COMPLICATIONS OF PAROTIDECTOMY

Complications of parotidectomy can be divided into early complications (including

those that occur intraoperatively and during the immediate postoperative period) and
late postoperative complications (Box 20-1). Each complication of parotidectomy is
discussed separately. Expected sequelae of parotidectomy should be differentiated
from complications and are also presented.
BOX 20-1
Complications of Parotidectomy

EARLY COMPLICATIONS
Facial nerve injury
Hemorrhage
Hematoma
Infection
External otitis
Sialocele
Seroma
Salivary fistula

LATE COMPLICATIONS
Frey syndrome
Trismus
Amputation neuroma (greater auricular nerve)
Tumor recurrence
Cosmetic deformity
Hypertrophic scar
Keloid
Earlobe malpositioning

Early Complications
Facial Nerve Injury
Facial nerve paralysis represents the major complication of parotid surgery. The risk of
this complication can be minimized with proper and careful surgical techniques.
At the time of surgery, paralysis agents (except for short-acting agents such as
succinylcholine at the time of anesthesia induction) should be avoided. If the local
injection of epinephrine along the proposed incision is used for vasoconstriction, then
the injection solution should contain no local anesthetic (e.g., lidocaine), which may
cause temporary neural blockade. The facial skin flap should be carefully raised to
avoid injury to the peripheral facial nerve branches beyond the anterior border of the
gland. Intraoperatively, the facial nerve should be carefully identified with the aid of
anatomic landmarks (Box 20-2). Wide surgical exposure is recommended to allow for
the adequate visualization of these landmarks. Adequate operative exposure reduces

the risk of inadvertent nerve injury during the dissection for facial nerve identification
and allows for safe hemostasis if bleeding occurs during dissection near the facial
nerve.
BOX 20-2
Anatomic Landmarks for Facial Nerve Identification
1.

Tragal pointer (The nerve is approximately 1-cm medial and anteroinferior to the tip of
the pointer.)

2.

Tympanomastoid suture (The nerve is approximately 68-mm medial to the suture.)

3.

Digastric muscle attachment to digastric groove (The nerve is just superior to and on the
same plane as the muscle attachment.)

4.

Nerve within the mastoid bone

5.

Retrograde dissection of the peripheral facial nerve branch

A disposable nonpulsed direct current nerve stimulator should be used judiciously for
facial nerve stimulation. However, this current can damage nerves, because it is
transmitted to the nerve for the duration of stimulator tip contact with the nerve. [13,]
[14]
Prolonged nerve contact with this type of stimulator may result in excessive current
delivery to the nerve. Repeated nerve stimulation with such a stimulator may be
responsible for temporary nerve paresis postoperatively.
Intraoperative nerve monitoring with commercially available electromyograph units can
provide valuable intraoperative information regarding facial nerve identity and integrity.
Such monitoring can be particularly useful for reoperation. In a retrospective review of
56 patients who received facial nerve monitoring during parotidectomy and of 61
patients who did not, a significant reduction in temporary facial paresis was observed in
the monitored group as compared with the unmonitored group (44% vs. 62%);
however, there was no significant difference in the rate of permanent facial paralysis.
[15]
Another retrospective review of 20 monitored and 33 unmonitored patients failed to
demonstrate a difference in temporary paresis between the monitored (20%) and
unmonitored (15%) groups.[16] A recent survey found that 60% of otolaryngologisthead
and neck surgeons and 79% of frequent U.S. parotid surgeons (i.e., those who perform
more than 10 parotidectomies per year) used a facial nerve monitoring system some or
all of the time during parotidectomy.[17] Interestingly, surgeons who used monitoring
were 21% less likely to have a history of a parotidectomy-related lawsuit. [17]
After the facial nerve is identified, it is followed peripherally. The surgeon must keep in
mind the initial steep lateral course of the nerve to the mid-gland level as well as the
anatomic variability of the facial nerve branches. Care must be taken to avoid nerve
stretch injury during dissection, and the manipulation of the nerve during dissection
should be minimized. Operating loupes or other magnification tools can be helpful for
nerve branch visualization.
After the removal of the surgical specimen, the integrity of the facial nerve is
determined both visually and with electrical stimulation. Nerve transection necessitates
immediate microsurgical neurorrhaphy.
Temporary facial nerve paralysis involving the entire facial nerve (Figure 20-4) or one
or more branches of the nerve is reported to occur in 5% to 65% of cases. [1823] The

