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the intraoral approach for cosmetic reasons. The intraoral approach is better than other approaches in avoiding skin incisions in the aesthetic view, although it provided a relatively bad exposure for tumor resection. This is why proper indications (benign lesions, relative small lesions, etc) for intraoral approach should be chosen before its clinical use. This intraoral approach is not recommended when the lesions are supposed to be malignant, of infiltrative growth, have a relative big size, and even incomplete envelope. Our group had strong reasons to believe that the intraoral approach would be an ideal option if the following conditions were met: (1) nerve monitoring was performed to avoid facial nerve injuries, (2) preoperative diagnosis was a benign lesion, (3) has a relatively small size, and (4) located on the anterior portion of the masseter muscle. As for our case, 3 big cavernous hemangiomas were found on the right side of the face. Through CT results, it was easy to clarify the area of the lesions and adjacent tissue around lesions. With the consideration of cutting the 3 big cavernous hemangiomas together, the paraoral surgical approach was our best option to provide a clear surgical vision. During the surgery, the facial nerves were dissected at the anterior pole and anus perineum of the right parotid gland. The 3 cavernous hemangiomas were totally removed without any complications. The pathologic results supported preoperative diagnosis. As for the etiology of hemangioma, it is still a medical puzzle under study. It is controversial to clarify the etiology of hemangioma from gene mutation, placenta factors, or development factors. Some evidences8 showed that wounds of dendritic cells play an important role in the formation of hemangioma through some cytokine, such as vascular endothelial growth factor. Some experts9 concluded that hemangioma originates from embryo of angioblasts. In a clinical perspective, hemangioma10 might have a strong relationship with developmental defect. In our case, we found congenital triYcavernous hemangiomas of the right buccal region, right accessory parotid gland, and masseter muscle region together, which has not happened segmentally, and not in embryo fusion regions.11 The theory of developmental defect was not supported by our case, whereas angioplasty theory was more evidential in our case. The theory shows that hemangioma originates from embryo isolation of angioblasts. Angioblasts are a primordium to become blood vessels but, somehow, could not manage to head through with other vasculature during development; then, a hemangioma develops. Three cavernous hemangiomas happened to develop in nearby areas: the right buccal region, right accessory parotid gland, and masseter muscle region. Thanks to communication problems, the remaining angioblasts continued to develop as 3 big cavernous hemangiomas, which are shown in Figures 1 to 4.
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7. Kurabayashi T, Ida M, Tetsumura A, et al. MR imaging of benign and malignant lesions in the buccal space. Dentomaxillofac Radiol 2002;31:344Y349 8. Nguyen VA, Fti rhapter C, Romani N, et al. Infantile hemangioma is proliferation of beta 4-negative endothelial cells adjacent to HLA-DR-positive cells with dendritic cell morphology Hum Pathol 2004;35:739Y744 9. Dadras SS, North PE, Bertoncini J, et al. Infantile hemangiomas are arrested in an early developmental vascular differentiation state. Mod Pathol 2004;17:1068Y1079 10. Burns AJ, Kaplan LC, Mulliken JB. Is there an association between hemangioma and syndromes with dysmorphic features? Pediatrics 1991;88:1257Y1267 11. Waner M, North PE, Scherer KA, et al. The nonrandom distribution of facial hemangiomas. Arch Dermatol 2003;139:869Y875
Surgical Treatment of Masseteric Venous Malformations and Outcomes Jae Hyun Kwon, MD, So Young Lim, MD, PhD, Jai-Kyong Pyon, MD, PhD, Goo-Hyun Mun, MD, PhD, Sa-Ik Bang, MD, PhD, Kap Sung Oh, MD, PhD
REFERENCES
Abstract: Intramuscular venous malformations are often misdiagnosed as other types of tumors with similar presentations. We describe here the typical presentation of a venous malformation within the masseter muscle, including the physical findings and imaging, and present our experience with the surgical excision of these lesions. This is a review of 10 patients with venous malformations localized to the masseter muscle who presented to our institution between 2008 and 2011. The patients included 6 females and 4 males. Of these venous malformations, 80% were noted in childhood, and the remainder manifested later in adolescence. Pain, swelling, and facial asymmetry were the presenting complaints. Magnetic resonance imaging, Doppler ultrasonography, and whole-body blood scintigraphy were used to characterize the lesions. All patients were treated by total resection of the lesion while preserving the marginal mandibular branch of the facial nerve. Magnetic resonance imaging showed the lesions to be isointense with surrounding muscle on T1-weighted images and hyperintense on T2-weighted images. Gross examination of the resected specimens revealed multicolored tissue with dilated vascular channels, frequently containing phleboliths. After the operation, all patients showed improvement in both symptoms and
1. Haggstrom AN, Drolet BA, Baselga E, et al. Prospective study of infantile hemangiomas: clinical characteristics predicting complications and treatment. Pediatrics 2006;118:882Y887 2. Johnson FE, Spiro RH. Tumors arising in accessory parotid tissue. Am J Surg 1979;138:576Y578 3. Chang CH, Mun GH, Lim SY, et al. Cavernous vascular tumor of the accessory parotid gland. J Craniofac Surg 2007;18:1493Y1496 4. Toh H, Kodama J, Fukuda J, et al. Incidence and histology of human accessory parotid glands. Anat Rec 1993;236:586Y590 5. Schmutzhard J, Schwentner IM, Andrle J, et al. Resection of accessory parotid gland tumors through a peroral approach with facial nerve monitoring. J Craniofac Surg 2007;18:1419Y1421 6. Tart RP, Kotzur IM, Mancuso AA, et al. CT and MR imaging of the buccal space and buccal space masses. Radiographics 1995;15:531Y550
From the Department of Plastic and Reconstructive Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Received June 23, 2013. Accepted for publication October 28, 2013. Address correspondence and reprint requests to Dr. So Young Lim, Department of Plastic and Reconstructive Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000504
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* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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appearance. This improvement was sustained at a mean follow-up of 21 months. Masseteric venous malformations typically present with a pattern of clinical and imaging findings that should allow surgeons to distinguish them from other diseases in the cheek area. Complete surgical excision is a treatment option for these patients and can be performed without facial nerve injury or excessive bleeding. This procedure can result in excellent outcomes for localized intramasseteric venous malformation.
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FIGURE 2. Operative view. The facial nerve could be clearly identified and dissected in the bloodless surgical field.
