Pleomorphic adenoma of the parotid: formal parotidectomy or limited surgery?

Pleomorphic adenoma of the parotid: formal parotidectomy or limited surgery?

The American Journal of Surgery (2013) 205, 109-118 Pleomorphic adenoma of the parotid: formal parotidectomy or limited surgery? Peter Zba¨ren, M.D.a...

4MB Sizes 0 Downloads 44 Views

The American Journal of Surgery (2013) 205, 109-118

Pleomorphic adenoma of the parotid: formal parotidectomy or limited surgery? Peter Zba¨ren, M.D.a,*, Vincent Vander Poorten, M.D., Ph.D.b, Robert L. Witt, M.D.c, Julia A. Woolgar, Ph.D.d, Ashok R. Shaha, M.D.e, Asterios Triantafyllou, Ph.D.d, Robert P. Takes, M.D., Ph.D.f, Alessandra Rinaldo, M.D.g, Alfio Ferlito, M.D., D.L.O., D.Path.g a

Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital, Freiburgstrasse, 3010 Bern, Switzerland; bDepartment of Otorhinolaryngology, Head and Neck Surgery and Leuven Cancer Institute, University Hospitals Leuven, Leuven, Belgium; cHead and Neck Multidisciplinary Clinic, Helen F. Graham Cancer Center, Christiana Care, Newark, DE, USA; dOral Pathology, University of Liverpool Dental Hospital, Liverpool, UK; eHead and Neck Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA; fDepartment of Otolaryngology, Head and Neck Surgery, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands; gENT Clinic, University of Udine, Udine, Italy

KEYWORDS: Parotid gland; Adenoma pleomorphic; Parotidectomy; Superficial parotidectomy; Limited surgery

Abstract BACKGROUND: Optimal surgery for pleomorphic adenoma of the parotid is controversial. In the present review, we discuss the advantages and disadvantages of the various approaches after addressing the surgical pathology of the parotid pleomorphic adenoma capsule and its influence on surgery. DATA SOURCES: PubMed literature searches were performed to identify original studies. CONCLUSIONS: Almost all pleomorphic adenomas can be effectively treated by formal parotidectomy, but the procedure is not mandatory. Extracapsular dissection is a minimal margin surgery; therefore, in the hands of a novice or occasional parotid surgeon, it may result in higher rates of recurrence. Partial superficial parotidectomy may be a good compromise. The tumor is removed with a greater cuff of healthy parotid tissue than in extracapsular dissection. This may minimize the recurrence rate. On the other hand, the removal of healthy parotid tissue compared with formal parotidectomy is limited, thus minimizing complications such as facial nerve dysfunction and Frey syndrome. Ó 2013 Elsevier Inc. All rights reserved.

This paper was written by members and invitees of the International Head and Neck Scientific Group (www.IHNSG.com). There were no relevant financial relationships or any sources of support in the form of grants, equipment, or drugs. The authors declare no conflicts of interest. * Corresponding author. Tel.: 141-031-632-2931; fax: 141-031-632-8809. E-mail address: [email protected] Manuscript received November 21, 2011; revised manuscript April 16, 2012 0002-9610/$ - see front matter Ó 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjsurg.2012.05.026

Pleomorphic adenoma (PA) is the most common neoplasm of the salivary glands, comprising 45% to 60% of all salivary gland tumors.1–3 The tumor tends to recur after inappropriate treatment and may develop malignancy. Approximately 80% of all PAs arise in the parotid gland2 where they are frequently located in the inferior pole of the superficial lobe and less often in the deep lobe or in accessory parotid tissue.4,5 PAs of the parotid are diagnosed

110 in every age group and tend to grow slowly over prolonged time periods. The mean age at the initial diagnosis is 46 to 51 years,6–8 and women are affected more often than men.2,9 The surgical treatment of parotid PA has been debated over the past 100 years, but controversy remains with some endorsing formal parotidectomy (superficial or total parotidectomy) and others favoring limited surgery (partial superficial parotidectomy or extracapsular dissection [ECD]). Total/superficial parotidectomy requires dissection of the full facial nerve. Whereas total parotidectomy removes the parotid tissue lateral and medial to the nerve, superficial parotidectomy removes the parotid tissue lateral to it. Partial superficial parotidectomy (PSP) dissects less than the full facial nerve; the tumor is removed with 2 cm of normal parotid tissue.10 In ECD, the facial nerve is not dissected at all; a 2- to 3-mm rim of healthy tissue is removed together with the tumor.11 In this review, we discuss the advantages and disadvantages of the various approaches after addressing the surgical pathology of the parotid PA capsule and its influence on surgery.

Surgical Pathology of the Parotid Pleomorphic Adenoma Capsule The capsule is 1 of the 3 structural components of PA. The other 2 are parenchyma (tumor epithelial cells) and stroma (Fig. 1). The parenchymal:stromal ratio varies, and parenchyma-rich and stroma-rich variants have been recognized.12,13 It is not established whether the capsule is newly formed or reflects pre-existing connective tissue compressed by the growing tumor. Morphologically, the capsule consists of variably thick, dense, fibrous tissue that may be discontinuous or absent or become invaded and even penetrated by a tumor (Figs. 2–5). Subcapsular accumulation of myxoid stroma is a common feature of parotid PA, but small collections of tumor cells often remain attached to the capsular undersurface therein (Fig. 6). The capsule may contain elastic fibers and incorporate adipocytes or

The American Journal of Surgery, Vol 205, No 1, January 2013 atrophic parotid elements that may be difficult to be distinguished from an invading tumor. Attempts have been made to correlate capsular features with the parenchymal:stromal ratio or the location of the tumor. The capsule is .015- to 1.75-mm thick. It is thicker in parenchyma-rich tumors than in stroma-rich tumors.14–16 Tumors located in the deep lobe have a thicker capsule than those in the superficial lobe.17 Half to two thirds of stromarich tumors show a variable/focal absence of the capsule.15,18 Tumors bulge or grow through capsular breaches to extend to adjacent parotid or soft tissues (Fig. 7). The phenomenon is easily appreciated when adipose tissue is nearby and accounts for the characteristic bosselated gross appearance of many PAs. Where the capsule is absent, tumor invades adjacent parotid or adipose tissue either as a broad advancing front or as small mammillations bulging out from the main mass. Appreciating capsular features in PA naturally leads to consideration of the so-called tumor satellites. On the histologic section examined, satellites are perceived as variably sized tumor nodules of a variable parenchymal:stromal ratio, which appear separated by normal glandular, fibrous, or adipose tissue from the variably encapsulated, main mass15,16,18–23 (Figs. 8–10). The distance between the latter and satellites varies. The growing of a tumor through capsular breaches and/or capsular invasion/penetration would account for most of the satellites, particularly those of small size and at short distances from the main mass (Fig. 8). Thus, satellites would correspond with section profiles of extracapsular tumor extension; continuity with the main mass is outside of the plane of that section. Along with various authorities, we support this view. Eneroth24 observed that 50% of presumed satellites were continuous with the main tumor on serial histologic sectioning. Very occasionally, large satellites at an increased distance from the main tumor may be seen. These may be alternatively attributed to the multifocal/multicentric origin of PAs. The notion of a multicentric PA has been criticized. Nevertheless, envisaging separately arising tumor nodules that may eventually merge via continuous growth could explain the marked