facial nerve branch that is most at risk for temporary paralysis is the marginal
mandibular branch.[1921,23] This is thought to be the result of the high length-to-diameter
ratio of this nerve branch and of the relative lack of interconnections with other
branches of the facial nerve as compared with other facial nerve branches (e.g., the
buccal and zygomatic branches). Paralysis of the marginal mandibular branch results
in a loss of ipsilateral lower lip depressor function (Figure 20-5). Recovery from
temporary facial paresis occurs within 6 months in the majority of patients. [19,][20,][23]
Figure 20-4 Right facial paralysis after parotidectomy.

Figure 20-5 Paresis of the right marginal mandibular branch of the facial nerve. Note the
lack of lip depressor function.

Permanent facial nerve paralysis occurs less commonly than temporary paresis.
Permanent paralysis after partial parotidectomy for benign tumors is uncommon and
generally reported to occur in less than 5% to 6% of cases. [1922] A higher incidence of
both temporary and permanent facial paralysis occurs with total parotidectomy as
compared with superficial parotidectomy, perhaps as a result of the increased nerve
manipulation that is necessary for complete gland removal. [18,2023] In addition,
permanent facial paralysis is more common with reoperation for recurrent tumors. [21,][24,]
[25]
The performance of a neck dissection at the time of parotidectomy is associated
with a higher incidence of permanent paralysis of the marginal mandibular branch of
the facial nerve.[20] Care must be taken to protect the exposed facial nerve if
parotidectomy is performed before the neck dissection. Another protective option is to
perform the neck dissection before the parotidectomy.
Perzik[26] reported a 100% incidence of temporary facial paralysis with parotidectomy
for chronic sialadenitis. This is not the experience of the authors, and other reports
have shown no higher incidence of paralysis for parotidectomies performed for chronic
inflammation than with those performed for benign neoplasms. [18,][27,][28] In addition, total
parotidectomy does not appear to be associated with a higher incidence of permanent
paralysis than superficial parotidectomy when surgery is performed for chronic
parotitis.[28]
Facial paralysis involving the orbicularis oculi muscle often results in incomplete eye
closure. Conjunctivitis, keratitis, and corneal ulceration can result from eye exposure.
Epiphora results from the loss of the normal pumping action of the eyelids and lower-lid
laxity or ectropion (Figure 20-6). With facial paralysis involving the orbicularis oculi,
eye-protection measures should be instituted immediately and should include the
frequent instillation of artificial tears during the day and lubricant ophthalmic ointment
and eyelid closure with tape or the application of a moisture chamber (Figure 20-7) at
night. If prolonged or permanent paralysis is anticipated, upper-lid gold-weight
implantation is a useful technique to provide adequate eye closure. [29] In addition,
lower-lid tightening procedures may be beneficial. The patient should be questioned

periodically about eye symptoms and examined for signs of eye injury. Ophthalmologic
consultation should be obtained immediately if any eye complication is suspected.
Figure 20-6 Ectropion of the lower eyelid after intentional sacrifice of the facial nerve for a
malignant parotid neoplasm.

Figure 20-7 Eye-moisture chamber for nocturnal eye protection.

The management of permanent facial paralysis is beyond the scope of this chapter.
Facial reanimation procedures include nerve crossover techniques such as facial
hypoglossal anastomosis, cross-face nerve transplantation, masseter or temporalis
muscle transfer, and free-tissue transfer. Brow lift, rhytidectomy, blepharoplasty,
cheiloplasty, contralateral frontal neurectomy, and botulinum toxin injections to achieve
forehead symmetry for frontal paralysis are some of the other reconstructive
techniques that may help to improve the cosmetic deformities associated with facial
paralysis.
Hemorrhage and Hematoma
Hemorrhage is an uncommon intraoperative complication. Patients should be
instructed to avoid aspirin and nonsteroidal anti-inflammatory medications for several
weeks before surgery. Patients taking clopidogrel and warfarin should have medical
clearance to stop these medications at least 1 week before surgery. If these
medications cannot be safely discontinued, then replacement with low-molecularweight heparin therapy is recommended. Heparin can be stopped immediately before
surgery and resumed after all sanguinous wound drainage has ceased. The proper
identification, division, and ligation of blood vessels during surgical dissection usually
prevents significant intraoperative bleeding. During total parotidectomy and the
removal of the deep lobe, the internal maxillary artery and its branches are the primary
vessels of concern for significant bleeding.
During the removal of tumors of the superficial lobe, the posterior facial vein, which
courses deep to the facial nerve, can usually be preserved. The ligation of this vessel
can contribute to the venous congestion of the gland and to increased venous bleeding
from the cut surface of the gland during dissection.
Intraoperative bleeding should be controlled with careful technique using ligatures or
bipolar electrocautery. Care should be taken to avoid suction or clamp compression
injury to the facial nerve during attempts at hemostasis. Unipolar electrocautery should
be used with extreme care because of the risk of electrical current transmission to the
facial nerve. There continues to be interest among parotid surgeons to identify surgical
instruments that provide hemostasis without excessive facial nerve stimulation during

