UNIVERSITE DE GENEVE FACULTE DE MEDECINE
Département des Neurosciences Cliniques
et Dermatologie Professeur P. Montandon
Clinique et Policlinique d'Oto-rhino- laryngologie et Chirurgie Cervico-Faciale
Division de Chirurgie Cervico-Faciale Professeur W. Lehmann
PAROTIDECTOMY COMPLICATIONS.
NEW TECHNIQUES FOR THEIR OBJECTIVE EVALUATION, PREVENTION AND TREATMENT
Travail présenté par le Docteur Pavel Dulguerov
pour obtenir le titre de Privat Docent
Genève 1999
TABLE OF CONTENTS
Table of contents ... 1
Table of illustrations ... 4
Acknowledgements ... 7
SUMMARY ... 9
1. INTRODUCTION ... 13
1.1. History of parotid surgery ... 14
1.2. Anatomy ... 19
1.2.1. Parotid fascia ... 24
1.2.2. Contents of the parotid space ... 29
1.2.3. Histology ... 30
1.2.4. Parotid lobes ... 32
1.2.5. Facial nerve anatomy ... 34
1.2.5.1 Marginal mandibular branches. ... 37
1.2.5.2. Cervical branches. ... 38
1.2.5.3. Buccal branches... 38
1.2.5.4. Zygomatic branches. ... 38
1.2.5.5. Temporal branches. ... 38
1.3. Indications of parotidectomy ... 41
1.3.1. Histopathology of parotid lesions ... 42
1.3.2. Preoperative work-up of parotid lesions ... 44
1.4. Surgical techniques of parotidectomy ... 45
1.4.1. Parotid surgery mandates ... 45
1.4.2. Nomenclature of parotid operations ... 46
1.4.3. General techniques of parotidectomy ... 48
1.4.3.1. Anesthesia ... 48
1.4.3.2. Patient positioning ... 49
1.4.3.3. Infiltration ... 49
1.4.3.4. Patient preparation ... 49
1.4.3.5. Draping ... 49
1.4.3.6. Incision ... 49
1.4.3.7. The superficial skin flap ... 50
1.4.3.8. Dissection of the posterior parotid ... 51
1.4.4. Techniques for facial nerve identification ... 52
1.4.5. The superficial parotidectomy ... 57
1.4.6. The total parotidectomy ... 60
1.4.7. Wound closure ... 60
2. PAROTIDECTOMY COMPLICATIONS ... 61
2.1. Facial nerve ... 62
2.1.1. Historical background ... 62
2.1.2. Techniques of evaluation of facial nerve function ... 64
2.1.3. Topographic facial nerve function testing ... 66
2.1.3.1. Burres' linear measurement studies ... 66
2.1.3.2. Multi-camera linear measurement studies ... 71
2.1.3.3. Other linear measurement studies ... 71
2.1.3.4. Image subtraction techniques ... 73
2.1.3.5. Miscellaneous techniques ... 76
2.1.3.6. Conclusions ... 78
2.1.4. Facial nerve paralysis grading classifications ... 79
2.1.5. Physiopathology of facial nerve paralysis ... 86
2.1.5.1. Ischemia ... 86
2.1.5.2. Mechanical trauma – compression injuries ... 88
2.1.5.3. Mechanical trauma –crushing ... 89
2.1.5.4. Mechanical trauma –stretching ... 90
2.1.5.5. Cold injury ... 91
2.1.5.6. Damage from electrocautery ... 92
2.1.5.7. Damage from repeated stimulations ... 93
2.1.5.8. Nerve toxic substances ... 93
2.1.5.9. Parotidectomy data ... 93
2.1.6. Incidence of postparotidectomy facial nerve paralysis ... 94
2.1.7. Prevention of facial paralysis during parotidectomy ... 99
2.2. Frey syndrome ... 100
2.2.1. Historical background ... 100
2.2.2. Etiology ... 105
2.2.3. Anatomy and physiology ... 108
2.2.4. Pathogenesis of Frey syndrome ... 110
2.2.5. Investigation of Frey syndrome ... 113
2.2.6. Incidence of Frey syndrome ... 116
2.2.7. Treatment of Frey syndrome ... 120
2.2.8. Prevention of Frey syndrome ... 124
2.3. Wound complications ... 127
2.3.1. Parotidectomy incisions ... 127
2.3.2. Retromandibular post-parotidectomy depression ... 130
2.3.3. Salivary fistula and post-parotidectomy wound collections ... 131
2.3.4. Skin anesthesia ... 132
2.4. Recurrence ... 135
2.4.1. Histology and recurrence ... 135
2.4.2. Initial surgery and recurrence ... 136
2.4.3. Age at initial surgery and recurrence ... 138
2.4.4. About small tumors and capsules ... 138
2.4.5. Malignant degeneration of pleomorphic adenoma ... 138
2.4.6. Surgery for recurrences and its complications ... 139
2.4.7. Re-recurrence of pleomorphic adenomas ... 140
2.4.8. Radiation of pleomorphic adenomas ... 140
3. OBJECTIVES ... 141
4. PATIENTS AND METHODS ... 142
4.1. Population ... 142
4.2. Surgery ... 142
4.3. Post-operative evaluation ... 144
4.4. Videomimicography ... 146
4.4.1. Description ... 146
4.4.2. Subjects ... 149
4.4.3. Normative measures ... 149
4.4.4. Statistical analysis. ... 151
4.5. Facial gustatory sweating evaluation ... 152
4.5.1. Blotting paper technique ... 153
4.5.2. Iodine-sublimated paper histogram (ISPH) ... 154
4.6. Frey syndrome treatment with botulinum toxin ... 155
5. RESULTS ... 157
5.1. Videomimicography – the best measures ... 157
5.2. Videomimicography – variability in normals ... 160
5.2. Videomimicography – correlation with the House-Brackmann scale ... 161
5.2. Gustatory sweating – normative data ... 165
5.3. Parotidectomy - General data ... 167
5.4. Parotidectomy complications - facial nerve paralysis ... 170
5.4.1. Classification according to the House-Brackmann scale ... 170
5.4.1.1. Entire population ... 170
5.4.1.2. Role of sectioning of facial nerve branches ... 171
5.4.1.3. Patient's age and postoperative facial function ... 172
5.4.1.4. Type of parotidectomy and postoperative facial function ... 173
5.4.1.5. Histopathology and postoperative facial function... 174
5.4.1.6. Size of lesion and postoperative facial function ... 176
5.4.1.7. Duration of parotidectomy and postoperative facial function ... 177
5.4.1.8. Type of intraoperative monitoring technique and postoperative facial function ... 177
5.4.1.9. Patients with poor postoperative facial function ... 178
5.4.2. Videomimicography results ... 179