Key Words: Venous malformation, masseter muscle, intramuscular
V
ascular malformations are abnormal blood vessels that are generally slow growing but that may grow acutely in response to infection or trauma. 1 These are subdivided into capillary malformations, venous malformations, lymphatic malformations, arteriovenous malformations, and arteriovenous fistulas. This categorization is defined by the predominant anomalous channel present in the malformation.1,2 Among them, venous malformations are the most common vascular malformations, and more than 40% of these present in the head and neck region.1 Patients with more superficial venous malformations may present with a bluish hue overlying the lesion, and these patients may seek medical help for significant functional and cosmetic deformities depending on the size and the extent of the malformation. In contrast, pure intramuscular venous malformations often present in a more delayed manner and have no bluish hue because of the lack of obvious skin involvement. Intramuscular malformations generally present without any deformity until these are larger in size. Although superficial vascular malformations are relatively common in the head and the neck, intramuscular vascular malformations are rare. Less than 1% of vasoformative tumors occur in skeletal muscle, and only 15% of those occur in the musculature of the head and the neck.3 However, the exact incidence of masseteric venous malformations is unknown yet. Because of the rarity, deep location, and unfamiliar presentation of these lesions, inaccurate preoperative diagnosis and inappropriate treatment planning are common. However, diagnosis is greatly facilitated by training clinicians to recognize the stereotypical presentation of venous malformations of the masseter muscle.3,4 Often, there is gradual increase in facial asymmetry, which worsens with jaw clenching. In addition, small lesions may not be apparent with the jaw in a relaxed position. Some patients may also have discomfort with eating or chewing. On physical examination, a firm and nontender mass may be palpated when the jaw is clenched. An increase in the asymmetry of the cheeks may also be more apparent with proper positioning. Masseteric venous malformations also have a typical appearance on magnetic resonance imaging (MRI), and plain radiographs allow for the identification of phleboliths in the lesion.5 Once identified, treatment of these lesions may include observation, surgical excision, or sclerotherapy.2 Each treatment option has advantages and disadvantages, but complete removal of the lesion by one procedure might be possible only through surgery. Surgical removal does have the potential to cause significant morbidity in part
FIGURE 1. Preoperative photograph showing left cheek contour deformity due to masseteric venous malformation (left) and postoperative view at the 20-month follow-up (center). Esthetically satisfy ing scar was identified (right).
because of the location of the lesion in the masseter muscle.6 Here, we present 10 cases of successful surgical excisions of masseteric venous malformations without significant complications.
PATIENTS AND METHODS Intramuscular venous malformations were identified through a review of all patients seen from January 2008 to December 2011 at our institution. Patients were considered eligible for this study if they had presented with contour deformities (Fig. 1), pain with jaw clenching, and a cheek mass on physical examination and if the diagnosis has been confirmed by MRI and whole-body blood scan showing venous enhancement within well-delineated, hyperintense lesions confined to the masseter muscle on T2-weighted images. All of the patients in our study underwent surgery under general anesthesia and endotracheal intubation using a modified Blair incision.7 Dissection proceeded from the parotid fascia in the anterior direction. After that, the facial nerve branches were identified and dissected in the antegrade direction. The marginal mandibular branch and sometimes the buccal branch of the facial nerve were clearly identified by microscopic inspection and a nerve integrity monitor and were preserved without any definite injuries. Through careful dissection between the masseter muscle fibers along the longitudinal axis, the venous malformation lesions were exposed and excised meticulously with some surrounding normal muscle cuff to prevent rupture, which would cause massive bleeding and subsequent blurring of the field. Wound closure was accomplished without difficulty (Fig. 2).
TABLE 1. Clinical Features of 10 Patients With Masseteric Venous Malformations
Patient No. Sex Age, y
Clinical Features
1 2 3 4 5 6
M M F F F F
18 13 8 21 9 16
Persistent painful cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling
7 8 9 10
F M M F
15 10 8 17
Persistent cheek swelling Intermittent preauricular swelling Persistent painful cheek swelling Persistent diffuse cheek swelling
Provisional Diagnosis Before Radiologic Examination Venous malformation Venous malformation Hemangioma Parotid tumor Hemangioma Venolymphatic malformation Venous malformation Venous malformation Venous malformation Unilateral masseteric hypertrophy
F, female; M, male.
* 2014 Mutaz B. Habal, MD
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TABLE 2. Radiologic Evaluation Results Patient No. 1 2 3 4 5 6 7 8 9 10
Duplex US
MRI
Whole-Body Blood Scan
Venous malformation with phlebolith Multiple abnormal venous structure with phlebolith
Venous malformation Venous malformation Venolymphatic malformation Venous malformation Venous malformation Venous malformation Venous malformation Venous malformation Venous malformation Venolymphatic malformation Venous malformation
Venous malformation Venous malformation
Venous Venous Venous Venous
malformation with phlebolith malformation with phlebolith malformation with phlebolith malformation with phlebolith Venous malformation Venous malformation with phlebolith Venous malformation Venous malformation with phlebolith
Venous Venous Venous Venous Venous Venous Venous Venous
malformation malformation malformation malformation malformation malformation malformation malformation
US, ultrasonography.
The treatment outcomes were assessed through review of medical records and outpatient clinic visits. Both changes in contour and improvements in symptoms were evaluated.
RESULTS A total of 10 patients with a primary diagnosis of venous malformation were identified. The patients included 6 females and 4 males, with ages ranging from 8 to 21 years. The lesions were noted in childhood in 8 patients and in adolescence in 2 patients. The mean age at presentation to our institution was 12.5 years (Table 1). The most common symptoms were contour deformity (Fig. 1) and pain. There were no episodes of intralesional bleeding, localized intravascular coagulopathy, or associated skeletal problems, despite these having been previously described in the literature.2 Radiologic evaluation of masseteric venous malformation usually included duplex ultrasonography, MRI, angiography, and whole-body blood scan. Although not every patient was evaluated using the same studies, MRI and whole-body blood scan were applied to all patients in common. Except 1 patient who was diagnosed with venolymphatic malformation on MRI, diagnoses of all patients coincided (Table 2). The lesions were completely resected en bloc in all patients using the method described above. Compressive garments were applied to the surgical site for approximately 2 weeks postoperatively to prevent postoperative bleeding and hematoma formation in the remaining dead space (Fig. 3). This also served to minimize the extent and the duration of facial swelling. Tissue from all 10 patients was available for pathologic examination. The histologic specimens were usually variegated yellow and red and had dilated venous channels, frequently containing phleboliths. In 4 patients, the phleboliths were also identified grossly. On light microscopy, the excised lesions were observed to be composed of small- to medium-sized vascular channels with thin
FIGURE 3. Compressive garments were applied for 2 weeks postoperatively to prevent potential postoperative bleeding and hematoma.