parotidectomy. A retrospective review comparing 44 patients who underwent

parotidectomy with the Harmonic Scalpel (Ethicon Endo-Surgery, Inc., Cincinnati, Ohio)
with 41 patients who had conventional parotidectomy observed significantly less
intraoperative blood loss and a reduced incidence of facial nerve paresis in the
Harmonic Scalpel group.[30]Similarly, a retrospective series of 50 patients who
underwent parotidectomy with the Hemostatix Scalpel (Hemostatix Medical
Technologies, Bartlett, TN) were found to have significantly shorter operative times and
less intraoperative blood loss as compared with patients undergoing conventional
parotidectomy.[31] Another study of 77 parotidectomy patients asserted that the
Hemostatix Scalpel was an independent risk factor for facial nerve paralysis. However,
the larger Hemostatix #10 blade was used in this series rather than the more widely
accepted #15 blade.[32]
Postoperative hematoma formation is unusual, and it is reported to occur in 3% to 7%
of cases.[19,][21,][22] Hematoma is typically related to inadequate hemostasis or increased
venous blood pressure during emergence from anesthesia. Hematoma results in
wound and facial swelling (Figure 20-8), and the patient will often complain of pain.
Hemorrhage may occur from the wound and drain sites. Although some minor
hematomas can be evacuated at the bedside, hematoma formation usually requires a
return to the operating room for hematoma evacuation and wound exploration. Any
identified bleeding sites are carefully controlled with ligatures or bipolar electrocautery
with the identification and protection of the facial nerve.
Figure 20-8 Hematoma after left parotidectomy and neck dissection. Note the swelling of the
wound and bleeding from the wound and drain sites.

Infection
Parotidectomy is considered a clean surgical procedure. Postoperative infection is
uncommon, and it is reported to occur in less than 3% of patients. [19,][22] Infection is an
unusual complication of parotidectomy, probably because of the rich vascular supply to
the parotid region. Infection is avoided by adherence to sterile surgical technique and
the careful handling of tissues intraoperatively. Care must be taken during
parotidectomy to avoid entry into the external auditory canal and to avoid oral flora
contamination of the wound. Cellulitis (Figure 20-9) is treated with an intravenous
antibiotic with activity against gram-positive organisms until the tissue edema and
erythema begin to fade (usually 2448 hours). This is followed by a course of oral
antibiotics. Abscess formation requires incision and drainage as well as appropriate
antibiotics.
Figure 20-9 Cellulitis after parotidectomy.

Johnson and Wagner[33] examined the benefit of prophylactic antibiotics for

parotidectomy for cases in which no infection existed before surgery and found no

difference in infection rates with or without perioperative antibiotics. However,

perioperative prophylactic antibiotics are recommended for patients who have had
recent parotid gland infection or recent surgery.
External Otitis
External otitis can occur postoperatively, and it is related to blood collection in the
external auditory canal intraoperatively. Blood provides an excellent medium for
bacterial growth in the ear canal. External otitis can be prevented by carefully placing a
petrolatum gauze pack in the ear canal at the beginning of the procedure to prevent the
entry of blood (Figure 20-10). If blood enters the ear canal intraoperatively, saline
irrigation and careful suctioning of the ear canal are performed at the completion of
surgery. The treatment of postoperative external otitis consists of the careful removal of
blood and debris from the external auditory canal and the instillation of antibiotic
eardrops.
Figure 20-10 Petrolatum gauze pack placed in the external auditory canal to prevent the
entry of blood.