5.5. Parotidectomy complications – Frey syndrome ... 180
5.6. Parotidectomy – wound complications ... 183
5.7. Frey syndrome treatment with botulinum toxin ... 185
5.8. Recurrences ... 185
6. DISCUSSION ... 188
6.1. Videomimicography ... 188
6.1.1. What facial movements? ... 188
6.1.2. How should the movements be performed ? ... 189
6.1.3. What should be measured ? ... 189
6.1.4. How should the facial measurements performed? ... 190
6.1.4.1. Not impede facial movement and not touching the face. ... 191
6.1.4.2. Reproducibility for a given individual, both in normal and pathologic cases. 191 6.1.4.3. Synchronous data from the left and right side of the face. ... 192
6.1.4.4. Automatic measurements to avoid manipulation errors and observer bias. ... 192
6.1.4.5. Rapid, simple and low cost. ... 192
6.1.4.6. Well tolerated by patients. ... 193
6.1.4.7. Absolute values, not just percentages. ... 193
6.1.4.8. Stored for later comparison and evaluations. ... 193
6.1.4.9. Not require markings on the face. ... 193
6.2. Objective evaluation of Frey syndrome ... 194
6.3. Post-parotidectomy facial nerve paralysis ... 195
6.4. Frey syndrome: prevention, detection, and treatment ... 198
6.5. Wound complications ... 202
6.6. Recurrence ... 202
7. CONCLUSIONS ... 204
8. REFERENCES ... 205
APPENDIX 1 ... 228
TABLE OF ILLUSTRATIONS
Figure number Page
FIGURE 1:SCHEMATIC REPRESENTATION OF THE PAROTID GLAND AS A TRUNCATED QUADRANGULAR PYRAMID. ... 19
FIGURE 2:SCHEMATIC REPRESENTATION OF THE PAROTID GLAND. ... 22
FIGURE 3:HORIZONTAL SECTION THROUGH THE NECK AT THE LEVEL OF THE PAROTID GLAND. ... 23
FIGURE 4:SCHEMATIC REPRESENTATION OF THE FASCIAL LAYERS OF THE NECK ... 26
FIGURE 5:SCHEMATIC REPRESENTATION OF THE FASCIAL LAYERS AT THE LEVEL OF THE HARD PALATE ... 27
FIGURE 6:ANATOMICAL CROSS-SECTION SHOWING THE FASCIAL LAYERS LATERAL TO THE PAROTID GLAND ... 28
FIGURE 7:SCHEMATIC REPRESENTATION OF THE VESSELS AND NERVES WITHIN THE PAROTID SPACE. ... 31
FIGURE 8:SCHEMA OF THE DEVELOPMENT OF THE FACIAL NERVE AND PAROTID GLAND ... 33
TABLE I:SCHEMATIC DESCRIPTION OF THE BRANCHING PATTERNS OF THE FACIAL NERVE ... 36
FIGURE 9:BRANCHING PATTERNS OF THE EXTRATEMPORAL FACIAL NERVE ... 40
TABLE II:DISTRIBUTION OF SALIVARY GLAND TUMORS (BENIGN AND MALIGNANT) IN THE THREE MAIN SALIVARY GLANDS. ... 41
TABLE III:INCIDENCE OF MALIGNANCY IN SALIVARY GLAND TUMORS IN THE THREE MAIN SALIVARY GLANDS. ... 42
TABLE IV:PATHOLOGICAL CLASSIFICATION OF PAROTID TUMORS, THEIR INCIDENCE (IN PERCENT) AND BRIEF DESCRIPTION OF THEIR TREATMENT ... 43
FIGURE 10:POSITIONING OF THE PATIENT FOR PAROTID SURGERY ... 55
FIGURE 11:TYPICAL PAROTIDECTOMY INCISION ... 55
FIGURE 12:DISSECTION OF THE POSTERIOR PORTION OF THE PAROTID GLAND ... 56
FIGURE 13:EXPOSURE AND LANDMARKS FOR IDENTIFICATION OF THE FACIAL NERVE TRUNK ... 56
FIGURE 14:DISSECTION OF FACIAL NERVE BRANCHES DURING SUPERFICIAL PAROTIDECTOMY ... 59
FIGURE 15:THE OPERATIVE FIELD AT THE END OF SUPERFICIAL PAROTIDECTOMY ... 59
TABLE V:CLASSIFICATION OF FACIAL EVALUATION SYSTEMS AND THEIR USEFULNESS ACCORDING TO THE DEGREE OF RESIDUAL FACIAL MOTOR FUNCTION ... 65
FIGURE 16:FACIAL LANDMARKS FOR LINEAR MEASURES ... 69
TABLE VI:FACIAL MOVEMENTS AND THE MOST MEANINGFUL MEASURES TAKEN (LANDMARKS) ... 70
TABLE VII:VARIABILITY OF MOUTH AND EYE MOVEMENTS IN 11 NORMAL SUBJECTS USING MICROSCALING ... 77
TABLE VIII:BOTMAN AND JONGKEES – A GROSS FACIAL NERVE PARALYSIS CLASSIFICATION. ... 80
TABLE IX:PEITERSEN – A GROSS FACIAL NERVE PARALYSIS GRADING CLASSIFICATION. ... 81
TABLE X:ADOUR AND SWANSON – A REGIONAL WEIGHTED FACIAL PARALYSIS CLASSIFICATION. ... 81
TABLE XI:YANAGIHARA – A REGIONAL WEIGHTED FACIAL PARALYSIS CLASSIFICATION. ... 82
TABLE XII:STENNERT – A REGIONAL FACIAL NERVE PARALYSIS CLASSIFICATION. ... 83
TABLE XIII:HOUSE-BRACKMANN – A GROSS FACIAL NERVE PARALYSIS CLASSIFICATION. ... 84
FIGURE 17:ROSS –NEDZELSKI – THE LATEST DESCRIBED GROSS FACIAL NERVE PARALYSIS CLASSIFICATION. ... 85
FIGURE 18:MICROANATOMY OF PERIPHERAL NERVES AND THEIR VASCULAR SUPPLY. ... 87
FIGURE 19:STAIN-STRESS OF PERIPHERAL NERVES. ... 90
TABLE XIV:INCIDENCE OF FACIAL PARALYSIS, BOTH TEMPORARY AND PERMANENT IN THE LITERATURE ... 96
FIGURE 20:INCIDENCE OF TEMPORARY FACIAL PARALYSIS IN THE LITERATURE ... 97
FIGURE 21:INCIDENCE OF PERMANENT FACIAL PARALYSIS IN THE LITERATURE ... 98
FIGURE 22:FIRST PAGE OF DUPHENIX'S 1757 MANUSCRIPT ... 102
FIGURE 23:AUTONOMIC INNERVATION OF THE PAROTID GLAND AND FACIAL SKIN – OVERALL VIEW ... 107
FIGURE 24:AUTONOMIC INNERVATION OF THE PAROTID GLAND AND FACIAL SKIN - DETAIL ... 109
FIGURE 25:SCHEMATIC REPRESENTATION OF THE ABERRANT REGENERATION THEORY ... 112
FIGURE 26:FREQUENCY OF FREY SYNDROME FOLLOWING PAROTIDECTOMY ... 116
FIGURE 27:SEVERITY OF GUSTATORY SWEATING SYMPTOMS ... 117
FIGURE 28:MINOR-TEST SCORES IN DIFFERENT PAROTID SURGERY GROUPS ... 118
FIGURE 29:INCIDENCE OF FREY SYNDROME IN THE LITERATURE ... 119
TABLE XV:INCIDENCE OF FREY SYNDROME IN THE LITERATURE USING OBJECTIVE TESTING ... 120
TABLE XVI:GUIDELINES FOR TOPICAL TREATMENT OF FREY SYNDROME WITH TOPICAL ANTICHOLINERGICS ... 123
TABLE XVII:EFFECT OF VARIOUS SURGICAL TECHNIQUES FOR PREVENTING FREY SYNDROME ... 126
FIGURE 30:PAROTIDECTOMY INCISIONS ... 129
TABLE XVIII:EFFECT OF FIBRIN GLUE ON POSTPAROTIDECTOMY WOUND COMPLICATION ... 132
FIGURE 31:DISTRIBUTION OF THE FACIAL INNERVATION BY THE TRIGEMINAL NERVE ... 133
FIGURE 32:AVERAGE AND STANDARD DEVIATION OF POSTPAROTIDECTOMY RECURRENCE ... 137