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walls. They had the appearance of dysplastic veins characterized by flat endothelium and walls with irregular muscle. The lumens were filled with blood or were empty, and phleboliths were found in some specimens. All 10 patients showed improvement in both domains. We assumed that the dead space present after resection of the lesions and the surrounding muscle was subsequently filled with fibrotic tissue because no depression was encountered on follow-up period, and postoperative MRI demonstrated that the fibrotic tissue substituted for the dead space after excision of the lesions. There were no identifiable depressions, muscular dysfunction, or nerve dysfunction (Fig. 4) except in 1 patient who had transient paralysis of the buccal branch of the facial nerve. This paralysis resolved fully within 2 months without any intervention, and there were no lasting sequelae. The patients showed sustained improvement at a mean follow-up of 21 months (10Y27 mo), as shown in Table 3. Good cosmetic results were also achieved because all of the scars were nearly invisible (Fig. 1).
DISCUSSION Vascular malformations are sometimes difficult to differentiate from tumors composed of abnormal blood vessels, which are another large category of congenital lesions called hemangiomas.1 Whereas hemangiomas usually show a rapid growth or proliferative phase and an involutional phase, vascular malformations are instead generally
FIGURE 4. Function of the facial nerve was well preserved at the 1-month follow-up.
* 2014 Mutaz B. Habal, MD
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TABLE 3. Facial Weakness After Surgery, Duration of Follow-up, and Recurrence
Patient No.
Facial Weakness After Surgery
Duration of Follow-up, mo
1 2 3 4 5 6 7 8 9 10
None None None Temporary (2 mo) None None None None None None
22 23 27 10 14 19 22 26 27 20
Recurrence None None None None None None None None None
present at birth and grow proportionally with the body without spontaneous involution.8 Despite this distinction, we note that some previous reports on intramuscular venous malformations have incorrectly described these lesions as intramuscular hemangiomas. Further classifying vascular malformations into high- and lowflow malformations is a useful clinical distinction. Arterial or mixed arterial-venous malformations are high flow and may be associated with a bruit or thrill. Venous and lymphatic malformations are lowflow lesions. Lymphatic malformations are masses of abnormal lymphatic channels commonly found in the head and neck region. These are different from venous malformations in that these are generally not associated with a bluish hue.9,10 Hemangiomas and venous malformations are frequently confused clinically because of their similar gross appearance. For that reason, venous malformations have been described incorrectly as hemangiomas and mistaken for tumors, especially outside the field of plastic surgery. However, these 2 lesions are distinctly different in clinical course and in histopathology. Venous malformations are typically slow-flow lesions that do not regress; these may be asymptomatic for as long as several years, although infection or trauma may result in an acute increase in size. In contrast, hemangiomas are the most common vascular tumor presenting during infancy and have a characteristic proliferative phase followed by slow involution in early childhood.11 Although venous malformations are benign lesions, depending on the areas of involvement, these may be associated with dysfunction and cosmetic deformity. In the presence of functional limitations or problems with cosmesis or pain, more aggressive treatment may be appropriate. In particular, intramuscular venous malformations are considered more likely to present with phleboliths than are venous malformations that do not involve the muscle, and these phleboliths can cause pain and firmness of the lesion. The pathophysiology of phlebolith formation in venous malformations is not well understood; however, it has been theorized that a slow-flow state due to muscular contraction may be associated with local intravascular coagulopathies contributing to phlebolith formation.12,13 Imaging studies are useful diagnostic tools. Plain radiographs of venous malformations usually demonstrated soft tissue swelling. Although osseous deformities and phleboliths have been identified and described in the literature,2 we did not routinely use radiographs in our study population. Doppler ultrasonography was used to distinguish slow-flow lesions from other fast-flow lesions. On ultrasound examination, intramuscular venous malformations were easily identifiable because of their typical composition of channels with slow blood flow augmented by compression of the adjacent tissue. On MRI, venous malformations were isointense with the surrounding muscle on T1weighted sequences and hyperintense on T2-weighted sequences (Fig. 5). Although angiography is considered the criterion standard
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for the diagnosis of vascular malformations, it is not preferred at our center because of the invasiveness of the procedure and the associated risks. Of the less invasive studies, MRI is the single most effective study for the diagnosis of vascular malformations because it easily distinguishes lesions from surrounding soft tissue and allows for determination of the extent of the lesion. However, MRI sometimes fails to differentiate venous malformations from lymphatic malformations because these 2 lesions both appear as low-flow solid masses. Wholebody blood pool scintigraphy using 99mTc-labeled red blood cells and SPECT are used to characterize congenital venous malformations because of several advantages, including safety, noninvasiveness, and lower cost compared with MRI and angiography. Whole-body blood scans are particularly useful for distinguishing venous malformations from lymphatic malformations because venous malformations show strong symmetric jugular vein uptake, whereas lymphatic malformations do not.14 More detailed care is needed when diagnosing masseteric venous malformations so as not to confound them with lipoma, pleomorphic adenoma or hemangioma, or lymphatic malformations of the salivary gland or cheek region because these all present as similar mass lesions and in the same area. None of these, including masseteric venous malformation, have characteristic skin lesions, such as a bluish hue. The differential diagnosis of venous malformations from other malformations is usually made by clinical history, physical examination, and imaging studies. Furthermore, it is important to make a differential diagnosis with parotid hemagiomas because these are the most common vascular malformation of the head and the neck in childhood. The differential diagnosis between masseteric venous malformations and pleomorphic adenomas of the parotid gland can be based on clinical examination and history. The onset of venous malformations occurs early in childhood, and the size of the lesion increases in proportion of the growth of the body, whereas the onset of pleomorphic adenoma occurs in adulthood. Hemangioma regresses spontaneously after 1 year of age. If patients feel pain and a palpable mass when clenching, lesions are usually intramasseteric masses rather than parotid gland masses. Masseteric venous malformations show changes in size with position, whereas lipoma, pleomorphic adenoma, and hemangioma do not. Magnetic resonance imaging is the most commonly used diagnostic tool to identify whether a mass is in the masseteric muscle or the parotid gland. Whole-body blood pool scintigraphy can be used as a definite diagnostic tool if MRI findings are unclear because only masseteric venous malformations show abnormal uptake. There are various management options available for venous malformations, and the selection of an approach is based on the involved structures and the extent of the lesion. Most cases of venous malformations involving subcutaneous tissue can be successfully managed conservatively with observation or compression. Lesions causing significant pain and/or functional compromise may be treated with sclerotherapy.8 Surgical debulking or removal may be considered, depending on the involved anatomic site and extent. Surgical treatment modalities are generally less effective and may cause complications when used to treat diffuse, large, and deep lesions. Sclerotherapy is a safer option than surgical intervention for
FIGURE 5. T2-weighted sequence MRI in the preoperative (left) and postoperative (right) periods. The lesion was completely removed, and there was no recurrence at the 20-month follow-up.