Flap Necrosis
Flap necrosis is an uncommon complication of parotidectomy.[19] Necrosis occurs most
commonly in the distal tip of the inframastoid portion of the parotid flap (Figure 20-11).
Proper flap design and plane of elevation, careful handling of the flap, and the
avoidance of flap desiccation intraoperatively are all important factors for the
prevention of this complication. Other factors that may be responsible for the
development of this complication include the impairment of the flap's blood supply as a
result of smoking, diabetes mellitus, or prior radiation therapy. Patients who smoke
should be strongly encouraged to quit smoking several weeks before surgery to reduce
the risk of skin-flap necrosis.[34,][35] Venous congestion of cervicofacial rotation flaps can
be reduced with the rapid institution of leech therapy for flap salvage (Figure 20-12).
Figure 20-11 Parotid flap necrosis in a patient with diabetes mellitus.

Figure 20-12 Venous congestion in a cervical facial rotation flap of a heavy smoker treated
with leech therapy.

The treatment of parotid flap necrosis includes the debridement of necrotic tissue in the
wound. Depending on the size of the defect, secondary wound closure, closure by
secondary intention, or split-thickness skin grafting are options for wound closure.
Sialocele and Seroma

Sialocele represents a collection of saliva under the parotid flap and presents as a
nontender, cystic mass (Figure 20-13, A). Sialocele occurs after partial parotidectomy
related to salivary leakage from the cut surface of the gland remnant. This complication
occurs in approximately 5% to 10% of patients after partial parotidectomy.[18,][19,][22]
Figure 20-13 A, Sialocele after partial parotidectomy. B, Needle aspirate of sialocele fluid.

Seroma is clinically similar to sialocele but differs in that it has lower amylase content
on fluid analysis. However, such differentiation has little practical importance for the
management of these two uncommon complications. Postoperative seroma is unusual
if closedsuction drainage is employed until the wound drainage falls below 30 cc in a
24-hour period. However, a reduction in drain output of this degree may take several
days and result in a prolonged hospital stay in patients who underwent extensive
dissection or who have particularly large parotid glands. A recent randomized,
controlled study found significantly less postoperative drainage volume and fewer
postoperative seromas among 30 patients treated with a fibrin tissue glue to the wound
bed before closure as compared with 30 patients who underwent standard closure
alone.[36] The use of tissue sealants during parotidectomy may increase in the future to
allow for shorter hospital stays.
The management of sialocele and seroma includes needle aspiration of the fluid
collection after careful antibacterial skin preparation. Aspirated fluid is usually clear and
yellow (Figure 20-13, B). Pressure dressings are of little value for this problem, and
they are cumbersome to the patient. Patients should be counseled regarding potential
reoccurrence after needle aspiration but reassured that sialoceles are rarely a chronic
problem. Alternatively, the fluid collection may be observed, and fluid reabsorption will
often occur spontaneously. Large, persistent fluid collections may necessitate Penrose
or suction drain replacement.
Salivary Fistula
Salivary fistula is manifested by salivary drainage from the wound (Figure 20-14). It is
an uncommon complication of subtotal parotidectomy, occurring in less than 3% of
cases.[18,][21] Salivary fistulas are generally selflimited and usually close spontaneously
with local care within several weeks. A fistula will rarely persist for months or
chronically. The skin surrounding a chronic fistula is often excoriated and scarred as a
result of the irritative effect of saliva. [37]
Figure 20-14 Salivary fistula after partial parotidectomy.

A chronic salivary fistula usually requires additional treatment to effect closure.

Completion total parotidectomy is curative for chronic salivary fistula but involves the
risk of facial nerve injury.[38] Anticholinergic medications have been reported to have a
beneficial effect on the reduction of salivary flow with resultant fistula resolution. [39,]
[40]
Transdermal scopolamine may have a similar effect on salivary flow reduction.
[41]
Tympanic neurectomy, which interrupts the parasympathetic innervation to the
parotid gland, has also been advocated as a successful method for the closure of

chronic salivary fistulas.[37,][42] Recent reports have shown benefit with the use of
botulinum toxin for salivary fistula.[43,][44] Ultrasonography is useful for proper injection
into the remaining parotid gland parenchyma (Figure 20-15).
Figure 20-15 Ultrasound-guided botulinum toxin injection for postparotidectomy salivary
fistula.