Figure 1 Structural components of variously bosselated PAs (Pa). T, tumor parenchyma; *, stroma; C, capsule. The capsule in A is thicker than in B. Pairs of arrowheads are used so that the difference in the capsular thickness is appreciated. Unless otherwise specified, the photomicrographs in this article are from sections of routinely processed tissue, which were stained with hematoxylin-eosin. It was not deemed necessary to give objective magnifications. Zooming on the electronic format of the photomicrographs would allow appreciation of the detail, which is difficult to see on prints.

P. Zba¨ren et al.

Pleomorphic adenoma of the parotid

Figure 2 A thin capsule (C) separates a stroma-rich tumor (T) from parotid lobules in the lower right. A collecting duct (arrow) has been incorporated within the capsule.

lobulation of some PAs (Fig. 11A). Such configuration also characterizes recurrent PAs (Fig. 11B), but a history of previous surgery would allow distinction. There has been considerable variation regarding the occurrence of tumor satellites in parotid PAs.18,25 Methodology, including serial histologic sectioning, and the mode of origin should be considered while assessing these data.

Historic Survey of Surgical Treatment of Pleomorphic Adenoma During the first half of the 20th century, parotid surgery was more concerned about damaging the facial nerve trunk/ branches than recurrence. Although publications do not often detail the technique,26,27 incision of the PA capsule and enucleation of the contents (intracapsular enucleation, Fig. 12A) were often practiced to avoid exposure of the nerve.28 Except for intracapsular enucleation, enucleation

Figure 3 A dense fibrous capsule (C) surrounds a parenchymarich tumor (T). An aggregate of packed lymphoid cells (asterisk) is associated with the capsule. Such aggregates are not uncommon in PA.

111

Figure 4 A nonencapsulated, stroma-rich tumor (T) extends to the adjacent parotid acini (A).

at the level of loose connective tissue situated between the tumor and adjacent parotid (extracapsular enucleation, Fig. 12B) or removal of the tumor together with a margin of surrounding salivary tissue (ECD, Fig. 12C) had been considered.29 Recurrence was high after intracapsular enucleation, and postoperative irradiation was given in an attempt to decrease it.29–33 The radioresistance of PAs was eventually appreciated, and removal of the tumor capsule (extracapsular enucleation) was advocated to decrease recurrence.28 In the early 1950s, Martin34 and, in the late 1950s, Patey and Thackray21 combined surgical and histologic observations to recommend the use of superficial parotidectomy for PAs of the superficial lobe21,34 on the grounds that tumor satellites may be missed during enucleation. This was widely endorsed, and even total parotidectomy has been advocated.35 In the ensuing decades, superficial or total parotidectomy was established as the standard treatment of parotid PA15,36–38 and affected a dramatic decrease in recurrence. However, undesired complications were experienced, and it was gradually appreciated that 50% to 60% of the tumors were in contact with 1 or more branches

Figure 5 A tumor of an equal parenchymal:stromal ratio (T) penetrates the thick capsule (C). Penetration is in the form of a spur-like projection (arrowhead). The linear segment corresponds to the thickness of the capsule. Compare with Figure 2.

112

The American Journal of Surgery, Vol 205, No 1, January 2013

Diagnosis of Pleomorphic Adenoma

Figure 6 The myxoid matrix (M) between the tumor (T) and the capsule (C). Note the tumor cells attached to the capsule (arrowheads). *Subcapsular splitting attributable to a retraction artifact.

of the facial nerve.39 In order to preserve the nerve, dissection at the interface between nerve branches and the tumor has to be minimal; hence, superficial or total parotidectomy virtually corresponded to extracapsular enucleation in regards to the tumor part lying on branches of the facial nerve. This would explain why 40% to 80% of parotid PAs in recent series are regarded as partially enucleated.14,18,40–42 Postoperative complications in conjunction with the appreciation that superficial or total parotidectomy partially corresponds to extracapsular enucleation led to rethinking.43–51 The original ECD was reappraised,29 whereas other authors suggested PSP.9,52–60 Recent results suggest that recurrence after ECD/PSP is not higher than those after superficial or total parotidectomy (see later). Nevertheless, many specialists remain convinced that superficial parotidectomy is the minimal surgery for PA.15,36,61,62

PA is a slowly growing, usually demarcated, and mobile tumor located in the superficial parotid lobe in 80% to 87% of cases.5,18 About 80% of PAs in the superficial lobe are localized in the parotid tail.9 At the time of surgery, the majority of PAs are smaller than 4 cm. In a series of 280 tumors, only 6% were larger than 4 cm.18 It is imprudent to attempt establishing a diagnosis of PA on clinical features alone because 50% to 70% of parotid carcinomas are asymptomatic, T1/T2 tumors that may appear demarcated.6,63 If superficial parotidectomy is accepted as the minimal surgery for a small, nodular tumor, it does not seem necessary to establish preoperatively whether it is malignant or benign. In this context, the value of fineneedle aspiration cytology (FNAC) can be questioned.64–66 However, the need for preoperatively establishing the benign or malignant nature of a small mobile tumor becomes obvious if more limited surgery (PSP/ECD) is to be considered. To achieve this, ultrasound (US) examination and FNAC, alone or in combination (US-guided FNAC), have been used. US morphology of various parotid tumors has been compared with histopathology.67 US alone may detect malignancy with 72% sensitivity and 86% specificity68 and PAs with 80% sensitivity, 86% specificity, and 84% accuracy.69,70 The reported criteria to consider a malignant lesion were irregular shape, ill-defined and irregular margins, and inhomogeneous internal structure.69 Although FNAC aims at a preoperative diagnosis of malignancy so that inadequate limited surgery is avoided, it often fails to type primary salivary carcinomas.71–73 Regarding benign tumors, FNAC can support the use of limited surgery, whereas in the case of inflammatory processes it helps in avoiding unnecessary surgery.71 A number of studies reported 86% to 93% sensitivity, 92% to 100% specificity, and 90% to 98% accuracy of FNAC in detecting parotid malignancy.74–77 False-negative diagnosis seems to be the drawback of FNAC. In 2 series of 169 and 228 parotid tumors preoperatively assessed by FNAC, 78 and 97 were, respectively, diagnosed as PAs. Three of the 78 (4%) and 7 of the 97 (7%) cases were postoperatively proven by histopathology to be primary parotid carcinomas (ie, false-negative).78,79 Carcinomas ex-PA (Cas ex PA) are especially liable to false-negative diagnosis by FNAC.80–82 This is attributable to sampling errors, but US-guided FNAC is being increasingly used to decrease it. Regarding the diagnosis of PAs by FNAC, 97% sensitivity and 98% specificity have been reported.83 In experienced hands, available diagnostic procedures often allow accurate preoperative detection of malignancy and thus ensure their adequate surgical treatment.