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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certain malformations, and its success rates have been reported to be as high as 75%.8,15 Lesions that are ideal for sclerotherapy are known to be discrete, relatively superficial lesions with large vessels that are able to be punctured with a needle and that show potential for needle stabilization to prevent solution from leaking into surrounding tissues and a vessel volume and flow rate small enough to inhibit dilution of the agent.8,16 Although sclerotherapy is one of the useful modalities to treat masseteric venous malformation, it has a few shortcomings. Sclerotherapy may require multiple sessions under general anesthesia to achieve visible involution of the lesion in some cases. In addition, sclerotherapy yields less predictable results for intramuscular lesions than those in subcutaneous tissue because of their deep location and multiple intralesional thromboses, the disruption of which could have neurologic consequences. The results of treating intramuscular lesions with sclerotherapy are also less predictable than the results for lesions in subcutaneous tissues because injections are not as effective as in diffuse venous malformations. Therefore, as in the cases reviewed here, in which the lesion is well localized within a single muscle, we consider complete surgical excision as a treatment option. Although some clinicians emphasize the risks of surgical treatment of these lesions because of potentially severe complications such as facial nerve injury or massive bleeding, we were able to identify facial nerves by inspection and by using a nerve integrity monitor, which allowed for nerve preservation with minimal complications. We also recommend the application of compressive garments postoperatively to prevent postoperative hematoma and to limit swelling. A decision for surgical excision versus sclerotherapy should be made after predicting the consequences of each method. Although sclerotherapy does not require an extensive incision line or prolonged recovery period, it is usually not curative on a single procedure. In conclusion, we consider that surgical excisions can be one treatment option for venous malformations that are well localized within a single muscle group such as the masseter muscle. To minimize injury to the facial nerves, the operative field should be bloodless to allow for identification and dissection of the facial nerves. Masseteric venous malformations should thus be excised with a surrounding cuff of normal muscle so as to not rupture the venous lesions, and surgeons should pay particular attention to hemostasis of the cut edge of the muscle using bipolar electrocauterization. This study has some limitations. This study was retrospective, and the mean follow-up of 21 months is not enough to evaluate the recurrence of lesions. However, despite these shortcomings, we consider that our data support the advantages and the safety of surgical excision of masseteric venous malformation.
CONCLUSIONS Masseteric venous malformations have typical clinical and imaging characteristics that allow surgeons to distinguish them from other diseases. Complete surgical excision can be considered as a treatment option for these localized intramuscular lesions. Surgical excision can be performed without complications such as facial nerve injury or massive bleeding and can result in excellent outcomes.
REFERENCES 1. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982;69:412Y422 2. Hein KD, Mulliken JB, Kozakewich HP, et al. Venous malformations of skeletal muscle. Plast Reconstr Surg 2002;110:1625Y1635 3. Rai P, Setia S, Kalra N, et al. Intramuscular vascular malformation of the masseter muscle presenting with turkey wattle sign. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:618
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4. Demir Z, Oktem F, Celebioglu S. Rare case of intramasseteric cavernous hemangioma in a three-year-old boy: a diagnostic dilemma. Ann Otol Rhinol Laryngol 2004;113:455Y458 5. Lee SK, Kwon SY. Intramuscular cavernous hemangioma arising from masseter muscle: a diagnostic dilemma (2006: 12b). Eur Radiol 2007;17:854Y857 6. Smith WP, Prince S, Phelan S. The role of imaging and surgery in the management of vascular tumors of the masseter muscle. J Oral Maxillofac Surg 2005;63:1746Y1752 7. Wormald R, Donnelly M, Timon C. ‘Minor’ morbidity after parotid surgery via the modified Blair incision. J Plast Reconstr Aesthet Surg 2009;62:1008Y1011 8. Rosbe KW, Hess CP, Dowd CF, et al. Masseteric venous malformations: diagnosis, treatment, and outcomes. Otolaryngol Head Neck Surg 2010;143:779Y783 9. Perkins JA, Manning SC, Tempero RM, et al. Lymphatic malformations: review of current treatment. Otolaryngol Head Neck Surg 2010;142:795Y803, 803.e1 10. Perkins JA, Manning SC, Tempero RM, et al. Lymphatic malformations: current cellular and clinical investigations. Otolaryngol Head Neck Surg 2010;142:789Y794 11. Chang LC, Haggstrom AN, Drolet BA, et al. Growth characteristics of infantile hemangiomas: implications for management. Pediatrics 2008;122:360Y367 12. Kanaya H, Saito Y, Gama N, et al. Intramuscular hemangioma of masseter muscle with prominent formation of phleboliths: a case report. Auris Nasus Larynx 2008;35:587Y591 13. Dompmartin A, Acher A, Thibon P, et al. Association of localized intravascular coagulopathy with venous malformations. Arch Dermatol 2008;144:873Y877 14. Lee JY, Choi JY, Kim YH, et al. Characterization of congenital lymphatic and blood vascular malformations in the head and neck using blood pool scintigraphy and spect. Lymphology 2010;43:149Y157 15. Berenguer B, Burrows PE, Zurakowski D, et al. Sclerotherapy of craniofacial venous malformations: complications and results. Plast Reconstr Surg 1999;104:1Y11; discussion 12Y15 16. Deveikis JP. Percutaneous ethanol sclerotherapy for vascular malformations in the head and neck. Arch Facial Plast Surg 2005;7:322Y325
Severe Visual Loss and Cerebral Infarction After Injection of Hyaluronic Acid Gel Eung Gyu Kim, MD,* Tae Kyung Eom, MD,Þ Seok Joo Kang, MDÞ Abstract: We report a case of a 23-year-old man with cerebral infarction and permanent visual loss after injection of a hyaluronic acid gel filler for augmentation rhinoplasty. The patient was admitted to the hospital with complaints of loss of vision in the right eye, facial
From the Departments of *Neurology and †Plastic and Reconstructive Surgery, Baik Hospital, Inje University, Busan, Korea. Received October 23, 2013. Accepted for publication November 11, 2013. Address correspondence and reprint requests to Seok Joo Kang, MD, Department of Plastic and Reconstructive surgery, Busan Baik Hospital, Inje University School of Medicine, 75 Bokji-ro, Busan Jin-gu, Busan 614-735, Korea; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000537
