Plastic and Reconstructive Surgery Board Review Pearls of Wisdom 3th

CHAPTER 48 Facial Paralysis: Static and Dynamic reatment
473

Like the rontalis or upper brow paralysis, it is cosmetically and unctionally acceptable to paralyze which
normal perioral muscle or improved lower lip symmetry?
T e depressor labii in erioris. T is can be accomplished with botulinum toxin (temporary) or with partial
myectomy (permanent).

Describe the digastric trans er or treatment o marginal mandibular palsy.
T e technique involves preserving the mental attachment and tunneling the anterior belly and intermediate
tendon o the digastric through a subcutaneous tunnel to the lower lip. T e intermediate tendon is split and
attached to the mucocutaneous junction o the middle and lateral lower lip. Activation is not spontaneous unless
modi ed through a cross- acial nerve gra t. T e anterior belly receives its motor innervation rom the nerve to
mylohyoid, which arises rom the mandibular branch o the trigeminal nerve (V3) (see Fig. 48-3).
Figure 48-3 Digastric trans er or treatment o marginal mandibular palsy.
REFERENCES
Borschel GH, Kawamura DH, Kasukurthi R, Hunter DA, Zuker RM, Woo AS. T e motor nerve to the masseter muscle: An anatomic
and histomorphometric study to acilitate its use in acial reanimation. J Plast Reconstr Aesthet Surg. 2012;65:363–366.
Chan JY, Byrne PJ. Management o acial paralysis in the 21st century. Facial Plast Surg. 2011;27:346–357.
Chang CY, Cass SP. Management o acial nerve injury due to temporal bone trauma. Am J Otol. 1999;20:96–114.
Cocker NJ. Management o traumatic injuries to the acial nerve. Otolaryngol Clin North Am. 1991:24:215–227.
Dingman RO, Grabb WC. Surgical anatomy o the mandibular ramus o the acial nerve based on the dissection o 100 acial halves.
Plast Reconstr Surg ransplant Bull. 1962;29:266–272.
Dora shar AH, Borsuk DE, Bojovic B, et al. Sur ace anatomy o the middle division o the acial nerve: Zuker’s point. Plast Reconstr
Surg. 2013;131:253–257.
Evans GR, Brandt K, Ang K, et al. Peripheral nerve regeneration: the e ects o postoperative irradiation. Plast Reconstr Surg. 1997:
100:375–380.
Fattah A, Borschel GH, Manktelow R , Bezuhly M, Zuker RM. Facial palsy and reconstruction. Plast Reconstr Surg. 2012;129:340e–352e.
Hadlock A, Green eld LJ, Wernick-Robinson M, Cheney ML. Multimodality approach to management o the paralyzed ace.
Laryngoscope. 2006;116:1385–1389.
Kesser B. Anatomy o the acial nerve and associated structures. In: Slattery WH, Azizzadeh B, eds. T e Facial Nerve. New York, NY:
T ieme; 2014:1–22.
Klebuc MJ. Facial reanimation using the masseter-to- acial nerve trans er. Plast Reconstr Surg. 2011;127:1909–1915.
Kumar D. Moebius syndrome. J Med Genet. 1990:27:122–126.
Labbé D, Huault M. Lengthening temporalis myoplasty and lip reanimation. Plast Reconstr Surg. 2000;105:1289–1297; discussion
1298.