Recurrence Figure 7 Fungiform growth of a tumor (T) through a gap in the continuity of the capsule (C). The gap is indicated by arrowheads. Although most of the tumor appears stroma rich, parenchyma-rich areas (arrows) are subadjacent to the capsule.

A recurrent parotid PA is almost always multifocal (Fig. 11B). Multiple tumor nodules are increasingly found with each episode of recurrence.6,19,84–88 Their distribution

P. Zba¨ren et al.

Pleomorphic adenoma of the parotid

113

Figure 8 (A), (B), and (C) show stroma-rich satellite nodules (arrowheads) at variable distances from the nonencapsulated stroma-rich main tumor (T). The nodules are separated from the latter by fat (F) or a mixture of fat and parotid acini (A). The arrow indicates a collection of acini being incorporated within the advancing tumor.

is often widespread. Hypotheses to explain recurrence include a multicentric origin of the tumor, capsular features, accidental tumor rupture, and surgical procedure. During the first half of the 20th century, a multicentric origin had been the favored explanation.89,90 The hypothesis was questioned by Foote and Frazell,23 who examined 447 PAs and could not confirm a single case of initial multicentricity. As noted previously, initial multicentricity in PA appears to be a rare phenomenon,91 and Batsakis92 could find only a single possible example out of 240 cases. It has already been mentioned that a high percentage of PAs, particularly stroma-rich tumors, show focal absence of the capsule and the formation of satellite nodules. During enucleation, the nodules may escape unnoticed and be left behind.14,15,18,93,94 The significance of accidental capsule rupture may have been overestimated. Certainly, in the 1930s when parotid PA was usually treated by intracapsular enucleation, recurrence was 22% to 43%.26,27,95 However, recent studies suggest that differences in recurrence between patients with or without intraoperative capsular rupture (7% to 8% vs 2.5% to 4%, respectively) are not statistically significant.20,96 Other authors suggested that microscopically positive margins are associated with an increased recurrence, whereas intraoperative tumor spillage is not.58,97 Nevertheless, spillage occasionally accounts for tumor implantation.98

Figure 9 Both the satellite nodule (arrowhead) and the main tumor (T) show an equal parenchymal:stromal ratio. The nodule is partly surrounded by thin-walled vessels (V) and separated from the nonencapsulated main tumor by fatty lobules.

A significant factor is the surgical procedure.48,99 Even before the era of endorsing formal parotidectomy, recurrence rates of less than 10% were reported, but in these series PAs were apparently not removed by enucleation but rather by operative, surgical, or local excision.3,23,100,101 Witt10 surveyed the literature to record recurrence in relation to the extent of surgery. While comparing recurrence rates of different surgical procedures, a selection bias should be considered. Patients undergoing limited surgical procedures (PSP or ECD) may present with more accessible mobile and circumscribed tumors probably less prone to recurrence than patients undergoing formal parotidectomy. For instance, Klintworth et al11 performed ECD in only 40% of patients with benign parotid tumors. Recurrence amounted to 1.8% after total parotidectomy (9 analyzed articles, 828 PAs), 2.6% after lateral parotidectomy (23 articles, 2,366 PAs), .3% after PSP (5 artiles, 340 PAs), and 2.6% after ECD (11 articles, 1,113 PAs). Only after enucleation (intracapsular/extracapsular) was the recurrence high (25%) (14 articles, 797 PAs). It is noted that recurrence after PSP/ECD was not, as might have been expected, higher than after superficial/total parotidectomy.10 More recent studies confirmed low recurrence rates after PSP and ECD.43,53,102,103 However, the mean follow-up in the series with ECD was 194, 61, and ,60 months, respectively.43,102,103 In a further recent literature survey by Witt

Figure 10 A parenchyma-rich satellite nodule (arrowhead). Adjacent main tumor (T) is stroma-rich and partly surrounded by capsule (C).

114

The American Journal of Surgery, Vol 205, No 1, January 2013

Figure 11 (A) A markedly lobulated PA of the parotid. Compare with Figure 1 and with recurrent PA. (B) Although most of the recurrent tumor consists of variously confluent stroma-rich nodules (asterisk), 1 nodule is parenchyma rich (arrow).

and Rejto,104 the recurrence rates of ECD and PSP were compared. Recurrence occurred in 36 of 1,183 (3%) ECD cases and in 1 of 340 PSP (.3%) cases (P , .05).104 The recurrence rate was lower after PSP than after ECD. The widespread distribution of recurrent tumor nodules precludes radical surgery. This increases the risk of further recurrence and permanent facial nerve paralysis (see later). Estimated rates are 21% to 31% and 15% to 31%, respectively.6,8,85,87,88,105,106 The chance of a second recurrence after 1, 2, 5, 10, and 15 years was estimated at 16%, 23 %, 42%, 60%, and 75%, respectively.107 Therefore, adequate initial treatment of PAs is mandatory to minimize recurrence.

Carcinoma ex Pleomorphic Adenoma In Ca ex PA, epithelial malignancy develops in association with a primary PA or at the site of a previous one.108

Figure 12 dissection.