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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the intraoral approach for cosmetic reasons. The intraoral approach is better than other approaches in avoiding skin incisions in the aesthetic view, although it provided a relatively bad exposure for tumor resection. This is why proper indications (benign lesions, relative small lesions, etc) for intraoral approach should be chosen before its clinical use. This intraoral approach is not recommended when the lesions are supposed to be malignant, of infiltrative growth, have a relative big size, and even incomplete envelope. Our group had strong reasons to believe that the intraoral approach would be an ideal option if the following conditions were met: (1) nerve monitoring was performed to avoid facial nerve injuries, (2) preoperative diagnosis was a benign lesion, (3) has a relatively small size, and (4) located on the anterior portion of the masseter muscle. As for our case, 3 big cavernous hemangiomas were found on the right side of the face. Through CT results, it was easy to clarify the area of the lesions and adjacent tissue around lesions. With the consideration of cutting the 3 big cavernous hemangiomas together, the paraoral surgical approach was our best option to provide a clear surgical vision. During the surgery, the facial nerves were dissected at the anterior pole and anus perineum of the right parotid gland. The 3 cavernous hemangiomas were totally removed without any complications. The pathologic results supported preoperative diagnosis. As for the etiology of hemangioma, it is still a medical puzzle under study. It is controversial to clarify the etiology of hemangioma from gene mutation, placenta factors, or development factors. Some evidences8 showed that wounds of dendritic cells play an important role in the formation of hemangioma through some cytokine, such as vascular endothelial growth factor. Some experts9 concluded that hemangioma originates from embryo of angioblasts. In a clinical perspective, hemangioma10 might have a strong relationship with developmental defect. In our case, we found congenital triYcavernous hemangiomas of the right buccal region, right accessory parotid gland, and masseter muscle region together, which has not happened segmentally, and not in embryo fusion regions.11 The theory of developmental defect was not supported by our case, whereas angioplasty theory was more evidential in our case. The theory shows that hemangioma originates from embryo isolation of angioblasts. Angioblasts are a primordium to become blood vessels but, somehow, could not manage to head through with other vasculature during development; then, a hemangioma develops. Three cavernous hemangiomas happened to develop in nearby areas: the right buccal region, right accessory parotid gland, and masseter muscle region. Thanks to communication problems, the remaining angioblasts continued to develop as 3 big cavernous hemangiomas, which are shown in Figures 1 to 4.
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7. Kurabayashi T, Ida M, Tetsumura A, et al. MR imaging of benign and malignant lesions in the buccal space. Dentomaxillofac Radiol 2002;31:344Y349 8. Nguyen VA, Fti rhapter C, Romani N, et al. Infantile hemangioma is proliferation of beta 4-negative endothelial cells adjacent to HLA-DR-positive cells with dendritic cell morphology Hum Pathol 2004;35:739Y744 9. Dadras SS, North PE, Bertoncini J, et al. Infantile hemangiomas are arrested in an early developmental vascular differentiation state. Mod Pathol 2004;17:1068Y1079 10. Burns AJ, Kaplan LC, Mulliken JB. Is there an association between hemangioma and syndromes with dysmorphic features? Pediatrics 1991;88:1257Y1267 11. Waner M, North PE, Scherer KA, et al. The nonrandom distribution of facial hemangiomas. Arch Dermatol 2003;139:869Y875
Surgical Treatment of Masseteric Venous Malformations and Outcomes Jae Hyun Kwon, MD, So Young Lim, MD, PhD, Jai-Kyong Pyon, MD, PhD, Goo-Hyun Mun, MD, PhD, Sa-Ik Bang, MD, PhD, Kap Sung Oh, MD, PhD
REFERENCES
Abstract: Intramuscular venous malformations are often misdiagnosed as other types of tumors with similar presentations. We describe here the typical presentation of a venous malformation within the masseter muscle, including the physical findings and imaging, and present our experience with the surgical excision of these lesions. This is a review of 10 patients with venous malformations localized to the masseter muscle who presented to our institution between 2008 and 2011. The patients included 6 females and 4 males. Of these venous malformations, 80% were noted in childhood, and the remainder manifested later in adolescence. Pain, swelling, and facial asymmetry were the presenting complaints. Magnetic resonance imaging, Doppler ultrasonography, and whole-body blood scintigraphy were used to characterize the lesions. All patients were treated by total resection of the lesion while preserving the marginal mandibular branch of the facial nerve. Magnetic resonance imaging showed the lesions to be isointense with surrounding muscle on T1-weighted images and hyperintense on T2-weighted images. Gross examination of the resected specimens revealed multicolored tissue with dilated vascular channels, frequently containing phleboliths. After the operation, all patients showed improvement in both symptoms and
1. Haggstrom AN, Drolet BA, Baselga E, et al. Prospective study of infantile hemangiomas: clinical characteristics predicting complications and treatment. Pediatrics 2006;118:882Y887 2. Johnson FE, Spiro RH. Tumors arising in accessory parotid tissue. Am J Surg 1979;138:576Y578 3. Chang CH, Mun GH, Lim SY, et al. Cavernous vascular tumor of the accessory parotid gland. J Craniofac Surg 2007;18:1493Y1496 4. Toh H, Kodama J, Fukuda J, et al. Incidence and histology of human accessory parotid glands. Anat Rec 1993;236:586Y590 5. Schmutzhard J, Schwentner IM, Andrle J, et al. Resection of accessory parotid gland tumors through a peroral approach with facial nerve monitoring. J Craniofac Surg 2007;18:1419Y1421 6. Tart RP, Kotzur IM, Mancuso AA, et al. CT and MR imaging of the buccal space and buccal space masses. Radiographics 1995;15:531Y550
From the Department of Plastic and Reconstructive Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea. Received June 23, 2013. Accepted for publication October 28, 2013. Address correspondence and reprint requests to Dr. So Young Lim, Department of Plastic and Reconstructive Surgery, Samsung Medical Center, Sungkyunkwan University School of Medicine, 50 Irwon-dong, Gangnam-gu, Seoul 135-710, Republic of Korea; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000504
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* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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appearance. This improvement was sustained at a mean follow-up of 21 months. Masseteric venous malformations typically present with a pattern of clinical and imaging findings that should allow surgeons to distinguish them from other diseases in the cheek area. Complete surgical excision is a treatment option for these patients and can be performed without facial nerve injury or excessive bleeding. This procedure can result in excellent outcomes for localized intramasseteric venous malformation.
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FIGURE 2. Operative view. The facial nerve could be clearly identified and dissected in the bloodless surgical field.
