(Radiology. 1999;211:566-570.)
© RSNA, 1999
Low-Flow Vascular Malformations in the Head and Neck: Safety and Feasibility of MR Imaging–guided Percutaneous Sclerotherapy—Preliminary Experience with 14 Procedures in Three Patients1
Jonathan S. Lewin, MD,
Elmar M. Merkle, MD,
Jeffrey L. Duerk, PhD and
Robert W. Tarr, MD
1 From the Departments of Radiology (J.S.L., E.M.M., J.L.D., R.W.T.), Oncology (J.S.L.), and Biomedical Engineering (J.L.D.), University Hospitals of Cleveland, Case Western Reserve University, 11100 Euclid Ave, Cleveland, OH 44106, and the Department of Radiology, University of Ulm, Germany (E.M.M.). Received February 25, 1998; revision requested May 4; revision received October 13; accepted November 19. Supported in part by research collaborations with Siemens Medical Systems, Minrad, and Radionics. Also supported in part by grants from the Whitaker Foundation, American Cancer Society, Mary Ann S. Swetland Fund, M.E. and F.J. Callahan Foundation, and the Deutsche Forschungsgemeinschaft grant Me 1593/1-1. Address reprint requests to J.S.L.
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Abstract
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Fourteen percutaneous sclerotherapy procedures with magnetic resonance (MR) imaging guidance were performed in three patients with low-flow vascular malformations. All targeted vascular malformation compartments were filled with sclerosing agent without complications in a mean procedural time of 29 minutes. Follow-up imaging demonstrated reduction in size of the treated portions in all patients. In conclusion, sclerotherapy with MR imaging guidance can be performed safely and allows monitoring of injection.
Index terms: Arteriovenous malformations, cranial, 10.75 • Interventional procedures, 10.1299 • Magnetic resonance (MR), guidance, 10.1299 • Veins, abnormalities, 10.75 • Veins, therapeutic blockade, 10.1299
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Introduction
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The currently accepted classification of congenital vascular malformations is based on a number of histologic and clinical features described by Mulliken and Glowacki in 1982 (1). This classification differentiates vascular malformations (arterial, capillary, venous, lymphatic, and combined) from true hemangiomas on the basis of endothelial cell characteristics and the number of mast cells. Whereas true hemangiomas often involute with age, vascular malformations remain stable or slowly grow with the patient and typically require some form of therapy when cosmetic disfigurement, bleeding, or functional impairment occur.
From a therapeutic perspective, one of the most important differentiating characteristics of vascular malformations is their classification as "high flow" or "low flow" based on findings at physical examination, imaging, or both (2,3). Magnetic resonance (MR) imaging is an excellent noninvasive imaging technique for classification of vascular malformations, and it is often used to help therapeutic decision making and to provide posttherapy follow-up (3). High-flow vascular malformations, which produce signal voids on spin-echo (SE) images and high-signal-intensity flow-related enhancement on flow-compensated gradient-echo images (3), are often treated with embolization therapy via a transarterial approach (4,5). Alternatively, low-flow vascular malformations, which appear predominantly bright on T2-weighted SE images, without evidence of flow void are often successfully treated with sclerotherapy via a direct percutaneous approach (6). In superficial or easily palpable lesions, needles are inserted percutaneously without imaging guidance (6). Deep lesions may be localized with ultrasonography or computed tomography (CT), or they may be injected with use of x-ray fluoroscopic guidance (6).
This pilot study was performed to test the hypothesis that MR imaging–guided percutaneous sclerotherapy of low-flow vascular malformations in the head and neck is feasible, can be performed safely, and will allow direct visualization of sclerosing agent distribution and needle placement during injection of both superficial and deep components of vascular malformations.
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Materials and Methods
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Imaging System
MR imaging–guided procedures were performed by using a clinical 0.2-T C-arm imaging system (Magnetom Open; Siemens Medical Systems, Erlangen, Germany) supplemented with the following components: (a) an in-room liquid crystal monitor with 1,024 x 1,280-pixel resolution and radio-frequency shielding for image viewing at the side of the magnet; (b) MR imaging–compatible mouse and foot pedal to control the imager from within the magnet room; and (c) MR imaging–compatible surgical lighting, pulse oximetry, and noninvasive blood pressure monitoring.