FIGURE 33:VIDEOMIMICOGRAPHY SET UP. ... 145
FIGURE 34:VIDEOMIMICOGRAPHY FACIAL LANDMARKS. ... 147
FIGURE 35:ADJUSTMENT OF LANDMARKS LS AND LI FOR SMILING MOVEMENT ... 148
FIGURE 36:VIDEOMIMICOGRAPHY DISTANCE MEASUREMENTS. ... 150
FIGURE 37:VIDEOMIMICOGRAPHY SURFACE MEASUREMENTS. ... 151
FIGURE 38:PREFORMED STENCIL FOR FREY SYNDROME EVALUATION. ... 152
FIGURE 39:STANDARDIZED FOLDING OF THE BLOTTING PAPER STENCIL. ... 153
FIGURE 40:IODINE-SUBLIMATED PAPER STENCIL WETTED WITH WATER. ... 154
FIGURE 41:ISPH DATA SHEET OF A PATIENT WITH FREY SYNDROME ... 156
TABLE XIX:PERCENT CHANGE OF ALL MEASURES FOR EACH MOVEMENT IN NORMAL SUBJECTS. ... 157
FIGURE 42:PERCENT CHANGE FOR EYE CLOSURE IN NORMAL SUBJECTS ... 158
FIGURE 43:PERCENT CHANGE FOR FOREHEAD LIFTING IN NORMAL SUBJECTS ... 158
FIGURE 44:PERCENT CHANGE FOR NOSE WRINKLING IN NORMAL SUBJECTS ... 159
FIGURE 45PERCENT CHANGE FOR LIP PUCKERING IN NORMAL SUBJECTS ... 159
FIGURE 46:PERCENT CHANGE FOR SMILING IN NORMAL SUBJECTS ... 160
TABLE XX:ANOVA OF SIDE, DAY, SUBJECT AND REPEAT VARIABLE ... 161
TABLE XXI:PERCENT CHANGE OF THE BEST MEASURES FOR EACH FACIAL MOVEMENT WITHIN HB GRADE ... 162
TABLE XXII:ANOVA ANALYSIS OF THE TOTAL VARIABILITY OF THE BEST MEASURE FOR EACH FACIAL MOVEMENT AND THE GLOBAL FACIAL VALUES. ... 162
FIGURE 47:BOX-PLOT OF THE BEST MEASURES FOR EACH MOVEMENT AGAINST THE HB GRADE. ... 162
FIGURE 48:BOX-PLOT OF THE HB GRADE AGAINST VMGS (TOP) AND VMGI (BOTTOM). ... 164
TABLE XXIII:NORMATIVE DATA OF GUSTATORY SWEATING ... 165
FIGURE 49:NORMATIVE DATA FOR THE BLOTTING PAPER AND THE ISPH METHODS ... 166
FIGURE 50:HISTOGRAM OF AGE DISTRIBUTION ... 167
FIGURE 51:HISTOGRAM OF THE SIZE OF PAROTID LESIONS ... 168
TABLE XXIV:HISTOLOGY OF PAROTIDECTOMY SPECIMEN ... 169
TABLE XXV:FACIAL FUNCTION SCORES OF THE ENTIRE POPULATION ... 170
FIGURE 52:POSTOPERATIVE HB SCORES ACCORDING TO WHETHER FACIAL NERVE BRANCHES WERE SECTIONED ... 171
FIGURE 53:X-Y PLOT OF PATIENT'S AGE VS. POSTOPERATIVE HB SCORE ... 172
FIGURE 54:BAR CHART OF THE POSTOPERATIVE HB SCORES ACCORDING TO THE TYPE OF PAROTIDECTOMY ... 173
FIGURE 55:POSTOPERATIVE HB SCORES ACCORDING TO THE HISTOPATHOLOGY ... 174
FIGURE 56:POSTOPERATIVE HB SCORES ACCORDING TO THREE HISTOPATHOLOGIC GROUPS ... 175
FIGURE 57:POSTOPERATIVE HB SCORES ACCORDING TO THE SIZE OF THE LESION ... 176
FIGURE 58:X-YPLOT OF THE RELATION BETWEEN DURATION OF SURGERY AND POSTOPERATIVE HB SCORES ... 177
FIGURE 59:POSTOPERATIVE HB SCORES ACCORDING TO THE TYPE OF MONITOR. ... 178
TABLE XXVI:MAIN CHARACTERISTICS IN PATIENTS WITH POSTOPERATIVE HB SCORE >2 ... 178
TABLE XXVII:STATISTICAL RELATIONS BETWEEN PAROTIDECTOMY VARIABLES AND VMG INDEX ... 179
FIGURE 60:DISTRIBUTION OF THE GRADES OF THE CLINICAL FREY SYNDROME EVALUATION ... 180
FIGURE 61:OBJECTIVE FREY SYNDROME EVALUATION ... 181
FIGURE 62:SURFACE OF FREY SYNDROME USING THE ISPH METHOD ... 182
TABLE XXVIII:FREQUENCY OF THE DIFFERENT WOUND COLLECTION COMPLICATIONS AND TYPE OF IMPLANT ... 183
FIGURE 63:INCIDENCE OF POSTPAROTIDECTOMY FISTULA AND TYPE OF IMPLANT ... 184
FIGURE 64:INCIDENCE OF PAROTID WOUND COMPLICATIONS (OVERALL) AND TYPE OF IMPLANT ... 184
FIGURE 65:FREY SYNDROME QUANTITY BEFORE AND AFTER TREATMENT WITH BOTULINUM TOXIN ... 186 FIGURE 66:FREY SYNDROME SURFACE BEFORE AND AFTER TREATMENT WITH BOTULINUM TOXIN ... 186 TABLE XXIX:CHARACTERISTICS OF THE BOTULINUM TOXIN TYPE A DILUTION AND DOSES IN PUBLICATIONS ON
FREY SYNDROME TREATMENT WITH BOTULINUM TOXIN ... 201
ACKNOWLEDGEMENTS
I would like to thank:
The patients, subjects of this thesis, for their cooperation and patience during the various tests for which they did not always see the importance. This study has probably improved the care they received, but future patients will probably benefit the most.
Dr D. Wang, who was a visiting Research Fellow from Fuyong University, China. He worked very hard, and with remarkable patience, to perform the majority of the computer analysis of the data collected for the videomimicography test. He also suggested the use of the global indexes for this test and essentially made a old dream of mine a realty.
Mr. G. Rizzo for his help with the video recordings during the videomimicography. These recordings scheduled at various unpredictable times often disrupted his schedule. I would also like to thank him for his help and cooperation in the setup of the computer analysis of facial landmarks, and for scanning the iodinated paper stencils used in the Frey syndrome evaluation. Without his cooperation, this work would have taken much more time to complete.
Mrs. L. Johnson, Head Nurse of the ENT Operating Room for her encouragement and interest in this study. Without her cooperation and efficacy, the purchase of the EMG
intraoperative monitoring system would probably have been delayed for months in the administrative bureaucracy of our institution.
Professor W. Lehmann, Chief of the Head and Neck Surgery Division, for his enthusiasm and encouragement during this study. In large part, the ideas presented in this thesis were born and perfected during our discussions. In addition, a large number of the patients were operated on by him, and his surgical skill is reflected in the excellent results obtained.
Dr. D. Quinodoz, who generously participated in the elaboration of the functional sweat tests and who collected the patient data for the treatment of Frey’s syndrome patients with botulinum toxin.