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Levine RE, Shapiro JP. Reanimation o the paralyzed eyelid with the enhanced palpebral spring or the gold weight: modern replacements
or tarsorrhaphy. Facial Plast Surg. 2000;16(4):325–336.
Manktelow R . Use o the gold weight or lagophthalmos. Operat ech Plast Reconstr Surg. 1999;6:157–158.
Manktelow R , omat LR, Zuker RM, Chang M. Smile reconstruction in adults with ree muscle trans ers innervated by the masseter
motor nerve: E ectiveness o cerebral adaptation. Plast Reconstr Surg. 2006;118:885–899.
Maurizio B. Di erential diagnosis o acute acial paralysis. In: Slattery WH, Azizzadeh B, eds. T e Facial Nerve. New York, NY: T ieme;
2014:57–62.
May M. rauma to the acial nerve. Otolaryngol Clin North Am. 1983:16:661–670.
May M, Sobol SM, Mester SJ. Hypoglossal- acial nerve interpositional-jump gra t or acial reanimation without tongue atrophy.
Otolaryngol Head Neck Surg. 1991;104:818–825.
McLaughlin CR. Surgical support in permanent acial paralysis. Plast Reconstr Surg (1946). 1953;11:302–314.
Meltzer NE, Alam DS. Facial paralysis rehabilitation: state o the art. Curr Opin Otolaryngol Head Neck Surg. 2010;18:232–237.
Peitersen E. T e natural history o Bell’s palsy. Am J Otol. 1982;4:107–111.
Pitanguy I, Ramos AS. T e rontal branch o the acial nerve: the importance o its variations in ace li ting. Plast Reconstr
Surg.1966;38:352–356.
Rubin LR, Lee GW, Simpson RL. Reanimation o the long-standing partial acial paralysis. Plast Reconstr Surg. 1986;77:41–49.
Seckel BR. Facial danger zone 2. In: Seckel BR, ed. Facial Danger Zones Avoiding Nerve Injuries in Plastic Surgery. St. Louis, MO:Quality
Medical Publishing;1994;12–17.
an S . Anterior belly o digastric muscle trans er: a use ul technique in head and neck surgery. Head Neck. 2002;24:947–954.
erzis JK. “Babysitters.” An exciting new concept in acial reanimation. In: Proceedings of the 6th International Symposium on the Facial
Nerve. Rio de Janeiro, Brazil: Kugler and Ghendini Publications; 1990.
erzis JK, Kalantarian B. Microsurgical strategies in 74 patients or restoration o dynamic depressor muscle mechanism: a neglected
target in acial reanimation. Plast Reconstr Surg. 2000;105:1917–1931.
erzis JK, Karypidis D. T e outcomes o dynamic procedures or blink restoration in pediatric acial paralysis. Plast Reconstr Surg
2010;125:629–644.
erzis JK, Kyere SA. Minitendon gra t trans er or suspension o the paralyzed lower eyelid: our experience. Plast Reconstr Surg 2008;
121:1206–1216.
ucker H, May M. T e acial nerve and extracranial surgery. In: May M, Schaitkin B, eds. T e Facial Nerve May’s Second Edition.
2nd ed. New York, NY: T ieme; 2000;491–503.
Yavuzer R, Jackson I . Partial lip resection with orbicularis oris transposition or lower lip correction in unilateral acial paralysis.
2001;108:1874–1879.
Zuker RM, Manktelow R , Hussain G. Facial paralysis. In: Mathes SJ, ed. Plastic Surgery. Vol 3. 2nd ed. Philadelphia, PA: Saunders;
2005:883–915.

475
Priyesh Patel, MD and
Rakesh K. Chandra, MD

Describe the anatomy o the branchial apparatus (see Fig. 49-1).
Head and Neck
Embryology
CHAPTER 49
Figure 49-1 Branchial arches.
T e branchial apparatus consists o ve paired mesodermal arches that are separated by invaginations o ectoderm
and endoderm known, respectively, as cle ts and pouches. Each arch has a cartilage bar, an artery, and a nerve.
T e derivatives o the cartilage o each arch orm the acial skeleton and laryngeal ramework, while the artery and
nerve supply and innervate the derivatives o the arch.

What is derived rom the ectoderm/branchial cle ts?
T e ectoderm o the rst cle t orms the major salivary glands, the mucosa o the oral cavity, and the lining o
the anterior two-thirds o the tongue, while the ectoderm o the second, third, and ourth arches use to orm a
common cervical sinus (o His), which normally degenerates.

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What is derived rom the endoderm/branchial pouches?
T e endoderm o the branchial pouches orms the middle ear, the glandular structures o the oropharynx, the
parathyroid glands, and the thymus.

What is the nerve o the rst branchial arch?
T e trigeminal nerve.

What is the artery o the rst branchial arch?
T e artery o the rst arch partly degenerates and partly remains as the maxillary artery.