Key Words: Venous malformation, masseter muscle, intramuscular
V
ascular malformations are abnormal blood vessels that are generally slow growing but that may grow acutely in response to infection or trauma. 1 These are subdivided into capillary malformations, venous malformations, lymphatic malformations, arteriovenous malformations, and arteriovenous fistulas. This categorization is defined by the predominant anomalous channel present in the malformation.1,2 Among them, venous malformations are the most common vascular malformations, and more than 40% of these present in the head and neck region.1 Patients with more superficial venous malformations may present with a bluish hue overlying the lesion, and these patients may seek medical help for significant functional and cosmetic deformities depending on the size and the extent of the malformation. In contrast, pure intramuscular venous malformations often present in a more delayed manner and have no bluish hue because of the lack of obvious skin involvement. Intramuscular malformations generally present without any deformity until these are larger in size. Although superficial vascular malformations are relatively common in the head and the neck, intramuscular vascular malformations are rare. Less than 1% of vasoformative tumors occur in skeletal muscle, and only 15% of those occur in the musculature of the head and the neck.3 However, the exact incidence of masseteric venous malformations is unknown yet. Because of the rarity, deep location, and unfamiliar presentation of these lesions, inaccurate preoperative diagnosis and inappropriate treatment planning are common. However, diagnosis is greatly facilitated by training clinicians to recognize the stereotypical presentation of venous malformations of the masseter muscle.3,4 Often, there is gradual increase in facial asymmetry, which worsens with jaw clenching. In addition, small lesions may not be apparent with the jaw in a relaxed position. Some patients may also have discomfort with eating or chewing. On physical examination, a firm and nontender mass may be palpated when the jaw is clenched. An increase in the asymmetry of the cheeks may also be more apparent with proper positioning. Masseteric venous malformations also have a typical appearance on magnetic resonance imaging (MRI), and plain radiographs allow for the identification of phleboliths in the lesion.5 Once identified, treatment of these lesions may include observation, surgical excision, or sclerotherapy.2 Each treatment option has advantages and disadvantages, but complete removal of the lesion by one procedure might be possible only through surgery. Surgical removal does have the potential to cause significant morbidity in part
FIGURE 1. Preoperative photograph showing left cheek contour deformity due to masseteric venous malformation (left) and postoperative view at the 20-month follow-up (center). Esthetically satisfy ing scar was identified (right).
because of the location of the lesion in the masseter muscle.6 Here, we present 10 cases of successful surgical excisions of masseteric venous malformations without significant complications.
PATIENTS AND METHODS Intramuscular venous malformations were identified through a review of all patients seen from January 2008 to December 2011 at our institution. Patients were considered eligible for this study if they had presented with contour deformities (Fig. 1), pain with jaw clenching, and a cheek mass on physical examination and if the diagnosis has been confirmed by MRI and whole-body blood scan showing venous enhancement within well-delineated, hyperintense lesions confined to the masseter muscle on T2-weighted images. All of the patients in our study underwent surgery under general anesthesia and endotracheal intubation using a modified Blair incision.7 Dissection proceeded from the parotid fascia in the anterior direction. After that, the facial nerve branches were identified and dissected in the antegrade direction. The marginal mandibular branch and sometimes the buccal branch of the facial nerve were clearly identified by microscopic inspection and a nerve integrity monitor and were preserved without any definite injuries. Through careful dissection between the masseter muscle fibers along the longitudinal axis, the venous malformation lesions were exposed and excised meticulously with some surrounding normal muscle cuff to prevent rupture, which would cause massive bleeding and subsequent blurring of the field. Wound closure was accomplished without difficulty (Fig. 2).
TABLE 1. Clinical Features of 10 Patients With Masseteric Venous Malformations
Patient No. Sex Age, y
Clinical Features
1 2 3 4 5 6
M M F F F F
18 13 8 21 9 16
Persistent painful cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling Persistent cheek swelling
7 8 9 10
F M M F
15 10 8 17
Persistent cheek swelling Intermittent preauricular swelling Persistent painful cheek swelling Persistent diffuse cheek swelling
Provisional Diagnosis Before Radiologic Examination Venous malformation Venous malformation Hemangioma Parotid tumor Hemangioma Venolymphatic malformation Venous malformation Venous malformation Venous malformation Unilateral masseteric hypertrophy
F, female; M, male.
* 2014 Mutaz B. Habal, MD
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TABLE 2. Radiologic Evaluation Results Patient No. 1 2 3 4 5 6 7 8 9 10
Duplex US
MRI
Whole-Body Blood Scan
Venous malformation with phlebolith Multiple abnormal venous structure with phlebolith
Venous malformation Venous malformation Venolymphatic malformation Venous malformation Venous malformation Venous malformation Venous malformation Venous malformation Venous malformation Venolymphatic malformation Venous malformation
Venous malformation Venous malformation
Venous Venous Venous Venous
malformation with phlebolith malformation with phlebolith malformation with phlebolith malformation with phlebolith Venous malformation Venous malformation with phlebolith Venous malformation Venous malformation with phlebolith
Venous Venous Venous Venous Venous Venous Venous Venous
malformation malformation malformation malformation malformation malformation malformation malformation
US, ultrasonography.
The treatment outcomes were assessed through review of medical records and outpatient clinic visits. Both changes in contour and improvements in symptoms were evaluated.
RESULTS A total of 10 patients with a primary diagnosis of venous malformation were identified. The patients included 6 females and 4 males, with ages ranging from 8 to 21 years. The lesions were noted in childhood in 8 patients and in adolescence in 2 patients. The mean age at presentation to our institution was 12.5 years (Table 1). The most common symptoms were contour deformity (Fig. 1) and pain. There were no episodes of intralesional bleeding, localized intravascular coagulopathy, or associated skeletal problems, despite these having been previously described in the literature.2 Radiologic evaluation of masseteric venous malformation usually included duplex ultrasonography, MRI, angiography, and whole-body blood scan. Although not every patient was evaluated using the same studies, MRI and whole-body blood scan were applied to all patients in common. Except 1 patient who was diagnosed with venolymphatic malformation on MRI, diagnoses of all patients coincided (Table 2). The lesions were completely resected en bloc in all patients using the method described above. Compressive garments were applied to the surgical site for approximately 2 weeks postoperatively to prevent postoperative bleeding and hematoma formation in the remaining dead space (Fig. 3). This also served to minimize the extent and the duration of facial swelling. Tissue from all 10 patients was available for pathologic examination. The histologic specimens were usually variegated yellow and red and had dilated venous channels, frequently containing phleboliths. In 4 patients, the phleboliths were also identified grossly. On light microscopy, the excised lesions were observed to be composed of small- to medium-sized vascular channels with thin
FIGURE 3. Compressive garments were applied for 2 weeks postoperatively to prevent potential postoperative bleeding and hematoma.