Mr. G. Cosenday, engineer with the Geneva Cochlear Implant Center, for developing the histogram algorithms necessary for the iodine-sublimated paper method. His rapidity in providing last minute results was especially appreciated.
Dr. A. Vaezi who was able to propose within a very short timeframe, solutions to the
reproducibility problems, which interfered with the blotting paper method. He actively participated in standardizing the perspiration tests.
Dr. P. Piletta and Dr. A. Arechalde from the Dermatology Clinic for preparing the iodinated paper stencils, as well as the temperature and skin coloration tests which were used for the
objective evaluation of Frey’s syndrome.
Mr. A. Rohr who replaced Mr. Rizzo, sometimes at the last minute, in various activities with his typical eagerness. He was also responsible for the modification of the VMG chair.
Dr. D. Salomon, “Medicin-Adjoint” of the Dermatology Clinic and Dr. M. Pelizzone,
“Maître d’Enseignement and Recherche” at the Geneva Cochlear Implant Center, whose ideas contributed to the initial steps which led to the new objective tests of Frey’s syndrome.
Professor P. Montandon, Dr. J. P. Guyot and Dr. S. Auderson who kindly allowed their patients to be included in this study.
Mrs. J. Newsom, my mother-in-law, whose editorial experience and professional expertise clarified several passages and greatly improved the English text
SUMMARY
OBJECTIVE: To review the literature on postparotidectomy complications (facial nerve paralysis, Frey syndrome, "wound complications", and recurrence) and to obtain meaningful data on their incidence, physiopathology, and favoring factors. To analyze the incidence of
postparotidectomy complications in a prospective trial. To develop new objective evaluation methods for facial motor function and Frey syndrome.
METHODS: Seventy patients underwent parotidectomy between April 1994 and 1998.
Several improvements of standard parotidectomy were introduced in order to decrease postparotidectomy complications.
1) Videomimicography. A new objective facial neuromuscular evaluation method, called videomimicography (VMG) is proposed. VMG uses landmarks placed on the face, and digital video recording of subjects during five standard facial movements (forehead wrinkling, eye closure, nose wrinkling, lip puckering, and smiling) performed with maximal strength. Digital video frames are directly fed in a computer and a custom-modified public domain software used for analysis. In five normal subjects, the "best measures" for each movement were assessed. The reproducibility of VMG was studied with ANOVA comparing intersubject, side, and same or different day test-retest variability. Two global values of facial paralysis were derived from these measures: the VMG score and the VMG index. The "best measures" and the VMG score and VMG index were then
correlated with the facial paralysis House-Brackmann grade in 29 patients with facial paralysis.
2) Facial nerve. An intraoperative facial nerve monitoring was used in all patients. Two devices were used: a custom mechanical transducer (35 patients - 1994-6) and a commercial EMG- based apparatus (35 patients - 1996-8). All patients were analyzed, including those with cancer and those with deliberate or accidental sectioning of facial nerve branches. The outcome variables studied were the motor facial function at 1 week postoperatively (temporary paralysis) and at 6-12 months (definitive paralysis). The facial nerve was evaluated according to the House-Brackmann grading scale (HB) and according to VMG.
3) Frey syndrome. Implants were placed under the skin at the end of parotidectomy. The choice of the implant was left to the individual surgeon: 24 patients had no implant and 46 patients had the following implants – 7 lyophilized dura, 7 Ethisorb®, 32 e-PTFE sheets. The incidence of
Frey syndrome was evaluated 12 months after the operation. A clinical Frey syndrome was present if the patients complained of gustatory sweating or flushing. An objective Frey syndrome was present if patients tested positive with the two newly developed tests for the evaluation of Frey syndrome. The blotting-paper technique (BP) used the difference in weight of a blotting stencil before and after gustatory stimulation to measure sweating quantity. The iodine-sublimated paper (ISPH) is based on the change of color of an iodine-sublimated paper stencil by the reduction of an iodine-starch mixture by water. The stencils were digitized and the darkness was used as a measure of Frey syndrome surface as well as an important topographic indicator. The gustatory stimulus for all patients was a slice of lemon sucked for 1 minute. Some patients with an important and
disabling Frey syndrome were offered treatment with an intradermal injection with botulinum toxin. The results of this treatment were evaluated by the BP and ISPH techniques before and 2 weeks after treatment.
4) Wound complications. The following wound complications were evaluated after
parotidectomy: hematoma, seroma, and salivary fistula. Patients were examined daily when in the hospital and at each postoperative visit.
5) Recurrence. All patients were examined clinically at 12 months for a possible recurrence.
In addition, the charts were reviewed and patients called to assess a possible long-term recurrence.
The following variables were also noted: patients sex and age, the site of the lesion, the type of parotidectomy (superficial or total) performed, the possible section of a facial nerve branch, the duration of the procedure, the histopathology and size of the lesion. Their association with the outcome variables discussed above was examined with the appropriate statistical tests.
RESULTS:
1) Videomimicography. Surface areas, close to the moving portion of the face, were found to better evaluate each facial movement studied. The reproducibility of VMG was excellent, with 80- 90% of the total variability due to intersubject variability, while the facial side, and same or different day test-retest variability was small. The "best measures" and the VMG score and VMG index had a linear and highly statistically significant correlation with the House-Brackmann scale.
2) Facial nerve. The overall incidence of facial paralysis was 27% for temporary and 4% for permanent deficits. Most of the deficits were partial, and most often concerned the marginal mandibular branch. Temporary deficits with HB>2 scores were only present in patients with
parotid cancer or infection. Permanent deficits were present in 3 patients, all with cancer or infection. Factors significantly associated with an increased incidence of temporary facial paralysis include the extent of parotidectomy, the intraoperative sectioning of facial nerve branches, the histopathology of the lesion, and the duration of the operation.
3) Frey syndrome. Clinical Frey syndrome was present in 12 patients: 11 without implant (53%) and 1 with implant (2.6%). Objective tests were positive in 24 patients: 16 without implants (76%) and 8 with implants (20%). In the implanted patients, the objective tests were positive in 71% of lyophilized dura, 14% of Ethisorb®, and 8% of e-PTFE patients. In all 16 patients treated with botulinum toxin, an excellent result was achieved with disappearance of clinical symptoms and an important reduction on the objective tests.
4) Wound complications. Hematoma, seroma, and salivary fistula were present in respectively 7%, 6%, and 21% of patients. Salivary fistula were more frequent with Ethisorb®
(57%) and e-PTFE (25%).
5) Recurrence. 4 recurrences were noted, 2 (3.6%) in patients with pleomorphic adenoma, and 2 in patients with cancer (25%).
CONCLUSIONS:
1) The videomimicography is a promising evaluation method of facial paralysis. The test is quantitative, objective, reproducible, and rather simple.
2) The routine use of a facial nerve monitoring device was found extremely helpful during parotid surgery. In this study of unselected patients, the overall incidence of facial paralysis is 27%
for temporary deficits and 4% for long-term deficits. Important temporary facial nerve deficits (HB>2) were not found in patients undergoing parotidectomy for benign tumors. Permanent deficits were present only in patients who had a section of nerve branches. Factors associated with an increased incidence of temporary facial paralysis include the extent of parotidectomy, the
intraoperative sectioning of facial nerve branches, the histopathology and the size of the lesion, and the duration of the operation. A review of the physiopathological factors possibly responsible for facial nerve deficit points to nerve stretching as the most probable etiology.