What are the derivatives o the cartilage o the rst arch?
Meckel’s cartilage is the cartilage o the rst arch and its derivatives are the mandible, the malleus (except or the
manubrium), and the incus (except or the long process).

What are the muscular derivatives o the rst branchial arch?
T e muscular derivatives are the muscles o mastication (temporalis, masseter, medial and lateral pterygoids), the
tensor tympani, the mylohyoid, anterior belly o the digastric, and the tensor veli palatini.

What is the nerve o the second branchial arch?
T e acial nerve.

What is the artery o the second branchial arch?
T e stapedial artery, which usually degenerates in normal development but occasionally persists in adulthood.

What are the derivatives o the cartilage o the second arch?
Reichert’s cartilage is the cartilage o the second arch and its derivatives are the manubrium o the malleus, the
long process o the incus, the stapes suprastructure, the styloid process, the stylohyoid ligament, and the body and
lesser cornu o the hyoid bone.

What are the muscular derivatives o the second branchial arch?
T e muscular derivatives o the second arch are the muscles o acial expression, the platysma, stylohyoid, posterior
belly o the digastric, and the stapedius muscle.

What is the nerve o the third branchial arch?
T e glossopharyngeal nerve.

What is the artery o the third branchial arch?
T e internal carotid artery.

What are the derivatives o the cartilage o the third arch?
T e body and greater cornu o the hyoid are the skeletal derivatives o the third arch.

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What are the muscular derivatives o the third branchial arch?
T e stylopharyngeus is the only muscle o the third arch.

What is the nerve o the ourth branchial arch?
T e superior laryngeal nerve.

What is the artery o the ourth branchial arch?
T e aortic arch is derived rom the le t arch, and the right subclavian artery is derived rom the right arch. I the
right ourth arch artery degenerates, the right subclavian artery will arise rom the dorsal aorta and run posterior to
the esophagus (retroesophageal subclavian).

What are the derivatives o the cartilage o the ourth arch?
T e thyroid and cunei orm cartilage o the larynx.

What are the mesodermal derivatives o the ourth branchial arch?
T e in erior pharyngeal constrictor, cricopharyngeal, and cricothyroid are the muscular derivatives o the ourth
arch.

What is derived rom the th branchial arch?
T e th arch degenerates and has no derivatives in the human.

What is the nerve o the sixth branchial arch?
T e recurrent laryngeal nerve.

What is the artery o the sixth branchial arch?
T e pulmonary artery.

What are the derivatives o the cartilage o the sixth arch?
T e skeletal derivatives are the cricoid, arytenoids, and corniculate cartilage.

What are the muscular derivatives o the sixth branchial arch?
T e intrinsic muscles o the larynx.

What are branchial cle t anomalies?
Branchial cle t anomalies occur as cystic masses in the anterior triangle o the neck that arise rom the ailure
o their respective branchial cle t remnants to obliterate during development. T e etiology o the masses is not
known, but the most common theory is that they are the result o entrapped remnants o the cervical sinus o His.

How are the types o branchial cle t anomalies?
Branchial cle t anomalies may occur as cysts, sinuses (with a blind-ended connection to either the pharynx or the
skin), or as stulas (with a connection between the pharynx and the skin). Branchial cle t anomalies are lined with
squamous and respiratory epithelia.

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How do branchial cle t cysts present?
Branchial cle t cysts most commonly present as uctuant, nontender masses o the anterior cervical triangle. T ey
may intermittently become in ected during upper respiratory in ections, and can present as a neck abscess. I a
cutaneous connection via a sinus or stula is present, mucoid discharge can o ten be expressed rom the opening,
and the opening may have increased or purulent drainage during an upper respiratory tract in ection.

How do branchial cle t sinuses or stulas present?
A branchial cle t sinus or stula with a connection to the pharynx may present as recurrent unilateral in ections o
the tonsil or pyri orm sinuses.

Describe the classi cation o branchial cle t anomalies.
Branchial cle t cysts arise rom the rst, second, and third branchial cle ts. Branchial cle t anomalies are classi ed
by anatomical location. T ey occur between the derivatives o two branchial arches and are named or the arch
whose structures they lie deep to. T ere are two types o rst branchial cle t cysts (type I and type II).