The proportion of benign versus malignant components can be quite variable; therefore, the preoperative diagnosis of a Ca ex PA may be difficult.80 Approximately 50% can be identified by FNAC.80,82 Information on pathogenesis is elusive. The tumor may be malignant from the onset or when carcinomatous transformation occurs.109 Investigation of molecular events may be enlightening, but such events are outside the scope of this review. Ca ex PA comprises 5% to 25% of primary parotid carcinomas.1,63,108,110–113 Based on a series of 623 tumors, Eneroth et al114 showed a positive relationship between preoperative duration and the risk of developing Cas ex PA. While only 1.6% of tumors present for 0 to 4 years developed carcinoma, the percentage rose to 2.4% in tumors lasting 5 to 9 years, 5.9% in tumors lasting 10 to 14 years, and 9.4% in tumors older than 15 years.114 Thackray and Lucas115 estimated that 25% of parotid PAs may undergo malignant transformation if left untreated. Regarding recurrent PAs, the rate of

Diagrammatic representations outlining (A) intracapsular enucleation, (B) extracapsular enucleation, and (C) extracapsular

P. Zba¨ren et al.

Pleomorphic adenoma of the parotid

carcinoma ranges from 7% to 16%.8,85,88,116–118 The increased development of carcinoma in recurrent PAs is another reason why surgery should be ab initio optimized.

Complications of Parotid Surgery Again, while comparing recurrence or complication rates of different surgical procedures, the selection bias should be considered that patients undergoing more limited surgical procedures may present with more accessible mobile and circumscribed tumors than patients undergoing formal parotidectomies. The main complication is facial nerve dysfunction because facial nerve paralysis compromises quality of life (QOL).119 Although 11% to 65% of patients experience temporary facial nerve dysfunction after superficial or total parotidectomy, permanent paralysis is seen in 0% to 19%.37,56,120–124 Various studies showed a positive relationship between the extent of parotid surgery and postoperative facial nerve function. Temporary facial nerve paralysis occurred in 38.4% of total parotidectomies and 25.6% of superficial parotidectomies but only in 5.9% of PSPs. Permanent facial nerve dysfunction followed 3.1% of total parotidectomies and .7% of superficial parotidectomies but did not occur after PSP.120 With ECD, temporary facial nerve paralysis followed in 3% to 12% and permanent dysfunction in 0% to 2.12%.10,11,104 In summary, the risk of temporary/ permanent facial nerve paralysis is lower after PSP/ECD than after superficial/total parotidectomy.11,120 Another complication is Frey syndrome/gustatory sweating. Clinically manifested Frey syndrome was seen in 18% and 43% of retrospectively and prospectively analyzed groups, respectively; the starch-iodine test was positive in all patients of both groups.125 After superficial and total parotidectomy, the syndrome is seen in 2% to 40% of patients but in only 0% to 5% after ECD48,50,120,126; hence, it is positively related to the extent of parotid surgery. Surgical procedures to avoid Frey syndrome after superficial or total parotidectomy have been proposed.127–131 A further unwanted sequela of superficial or total parotidectomy is a sensory deficit in the area of the great auricular nerve (skin overlying the parotid gland and the mastoid, the posteroinferior surface of the auricle, the ear lobule, and the concha).132 If the nerve is sacrificed during the procedures, almost all patients exhibit the symptom. The deficit does not markedly affect QOL,119,132,133 and preservation of the posterior branch of the great auricular nerve appears to diminish the deficit and improve recovery chances.53,58,132,134–138 Patients treated by PSP often present with a sensory deficit.53 It is less often observed after ECD because this procedure preserves most branches of the great auricular nerve.11,45 A prospective randomized study recorded a lower occurrence of facial nerve paralysis, Frey syndrome, and auricular dysesthesia after limited partial parotidectomy than after superficial or total parotidectomy; some of the differences were statistically significant.139 A recent prospective study

115 using the core quality of life questionnaire (QLQ-C30) in conjunction with the Head and Neck cancer-specific questionnaire module (QLQ-H&N35) of the European Organization for Research and Treatement of Cancer (EORTC) evaluating the global QOL indicated that it is not negatively affected by superficial parotidectomy.140

Summation of Advantages/Disadvantages of Formal Parotidectomy For several decades, superficial and total parotidectomy was successfully used to treat PAs, with an average recurrence rate below 2%. Because the majority of benign salivary gland tumors are located in the superficial lobe of the parotid, surgeons in training have the opportunity to practice straightforward, superficial parotidectomy therein and acquire skills that will enable them to deal with more challenging approaches. Technical advances, such as facial nerve monitoring and microscope-guided surgery, may contribute to the decrease in the risk of permanent facial nerve paralysis. On the other hand, many PAs contact branches of the facial nerve and should be dissected along the capsule to preserve these branches; thus, the surgeon focally performs extracapsular enucleation. After formal parotidectomy, comparatively many patients develop Frey syndrome and auricular dysesthesia, tissue defects may lead to cosmetic problems, and QOL may be affected. In the event of recurrence after formal parotidectomy, the risks of further recurrence and facial nerve paralysis are increased. Given the multifocal nature of recurrent PAs, radicality of surgery is difficult to achieve, furthermore the facial nerve trunk/branches become embedded in scar tissue because of exposure during the first operation.

Summation of Advantages/Disadvantages of More Limited Surgery Recurrence after PSP or ECD is not higher than that after formal parotidectomy in carefully selected patients with experienced surgeons. PAs located in the tail of the parotid are easily accessed by limited surgery. The risk of permanent facial nerve paralysis, Frey syndrome, or cosmetic problems is low for both PSP and ECD. Facial nerve trunk/branches are not (ECD) or only partly (PSP) embedded in scar tissue, which decreases the risk of permanent paralysis after surgery for recurrence. Limited approaches are more technically demanding and the prerogative of experienced surgeons. The preoperative use of US/FNAC is mandatory to avoid inappropriate limited surgery for malignant neoplasms.

Conclusions Both formal parotidectomy and more limited surgery serve a legitimate purpose, and their domains do not overlap.