3) The iodine-sublimated paper histogram (ISPH) test for facial gustatory sweating is an accurate, reliable, easy to perform, and well-tolerated objective test. The topographic information is essential for Frey syndrome treatment involving local application of a medication. In addition, the
quantitative data provided are indispensable to evaluate the results of a given treatment. The incidence of clinical Frey syndrome after parotidectomy is 40-50%. When objective tests are used (ISPH), the incidence is around 80%. The use of an implant placed in the wound as a prevention barrier reduces the incidence of clinical Frey syndrome to 2-3%. When objective tests (ISPH) are used, the incidence with e-PTFE is reduced to 10%. The best Frey syndrome prevention barrier appears to be a non-resorbable implant.
4) Some of the implants used (mainly Ethisorb®, but also e-PTFE) result in a high incidence of parotid fistula. Therefore, the search for the best implant should continue.
5) The treatment of Frey syndrome by intradermal injection of botulinum toxin type A appears simple, effective, reliable, fast, and devoid of major side effects.
1. INTRODUCTION
Parotide est une tumeur contre nature, occupant les glandules et parties d'autour, qui sont sous les oreilles dites Emonctoires du cerveau : lesquelles, parce qu'elles sont laxes et rares, facilement reçoivent les excremens d'iceluy.
Ambroise Paré, 1572
The first reference to parotid pathology is attributed to Hippocrates (460-370 BC) who described purulent and non-purulent parotitis [212; 390]. Any further understanding of parotid pathology is hampered until the anatomical description of the gland and its role in secretion of saliva. In fact, as pointed out by Hyrtl in the early 19th century, even the term parotid designated a disease and not an anatomical structure [212].
The recognition of the existence and role of the major salivary glands dates back to the second half of the 17th century. Thomas Wharton (1614-1673) in a monograph named
"Adenographia. Siva glandularum totius corporis descriptio" gives the first description of the
submandibular gland and its drainage duct that still bears his name [189; 212; 390; 546]. At the same period, Niels Steenson also known as Nicolaus Stenonius (1638-1686) discovers the parotid duct and describes the anatomy of parotid gland [189; 212; 390; 496]. It is interesting to note, that Stenonius, after numerous contributions to medicine, embraced Catholicism and was made apostolic vicar. In 1988, he was beatified by Pope Jean Paul II [127]. During the 17th century, Malpighi studies the histology of salivary glands and coins the term "acini" [189].
Definitive demonstration of the control of salivary secretion by nerves is provided in 1850 by Carl Ludwig by stimulating the chorda tympani nerve [189]. In the second half of the 19th century, the role of the sympathetic and parasympathetic systems in salivary secretion was studied by Claude Bernard and John Langley [189; 358].
1.1. History of parotid surgery
L'ablation de la parotide est une opération grave, d'exécution difficile, dangereuse à cause de l'hémorragie qui l'accompagne lorsqu'elle n'est pas faite méthodiquement, entraînant fatalement une paralysie faciale définitive
Charles Lenormant, 1919 [312].
The first parotidectomy was apparently carried out by the British surgeon John Hunter in 1785 for a large tumor weighting 4 kilograms [358; 390]. Despite the heroic conditions in which these operations were carried out, several surgeons have undertaken parotidectomies in the first half of the 19th century: Carmichael [82] in Ireland, Bérard [43] in France, McClellan [341], Mott [366], and Sweat [506] in the United States. In 1860 already, Brainard [58] reviewed 91
parotidectomies from 64 surgeons. Still numerous physicians doubted the feasibility of parotidectomy and McCoy wrote in 1844: “ I need to say nothing about the operation of the parotid gland, for if you consider its anatomical relation you will be convinced that its removal is quite beyond the power of surgery” [390].
In most operations on the parotid gland in the 19th century the principal problem was bleeding and the main aim, the survival of the patient. The surgical technique became established and J.-L. Faure [165] described 8 pedicles that have to be ligated and sectioned to free the gland and control bleeding. Pedicle number 5 is called the stylomastoid pedicle and is composed mainly of the facial nerve! These parotidectomies were often radical operations with removal of a various portions of the mandibular ramus, in order to completely resect the deep portion of the gland [165].
Surgical treatment of parotid tumors would be straightforward, by removing the entire gland, if not for the presence of the facial nerve in the middle of the glandular parenchyma. The
possibility of accomplishing a parotidectomy without sacrificing the facial nerve was first suggested by Thomas Carwardine in 1907 [84], followed by Duval [149], Barbat [24], Sistrunk [481], and Adson and Ott [3]. The French surgical school with Duval and Redon contributed greatly to the techniques of facial nerve identification and preservation. As early as 1914, Duval [149] performs the identification and preservation of the upper facial nerve branches in benign parotid tumors by removing the inferior aspect of the mastoid process and identifying the nerve before its division. In 1916, Barbat [24] described one case in which the marginal mandibular branch is identified and followed to identify the facial nerve trunk, before removing the tumor. This report is rarely cited
[115], but an identical technique was popularized by Sistrunk in 1921 [481] and Adson and Ott in 1923 [3], to who credit is sometimes given [16; 79; 252; 276; 335; 527]. Sistrunk used enucleation for the majority of his cases, but stated that "In operating on some of the recurring growths and the larger growths that are deeply placed in the substance of the gland I have, in some instances, been able to save the nerve by the following procedure: I have exposed the facial nerve by first isolating the inframandibular branch of the nerve which runs along the angle of the jaw and dissecting this upward through the substance of the parotid gland to the point where the nerve divides…" [481].
The article of Adson and Ott, although published later, recommends the identification of the mandibular branch and dissection of the facial nerve in all cases [3]. This paper is a remarkable description of the surgical technique of total parotidectomy with facial nerve preservation [3]. A case report using this technique was published by Saltstein in 1936 [455].
The debate for the following 40 years will center on mixed tumors, probably because they represent more than 60% of parotid masses (see §1.3.). Because of the high number of recurrences in early publications [5; 40; 74; 281; 335; 344; 429; 494], the controversy surrounds their exact histologic nature (benign vs. malignant, uni- vs. multicentric) and, therefore, their best treatment [5;
16; 17; 35; 40; 74; 213; 241; 247; 252; 253; 276; 334; 340; 344; 407; 410; 414; 436; 493; 494; 527; 528;
545]. Benedict and Meigs in 1930 [40] reviewed 225 parotid tumors and concluded that: 1) mixed tumors are essentially benign, but recur locally with great frequency; 2) mixed tumors rarely become malignant; 3) radiation is of benefit in some benign parotid tumors, but excision is the treatment of choice. Nevertheless, the debate on each the above points carried on until the 1980's.
While the benign histology of mixed tumors became progressively established [35; 63; 78;
156; 157; 178; 274; 334; 414; 429], recurrences were attributed to inadequate surgery [34; 35; 96;
152; 252; 253; 281; 335; 492]. At that time, the majority of parotidectomies performed for mixed tumors were enucleations as described in two large series from the late 1930's [247; 407]. As late as 1940 Patey, to whom parotid surgery owes much, wrote: "There are three possible planes in which a parotid tumor can be removed. In the first place, the rather delicate capsule may be opened and the contained tumour tissue expressed… Secondly, the tumour may be enucleated in the layer of loose alveolar tissue which lies between it and the surrounding normal salivary glandular tissue…
Finally, the tumour may be removed with a margin of surrounding salivary glandular tissue by cutting through or outside the gland. This procedure involves almost of necessity the cutting of some or all of the branches of the facial nerve, depending on the amount of gland removed." [407].
Papers supporting enucleation for parotid tumors have continued until the 1980's [13; 224; 232;
343; 493].
Bailey [16] is often credited as having described modern parotidectomy [273; 410; 527], but his technique shows minor improvements compared to Adson and Ott's 1923 description [3].