Describe the anatomical location o a type I rst branchial cle t cyst.
A type I rst branchial cle t cyst is a duplication o the external auditory canal and exists as a stulous tract lying
in close association with the lower portion o the parotid gland. T ey o ten have tracts that terminate in the
external auditory canal, or the middle ear.

Describe the anatomical location o a type II rst branchial cle t cyst.
A type II rst branchial cle t cyst is typically located in the anterior triangle o the neck just in erior to the angle
o the mandible. T e tract o a type II rst branchial cle t cysts extends superiorly through the substance o the
parotid gland, over the angle o the mandible to the bony cartilaginous junction o the external auditory canal.
ype II cysts are intimately related to the acial nerve, putting it at risk or injury during excision.

Describe the anatomical location o second branchial cle t cyst.
Second branchial cle t cysts are located deep to the structures o the second arch (the platysma and acial nerve),
and super cial to the structures o the third arch (the internal carotid artery and the glossopharyngeal nerve). T e
tract o the second branchial cle t cyst ascends between the internal and external carotid arteries and opens into
the pharynx at the tonsillar ossae.

Describe the anatomical location o a third branchial cle t cyst.
T ird branchial cle t cysts are located in the anterior triangle o the neck deep to the structures o the third arch
(glossopharyngeal nerve and the internal carotid artery), and super cial to the structures o the ourth arch
(superior laryngeal nerves). T e cyst enters the pharynx in the region o the thyrohyoid membrane or piri orm
sinus.

What are the embryologic components o the mid ace (see Fig. 49-2)?
T e maxillary prominence, the lateral nasal prominence, and the medial nasal prominence are paired embryologic
structures that use in the midline along with the rontonasal prominence to orm the nose and upper lip. T ese
prominences are made o neural crest–derived mesenchymal cells o the rst branchial arch.

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Describe the embryogenesis o the nose and upper lip (see Fig. 49-2).
Nasal placodes invaginate to orm nasal pits during the th week o development. Medial and lateral nasal
prominences are created on either side o the nasal pits. During the next 2 weeks, the maxillary prominences
continue to grow in a medial direction and push the nasal prominences toward the midline. T e medial nasal
prominences use in the midline to orm the tip o the nose and the philtrum o the upper lip. T e lateral nasal
prominences orm the ala o the nose, and use with the maxillary prominence that orms the cheeks and lateral
portions o the upper lip. T e rontonasal prominence, which is located superiorly, uses with the medial and
lateral nasal prominences and orms the remaining portion o the nasal dorsum.

Discuss the dif erential diagnosis o the congenital midline nasal mass.
T e dif erential diagnosis o the congenital midline nasal mass includes nasal dermoid cysts, nasal gliomas, and
nasal encephaloceles.

How do dermoid cysts present?
Dermoid sinus cysts present as a mass on the dorsum o the nose or intranasally, with a pit or sinus tract opening
on the nasal dorsum, hair around the external opening, and discharge o pus or sebaceous material.

How do gliomas present?
Nasal gliomas are rm masses that are nonpulsatile, present on the nasal dorsum and/or arise rom the lateral
nasal wall, have telangiectasias o the overlying skin, and do not enlarge with bilateral compression o the internal
jugular veins (Furstenberg test).

How do encephaloceles present?
Encephaloceles may present as nasal broadening and/or as a blue, pulsatile, compressible mass near the nasal
bridge or as an intranasal mass arising at the cribri orm plate. Encephaloceles may be observed to transilluminate,
or enlarge with crying or bilateral compression o the internal jugular veins.

Where do congenital nasal masses arise rom?
During ormation o the skull base and nose, the mesenchymal structures are ormed rom several neural crest–
derived centers that will eventually use and ossi y. Be ore their usion there are recognized spaces including the
onticulus rontalis, the prenasal space, and the oramen cecum rom which congenital nasal masses are thought
to arise. T e onticulus rontalis is the space between the rontal and nasal bones. T e prenasal space is between
the nasal bones and the nasal capsule—the precursor o the septum and nasal cartilages. T e oramen cecum is a
midline opening present in the developing skull base in the basal rontal region.
Figure 49-2 Seven-week embryo.