Procedures
Fourteen MR imaging–guided procedures were performed in three patients (two women, aged 27 and 45 years, and one man, aged 31 years) with low-flow vascular malformations of the masticator, parotid, parapharyngeal, or carotid spaces in the head and neck. The clinical symptoms and previously attempted therapy are described in Table 1. All procedures were performed after written informed consent was obtained, with a protocol approved by the institutional review board for human investigation.
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TABLE 1. Initial Symptoms, Clinical Findings, and Outcome in Three Patients with Low-Flow Vascular Malformations after MR Imaging–guided Percutaneous Sclerotherapy
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First, lesion characterization and target localization were performed with turbo SE T2-weighted imaging (repetition time msec/echo time msec = 4,655/102; two signals acquired; echo train length, seven or 17) and SE T1-weighted imaging (504/15, two signals acquired). Then, a skin puncture site was chosen by moving a syringe full of water along the skin surface overlying the malformation during rapid continuous gradient-echo MR imaging until the site of the syringe tip corresponded to the desired puncture site on the images. This continuous gradient-echo MR imaging mode consisted of the sequential acquisition, reconstruction, and display of multiple sets of three to five parallel contiguous 5-mm-thick image sections centered on the predicted needle position with use of a fast imaging with steady-state precession, or FISP, sequence (18/7, one signal acquired, 90° flip angle, 128 x 256 matrix, 20–25-cm field of view, 
rectangular to full field of view, imaging time of 6–9 seconds for three sections) (7).
Once the puncture site was chosen and marked, the skin was prepared with antiseptic solution and draped. Local anesthesia was administered by means of superficial infiltration of 1% lidocaine. A 22-gauge MR imaging–compatible needle (E-Z-Em, Westbury, NY) was then advanced by means of direct visualization into the targeted component of the vascular malformation by using the continuous imaging mode described previously. After the needle was placed at the target site, the position was confirmed by means of either T1-weighted turbo SE imaging (500/24; three signals acquired; echo train length, five; 250 x 256 matrix; 200–250-mm field of view; three 5-mm-thick sections; 79-second total acquisition time) or T2-weighted turbo SE imaging (2,000/105; one signal acquired; echo train length, 17; 238 x 256 matrix; 265-mm field of view; five 5-mm-thick sections; 31-second total acquisition time).
A sclerosing agent–contrast material mixture was made by mixing a sclerosing agent (ethanolamine oleate [Ethamolin; Cypros Pharmaceutical, Carlsbad, Calif] or sodium tetradecyl sulfate [Sotradecol 3%; Elkins-Sinn, Cherry Hill, NJ]) with 1.25–2.50 µm of contrast material (gadopentetate dimeglumine, Magnevist; Berlex Laboratories, Wayne, NJ]) per milliliter of sclerosing agent. During each treatment session, a total of 4–10 mL of this mixture was injected into the low-flow malformation. This concentration was obtained by mixing a volume of 0.1 mL of diluted gadopentetate dimeglumine with 2 mL of sclerosing agent and was chosen to approximate the concentration of 2 µm/mL typically used during MR arthrography (8). The total volume injected during each treatment session is listed in Table 2.
The targeted component of the lesion was injected with this sclerosing agent–contrast material mixture and monitored by means of continuous gradient-echo MR imaging. Injection was stopped when the punctured portion of the malformation was completely filled or when any extravasation was seen. The images obtained during injection were also monitored for evidence of noticeable venous outflow of the sclerosing agent. The needle was then repositioned as guided with continuous direct MR imaging, and injection was repeated until all desired compartments of the malformation appeared filled with the mixture. Owing to the size of the lesions, sclerotherapy was planned in a staged manner, and specific portions of the malformation were targeted for treatment in each of multiple stages. A staged approach was chosen to limit the inflammatory response and patient discomfort that might occur with injection of larger volumes of the mixture. Extreme care was taken to prevent subcutaneous or submucosal extravasation of the sclerosing agent. The patients were followed up with clinical and MR imaging examinations 4–17 weeks after treatment.