116 Almost all PAs can be effectively treated by formal parotidectomy, but the procedure is not mandatory. Small, mobile PAs located in the superficial lobe/tail of the parotid gland can be removed by limited surgery with few complications. The preoperative use of US/FNAC decreases the risk of applying limited surgery to remove a malignant neoplasm. In the first half of the 20th century, surgeons were concerned about injuring the facial nerve. Therefore, they operated only on or within the PA capsule. As a consequence, recurrence was high and up to 45%. Based on cumulative experience and technical advances, contemporary parotid and facial nerve surgeons are conscious of the technical demands of limited surgery and are not inhibited by unwarranted fear of the facial nerve branching, thus preventing the quality of PA treatment from declining to the level of the first half of the 20th century. ECD is a minimal margin surgery. Therefore, in the hands of a novice or occasional parotid surgeon, it may result in higher rates of recurrence. PSP may be a good compromise. On the one hand, surgeons in training have the opportunity to acquire skills of standard parotid surgery (facial nerve dissection), and the tumor is removed with a greater cuff of healthy parotid tissue than in ECD. This may minimize the recurrence rate. On the other hand, the removal of healthy parotid tissue compared with formal parotidectomy is limited, thus minimizing complications such as facial nerve dysfunction and Frey syndrome. A multicenter prospective randomized study may be helpful in deciding the optimal treatment of PAs; however, conducting such a study may be difficult.

References 1. Spiro RH. Salivary neoplasms: overview of a 35-year experience with 2,807 patients. Head Neck Surg 1986;8:177–84. 2. Eveson JW, Cawson RA. Salivary gland tumours. A review of 2410 cases with particular reference to histological types, site, age and sex distribution. J Pathol 1985;146:51–8. 3. Woods JE, Chong GC, Beahrs OH. Experience with 1360 primary parotid tumors. Am J Surg 1975;130:460–2. 4. Lin DT, Coppit GL, Burkey BB, et al. Tumors of the accessory lobe of the parotid gland: a 10-year experience. Laryngoscope 2004;114:1652–5. 5. Batsakis JG. Deep-lobe parotid gland tumors. Ann Otol Rhinol Laryngol 1984;93:415–6. 6. Renehan A, Gleave EN, McGurk M. An analysis of the treatment of 114 patients with recurrent pleomorphic adenomas of the parotid gland. Am J Surg 1996;172:710–4. 7. McGregor AD, Burgoyne M, Tan KC. Recurrent pleomorphic salivary adenoma-the relevance of age at first presentation. Br J Plast Surg 1988;41:177–81. 8. Maran AG, Mackenzie IJ, Stanley RE. Recurrent pleomorphic adenomas of the parotid gland. Arch Otolaryngol 1984;110:167–71. 9. Yamashita T, Tomoda K, Kumazawa T. The usefulness of partial parotidectomy for benign parotid gland tumors. A retrospective study of 306 cases. Acta Otolaryngol Suppl 1993;500:113–6. 10. Witt RL. The significance of the margin in parotid surgery for pleomorphic adenoma. Laryngoscope 2002;112:2141–54. 11. Klintworth N, Zenk J, Koch M, et al. Postoperative complications after extracapsular dissection of benign parotid lesions with particular reference to facial nerve function. Laryngoscope 2010;120:484–90. 12. Ellis G, Auclair P. Tumors of the Salivary Glands. In: Atlas of Tumor Pathology, third series, fasciale 17. Washington DC: Armed Forces Institute of Pathology; 1995. p. 39–153.

The American Journal of Surgery, Vol 205, No 1, January 2013 13. Seifert G, Brocheriou C, Cardesa A, et al. WHO International Histological Classification of Tumours. Tentative histological classification of salivary gland tumours. Pathol Res Pract 1990;186:555–81. 14. Webb AJ, Eveson JW. Pleomorphic adenomas of the major salivary glands: a study of the capsular form in relation to surgical management. Clin Otolaryngol 2001;26:134–42. 15. Stennert E, Guntinas-Lichius O, Klussmann JP, et al. Histopathology of pleomorphic adenoma in the parotid gland: a prospective unselected series of 100 cases. Laryngoscope 2001;111:2195–200. 16. Naeim F, Forsberg MI, Waisman J, et al. Mixed tumors of the salivary glands. Arch Pathol Lab Med 1976;100:271–5. 17. Fliss DM, Rival R, Gullane P, et al. Pleomorphic adenoma: a preliminary histopathologic comparison between tumors occurring in the deep and superficial lobes of the parotid gland. Ear Nose Throat J 1992;71:254–7. 18. Zba¨ren P, Stauffer E. Pleomorphic adenoma of the parotid gland: histopathologic analysis of the capsular characteristics of 218 tumors. Head Neck 2007;29:751–7. 19. Stennert E, Wittekindt C, Klussmann JP, et al. Recurrent pleomorphic adenoma of the parotid gland: a prospective histopathological and immunohistochemical study. Laryngoscope 2004;114:158–63. 20. Henriksson G, Westrin KM, Cartso¨o¨ B, et al. Recurrent primary pleomorphic adenoma of salivary gland origin intrasurgical rupture, histopathologic features, and pseudopodia. Cancer 1998;82:617–20. 21. Patey DH, Thackray AC. The treatment of parotid tumours in the light of a pathological study of parotidectomy material. Br J Surg 1958;55:477–87. 22. Kuhn AJ, Devine KD, ReMine WH. Multiple benign mixed tumors. Proc Staff Meet Mayo Clin 1956;31:544–51. 23. Foote FW Jr, Frazell EL. Tumors of the major salivary glands. Cancer 1953;6:1065–133. 24. Eneroth CM. Histological and clinical aspects of parotid tumours. Acta Otolaryngol Suppl 1964;191:1–99. 25. Orita Y, Hamaya K, Miki K, et al. Satellite tumors surrounding primary pleomorphic adenomas of the parotid gland. Eur Arch Otorhinolaryngol 2010;267:801–6. 26. McFarland J. Three hundred mixed tumors of the salivary gland, of which sixty-nine recurred. Surg Gynecol Obstet 1936;63:457–69. 27. Bendedict EB, Meigs JV. Tumors of the parotid gland. Surg Gynec Obstet 1930;51:626–47. 28. Bailey H. The treatment of tumours of the parotid gland with special reference to total parotidectomy. Br J Surg 1941;28:337–46. 29. Patey DH. The treatment of mixed tumours of the parotid gland. Br J Surg 1940;28:29–38. 30. McEvedy BV, Ross WM. The treatment of mixed parotid tumours by enucleation and radiotherapy. Br J Surg 1976;63:341–2. 31. Van Miert PJ, Dawes JDK, Harkness DG. The treatment of mixed parotid tumours. A report of 183 cases. J Laryngol Otol 1968;82: 459–68. 32. Smiddy FG. Treatment of mixed parotid tumours. Br Med J 1956;11: 322–5. 33. McFarland J. Treatment of mixed tumors of salivary glands by roentgen rays and radium. AJR Am J Roentgenol 1941;46:506–17. 34. Martin H. The operative removal of the parotid salivary gland. Surgery 1952;31:670–82. 35. Klopp CT, Winship T. Treatment of mixed tumors of the parotid gland by subtotal parotidectomy. Arch Surg 1950;61:477–86. 36. Arshad AR. Benign parotid lesions: is near total parotidectomy justified? Ann Acad Med Singapore 2006;35:889–91. 37. Laccourreye H, Laccourreye O, Cauchois R, et al. Total conservative parotidectomy for primary benign pleomorphic adenoma of the parotid gland: a 25-year experience with 229 patients. Laryngoscope 1994;104:1487–94. 38. Beahrs OH, Woolner LB, Carveth SW, et al. Surgical management of parotid lesions. Review of seven hundred sixty cases. Arch Surg 1960;80:890–904. 39. Donovan DT, Conley JJ. Capsular significance in parotid tumor surgery: reality and myths of lateral lobectomy. Laryngoscope 1984;94:324–9.