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What is the primary palate?
T e primary palate is ormed by the usion o the medial nasal prominence. T e primary palate is located anterior
to the incisive oramen, and contains the our central incisors.

What is the secondary palate?
Development o the secondary palate begins a ter development o the primary palate is complete. T e secondary
palate is ormed rom laterally based palatal shelves o the maxillary prominences.

Describe the embryogenesis o the palate.
Both the primary and secondary palates are initially directed obliquely downward on either side o the developing
tongue. As the maxillary prominences move medially, and as the developing tongue descends, the palatal shelves
achieve their correct orientation in a horizontal plane. T e palatal shelves then use rom anterior (incisive
oramen) to posterior (uvula).

Describe the embryogenesis o the auricle.
T e external ear begins as six proli erations o mesenchymal tissue (known as Hillocks o His) located on either
side o the dorsal end o the rst branchial cle t. T e rst three hillocks are located on the rst branchial arch and
the last three hillocks are located on the second brachial arch.

What arises rom the rst three Hillocks o His?
T e rst three Hillocks o His orm the tragus (1) and the helix (2, 3).

What arises rom the last three Hillocks o His?
T e last three Hillocks o His orm the descending helix, antihelix (4, 5), and the antitragus (6).

Describe the embryogenesis o the tongue.
T e anterior two-thirds o the tongue is derived rom components o the rst pharyngeal arch, which includes two
paired lateral lingual swellings, and one medial swelling known as the tuberculum impar. T e posterior one-third
o the tongue is ormed by the second, third, and ourth arches. T e third arch component overgrows the second
arch and the ourth arch component orms the most posterior portion o the tongue and the epiglottis.

How does embryology explain tongue sensory innervation?
T e embryologic origin and development o the tongue explain why the anterior two-thirds is innervated by
the lingual nerve (branch o trigeminal, nerve to rst arch) and the posterior one-third is innervated by the
glossopharyngeal nerve (nerve to the third arch).

How do thyroglossal duct cysts present?
T yroglossal duct cysts typically present as asymptomatic midline neck mass. T ey are located near the level o the
hyoid bone and elevate and descend with swallowing. T yroglossal duct cysts are managed with excision o the
cyst and the central portion o the hyoid bone (Sistrunk procedure).

What do the paranasal sinuses develop rom?
T e maxillary, ethmoid, and rontal sinuses are derived rom evaginations o the lateral nasal wall. T e sphenoid
sinus originates as a posterior evagination o the nasal capsule.

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Which sinuses are present at birth?
T e ethmoid and maxillary sinuses are the only sinuses present at birth.

Describe the development o the maxillary sinus?
T e maxillary sinus is the rst sinus to develop, beginning as an outpouching o the lateral nasal wall in the 10th
week. T is outpouching is superior to the in erior turbinate and posterior to the developing uncinate. Maxillary
sinus growth in its later stages involves invasion into the alveolar process a ter the eruption o permanent
dentition. T e sinus grows and matures at age 3, with another period o growth between ages 7 and 18.

Describe the development o the ethmoid sinus?
T e ethmoid sinus develops in the 12th week and at birth there are three to our ethmoid air cells present. T ese
cells pneumatize urther between ages 3 and 12.

Describe the development o the rontal sinus?
Fontal sinus development involves upward extension o the nasal capsule and invasion o the rontal bone. T e
rontal sinus is not present at birth and does not appear until 5 to 6 years old. It reaches adult size by age 12 to 20.