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walls. They had the appearance of dysplastic veins characterized by flat endothelium and walls with irregular muscle. The lumens were filled with blood or were empty, and phleboliths were found in some specimens. All 10 patients showed improvement in both domains. We assumed that the dead space present after resection of the lesions and the surrounding muscle was subsequently filled with fibrotic tissue because no depression was encountered on follow-up period, and postoperative MRI demonstrated that the fibrotic tissue substituted for the dead space after excision of the lesions. There were no identifiable depressions, muscular dysfunction, or nerve dysfunction (Fig. 4) except in 1 patient who had transient paralysis of the buccal branch of the facial nerve. This paralysis resolved fully within 2 months without any intervention, and there were no lasting sequelae. The patients showed sustained improvement at a mean follow-up of 21 months (10Y27 mo), as shown in Table 3. Good cosmetic results were also achieved because all of the scars were nearly invisible (Fig. 1).
DISCUSSION Vascular malformations are sometimes difficult to differentiate from tumors composed of abnormal blood vessels, which are another large category of congenital lesions called hemangiomas.1 Whereas hemangiomas usually show a rapid growth or proliferative phase and an involutional phase, vascular malformations are instead generally
FIGURE 4. Function of the facial nerve was well preserved at the 1-month follow-up.
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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& Volume 25, Number 2, March 2014
TABLE 3. Facial Weakness After Surgery, Duration of Follow-up, and Recurrence
Patient No.
Facial Weakness After Surgery
Duration of Follow-up, mo
1 2 3 4 5 6 7 8 9 10
None None None Temporary (2 mo) None None None None None None
22 23 27 10 14 19 22 26 27 20
Recurrence None None None None None None None None None
present at birth and grow proportionally with the body without spontaneous involution.8 Despite this distinction, we note that some previous reports on intramuscular venous malformations have incorrectly described these lesions as intramuscular hemangiomas. Further classifying vascular malformations into high- and lowflow malformations is a useful clinical distinction. Arterial or mixed arterial-venous malformations are high flow and may be associated with a bruit or thrill. Venous and lymphatic malformations are lowflow lesions. Lymphatic malformations are masses of abnormal lymphatic channels commonly found in the head and neck region. These are different from venous malformations in that these are generally not associated with a bluish hue.9,10 Hemangiomas and venous malformations are frequently confused clinically because of their similar gross appearance. For that reason, venous malformations have been described incorrectly as hemangiomas and mistaken for tumors, especially outside the field of plastic surgery. However, these 2 lesions are distinctly different in clinical course and in histopathology. Venous malformations are typically slow-flow lesions that do not regress; these may be asymptomatic for as long as several years, although infection or trauma may result in an acute increase in size. In contrast, hemangiomas are the most common vascular tumor presenting during infancy and have a characteristic proliferative phase followed by slow involution in early childhood.11 Although venous malformations are benign lesions, depending on the areas of involvement, these may be associated with dysfunction and cosmetic deformity. In the presence of functional limitations or problems with cosmesis or pain, more aggressive treatment may be appropriate. In particular, intramuscular venous malformations are considered more likely to present with phleboliths than are venous malformations that do not involve the muscle, and these phleboliths can cause pain and firmness of the lesion. The pathophysiology of phlebolith formation in venous malformations is not well understood; however, it has been theorized that a slow-flow state due to muscular contraction may be associated with local intravascular coagulopathies contributing to phlebolith formation.12,13 Imaging studies are useful diagnostic tools. Plain radiographs of venous malformations usually demonstrated soft tissue swelling. Although osseous deformities and phleboliths have been identified and described in the literature,2 we did not routinely use radiographs in our study population. Doppler ultrasonography was used to distinguish slow-flow lesions from other fast-flow lesions. On ultrasound examination, intramuscular venous malformations were easily identifiable because of their typical composition of channels with slow blood flow augmented by compression of the adjacent tissue. On MRI, venous malformations were isointense with the surrounding muscle on T1weighted sequences and hyperintense on T2-weighted sequences (Fig. 5). Although angiography is considered the criterion standard
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for the diagnosis of vascular malformations, it is not preferred at our center because of the invasiveness of the procedure and the associated risks. Of the less invasive studies, MRI is the single most effective study for the diagnosis of vascular malformations because it easily distinguishes lesions from surrounding soft tissue and allows for determination of the extent of the lesion. However, MRI sometimes fails to differentiate venous malformations from lymphatic malformations because these 2 lesions both appear as low-flow solid masses. Wholebody blood pool scintigraphy using 99mTc-labeled red blood cells and SPECT are used to characterize congenital venous malformations because of several advantages, including safety, noninvasiveness, and lower cost compared with MRI and angiography. Whole-body blood scans are particularly useful for distinguishing venous malformations from lymphatic malformations because venous malformations show strong symmetric jugular vein uptake, whereas lymphatic malformations do not.14 More detailed care is needed when diagnosing masseteric venous malformations so as not to confound them with lipoma, pleomorphic adenoma or hemangioma, or lymphatic malformations of the salivary gland or cheek region because these all present as similar mass lesions and in the same area. None of these, including masseteric venous malformation, have characteristic skin lesions, such as a bluish hue. The differential diagnosis of venous malformations from other malformations is usually made by clinical history, physical examination, and imaging studies. Furthermore, it is important to make a differential diagnosis with parotid hemagiomas because these are the most common vascular malformation of the head and the neck in childhood. The differential diagnosis between masseteric venous malformations and pleomorphic adenomas of the parotid gland can be based on clinical examination and history. The onset of venous malformations occurs early in childhood, and the size of the lesion increases in proportion of the growth of the body, whereas the onset of pleomorphic adenoma occurs in adulthood. Hemangioma regresses spontaneously after 1 year of age. If patients feel pain and a palpable mass when clenching, lesions are usually intramasseteric masses rather than parotid gland masses. Masseteric venous malformations show changes in size with position, whereas lipoma, pleomorphic adenoma, and hemangioma do not. Magnetic resonance imaging is the most commonly used diagnostic tool to identify whether a mass is in the masseteric muscle or the parotid gland. Whole-body blood pool scintigraphy can be used as a definite diagnostic tool if MRI findings are unclear because only masseteric venous malformations show abnormal uptake. There are various management options available for venous malformations, and the selection of an approach is based on the involved structures and the extent of the lesion. Most cases of venous malformations involving subcutaneous tissue can be successfully managed conservatively with observation or compression. Lesions causing significant pain and/or functional compromise may be treated with sclerotherapy.8 Surgical debulking or removal may be considered, depending on the involved anatomic site and extent. Surgical treatment modalities are generally less effective and may cause complications when used to treat diffuse, large, and deep lesions. Sclerotherapy is a safer option than surgical intervention for
FIGURE 5. T2-weighted sequence MRI in the preoperative (left) and postoperative (right) periods. The lesion was completely removed, and there was no recurrence at the 20-month follow-up.