Late Complications
Frey Syndrome
Frey syndrome (gustatory sweating, auriculotemporal syndrome) is a relatively
common late complication of parotidectomy. This complication is thought to occur in
relation to the aberrant regeneration of the postganglionic secretomotor
parasympathetic nerve fibers, which are carried in the auriculotemporal nerve from the
otic ganglion to the parotid to the severed postganglionic sympathetic fibers that supply
the sweat glands of the skin (Figure 20-16). As a result, sweating, dermal flush, or both
occur in the distribution of the auriculotemporal nerve during salivary stimulation.
Figure 20-16 Proposed aberrant regeneration mechanism of Frey syndrome. A, Normal
parotid gland and sweat gland parasympathetic and sympathetic innervation. B, Aberrant
regeneration of severed parotid postganglionic parasympathetic nerve fibers to severed sweat
gland postganglionic sympathetic fibers.

The Minor starchiodine test will objectively demonstrate the area affected by Frey
syndrome.[45] An iodine solution consisting of 3 g of iodine, 20 g of castor oil, and 200
ml of absolute alcohol is applied to the skin of the face and neck. After the solution
dries, the face is dusted with starch powder. The patient is given a sialogogue such as
lemon candy. In areas of sweating, the starch and iodine react, producing a dark-blue
discoloration (Figure 20-17). An alternative simple method for the objective assessment
of Frey syndrome is to apply one ply of a two-ply tissue to the patient's face after the
patient has been given a sialogogue. The tissue will adhere to areas of perspiration
(Figure 20-18).
Figure 20-17 Minor starchiodine test for Frey syndrome. Discoloration occurs in the affected
area after gustatory stimulation.

Figure 20-18 Simple assessment of Frey syndrome with facial tissue. The affected area is
demarcated by the wet area on the tissue.

The reported incidence of Frey syndrome after parotidectomy varies greatly depending
on how closely patients are questioned and examined for the condition. The incidence

of objectively documented Frey syndrome by the Minor starchiodine test approaches

95% to 100%.[4653] Reports indicate incidences of patient awareness of this problem of
between 20% and 65%.[18,19,4649] Symptomatic Frey syndrome, however, occurs in only
approximately 10% to 15% of patients.[18,][46,][50] Symptoms usually develop after a latent
period of many months to a year or more after surgery.[18,][51] The delayed development
of symptoms of up to 8.5 years after surgery has been reported. [49]
Frey syndrome may be preventable by the elevation of a thick skin flap at the time of
parotid exposure. Singleton and Cassisi[52] reported only a 2.6% incidence of this
complication with thick-flap elevation as compared with a 12.5% incidence with a
thinner flap. The use of a sternocleidomastoid muscle flap for the prevention of Frey
syndrome has been shown to be ineffective.[53,][54] Other reports have examined the use
of barriers placed at the time of parotidectomy to prevent Frey syndrome. Various
biologic barriers placed between the parotid bed and the skin, including lyophilized
dura, polyglactin 910-polydioxane, and expanded polytetrafluoroethylene, may reduce
the incidence of Frey syndrome, but they have not been widely accepted as a result of
an observed increase in postoperative seroma and salivary fistula with their use.
[55]
Acellular dermis has also been reported to significantly reduce the incidence of Frey
syndrome while improving postoperative facial contour. However, an increased rate of
postoperative seroma formation has also been noted with its use. [56,][57]
After they understand the condition, many patients choose to tolerate the symptoms of
Frey syndrome and do not opt for treatment. [19,][21] Some patients benefit from the daily
or twice-daily application of antiperspirants to the affected area. [49,][58] Treatment with
anticholinergic medications is based on the fact that the postganglionic sympathetic
innervation to the sweat gland is cholinergic rather than adrenergic. However, systemic
anticholinergic medications are associated with a high incidence of side effects such as
dry mouth and blurred vision, which are usually undesirable.
Topical 1% or 2% glycopyrrolate applied to the affected area of gustatory sweating has
been shown in double-blind studies to be an effective treatment with a low incidence of
side effects.[49,][59] The relief of symptoms lasts for several days after the application of
topical glycopyrrolate. This medication is not available commercially as a topical
preparation; therefore a lotion or cream must be made specially by a pharmacist.
Contraindications to the use of this medication include glaucoma, pyloric obstruction,
and prostate hypertrophy.
Currently a common and effective method for the management of Frey syndrome is
botulinum toxin injections. The recommended administration of botulinum toxin A for
Frey syndrome is 2.5 IU/0.1 ml injected subcutaneously into each 1.0 cm 2 of affected
area, with total dosages ranging from 80 IU to 100 IU. [60,][61] The majority of patients
treated with botulinum toxin A will have an objective return of gustatory sweating by
starch iodine testing by 18 months after the injection; however, subjective symptoms
are usually reported to be less severe.[6062] Patients with a symptomatic recurrence of
Frey syndrome often benefit from repeat injections. [61]
The surgical correction of Frey syndrome includes fascial graft interposition between
an elevated skin flap and the gland.[63,][64] This technique has been shown to have longterm benefit for some patients, but there have been few reports of this procedure.
[63]
Extreme care must be taken to avoid facial nerve injury during skin-flap elevation
with this approach. As a result of the efficacy of the nonsurgical management of Frey
syndrome, surgical management is presently an uncommon remedy.
Gustatory rhinorrhea has occasionally been reported after parotidectomy.[6567] Patients
complain of ipsilateral rhinorrhea with eating. A proposed pathway for this symptom is

