the size of superficial veins, combined with a reduction in facial swelling (arrowheads).

 


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  		Figure 3b. Images obtained in a 57-year-old woman with extensive bilateral distribution of low-flow vascular malformations within the masticator, parapharyngeal, parotid, and carotid spaces. (a) Preinterventional transverse T2-weighted fast SE MR image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the targeted portion of the vascular malformation (arrow) within the right masticator space, leading to facial disfigurement and fatty and atrophic changes within right masseter muscle. (b) Early follow-up MR image obtained with the same transverse T2-weighted fast SE sequence 5 weeks after MR-guided sclerotherapy showed intravascular thrombus formation (arrow) and decrease in size of perfused vascular malformation; however, the incomplete sclerosed vascular malformation shows the tendency to compensate for the loss of perfused portions by an increase of perfusion in neighboring veins (arrowheads). (c) Late follow-up MR image obtained analogously with the same transverse T2-weighted fast SE sequence 11 weeks after MR-guided sclerotherapy showed further shrinkage (arrow) of the treated portion and decrease in the size of superficial veins, combined with a reduction in facial swelling (arrowheads).

 


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  		Figure 3c. Images obtained in a 57-year-old woman with extensive bilateral distribution of low-flow vascular malformations within the masticator, parapharyngeal, parotid, and carotid spaces. (a) Preinterventional transverse T2-weighted fast SE MR image (4914/102; 19 sections; section thickness, 5 mm; matrix, 252 x 256; field of view, 200 x 200 mm; number of signals acquired, two; acquisition time, 6 minutes) shows the targeted portion of the vascular malformation (arrow) within the right masticator space, leading to facial disfigurement and fatty and atrophic changes within right masseter muscle. (b) Early follow-up MR image obtained with the same transverse T2-weighted fast SE sequence 5 weeks after MR-guided sclerotherapy showed intravascular thrombus formation (arrow) and decrease in size of perfused vascular malformation; however, the incomplete sclerosed vascular malformation shows the tendency to compensate for the loss of perfused portions by an increase of perfusion in neighboring veins (arrowheads). (c) Late follow-up MR image obtained analogously with the same transverse T2-weighted fast SE sequence 11 weeks after MR-guided sclerotherapy showed further shrinkage (arrow) of the treated portion and decrease in the size of superficial veins, combined with a reduction in facial swelling (arrowheads).

 
After the intervention, two patients with paraspinal vascular malformations and chronic pain syndromes substantially reduced the dosage of pain medication they required. Both patients subjectively recognized an increase in mobility.

Predominant symptoms of the three low-flow vascular malformations in the extremities included hemorrhage, pain, and functional impairment. Whereas MR-guided sclerotherapy allowed us to successfully address all three symptoms within the knee and elbow, the extensive vascular malformation within the foot could only be successfully treated in the superficial portions.

The patient interviews that were conducted immediately after the procedure allowed us to evaluate sensations of experienced discomfort or pain during the sclerotherapeutic procedure and showed that MR-guided sclerotherapy itself produced minimal individual discomfort. All patients experienced pain and marked acute soft-tissue swelling after MR-guided sclerotherapy; this was treated locally with application of an ice pack and oral acetaminophen. No regional venous draining of the sclerosing agent was observed either during or directly after the procedure. No severe complications—such as skin necrosis, neuropathy, muscle atrophy and contracture, deep venous thrombosis, pulmonary embolus, disseminated intravascular coagulation, or cardiopulmonary collapse—were observed. Increased sensitivity in the area of the treated portion of the vascular malformation subsided during the following 2 weeks.

Quantitative Assessment of Therapy and Outcome
The length of time that MR-guided sclerotherapy required was differentiated into three phases: (a) preinterventional imaging, (b) duration of the interventional procedure, and (c) postinterventional imaging (Table 2). The pre- and postinterventional imaging time periods showed linear, yet inverse, progressions over time. Thus, the marginal prolongation of preinterventional imaging was compensated for by minor acceleration of postinterventional visualization.


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  		TABLE 2. Procedure Time and Regression Analysis

 
A significant acceleration was observed in the length of time of the actual MR-guided procedure. The curve fit of the regression analysis proved that an acceleration to a cubic function over time had been achieved (Fig 4), thereby significantly shortening the overall duration of the MR-guided sclerotherapy over the 5-year evaluation period.



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  		Figure 4. Curve estimation procedure was used to produce the cubic curve estimation regression plot, in which development of the average length of time of the MR-guidance and monitoring phase of percutaneous sclerotherapy was statistically analyzed over the 5-year period (correlation, 0.938; P < .001; mean duration, 31 minutes 50 seconds).