P. Zba¨ren et al.

Pleomorphic adenoma of the parotid

40. Ghosh S, Panarese A, Bull PD, et al. Marginally excised parotid pleomorphic salivary adenomas: risk factors for recurrence and management. A 12.5-year mean follow-up study of histologically marginal excisions. Clin Otolaryngol 2003;28:262–6. 41. Bron LP, O’Brien CJ. Facial nerve function after parotidectomy. Arch Otolaryngol Head Neck Surg 1997;123:1091–6. 42. Dallera P, Marchetti C, Campobassi A. Local capsular dissection of protid pleomorphic adenomas. Int J Oral Maxillofac Surg 1993;22: 154–7. 43. Fukushima M, Miyaguchi M, Kitahara T. Extracapsular dissection: minimally invasive surgery aplied to patients with parotid pleomorphic adenoma. Acta Otolaryngol 2011;131:653–9. 44. George KS, McGurk M. Extracapsular dissection-minimal resection for benign parotid tumours. Br J Oral Maxillofac Surg 2011;49:451–4. 45. Smith SL, Komisar A. Limited parotidectomy: the role of extracapsular dissection in parotid gland neoplasms. Laryngoscope 2007;117:1163–7. 46. Piekarski J, Nejc D, Szymczak W, et al. Results of extracapsular dissection of pleomorphic adenoma of parotid gland. J Oral Maxillofac Surg 2004;62:1198–202. 47. McGurk M, Thomas BL, Renehan AG. Extracapsular dissection for clinically benign parotid lumps: reduced morbidity without oncological compromise. Br J Cancer 2003;89:1610–3. 48. Hancock BD. Clinically benign parotid tumours: local dissection as an alternative to superficial parotidectomy in selected cases. Ann R Coll Surg Engl 1999;81:299–301. 49. Iizuka K, Ishikawa K. Surgical techniques for benign parotid tumors: segmental resection vs extracapsular lumpectomy. Acta Otolaryngol Suppl 1998;537:75–81. 50. McGurk M, Renehan A, Gleave EN, et al. Clinical significance of the tumour capsule in the treatment of parotid pleomorphic adenomas. Br J Surg 1996;83:1747–9. 51. Gleave EN, Whittaker JS, Nicholson A. Salivary tumoursdexperience over thirty years. Clin Otolaryngol 1979;4:247–57. 52. Johnson JT, Ferlito A, Fagan JJ, et al. Role of limited parotidectomy in management of pleomorphic adenoma. J Laryngol Otol 2007;121: 1126–8. 53. Witt RL. Minimally invasive surgery for parotid pleomorphic adenoma. Ear Nose Throat J 2005;84:308–11. 54. O’Brien CJ. Current management of benign parotid tumorsdthe role of limited superficial parotidectomy. Head Neck 2003;25:946–52. 55. Rea JL. Partial parotidectomies: morbidity and benign tumor recurrence rates in a series of 94 cases. Laryngoscope 2000;110:924–7. 56. Witt RL. Facial nerve function after partial superficial parotidectomy: an 11-year review (1987-1997). Otolaryngol Head Neck Surg 1999; 121:210–3. 57. Helmus C. Subtotal parotidectomy: a 10-year review (1985 to 1994). Laryngoscope 1997;107:1024–7. 58. Leverstein H, van der Wal JE, Tiwari RM, et al. Surgical management of 246 previously untreated pleomorphic adenomas of the partotid gland. Br J Surg 1997;84:399–403. 59. Maynard JD. Management of pleomorphic adenoma. Br J Surg 1988; 75:305–8. 60. Hugo NE, McKinney P, Griffith BH. Management of tumors of the parotid gland. Surg Clin North Am 1973;51:105–11. 61. Guntinas-Lichius O, Kick C, Klussmann JP, et al. Pleomorphic adenoma of the parotid gland: a 13-year experience of consequent management by lateral or total parotidectomy. Eur Arch Otorhinolaryngol 2004;261:143–6. 62. Valentini V, Fabiani F, Perugini M, et al. Surgical techniques in the treatment of pleomorphic adenoma of the parotid gland: our experience and review of literature. J Craniofac Surg 2001;12:565–8. 63. Zba¨ren P, Schu¨pbach J, Nuyens M, et al. Carcinoma of the parotid gland. Am J Surg 2003;186:57–62. 64. Fee WE Jr, Tran LE. Evaluation of a patient with a parotid tumor. Arch Otolaryngol Head Neck Surg 2003;129:937–8. 65. Batsakis JG, Sneige N, El-Naggar AK. Fine-needle aspiration of salivary glands: its utility and tissue effects. Ann Otol Rhinol Laryngol 1992;101:185–8.