Bailey used what he called a "modified Blair" incision (see § 2.3.1.), the anterior skin flap is elevated of the gland at the beginning of the procedure, and the external carotid artery is ligated [16]. The superficial lobe is mobilized progressively starting from the inferior and anterior poles of the gland and the dissection proceeds in posterior direction "between the two lobes.” Although the facial nerve is supposed to be preserved, in Bailey's papers it is unclear, where and when it is identified.
The major progress in Bailey's writing is the emphasis on complete superficial or total
parotidectomy, instead of enucleation, for the surgical treatment of parotid tumors [16; 17; 248].
The first descriptions of an early identification of the facial nerve trunk followed by
anterograde dissection along facial nerve branches is due to Janes, from the University of Toronto in 1940 [252]. He often removed "the tip of the mastoid process with an osteotome for easier access. The main trunk of the facial nerve is then exposed by blunt dissection as it emerges from the stylomastoid foramen… Once the nerve has been exposed it is usually surprisingly easy, except in inflammatory or malignant lesions, to dissect it free from the surrounding tissue, identifying the branches as they arise from the main trunk." [252]. Although the dates of the publications show beyond any doubt that Janes was first to describe the technique, Janes in a later article [253], stated, with great modesty, that the first parotidectomies with identification of facial nerve trunk and anterograde dissection of facial nerve branches was done for the first time around 1935 by himself in Canada, Redon in Paris, and Bailey in England!
Redon in 1945 [435], Marshall and Miles in 1947 [334], Clausen and Henley [96] in 1948, Klopp and Winship [276], and Brown et al. [63] in 1950, Hayes Martin [335] and Louis Byars [79] in 1952, described a similar technique, except for the removal of the mastoid tip. After separating the parotid gland from the sternocleidomastoid muscle [276; 435] and then from the digastric muscle [63; 335; 435], the facial nerve trunk is identified as it exits the stylomastoid foramen and dissected forward from the parotid gland. A superficial conservative (as far as the facial nerve is concerned) parotidectomy is then performed. If necessary, the deep lobe can also be removed, accomplishing what is variably called a total parotidectomy or a subtotal parotidectomy [276]. The technique was rapidly accepted by others such as Finochietto [173], Fitzgibbon [175], Brintall et al. [59], Kidd [273], Patey [410], Utendorfer [527], Beahrs [33; 34]. Although some [63; 272; 273; 276; 315; 335;
527] refer to the 1941 publication of Bailey [16], and sometimes to Janes' article [34; 59; 276; 315;
334; 492; 527], rarely is Janes credited as a pioneer. For example, Patey in his 1968 publication
[410] giving credit to the "three big man of parotid surgery,” cites McFarland, Bailey, and Redon, without any mention of Janes.
The anterograde facial nerve dissection technique has become the standard approach in parotid surgery [437; 520], although some surgeons still perform retrograde facial nerve dissections [93; 232; 535], following the description of this procedure by State in 1949 [492].
Janes [252] and, later, State [492] and Redon [436] condemned parotid biopsy and enucleation. Basing his observation on the work of Delarue [120], Redon [435; 436] strongly believed in the existence of multicentric mixed tumors, an idea advanced by McFarland [347; 348]
and Patey [407]. This theory made him favor total parotidectomy as the routine surgical treatment of mixed tumors, an attitude still followed by French surgeons [6; 94; 211; 270; 288; 291; 520].
Great progress in the comprehension of mixed tumors was made by the serial sectioning of parotidectomy material by Patey and Thackray [414]: 1) the capsule surrounding the tumors was found to vary greatly in thickness, not only from case to case, but also in different areas of the same tumor; 2) the capsule was found sometimes to be incomplete with tumor adjacent to normal gland tissue; 3) mixed tumors were found to be nodular and to grow by polypoid extensions through the capsule; 4) these polypoid extensions were more common in small tumors; 5) no multifocal mixed tumors were found in 37 specimens [414]. After recurrence, mixed tumors were often multicentric in the entire operated field and in particular along the previous scar [414]. These conclusions have been confirmed by Gunnel [214], Kleinsasser [275], Naeim et al. [372], Danovan and Conley [113], Lawson [305], and Lam et al. [299]. Also, Patey and Thackray's finding explained McFarland's conclusion from the 1930's, that small mixed tumors recur more often than large ones, and
therefore that small tumors should not be operated on [347]. Because of McFarland's position as a prominent pathologist with special expertise in parotid tumors [344; 345; 346; 347; 348], the above statement haunted parotid surgeons [16; 17; 63; 253; 334; 407] until Patey and Thackray's study published in the late 1950's.
Since mixed tumors are benign, recurrences are often delayed, up to 10-20 years after the initial surgery. Therefore, after the progressive generalization of superficial parotidectomy as minimal procedure in the 1950's, series with low recurrence rates for mixed tumors appeared [35;
63; 205; 253; 273; 527]. Also, comparison between enucleation with superficial or total
parotidectomy showed lower rates than enucleation [35; 205; 253; 530] and have continued to the 1980's [104; 493; 498].
In view of the high recurrence rates of mixed tumors in earlier series, radiation therapy has been proposed as adjuvant therapy since the 1920's [74], either as external beam radiation [5; 13;
224; 247; 343; 407; 456; 528], curietherapy with radium implants [74; 343; 528], or an association of both [5; 247]. Although the available results do not show a reduction of recurrence rates by radiation [528] and several authors have recommended against its use [16; 17; 152; 253; 273; 347;
407], proponents of radiation have continued until the 1990's [13; 25; 194; 224; 315; 343; 456; 528].
On a somewhat different front, the progress in the treatment of malignant parotid tumors has been made by a more precise and adequate histopathological diagnosis [29; 30; 31; 32; 178; 478;
515], by the recognition that recurrence and survival have to be measured over a time period of 10- 20 years [47; 159], and by the elaboration of groups of malignancies [47; 261] requiring treatment approaches of increased aggressiveness. However, as already noted by Brown et al. [63] in 1950, in view of the difficulty to establish an exact pre- or intraoperative pathological diagnosis in parotid malignancies, and because of the lack of an adequate rehabilitation techniques in facial nerve paralysis [199; 451], the often used approach is to make every effort to conserve a nerve not paralyzed prior to surgery [409].
In summary, the progress in parotid surgery has been a better understanding of mixed tumors and a standardization of surgical procedures towards early identification and dissection of the facial nerve. However, some of the problems discussed in the 1930's are still not completely resolved today. While it is now generally accepted that pleomorphic adenomas are benign, the extent of primary surgery for pleomorphic adenoma is still debated [132]. Similarly, radiation for pleomorphic adenoma, after a long debate, is less often used but not abandoned. In addition, the frequency and importance of various surgical complications of parotidectomy are reported over a wide range, and few techniques have evolved in order to reduce them [135; 137]. Finally, if the preservation of the facial nerve in benign parotid tumors has become the standard of care, its handling in the various parotid malignancies is still debatable.
1.2. Anatomy
It follows from its anatomy and complex relations of the parotid, that its entire removal as a surgical procedure is an anatomical impossibility
Treves, 1907[519]
The parotid gland fills the parotid space. The exact three-dimensional anatomy of the parotid space is extremely complicated and variable, but, with simplification, has been schematized as a quadrangular pyramid which is upside-down and the summit of which is somewhat truncated [56] (Figure 1). Therefore, six different walls can be recognized to the parotid space [33].
Figure 1: Schematic representation of the parotid gland as a truncated quadrangular pyramid.
Four of the six walls are represented: Ant: anterior wall, Sup: superior wall, Post: posterior wall, Inf: inferior wall. The front of the figure represents the lateral wall and the back the medial wall.