 
Multivariate general linear model analysis with Bonferroni post hoc comparisons that used underlying patient age as an independent factor was used to calculate significance for the preinterventional, interventional, and postinterventional length of time (P = .642, .453, and .466, respectively). Patient sex was used as an independent factor, and significance was calculated for preinterventional, interventional, and postinterventional lengths of time (P = .861, .422, and .852, respectively).

The evaluation of alterations in flow patterns within the treated portions of low-flow vascular malformations proved the ability of MR imaging to successfully depict induced thrombosis and subsequent fibrosis (Fig 2). On T2-weighted images, a statistically significant decrease in the contrast-to-noise ratio within the treated vascular portions was observed at corresponding locations during follow-up examinations compared with measurements obtained with preinterventional imaging (Table 3). An analysis of the neighboring and further-perfused portions of a vascular malformation during follow-up examinations was compared with the pre- and postinterventional imaging datasets, which validated this statistical difference in contrast-to-noise ratio and excluded other imaging phenomena as the origin of differences in the measured signal intensities.


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  		TABLE 3. Quantitative and Statistical Analysis of Contrast-to-Noise Ratio

 
By using underlying patient age as an independent factor, a significance level of .633 was calculated. The sex-specific differentiation revealed a significance of .079; no sex-specific statistically significant differences in contrast-to-noise ratio were detected.

A decrease in the perfused volume of the treated portions of low-flow vascular malformations was observed in all patients. Whereas the initial sclerotherapy led to the most significant reduction in size in a treated region, necessary subsequent treatments were used to induce further shrinkage of the remaining perfused fractions by a further third of the preinterventional size (Table 4, Fig 3).


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  		TABLE 4. Volume Decrease in Treated Portions of Vascular Malformations

 
Patient age was evaluated as an independent factor by using the multivariate general linear model analysis with Bonferroni post hoc comparisons, and a significance level of .365 was calculated. The sex-specific differentiation revealed a significance of .423; no sex-specific statistically significant differences in contrast-to-noise ratio were detected.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
 
Congenital vascular malformations have a characteristic serpentine pattern of endothelium-lined vascular channels with internal striations and fibrofatty septations; they may also contain intravascular thrombosis, hemosiderin deposits, and phleboliths (19). Vascular malformations have a subcutaneous fatty prominence; however, a propensity for discontinuous multifocal involvement with a tendency to follow neurovascular distributions suggests a more diffuse congenital dysplasia rather than an isolated dysplasia to the malformed vascular spaces (20). In particular, low-flow vascular malformations are characterized by the absence of dilated feeding arteries and draining veins.

The abnormal mural muscular anatomy of congenital vascular malformations, which consists of sparse smooth-muscle clumps, is most probably responsible for the gradual vascular expansion (5). An escalated, malformed vascular growth might be induced by hemodynamic alterations caused by various previously performed treatment attempts (1); however, any form of vascular malformation expansion directly affects the surrounding tissue. Whereas adjacent musculature showed strains of fatty infiltration and subsequent atrophy, as well as fascial involvement and infiltration into associated tendons, adjacent bones might have intramedullary vascular components (20).

Thus, complex anatomy and its spatial relationships with adjacent structures, as well as various intravascular perfusion patterns and functionally induced morphologic changes, emphasized that successful planning and guiding of minimally invasive sclerotherapy requires an imaging modality that provides sufficient spatial and temporal resolution, lesion characterization, and a high degree of reproducibility. In this study, we sought to evaluate qualitatively and quantitatively the process and outcome of MR-guided percutaneous sclerotherapy by targeting low-flow vascular malformations.

Qualitative analysis showed that MR imaging succeeded in vascular malformation characterization, sclerotherapy target localization, and interventional guidance and monitoring. The process of vascular malformation characterization was crucial in identifying the portion of the extended network of interconnected dilated veins responsible for the predominant clinical symptoms. Furthermore, lesion characterization allowed us to predict therapeutic success by analyzing the drainage pattern of this causative portion, thereby contributing to the overall success of treating various clinical and subjective symptoms of patients with congenital vascular malformations.

The process of careful sclerotherapy target localization was partially responsible for the complete absence of any major or minor complications, as evaluations performed prior to every subsequent treatment after initial MR-guided sclerotherapy showed. Identifying subcutaneous vascular targets that were neither too superficial nor too profoundly hidden within the complex anatomy prevented the development of skin alterations and necrosis, as well as an accelerated systemic drainage of the sclerosing agent. The acute marked tissue swelling after every MR-guided intervention prohibited target selection in the proximity of highly sensitive neurovascular distributions (17).