117 66. Olsen KD. The parotid lumpddon’t biopsy it! An approach to avoiding misadventure. Postgrad Med 1987;81:225–9. 232–4. 67. Shimizu M, Ussmu¨ller J, Hartwein J, et al. A comparative study of sonographic and histopathologic findings of tumorous lesions in the parotid gland. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;88:723–7. 68. Schick S, Steiner E, Gahleitner A, et al. Differentiation of benign and malignant tumors of the parotid gland: value of pulsed doppler and color doppler sonography. Eur Radiol 1998;8:1462–7. 69. Bialek EJ, Jakubowski W, Karpinska G. Role of ultrasonography in diagnosis and differentiation of pleomorphic adenomas. Arch Otolaryngol Head Neck Surg 2003;129:929–33. 70. Bozzato A, Zenk J, Greess H, et al. Potential of ultrasound diagnosis for parotid tumors: analysis of qualitative and quantitative parameters. Otolaryngol Head Neck Surg 2007;137:642–6. 71. Salgarelli AC, Cappare` P, Bellini P, et al. Usefulness of fine-needle aspiration in parotid diagnostics. Oral Maxillofac Surg 2009;13: 185–90. 72. Alphs HH, Eisele DW, Westra WH. The role of fine needle aspiration in the evaluation of parotid masses. Curr Opin Otolaryngol Head Neck Surg 2006;14:62–6. 73. Zba¨ren P, Nuyens M, Loosli H, et al. Diagnostic accuracy of fineneedle aspiration cytology and frozen section in primary parotid carcinoma. Cancer 2004;100:1876–83. 74. Seethala RR, LiVolsi VA, Baloch ZW. Relative accuracy of fineneedle aspiration and frozen section in the diagnosis of lesions of the parotid gland. Head Neck 2005;27:217–23. 75. Postema RJ, van Velthuysen MLF, van den Brekel MWM, et al. Accuracy of fine-needle aspiration cytology of salivary gland lesions in the netherlands cancer institute. Head Neck 2004;26:418–24. 76. Stewart CJR, MacKenzie K, McGarry GW, et al. Fine-needle aspiration cytology of salivary gland: a review of 341 cases. Diagn Cytopathol 2000;22:139–46. 77. Schro¨der U, Eckel HE, Rasche V, et al. The value of fine needle aspiration biopsy in neoplasms of the parotid gland. HNO 2000;48:421–9. 78. Que Hee CG, Perry CF. Fine-needle aspiration cytology of parotid tumours: is it useful? ANZ J Surg 2001;71:345–8. 79. Zba¨ren P, Scha¨r C, Hotz MA, et al. Value of fine-needle aspiration cytology of parotid gland masses. Laryngoscope 2001;111:1989–92. 80. Zba¨ren P, Zba¨ren S, Caversaccio MD, et al. Carcinoma ex pleomorphic adenoma: diagnostic difficulty and outcome. Otolaryngol Head Neck Surg 2008;138:601–5. 81. Nouraei SAR, Hope KL, Kelly CG, et al. Carcinoma ex benign pleomorphic adenoma of the parotid gland. Plast Reconstr Surg 2005; 116:1206–13. 82. Klijanienko J, El-Naggar AK, Vielh P. Fine-needle sampling findings in 26 carcinoma ex pleomorphic adenomas: diagnostic pitfalls and clinical considerations. Diang Cytopathol 1999;21:163–6. 83. Carrilo JF, Ramirez R, Flores L, et al. Diagnostic accuracy of fine needle-aspiration biopsy in preoperative diagnosis of patients with parotid gland masses. J Surg Oncol 2009;100:133–8. 84. Papadogeorgakis N, Kalfarentzos EF, Petsinis V, et al. Multinodular neck recurrence of parotid gland pleomorphic adenoma: a case report. Oral Maxillofac Surg 2012;16:137–40. 85. Zba¨ren P, Tschumi I, Nuyens M, et al. Recurrent pleomorphic adenoma of the parotid gland. Am J Surg 2005;189:2003–7. 86. Leonetti JP, Marzo SJ, Petruzzelli GJ, et al. Recurrent pleomorphic adenoma of the parotid gland. Otolaryngol Head Neck Surg 2005; 133:319–22. 87. Maxwell EL, Hall FT, Freeman JL. Recurrent pleomorphic adenoma of the parotid gland. J Otolaryngol 2004;33:181–4. 88. Philips PP, Olsen KD. Recurrent pleomorphic adenoma of the parotid gland: report of 126 cases and a review of the literature. Ann Otol Rhinol Laryngol 1995;104:100–4. 89. Delarue J. Les tumeurs mixtes plurifocales de la glande parotide. Ann Anat Path 1956;1:34–58. 90. McFarland J. The histopathologic prognosis of salivary gland mixed tumors. Am J Med Sci 1942;203:502–19.

118 91. Krolls SO, Boyers RC. Mixed tumors of salivary glands. Long-term follow-up. Cancer 1972;30:276–81. 92. Batsakis JG. Quality assurance. Sisyphean or sibylline? Arch Pathol Lab Med 1990;114:1173–4. 93. Conley J, Clairmont AA. Facial nerve in recurrent benign pleomorphic adenoma. Arch Otolaryngol 1979;105:247–51. 94. Clairmont AA, Richardson GS, Hanna DC. The pseudocapsule of pleomorphic adenomas (benign mixed tumors): the argument against enucleation. Am J Surg 1977;134:242–3. 95. Stein I, Geschickter CF. Tumors of the parotid gland. Arch Surg 1934;28:492–526. 96. Natvig K, Soberg R. Relationship of intraoperative rupture of pleomorphic adenomas to recurrence an 11-25 year follow-up study. Head Neck 1994;16:213–7. 97. Buchman C, Stringer SP, Mendenhall WM, et al. Pleomorphic adenoma: effect of tumor spill and inadequate resection on tumor recurrence. Laryngoscope 1994;104:1231–4. 98. Ferlito A, Baldan M, Andretta M, et al. Implantation of parotid pleomorphic adenoma in the upper neck. ORL J Otorhinolaryngol Relat Spec 1991;53:165–76. 99. Bradley PJ. Pleomorphic salivary adenoma of the parotid gland: which operation to perform? Curr Opin Otolaryngol Head Neck Surg 2004;12:69–70. 100. Buxton RW, Maxwell JH, French AJ. Surgical treatment of epithelial tumors of the parotid gland. Surg Gynecol Obstet 1953;97:401–16. 101. Houck JW. Tumors of the salivary glands. Surgery 1939;6:565–84. 102. Uyar Y, Caglak F, Keles B, et al. Extracapsular dissection versus superficial parotidectomy in pleomorphic adenomas of the parotid gland. Kulak Burun Bogaz Ihtis Derg 2011;21:76–9. 103. Shehata EA. Extra-capsular dissection for benign parotid tumours. Int J Oral Maxillofac Surg 2010;39:140–4. 104. Witt RL, Rejto L. Pleomorphic adenoma: extracapsular dissection versus partial superficial parotidectomy with facial nerve dissection. Del Med J 2009;81:119–25. 105. Yugueros P, Goellner JR, Petty PM, et al. Treating recurrence of parotid benign pleomorphic adenomas. Ann Plast Surg 1998;40:573–6. 106. O’Dwyer PJ, Farrar WB, Finkelmeier WR, et al. Facial nerve sacrifice and tumor recurrence in primary and recurrent benign parotid tumors. Am J Surg 1986;152:442–5. 107. Wittekindt C, Streubel K, Arnold G, et al. Recurrent pleomorphic adenoma of the parotid gland: analysis of 108 consecutive patients. Head Neck 2007;29:822–8. 108. Ellis GL, Auclair PL. Malignant epithelial tumors. In: Atlas of Tumor Pathology, 3rd Series, Fascicle 17. Washington DC: Armed Forces Institute of Pathology; 1996. p. 155–373. 109. Olsen KD, Levis JE. Carcinoma ex pleomorphic adenoma: a clinicopathologic review. Head Neck 2001;23:705–12. 110. Antony J, Gopalan V, Smith RA, et al. Carcinoma ex pleomorphic adenoma: a comprehensive review of clinical, pathological and molecular data. Head Neck Pathol 2012;6:1–9. 111. Malata CM, Camilleri IG, McLean NR, et al. Malignant tumours of the parotid gland: a 12-year review. Br J Plast Surg 1997;50:600–8. 112. Gnepp DR. Malignant mixed tumors of the salivary glands: a review. Pathol Annu 1993;1:279–328. 113. Frankenthaler RA, Luna MA, Lee SS, et al. Prognostic variables in parotid gland cancer. Arch Otolaryngol Head Neck Surg 1991;117:1251–6. 114. Eneroth CM, Zetterberg A. Malignancy in pleomorphic adenoma. A clinical and microspectrophotometric study. Acta Otolaryngol 1994;77:426–32. 115. Thackray AC, Lucas RB. Tumors of the major salivary glands. In: Atlas of Tumor Pathology, 2nd Series, Fascicle 10. Washington DC: Armed forces Institute of Pathology; 1983. p. 107–17. 116. Jackson SR, Roland NJ, Clarke RW, et al. Recurrent pleomorphic adenoma. J Laryngol Otol 1993;107:546–9. 117. Niparko JK, Beauchamp ML, Krause CJ, et al. Surgical treatment of recurrent pleomorphic adenoma of the parotid gland. Arch Otolaryngol Head Neck Surg 1986;112:1180–4.