the regeneration of damaged preganglionic parasympathetic fibers in the lesser

superficial petrosal nerve through the greater superficial petrosal nerve to the Vidian
nerve, the sphenopalatine ganglion, and the long sphenopalatine nerve, which supplies
the nasal mucous glands.[65]
Trismus
Trismus occurs rarely after parotidectomy, and, if it occurs, it is usually mild and
transient (Figure 20-19). Trismus is most likely related to masseter inflammation and
fibrosis or other scarring. Radiation therapy may contribute significantly to this problem.
Trismus usually improves with mouth-opening exercises. Some patients may benefit
from physical therapy or the use of a commercially available mouth-opening device
(e.g., Therabite [Atos Medical, Hrby, Sweden]).
Figure 20-19 Trismus after total parotidectomy and postoperative radiation therapy for an
adenoid cystic carcinoma.

Hypertrophic Scar and Keloid

For the majority of patients, the parotidectomy incision heals well and is cosmetically
acceptable as a result of concealment in the natural skin creases. Care must be taken
during wound closure to carefully realign the wound to avoid the malpositioning of the
earlobe. Hypertrophic scarring or keloid will rarely complicate healing (Figure 20-20).
Scar revision, steroid injections, and other therapies are treatment options for the
management of hypertrophic scars.
Figure 20-20 A, Hypertrophic scar after parotidectomy. B, Keloid after parotidectomy.

Amputation Neuroma of the Greater Auricular Nerve

An amputation neuroma (Figure 20-21) will occasionally form at the severed end of the
greater auricular nerve after parotidectomy.[68,][69] The diagnosis of an amputation
neuroma is usually clinical. Patients may complain of localized or radiating pain related
to the mass. A tender nodule usually less than 1 cm in diameter is palpable over the
upper border of the sternocleidomastoid muscle. Palpation of the mass usually elicits
tenderness and paresthesias.[68] Eddey[51] reported a 3.8% incidence of neuroma
formation after parotidectomy. Hobsley[68] reported seven amputation neuromas that
were diagnosed an average of 4 years after surgery. The incidence of this problem may
be reduced with recent trends to preserve the greater auricular nerve during
parotidectomy. Simple excision of the neuroma is usually curative.
Figure 20-21 Excised amputation neuroma of the greater auricular nerve.

Expected Sequelae
The expected sequelae of parotidectomy are as follows:
Some degree of sensory loss in the distribution of the greater auricular nerve
Soft-tissue deficit in the area of resection
Scar
Sensory Loss in the Distribution of the Greater Auricular Nerve
All patients should be informed that sensory loss in the distribution of the greater
auricular nerve to some degree is an expected sequela of parotidectomy. The posterior
branch of this nerve can be preserved.[70,][71] In the authors' experience, this is possible
in more than 50% of cases (Figure 20-22). The area of sensory loss decreases, and,
with time, the sensory deficit becomes less noticeable to the patient. [72] Only
approximately 25% of patients complained of this symptom when they were questioned
postoperatively in the series reported by Eddey.[51] Patients with a sensory deficit
should be cautioned about the possibility of unnoticed injury to the ear by thermal or
other trauma (Figure 20-23).[73]
Figure 20-22 Preservation of the posterior branch of the greater auricular nerve. A, Nerve dissected
circumferentially. B, Nerve undermined with a cuff of parotid tissue. This method avoids nerve
stretch injury and contributes to improved facial contour.