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Results
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A total of 14 procedures were performed. The first patient required two staged procedures, and the second and third patients each required six procedures. The time between sequential staged treatment sessions ranged from 4 to 17 weeks. After all treatment sessions, each patient demonstrated an immediate swelling and mild inflammatory reaction of the treated area, which transiently increased and then subsided during the following 1–2 weeks. No patient required treatment with a corticosteroid to decrease inflammation. Pain was a constant finding after sclerotherapy, and pain in two patients required treatment with oral acetaminophen with codeine in the immediate postprocedural period. No cases of fever, infection, and skin or mucosal ulceration were observed. No patient reported respiratory distress as a clinical sign of pulmonary embolization of the sclerosing agent.
Table 2 provides the time each patient was in the MR imager during each procedure, including the overall time and the times for preliminary imaging for target characterization and localization, the interventional procedure, and the postprocedural imaging for documentation and exclusion of extravasation. The time required for the MR imaging–guided portions of the interventional procedure, starting with insertion of the 22-gauge MR imaging–compatible needle and ending with the final needle withdrawal, ranged from 14 to 53 minutes (mean, 29 minutes).
The sclerosing agent–contrast material mixture was clearly visible during injection as an enlarging bright region surrounding the needle tip (Fig 1). Successful needle placement, repositioning, and MR imaging–monitored injection of the mixture was accomplished in all cases without complication, and all targeted compartments of the low-flow vascular malformations could be filled with the mixture.
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Figure 1a. Patient 2. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately prior to the procedure demonstrates an area of high signal intensity (arrows) in the right masticator space, representing the low-flow vascular malformation targeted for treatment in this session. Additional compartments (arrowheads) of the malformation, anterior and medial to the largest component, were treated in subsequent stages. (b) Single frame from a continuous series of gradient-echo images (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) obtained during the treatment session, shows a small area of high signal intensity (arrow) representing the sclerosing agent–contrast material mixture collecting around the tip of the needle (arrowhead). (c) Gradient-echo image (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) later in the series. After repositioning of the needle (arrowhead) guided by means of the continuously acquired images, the targeted lesion continues to fill with sclerosing agent–contrast material mixture (arrows) without evidence of subcutaneous extravasation. (d) T1-weighted SE image (504/15, one signal acquired) obtained immediately after the interventional procedure. The treated portion of the low-flow vascular malformation is clearly visible as a high-signal-intensity region (arrows) representing sclerosing agent–contrast material mixture in the lesion. Heterogeneity partially reflects intermixed thrombus. (e) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately after the interventional procedure. The low-flow vascular malformation (arrows) now demonstrates areas of central low signal intensity in the treated portion owing to the susceptibility effect of concentrated contrast material and thrombus.
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Figure 1b. Patient 2. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately prior to the procedure demonstrates an area of high signal intensity (arrows) in the right masticator space, representing the low-flow vascular malformation targeted for treatment in this session. Additional compartments (arrowheads) of the malformation, anterior and medial to the largest component, were treated in subsequent stages. (b) Single frame from a continuous series of gradient-echo images (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) obtained during the treatment session, shows a small area of high signal intensity (arrow) representing the sclerosing agent–contrast material mixture collecting around the tip of the needle (arrowhead). (c) Gradient-echo image (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) later in the series. After repositioning of the needle (arrowhead) guided by means of the continuously acquired images, the targeted lesion continues to fill with sclerosing agent–contrast material mixture (arrows) without evidence of subcutaneous extravasation. (d) T1-weighted SE image (504/15, one signal acquired) obtained immediately after the interventional procedure. The treated portion of the low-flow vascular malformation is clearly visible as a high-signal-intensity region (arrows) representing sclerosing agent–contrast material mixture in the lesion. Heterogeneity partially reflects intermixed thrombus. (e) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately after the interventional procedure. The low-flow vascular malformation (arrows) now demonstrates areas of central low signal intensity in the treated portion owing to the susceptibility effect of concentrated contrast material and thrombus.