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
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certain malformations, and its success rates have been reported to be as high as 75%.8,15 Lesions that are ideal for sclerotherapy are known to be discrete, relatively superficial lesions with large vessels that are able to be punctured with a needle and that show potential for needle stabilization to prevent solution from leaking into surrounding tissues and a vessel volume and flow rate small enough to inhibit dilution of the agent.8,16 Although sclerotherapy is one of the useful modalities to treat masseteric venous malformation, it has a few shortcomings. Sclerotherapy may require multiple sessions under general anesthesia to achieve visible involution of the lesion in some cases. In addition, sclerotherapy yields less predictable results for intramuscular lesions than those in subcutaneous tissue because of their deep location and multiple intralesional thromboses, the disruption of which could have neurologic consequences. The results of treating intramuscular lesions with sclerotherapy are also less predictable than the results for lesions in subcutaneous tissues because injections are not as effective as in diffuse venous malformations. Therefore, as in the cases reviewed here, in which the lesion is well localized within a single muscle, we consider complete surgical excision as a treatment option. Although some clinicians emphasize the risks of surgical treatment of these lesions because of potentially severe complications such as facial nerve injury or massive bleeding, we were able to identify facial nerves by inspection and by using a nerve integrity monitor, which allowed for nerve preservation with minimal complications. We also recommend the application of compressive garments postoperatively to prevent postoperative hematoma and to limit swelling. A decision for surgical excision versus sclerotherapy should be made after predicting the consequences of each method. Although sclerotherapy does not require an extensive incision line or prolonged recovery period, it is usually not curative on a single procedure. In conclusion, we consider that surgical excisions can be one treatment option for venous malformations that are well localized within a single muscle group such as the masseter muscle. To minimize injury to the facial nerves, the operative field should be bloodless to allow for identification and dissection of the facial nerves. Masseteric venous malformations should thus be excised with a surrounding cuff of normal muscle so as to not rupture the venous lesions, and surgeons should pay particular attention to hemostasis of the cut edge of the muscle using bipolar electrocauterization. This study has some limitations. This study was retrospective, and the mean follow-up of 21 months is not enough to evaluate the recurrence of lesions. However, despite these shortcomings, we consider that our data support the advantages and the safety of surgical excision of masseteric venous malformation.
CONCLUSIONS Masseteric venous malformations have typical clinical and imaging characteristics that allow surgeons to distinguish them from other diseases. Complete surgical excision can be considered as a treatment option for these localized intramuscular lesions. Surgical excision can be performed without complications such as facial nerve injury or massive bleeding and can result in excellent outcomes.
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4. Demir Z, Oktem F, Celebioglu S. Rare case of intramasseteric cavernous hemangioma in a three-year-old boy: a diagnostic dilemma. Ann Otol Rhinol Laryngol 2004;113:455Y458 5. Lee SK, Kwon SY. Intramuscular cavernous hemangioma arising from masseter muscle: a diagnostic dilemma (2006: 12b). Eur Radiol 2007;17:854Y857 6. Smith WP, Prince S, Phelan S. The role of imaging and surgery in the management of vascular tumors of the masseter muscle. J Oral Maxillofac Surg 2005;63:1746Y1752 7. Wormald R, Donnelly M, Timon C. ‘Minor’ morbidity after parotid surgery via the modified Blair incision. J Plast Reconstr Aesthet Surg 2009;62:1008Y1011 8. Rosbe KW, Hess CP, Dowd CF, et al. Masseteric venous malformations: diagnosis, treatment, and outcomes. Otolaryngol Head Neck Surg 2010;143:779Y783 9. Perkins JA, Manning SC, Tempero RM, et al. Lymphatic malformations: review of current treatment. Otolaryngol Head Neck Surg 2010;142:795Y803, 803.e1 10. Perkins JA, Manning SC, Tempero RM, et al. Lymphatic malformations: current cellular and clinical investigations. Otolaryngol Head Neck Surg 2010;142:789Y794 11. Chang LC, Haggstrom AN, Drolet BA, et al. Growth characteristics of infantile hemangiomas: implications for management. Pediatrics 2008;122:360Y367 12. Kanaya H, Saito Y, Gama N, et al. Intramuscular hemangioma of masseter muscle with prominent formation of phleboliths: a case report. Auris Nasus Larynx 2008;35:587Y591 13. Dompmartin A, Acher A, Thibon P, et al. Association of localized intravascular coagulopathy with venous malformations. Arch Dermatol 2008;144:873Y877 14. Lee JY, Choi JY, Kim YH, et al. Characterization of congenital lymphatic and blood vascular malformations in the head and neck using blood pool scintigraphy and spect. Lymphology 2010;43:149Y157 15. Berenguer B, Burrows PE, Zurakowski D, et al. Sclerotherapy of craniofacial venous malformations: complications and results. Plast Reconstr Surg 1999;104:1Y11; discussion 12Y15 16. Deveikis JP. Percutaneous ethanol sclerotherapy for vascular malformations in the head and neck. Arch Facial Plast Surg 2005;7:322Y325
Severe Visual Loss and Cerebral Infarction After Injection of Hyaluronic Acid Gel Eung Gyu Kim, MD,* Tae Kyung Eom, MD,Þ Seok Joo Kang, MDÞ Abstract: We report a case of a 23-year-old man with cerebral infarction and permanent visual loss after injection of a hyaluronic acid gel filler for augmentation rhinoplasty. The patient was admitted to the hospital with complaints of loss of vision in the right eye, facial
From the Departments of *Neurology and †Plastic and Reconstructive Surgery, Baik Hospital, Inje University, Busan, Korea. Received October 23, 2013. Accepted for publication November 11, 2013. Address correspondence and reprint requests to Seok Joo Kang, MD, Department of Plastic and Reconstructive surgery, Busan Baik Hospital, Inje University School of Medicine, 75 Bokji-ro, Busan Jin-gu, Busan 614-735, Korea; E-mail: [email protected] The authors report no conflicts of interest. Copyright * 2014 by Mutaz B. Habal, MD ISSN: 1049-2275 DOI: 10.1097/SCS.0000000000000537
* 2014 Mutaz B. Habal, MD
Copyright © 2014 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