MR guidance and monitoring of the actual procedure successfully allowed MR-fluoroscopic visualization of needle advancement into the targeted portion of the congenital vascular malformation and subsequent injection of the gadopentate dimeglumine–tagged sclerosing agent. Throughout the entire process of needle placement and subsequent application of the gadopentate dimeglumine-tagged sclerosing agent, the patient was able to directly communicate sensations of discomfort or pain to the performing radiologist, who in return was able to respond immediately by changing the needle location or amount of sclerosing agent applied. Furthermore, the amount of injected sclerosing agent, which varied between 2 and 6 mL, emphasized the importance of continuous visualization for complete filling of the targeted portion without extravasation. Additionally, manual cutaneous compression prohibited early drainage of injected sclerosing agent into more delicate anatomic areas, such as the orbits. The results of patient interviews, which focused on sensations of experienced discomfort or pain and were conducted immediately after the procedure, showed that MR-guided sclerotherapy itself produced only minimal discomfort.

Quantitative analysis of MR-guided sclerotherapy and outcome focused on the length of time of the various therapeutic sessions and showed a significantly decreased duration of the minimally invasive intervention, which patients indicated was the most physically stressful and disturbing part of the entire treatment. The markedly shortened length of time of the actual procedure, combined with continuous patient verbal response, allowed effective and rapid comforting of patients who experienced distress. Significant shortening of the sclerotherapeutic treatment phase was further realized with an increasingly thorough analysis of the anatomic spatial relationships and flow patterns, thereby explaining the slight increase in preinterventional imaging. This increase did not lead to an overall increase in treatment time, however, as it was compensated for by a minor acceleration of the postinterventional imaging time due to an increasingly refined and optimized imaging protocol.

The postinterventional imaging sequence and MR imaging performed during subsequent treatment sessions were used to visualize the formation and subsequent organization of intravascular thrombi in accordance with a recent study (18) and the subsequent development of vascular fibrosis. MR imaging datasets acquired after intervention and during subsequent treatment sessions sensitively visualized thrombus formation and organization, as well as changes in intralesional blood-flow patterns, thereby contributing to the individual therapeutic success.

After intravascular thrombus formation and subsequent organization and fibrosis, the final scarring led to a significant shrinkage of the vascular malformation. Whereas the clinical symptoms of hemorrhage and skin discoloration were resolved soon after initial MR-guided sclerotherapy (Fig 2), resolution of the remainder of clinical symptoms relied on effective shrinkage of the targeted vascular portions (Fig 3). Volumetric analysis based on acquired MR datasets allowed effective assessment of initial lesion size and subsequent postinterventional volumetric decrease accompanied by resolution of the predominant symptoms.

Our study had limitations that must be addressed. No standardized questionnaire was used for qualitative analysis because of the various symptoms and locations of the congenital vascular malformations; rather, individual patient interviews that focused on the most relevant and disturbing symptoms were conducted. Furthermore, quantitative analysis that focused on the intravascular changes after MR-guided sclerotherapy did not include any advanced analysis of hemodynamic patterns, but this could be explored in future studies.

In conclusion, MR-guided sclerotherapy is successful in the treatment of patients with predominant symptoms of congenital low-flow vascular malformations in a safe and efficient manner and allows quantitative verification of therapeutic success during follow-up examinations.


   FOOTNOTES
 
Abbreviation: SE = spin echo

Authors stated no financial relationship to disclose.

Author contributions: Guarantors of integrity of entire study, D.T.B., J.S.L.; study concepts, D.T.B., E.M.M.; study design, D.T.B., E.M.M., J.S.L.; literature research, D.T.B., E.M.M.; clinical studies, J.S.L.; experimental studies, D.T.B.; data acquisition and analysis/interpretation, D.T.B., E.M.M., J.S.L.; statistical analysis, D.T.B.; manuscript preparation, definition of intellectual content, editing, and revision/review, D.T.B., E.M.M., J.S.L.; manuscript final version approval, J.S.L.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
DISCUSSION
 REFERENCES
 

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H. Hyodoh, M. Hori, H. Akiba, M. Tamakawa, K. Hyodoh, and M. Hareyama
Peripheral Vascular Malformations: Imaging, Treatment Approaches, and Therapeutic Issues
RadioGraphics, October 1, 2005; 25(suppl_1): S159 - S171.
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