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Figure 1c. Patient 2. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately prior to the procedure demonstrates an area of high signal intensity (arrows) in the right masticator space, representing the low-flow vascular malformation targeted for treatment in this session. Additional compartments (arrowheads) of the malformation, anterior and medial to the largest component, were treated in subsequent stages. (b) Single frame from a continuous series of gradient-echo images (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) obtained during the treatment session, shows a small area of high signal intensity (arrow) representing the sclerosing agent–contrast material mixture collecting around the tip of the needle (arrowhead). (c) Gradient-echo image (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) later in the series. After repositioning of the needle (arrowhead) guided by means of the continuously acquired images, the targeted lesion continues to fill with sclerosing agent–contrast material mixture (arrows) without evidence of subcutaneous extravasation. (d) T1-weighted SE image (504/15, one signal acquired) obtained immediately after the interventional procedure. The treated portion of the low-flow vascular malformation is clearly visible as a high-signal-intensity region (arrows) representing sclerosing agent–contrast material mixture in the lesion. Heterogeneity partially reflects intermixed thrombus. (e) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately after the interventional procedure. The low-flow vascular malformation (arrows) now demonstrates areas of central low signal intensity in the treated portion owing to the susceptibility effect of concentrated contrast material and thrombus.
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Figure 1d. Patient 2. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately prior to the procedure demonstrates an area of high signal intensity (arrows) in the right masticator space, representing the low-flow vascular malformation targeted for treatment in this session. Additional compartments (arrowheads) of the malformation, anterior and medial to the largest component, were treated in subsequent stages. (b) Single frame from a continuous series of gradient-echo images (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) obtained during the treatment session, shows a small area of high signal intensity (arrow) representing the sclerosing agent–contrast material mixture collecting around the tip of the needle (arrowhead). (c) Gradient-echo image (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) later in the series. After repositioning of the needle (arrowhead) guided by means of the continuously acquired images, the targeted lesion continues to fill with sclerosing agent–contrast material mixture (arrows) without evidence of subcutaneous extravasation. (d) T1-weighted SE image (504/15, one signal acquired) obtained immediately after the interventional procedure. The treated portion of the low-flow vascular malformation is clearly visible as a high-signal-intensity region (arrows) representing sclerosing agent–contrast material mixture in the lesion. Heterogeneity partially reflects intermixed thrombus. (e) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately after the interventional procedure. The low-flow vascular malformation (arrows) now demonstrates areas of central low signal intensity in the treated portion owing to the susceptibility effect of concentrated contrast material and thrombus.
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Figure 1e. Patient 2. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately prior to the procedure demonstrates an area of high signal intensity (arrows) in the right masticator space, representing the low-flow vascular malformation targeted for treatment in this session. Additional compartments (arrowheads) of the malformation, anterior and medial to the largest component, were treated in subsequent stages. (b) Single frame from a continuous series of gradient-echo images (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) obtained during the treatment session, shows a small area of high signal intensity (arrow) representing the sclerosing agent–contrast material mixture collecting around the tip of the needle (arrowhead). (c) Gradient-echo image (18/7, one signal acquired, 90° flip angle, 1.8-second imaging time) later in the series. After repositioning of the needle (arrowhead) guided by means of the continuously acquired images, the targeted lesion continues to fill with sclerosing agent–contrast material mixture (arrows) without evidence of subcutaneous extravasation. (d) T1-weighted SE image (504/15, one signal acquired) obtained immediately after the interventional procedure. The treated portion of the low-flow vascular malformation is clearly visible as a high-signal-intensity region (arrows) representing sclerosing agent–contrast material mixture in the lesion. Heterogeneity partially reflects intermixed thrombus. (e) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) obtained immediately after the interventional procedure. The low-flow vascular malformation (arrows) now demonstrates areas of central low signal intensity in the treated portion owing to the susceptibility effect of concentrated contrast material and thrombus.
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In all three patients, follow-up MR imaging and clinical examinations demonstrated reduction in size of the treated portions of the malformations (Fig 2). Two patients reported an improvement in impaired chewing function, and one patient experienced a complete cessation of previous nightly oral hemorrhage.