The anterior wall is made of the mandible and the adjoining masseter and internal pterygoid muscles. The parotid gland actually extends more superficially than the masseter in the direction of Stenson's duct. The proximity of these muscles to the parotid gland can explain the frequently encountered post-operative complaint of painful chewing. The limit between the anterior and medial wall is the sphenomandibular ligament, which is actually a thickening of the interpterygoid aponeurosis [424].
The medial wall is quite complex: here the parotid is bound by the deep parotid aponeurosis, which is attached to the sphenomandibular ligament and the stylomandibular ligament. Between the mandible and the spheno-mandibular ligament is a potential space called the retro-condylar space of Juvara [266] (also called the stylomandibular tunnel by Patey [413]), through which the auriculotemporal nerve and the internal maxillary artery enter/leave the parotid space [424]. Deep- lobe parotid tumors egress out of the parotid space and extend into the parapharyngeal space, through this retro-condylar space. As these tumors grow, they are blocked and assume a dumb-bell shape, a term coined by Patey [413]. Another weak spot, allowing for communication between the parotid and parapharyngeal spaces, is present between these ligaments.
The posterior wall is made of: 1) the styloid process and its muscles and ligaments, namely from medial to lateral: the stylopharyngeus muscle, the styloglossus muscle, the stylohyoid ligament and the stylohyoid muscle; 2) the posterior belly of the digastric muscle and; 3) the
sternocleidomastoid muscle. The styloid muscles and ligaments form the so-called styloid
"diaphragm" [83; 424; 514], which separates the parotid space from the carotid sheath. The facial nerve enters the parotid space between the digastric and stylohyoid muscle [424].
The extreme irregularity of the posterior and deep surfaces of the parotid space, and the absence of an obvious angle between them, has led to alternative descriptions of the shape of the parotid space [260]. A single posterior (in fact posteromedial) surface is described, along with the usual anterior and superior surfaces. The inferior surface is seen as an edge, and as a result, the gland is described as a triangular pyramid [33].
The superior wall has, actually, more of a triangular shape [256]. It is formed laterally by the zygomatic arch and by the cartilage of the external auditory canal. More medially, the upper limit of the parotid space is formed by the skull base, which is made, at this level by the tympanic portion of the temporal bone. The glenoid fossa of the temporal is just in front of this extension, so it is not surprising that it could be invaded in certain cases of parotid cancer [442].
The inferior wall is formed, posteriorly, by the convergence of the stylohyoid ligament and muscle with the digastric tendon at the superior edge of the hyoid bone. The anterior edge is the mandibular angle with the attachment of the stylomandibular ligament. Between these two bony landmarks is a fascial thickening, named the angular tract of the cervical fascia [192; 565], separating the parotid space from the submandibular space. This fascial thickening extends sometimes to the sternocleidomastoid muscle forming the so-called sternomandibular ligament [424; 514]. The lowest point of the parotid gland is 1.18 ± 0.51 cm below and 1.38 ± 0.32 cm behind the angle of the mandible [566].
The lateral wall is apparently simpler, since it is composed only of aponeurosis and skin.
Nevertheless, considerable debate exists on the exact nature of the aponeurotic coverage of the parotid and the arrangement of fascia in the preauricular region (see §1.2.1.).
The height of the parotid space has been measured to average 5.8 cm by Davis et al. [115]
and 4.2 ± 0.24 by Rudolph [452], while the width was estimated at 3.4 cm by Davis et al. [115] and 2.43 ± 0.31 cm by Rudolph [452].
Figure 2: Schematic representation of the parotid gland.
The drawing represents a section through the parotid gland and surrounding structures. The buccopharyngeal fascia (1) covers the lateral aspect of the pharynx represented by the superior constrictor muscle (17) and tonsil (15). The masseteric fascia (10) covers the internal pterygoid muscle (14), the masseter and encircles the buccal fat pad of Bichat (12). The deep parotid fascia (7) covers the medial and deep aspect of the gland. On the medial aspect the sphenomandibular (17) and stylomandibular ligament (2) are shown. The posterior wall is made of the styloid muscles and ligaments: stylohyoid ligament (3), stylohyoid muscle (4), as well as the digastric muscle (5). It continues as the superficial layer of the deep cervical fascia, covering the sternocleidomastoid muscle (6). The external carotid artery (8) and posterior facial vein (9) are seen in the deep aspect of the gland. The Stenson's duct (11) is seen passing forward from the gland to terminate by piercing the buccinator muscle (13). Reprinted from Proctor [424], without permission.
Figure 3: Horizontal section through the neck at the level of the parotid gland.
1) Maxilla – symphysis; 2) Orbicularis oris muscle; 3) + 15) Stenson's duct; 4) Platysma muscle; 5) Bichat's fat pad;
6) Masseter muscle; 7)+ 19) Mandible – ascending ramus; 8) Internal pterygoid muscle; 9) Cartilage of the external ear; 10) Styloid process; 11) + 22) Internal jugular vein; 12) + 24) Mastoid process; 13) Cerebellum; 14) Tongue;
16) Mandible – body; 17) Oropharynx; 18) Internal maxillary artery; 20) Internal carotid artery; 21) Retromandibular vein; 22) Vagus, glossopharyngeus, spinal, and hypoglossus nerves. P = parotid gland.
1.2.1. Parotid fascia
The fascias in the human trunk are divided into a superficial and a deep fascial layer [209;
514]. The superficial fascia is under the dermis and is usually a thin connective tissue layer. The superficial fascia extends from the vertex where it covers the epicranius muscle, continuing on to the face, neck, chest, and abdomen [209]. As a rule, vessels and nerves are located deep to the superficial fascia, except fine elements destined to the overlaying skin. The deep fascia also extends from the abdomen to the head.
In the neck, the superficial cervical fascia covers the superficial aspect of the platysma muscle and, according to Grodinsky and Holyoke, splits to also cover its deep surface [209]. Therefore, the superficial fascia constitutes a complete subcutaneous layer surrounding the entire
circumference of the neck. It is attached to overlaying skin within thin fibrous septa and continues on the face and scalp.
In the neck, the deep cervical fascia has a complicated structure and, unfortunately, the names chosen render the subject confusing and misleading. Grodinsky and Holyoke divide the deep cervical fascia in 3 layers: a superficial layer of the deep cervical fascia (SL-DCF), a middle layer, and a deep layer [209]. Obviously, confusion exists when speaking about a "superficial fascia"
in the neck: is it the superficial cervical fascia or the superficial layer of the deep cervical fascia.
Furthermore, while the Grodinsky's terminology has become standard nomenclature in
Otolaryngology – Head and Neck Surgery textbooks [206; 259; 471], it is not exactly followed in anatomical textbooks. Also, none of the anatomical descriptions done recently refer to Grodinsky and Holyoke's work [204; 265; 361; 502; 516; 567].
The deep layer of the deep cervical fascia surrounds the vertebra and the prevertebral and paravertebral musculature (Figure 4). The middle layer of the deep cervical fascia encloses the pre- laryngeal musculature, the thyroid gland, trachea, and esophagus-pharynx. This layer is most developed in the infra-hyoid portion of the neck and continues above that level as a fascial covering of the pharynx up to the base of skull, where it is called the buccopharyngeal fascia.