Figure 20-23 A, Burn to the pinna after parotidectomy. B, Dog bite of pinna. The patient
was unaware of this injury, which was sustained while playing with a frisky puppy.

Soft-Tissue Deficit
A soft-tissue deficit in the area of resection is another expected sequela of
parotidectomy. Most patients are not disturbed by this, and few request consideration
for reconstructive surgery for its correction. This deformity is more severe after total or
radical parotidectomy (Figure 20-24), and primary reconstruction may be beneficial to
restore facial contour. Multiple reconstructive procedures have been proposed for
correction when the defect is significant, including fat graft, [74,][75] microvascular
muscular free flaps,[76] sternocleidomastoid muscle rotational flaps,[77,][78] and fillers (e.g.,
AlloDerm [LifeCell, Branchburg, NJ]).
Figure 20-24 Soft-tissue deficit after total parotidectomy. Note the infra-auricular and facial
depression.

Scar
After parotidectomy, the wound generally heals with an inconspicuous scar. Careful
placement of the incision parallel to relaxed skin tension lines contributes to optimal
scar concealment. For young patients and women without a prominent preauricular

crease, an incision behind the tragus may offer better camouflage for the scar line
(Figure 20-25).
Figure 20-25 Posttragal incision for scar camouflage for a 15-year-old girl requiring a
parotidectomy for a benign salivary neoplasm.

Tumor Recurrence
Recurrent tumor is a dreaded late complication of parotidectomy. Some malignant
parotid tumors are known to have a relatively high rate of recurrence. Recurrences are
more likely with higher tumor stage and higher histopathologic grade and among those
patients with preoperative facial nerve paralysis. [7981] Long-term follow up is necessary,
particularly for adenoid cystic carcinoma and acinic cell carcinoma, because late
recurrence can occur with these parotid malignancies. [79] Postoperative radiation
therapy has been shown to reduce the risk of local recurrence of select malignant
parotid neoplasms as compared with surgery alone. [8183]
The recurrence of pleomorphic adenoma occurs less than 1% of the time after formal
parotidectomy.[84,][85] Alternatively, the enucleation of pleomorphic adenomas results in
recurrence rates of 30% to 50%.[84,][86,][87] Recurrences after partial parotidectomy tend
to occur later than those that occur after enucleation. [88] Recurrent pleomorphic
adenoma may also occur as a result of tumor rupture and spillage during surgery with
wound seeding.[89] The majority of recurrent pleomorphic adenomas are multifocal. [84,][88,]
[89]
The average interval between the initial surgery and the identification of tumor
recurrence is 10 years or more.[90,][91] Both physical examination and imaging studies
tend to underestimate the extent of disease (Figure 20-26).
Figure 20-26 Coronal magnetic resonance image demonstrating the multifocal recurrence of
pleomorphic adenoma of the left parotid.

Total parotidectomy with facial nerve preservation is recommended for the

management of the first recurrence of pleomorphic adenoma. [24,][84,][88]Niparko and
colleagues[92] reported a 53% incidence of control of initial recurrences with long-term
follow up. Fee and colleagues[24] showed diminished control rates with subsequent
recurrences after the initial recurrence. Increased risks of both temporary and
permanent facial nerve paralysis occur with surgery for recurrent pleomorphic
adenoma.[24,][88] The excision of the old scar tract or of areas of skin adhering to the
tumor may be necessary to ensure complete tumor resection (Figure 20-27). En
bloc tumor resection with facial nerve sacrifice and immediate facial nerve grafting may
be necessary for confluent recurrences that encase the facial nerve. [84,][92,][93]
Figure 20-27 Excision of skin with a frozen-section margin for a patient with a recurrent
malignant parotid cancer.

Postoperative radiation therapy appears to be beneficial after the resection of recurrent

pleomorphic adenoma.[9496] Radiation therapy has been shown to be effective for those
patients with microscopic residual pleomorphic adenoma after the surgical resection of
recurrence but not for patients with residual gross disease after excision. [95] Patients
must be informed that radiation therapy carries with it a low risk of subsequent
radiation-induced malignancy.[97]