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Figure 2a. Patient 3. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) shows an extensive area of high signal intensity (arrows) representing a large low-flow vascular malformation. (b) Frame from the continuous gradient-echo image series (18/7, one signal acquired, 90° flip angle) obtained during the patient's third treatment session. A high-signal-intensity area (arrows) is depicted around the needle tip, representing the sclerosing agent–contrast material mixture as the malformation is filled. (c) Follow-up study at 4 months. T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) reveals low signal intensity in the previously treated portions of the malformation and reduction in size of the treated components (arrows).
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Figure 2b. Patient 3. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) shows an extensive area of high signal intensity (arrows) representing a large low-flow vascular malformation. (b) Frame from the continuous gradient-echo image series (18/7, one signal acquired, 90° flip angle) obtained during the patient's third treatment session. A high-signal-intensity area (arrows) is depicted around the needle tip, representing the sclerosing agent–contrast material mixture as the malformation is filled. (c) Follow-up study at 4 months. T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) reveals low signal intensity in the previously treated portions of the malformation and reduction in size of the treated components (arrows).
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Figure 2c. Patient 3. (a) T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) shows an extensive area of high signal intensity (arrows) representing a large low-flow vascular malformation. (b) Frame from the continuous gradient-echo image series (18/7, one signal acquired, 90° flip angle) obtained during the patient's third treatment session. A high-signal-intensity area (arrows) is depicted around the needle tip, representing the sclerosing agent–contrast material mixture as the malformation is filled. (c) Follow-up study at 4 months. T2-weighted turbo SE image (4,655/102; two signals acquired; echo train length, seven) reveals low signal intensity in the previously treated portions of the malformation and reduction in size of the treated components (arrows).
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On the posttreatment images obtained immediately after injection, the following signal intensity changes were observed. On the T1-weighted images, a high-signal-intensity area representing the injected sclerosing agent–contrast material mixture filled the targeted components of the malformation in all cases (Fig 1d). A similar effect was also seen on T2-weighted images, on which the injected mixture appeared as low-signal-intensity areas owing to the susceptibility effect of concentrated contrast agent (Fig 1e). Follow-up T1- and T2-weighted images, obtained between 4 and 17 weeks after the procedure, showed decrease in size and reduction in signal intensity in the previously injected portion of the malformation (Fig 2c). On T1-weighted images, no increased signal intensity was observed from residual injected sclerosing agent–contrast material mixture or subacute thrombus.
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Discussion
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Vascular malformations of the head and neck are lesions that often involve multiple contiguous anatomic spaces and encase critical neurovascular structures, making surgical treatment difficult and often unsuccessful. Percutaneous and transarterial sclerotherapy have been advocated as effective alternatives or adjuncts to surgery. For low-flow malformations, those without a noticeable arterial component, percutaneous injection of the lesion with x-ray fluoroscopic guidance is usually performed.
The striking conspicuity of these lesions on MR images, as well as the capacity for interactive multiplanar imaging, increased access to the patient, and rapid temporal resolution provided by currently available open-configuration MR imaging systems (9–11), suggest that MR imaging guidance may be well suited for imaging-guided sclerotherapy of these lesions. The relatively short procedural times in our investigation, with a mean of 29 minutes per intervention, support the hypothesis that this technology will allow this form of therapy to be performed in a clinically feasible time frame.
Direct observation of distribution of the sclerosing agent during injection is a key feature of this technique. This requires not only sufficient temporal resolution but also the ability to directly visualize the sclerosing agent in the malformation. This has been achieved by adding very dilute gadopentetate dimeglumine to the sclerosing agent. The very small volume of contrast agent necessary for visualization at MR imaging reduces undesired dilution of the sclerosing agent, with only 0.1 mL of diluted gadopentetate dimeglumine added for each 2 mL of sclerosing agent. This leaves the sclerosing agent at nearly full strength, in contrast to the dilutional effect of mixing the larger volumes of iodinated contrast material necessary to render sclerosing agents visible at fluoroscopy. Owing to the extremely strong chelation of gadolinium in the gadopentetate dimeglumine complex at physiologic pH and the slightly basic pH of the sclerosing agents (pH of between 8 and 9), there is no risk of release of free gadolinium with this technique (Frenzel T, oral communication, 1998). Use of this sclerosing agent–contrast material mixture makes tracking of the injected agent simple during treatment, and reduces the risk of subcutaneous or submucosal injection that can lead to tissue necrosis.