The American Journal of Surgery, Vol 205, No 1, January 2013 118. Mann W, Beck C, Karatay MC. Recurrent benign tumors of the parotid gland and their tendency for becoming malignant. Laryngol Rhinol Otol 1985;64:133–5. 119. Nitzan D, Kronenberg J, Horowitz Z, et al. Quality of life following parotidectomy for malignant and benign disease. Plast Reconstr Surg 2004;114:1060–7. 120. Koch M, Zenk J, Iro H. Long-term results of morbidity after parotid gland surgery in benign disease. Laryngoscope 2010;120:724–30. 121. Guntinas-Lichius O, Klussmann JP, Wittekindt C, et al. Parotidectomy for benign parotid disease at a university teaching hospital: outcome of 963 operations. Laryngoscope 2006;116:534–40. 122. Gaillard C, Pe´rie´ S, Susini B, et al. Facial nerve dysfunction after parotidectomy: the role of local factors. Laryngoscope 2005;115: 287–91. 123. Dulguerov P, Marchal F, Lehmann W. Postparotidectomy facial nerve paralysis: possible etiologic factors and results with routine facial nerve monitoring. Laryngoscope 1999;109:754–62. 124. O’Brien CJ, Malka VB, Mijailovic M. Evaluation of 242 consecutive parotidectomies performed for benign and malignant disease. Aust N Z J Surg 1993;63:870–7. 125. Linder TE, Huber A, Schmid S. Frey’s syndrome after parotidectomy: a retrospective and prospective analysis. Laryngoscope 1997; 107:1496–501. 126. Prichard AJN, Barton RPF, Narula AA. Complications of superficial parotidectomy versus extracapsular lumpectomy in the treatment of benign parotid lesions. J R Coll Surg Edinb 1992;37:155–8. 127. Sanabria A, Kowalski LP, Bradley PJ, et al. Sternocleidomastoid muscle flap in preventing Frey’s syndrome after parotidectomy: a systematic review. Head Neck 2012;34:589–98. 128. Kim JT, Naidu S, Kim YH. The buccal fat: a convenient and effective autologous option to prevent Frey syndrome and for facial contouring following parotidectomy. Plast Reconstr Surg 2010;125: 1706–9. 129. De Bree R, van der Waal I, Leemans CR. Management of Frey syndrome. Head Neck 2007;29:733–8. 130. Asal K, Ko¨ybasioglu A, Inal E, et al. Sternocleidomastoid muscle flap reconstruction during parotidectomy to prevent Frey’s syndrome and facial contour deformity. Ear Nose Throat 2005;84:173–6. 131. Dulguerov P, Quinodoz D, Cosendai G, et al. Frey syndrome treatment with botulinum toxin. Otolaryngol Head Neck Surg 2000;122: 821–7. 132. Patel N, Har-El G, Rosenfeld R. Quality of life after great auricular nerve sacrifice during parotidectomy. Arch Otolaryngol Head Neck Surg 2001;127:884–8. 133. Porter MJ, Wood SJ. Preservation of the great auricular nerve during parotidectomy. Clin Otolaryngol Allied Sci 1997;22:251–3. 134. Yokoshima K, Nakamizo M, Ozu C, et al. Significance of preserving the posterior branch of the great auricular nerve in parotidectomy. J Nihon Med Sch 2004;71:323–7. 135. Hui Y, Wong DS, Wong LY, et al. A prospective controlled doubleblind trial of great auricular nerve preservation at parotidectomy. Am J Surg 2003;185:574–9. 136. Vieira MB, Maja AF, Ribeiro JC. Randomized prospective study of the validity of the great auricular nerve preservation in parotidectomy. Arch Otolaryngol Head Neck Surg 2002;128:1191–5. 137. Biglioli F, D’Orto O, Bozzetti A, et al. Function of the great auricular nerve following surgery for benign parotid disorders. J Craniomaxillofac Surg 2002;30:308–17. 138. Christensen NR, Jacobsen SD. Parotidectomy. Preserving the posterior branch of the great auricular nerve. J Laryngol Otol 1997;111: 556–9. 139. Roh JL, Kim HS, Park CI. Randomized clinical trial comparing partial parotidectomy versus superficial or total parotidectomy. Br J Surg 2007;94:1081–7. 140. Beutner D, Wittekindt C, Dinh S, et al. Impact of lateral parotidectomy for benign tumors on quality of life. Acta Otolaryngol 2006; 126:1091–5.