The SL-DCF forms, like the superficial cervical fascia, a complete aponeurotic layer
surrounding the entire neck circumference. It is superficial to the pre-laryngeal musculature, splits to cover both sides of the sternocleidomastoid muscle, reunites to split again to ensheath the trapezius muscle, and continues on to the spines of the cervical vertebrae (Figure 4). The SL-DCF attaches to the hyoid and then splits to form the capsule of the submandibular gland. Further
superiorly and laterally, the SL-DCF attaches to the mandible and splits to encircle the masseter, mandible ramus and pterygoid muscles bounding the so-called masticatory space [209] (Figure 3 and 4). Similarly, the SL-DCF covers the deep aspect of the parotid space. The SL-DCF continues in a superior direction over the zygomatic bone and temporalis muscle as the deep temporal fascia [503].
Therefore, as far as the parotid region is concerned, the main layers involved are the superficial cervical fascia and the SL-DCF [209; 514]. The main subject of dispute is the relative contribution of the SL-DCF to the superficial parotid aponeurosis. Grodinsky and Holyoke [209], and Testut [514] favor the presence of a complete aponeurotic layer from the SL-DCF covering the parotid gland. On the other hand, Coller and Yglesias found a capsule only on the deep side of the parotid gland, the superficial side being covered only by the superficial layer [103].
Renewed interest to this apparently scholastic dispute was brought by the description of the so-called superficial musculo-aponeurotic system, or SMAS, by Mitz and Peyronie [361; 513]. The SMAS is a key concept in modern rhytidectomy [438]. Early facelift techniques were essentially skin mobilization through undermining and excision [23; 263], while second generation facelift techniques [402; 483] involve dissection of the SMAS down to the platysma and its
cephaloposterior advancement. Because of the clinical relevance, the exact anatomical fascial layering and the relation to facial nerve branching has generated a large controversy. Recently, the SMAS technique has been claimed to provide better postparotidectomy esthetic results [7; 264; 428]
and to prevent Frey syndrome [7; 51; 428; 562].
According to Mitz and Peyronie [361], the SMAS: 1) is a continuation of the superficial cervical fascia - platysma complex; 2) attaches anteriorly to the muscles of facial expression; 3) separates the subcutaneous fat in two layers; 4) is independent of the "parotid fascia" which is located deep to the SMAS. On the other hand, Jost and Levet [265] show different facial layers: 1) a superficial fascia under the skin; 2) a layer continuing the platysma and covering the parotid gland, which is called the "parotid fascia". The "deep fascia" (no precise reference to a corresponding neck structure) is located only on the deep aspect of the parotid gland (Figure 5 and 6).
A lack of generally accepted agreement persists [438; 537]. It is now accepted that the SMAS layer is a continuation of the platysma neck layer [163; 204; 438; 502; 516; 537]. What is disputed is whether there is a distinct superficial fascial layer lateral to the SMAS [265; 516], whether the parotid fascia is a separate layer deep to the SMAS [163; 361; 502], or whether a single
subcutaneous layer is present [537]. The more recent description by Gosain et al. [204] might bring
a consensus: 1) laterally to the SMAS the fibrous septa joining the superficial fascia to the skin are well developed over the parotid and could have been interpreted by Jost and Levet as a separate fascia; 2) the SMAS is below the fat and represents a continuation of the platysma - superficial cervical fascia; 3) a distinct parotid fascia is present covering the gland, but it is extremely thin, explaining why it could have been missed by previous investigators. In addition, significant individual variation is present in the thickness of these different layers [204].
Figure 4: Schematic representation of the fascial layers of the neck
The three layers of the superficial layer of the deep cervical fascia are drawn: in red the superficial layer, in blue the middle or visceral layer, and in green the deep layer.
Figure 5: Schematic representation of the fascial layers at the level of the hard palate The facial extension of the superficial layer of the deep cervical fascia is shown to surround the parotid gland and masseteric space on both superficial and deep face. Reprinted without permission from Grodinsky and Holyoke [209]. Abbreviations: MAX.S. = Maxilla sinus; MAND. = Mandible; MASS.M. = Masseter muscle; PT.INT.M. = Pterygoid internal muscle; PT.EXT.M. = Pterygoid external muscle; MASTIC.SP. = Masticator space; PAROT.GL.
= Parotid gland; E.C.A. = External carotid artery; P.F.V. = Posterior facial vein; MAST.PROC. = Mastoid process;
DIG.POST.M. = Posterior belly of the digastric muscle; ST.CL.M. = Sternocleidomastoid muscle;
LAT.PHARYNG.SP. = Lateral pharyngeal space; TEN.VEL.PAL.M. = Tensor velopalatini muscle;
LEV.VEL.PAL.M. = Levator velopalatini muscle; AUDIT.TUBE = Auditory tube; PHARYNX VISC. F. = Pharyngeal visceral fascia; ALAR F. = Alar fascia; PREVERT.F. = Prevertebral fascia; SCAL.F. = Scalene fascia;
I.J.V. = Internal jugular vein; C.A. = Carotid artery.
Figure 6: Anatomical cross-section showing the fascial layers lateral to the parotid gland Abbreviation: M – mandible and masseter muscle, P – parotid gland, S – submandibular gland, SCM – sternocleidomastoidien, SF – superficial fascia, T – temporalis muscle, Z – zygomatic bone. The discussion is centered about the fascia layers included in the fascia marked by ?. It should contain the SMAS, which is the facial extension of the platysma and its fascia, and the facial extension of the SL-DCF. Whether this fascial layer can be divided into 2 layers, with a separate parotid fascia is debatable. The superficial fascia below the epidermis is clearly seen.
1.2.2. Contents of the parotid space
The majority of the parotid space is occupied by the parotid gland. Other anatomical structures (Figure 7) enclosed by the parotid fascia include a) arteries: the external carotid artery and its terminal branches; b) veins: the external jugular vein and its branches; c) lymphatic vessels and ganglions; d) nerves: the facial nerve, the great auricular nerve, and the auriculotemporal nerve.
The external carotid artery ascends behind the digastric muscle [424] to enter the parotid space between the stylohyoid muscle and ligament [424]. It travels on the posterior and middle wall of the parotid space and gives off, within the parotid space, postauricular, including stylomastoid, and parotid branches. The terminal bifurcation of the external carotid artery into superficial temporal artery and internal maxillary artery usually takes place in the parotid space [424]. The superficial temporal artery ascends lateral to the zygoma, joined by the temporal branches of the facial nerve (§1.2.5.), while the internal maxillary artery pierces the deep parotid aponeurosis, in the retrocondylar space of Juvara [424], to enter the parapharyngeal space.
The retromandibular vein (retrofacial, posterior facial vein) is formed by the union of the superficial temporal vein and the internal maxillary vein(s) at the level of the maxillary condyle [260;
297; 514]. The vein is entirely within the parotid gland and is located within 5 mm of the branching of the facial nerve [277; 297]. The postauricular and occipital veins join the retromandibular vein either within the parotid space, or just inferior to it. The retromandibular vein gives of a
communicating branch for the facial vein and continues in the neck as the external jugular vein [424]. Dargent and Duroux [114] attempted to schematize the venous drainage around the parotid gland and found this so-called textbook pattern in 71%, the remaining cases having large veins in front of the facial nerve and its branches.
Numerous lymphatic ganglions are located within the parotid space. They drain the scalp and the face. During development (see §1.2.4), the parotid tissue develops before the parotid and cervical fascias [196; 260], resulting in the encapsulation of lymphatic ganglions within the parotid gland [381].
The auriculotemporal nerve enters the parotid space through the retrocondylar space of Juvara [33; 424] and travels along the medial, than posterior aspect of the gland, crossing behind the superficial temporal vessels [260]. It than passes between the gland and the bony and cartilaginous external ear canal [33; 412], to provide the sensory innervation of the facial skin in front of the