Although percutaneous injection of sclerosing agents has a relatively long history of safe application for the treatment of low-flow vascular malformations, complications have been reported with this form of therapy. The frequency of complication depends in part on the type of sclerosing agent applied. Local tissue injury, such as skin necrosis or peripheral nerve damage, is the most common complication of percutaneous sclerotherapy (2,4,12–14). With use of ethanol as a sclerosing agent, the reported complication rate ranges from 0% to 15% depending on the type of lesion. Because a combined approach was often chosen, it is difficult to determine whether the reported complications resulted from the percutaneous or transarterial portion of the procedures (4,12,13,15). Owing to the neurotoxic effects of absolute ethanol, Gomes (15) recommended that the use of ethanol should be avoided in proximity to major nerve trunks. With use of sodium tetradecyl sulfate as a sclerosing agent, only minor complications, primarily small skin ulcers (average diameter, 12 mm) have been reported, at a rate of 9.6% (2).
In our series, this low frequency of reported complications, reduced risk of nerve damage, and higher level of patient comfort formed the basis for our decision to use sodium tetradecyl sulfate and the similar agent, ethanoloamine oleate, rather than ethanol. The relative safety of these agents, as well as the ability to monitor distribution during injection, likely contributed to the absence of skin necrosis, nerve damage, or other complication in our series. We believe the increased safety of these agents outweighs the potential decrease in efficacy when compared with ethanol. However, if ethanol is chosen for percutaneous sclerotherapy, monitoring of injection with MR imaging should also be possible with appropriate modifications in the imaging technique.
A final issue that merits specific mention is the economic effect of this form of imaging guidance. At our institution, percutaneous sclerotherapy for vascular malformations was previously performed with CT guidance, with global charges of approximately $2,300 per treatment session, including all materials, scanner time, and professional fees. The charges incurred with MR imaging guidance are slightly higher, totaling approximately $2,600 per treatment session. We believe that the 13% increase in expense is justified by the improvement in visualization of the malformation and the ability to continuously monitor the injection, but this added cost may be prohibitive in some situations. Access to an MR imaging system with interventional capabilities may also present a limiting factor at many institutions, and purchase of a system solely for this type of procedure would be difficult to justify. However, open-configuration MR imaging systems are the fastest growing sector in the U.S. MR imaging market, and an increasing number of radiology practices have access to an open-configuration unit. The components and modifications necessary to perform this type of procedure can be added for less than $150,000, making the adoption of MR imaging–guided methods much more economically feasible.
Finally, procedures such as this displace diagnostic studies from the MR imager, and any decrease in patient throughput may present a problem for sites with high imager use. With the open-configuration MR imager at our teaching institution, we typically schedule patients for 1-hour time slots for routine studies and 1
-hour time slots for multipart or more complicated diagnostic studies. The imager time required for percutaneous sclerotherapy of low-flow vascular malformations is only slightly longer than that for routine diagnostic imaging and, in our experience, has not resulted in a noticeable reduction in patient throughput.
In conclusion, our preliminary results suggest that MR imaging–guided percutaneous sclerotherapy of low-flow vascular malformations in the head and neck is feasible, can be performed safely, and allows direct visualization of sclerosing agent distribution and needle placement during injection of both superficial and deep components of vascular malformations.
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Footnotes
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Abbreviation: SE = spin echo
Author contributions: Guarantor of integrity of entire study, J.S.L.; study concepts, all authors; study design, J.S.L., E.M.M.; definition of intellectual content, all authors; literature research, J.S.L., E.M.M.; clinical studies, J.S.L., R.W.T.; data acquisition, J.S.L., E.M.M., R.W.T.; data analysis, J.S.L., E.M.M., J.L.D.; manuscript preparation, editing, and review, all authors.
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Abstract
Introduction