Describe the development o the sphenoid sinus?
T e sphenoid sinus remains largely undeveloped until middle childhood, with a rapid period o pneumatization
and development occurring a ter age 7 until age 12 to 15.
REFERENCES
Chandler JR, Mitchell B. Branchial cle t cyst, sinuses, and stulas. Otolaryngol Clin North Am. 1981;14:175–186.
Friedman O, Wang D, Miluzuk HA. Cle t lip and palate. In: Cummings CW, Flint PW, Harker LA et al., eds. Otolaryngology-Head
and Neck Surgery. 4th ed. Philadelphia, PA: Elsevier Mosby; 2005:4052–4085.
Goding GS, Eisele DW. Embryology o the ace, head and neck. In: Papel ID, ed. Facial Plastic and Reconstructive Surgery. 2nd ed.
New York, NY: T ieme; 2002:785–794.
Graney DO, Sie KC. Developmental anatomy. In: Cummings CW, Flint PW, Harker LA, et al., eds. Otolaryngology-Head and Neck
Surgery. 4th ed. Philadelphia, PA: Elsevier Mosby; 2005:3938–3951.
Kubal WS. Sinonasal anatomy. Neuroimaging Clin N Am. 1998;8:143–156.
Sadler W. Ear. In: Gruenwald P, ed. Langman’s Medical Embryology. 7th ed. Baltimore, MD: Williams & Wilkins; 1995:347–357.
Sadler W. Head and neck. In: Gruenwald P, ed. Langman’s Medical Embryology. 7th ed. Baltimore, MD: Williams & Wilkins; 1995:
312–346.

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483
Ryan Gobble, MD and
Samuel J. Lin, MD, MBA, FACS

A patient presents with numbness o le t lower lip and a mass in oor o mouth. Examination demonstrates
2.5-cm biopsy-proven squamous cell carcinoma (SCC) o the oor o mouth with invasion o the mandible
on C scan and no lymph node involvement or distant metastases. According to the NM classi cation, how
would you stage this patient?
4aN0M0 (stage IVA). Based upon size this would be a 2 tumor, however, invasion o the mental nerve
(numbness) and through mandibular cortex makes this a 4 tumor.

Which surgical procedures are available or treating the mandible o the patient in Question 1?
Segmental mandibulectomy. Marginal mandibulectomy can be used when the tumor abuts the mandibular cortex
but does not directly invade it.

How would you treat the neck o the patient in Question 1?
T e options are surgery + /− radiotherapy versus radiotherapy alone. raditionally or midline 4 tumors, bilateral
neck dissections with postoperative radiotherapy to the both primary and bilateral necks.

What are the risk actors or increased risk o lymph node metastases?
High-grade histology, large lesions ( 4), spread involving the nonkeratinized (wet) mucosa o the lip or buccal
mucosa in patients with recurrent disease, and invasion o the orbicularis oris muscle. T ese patients all need
elective lymph node radiation or neck dissection.

How would you treat the surgical de ect i a segmental mandibulectomy were required or tumor clearance?
Free bula ap or bone reconstruction taken with a cutaneous skin paddle to reconstruct the oor o mouth
de ect.

How would you treat the surgical de ect i a rim/marginal resection only were required or tumor clearance?
A ree radial orearm ap or anterolateral thigh ap or intraoral lining.
Head and Neck Cancer
CHAPTER 50

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A 50-year-old patient presents with 1.5-cm tumor o the anterior tonsillar pillar with biopsy-proven SCC.
T e patient has no clinically palpable nodes or evidence o metastasis on work-up. How would you stage this
tumor?
1N0M0 (stage I).

What will be your treatment strategy?
Radiation or surgical resection is equally e ective in stage I and II oropharyngeal cancers. Elective cervical lymph
node dissection should be considered in anterior tonsillar pillar, tonsil and base o tongue lesions as the incidence
o lymph node metastases is up to 70%.

What level o lymph nodes is the rst to be involved?
Level 2 (jugulodigastric nodes) ollowed sequentially by levels III, IV, and V.

A 50-year-old patient presents with a 2-cm nonpulsatile mass in the level III o the neck. What is your
management plan?
FNA biopsy and C scan o head and neck.

I both C and FNA are negative in the patient above, what is your plan?
Open biopsy with rozen sectioning and progression to neck dissection i diagnosis o SCC is obtained. Pan
endoscopies o naso/oro/hypo-pharynx, larynx, esophagus, stomach. I all look normal, multiple biopsies are
per ormed including tonsils, base o tongue, nasopharynx, and piri orm ossa. reatment o the primary depends
on the results o these biopsies.

A patient presents with a 1-cm biopsy-proven tongue SCC and a palpable node in level II with no distant
metastases. According to the NM classi cation, how would you stage this patient clinically?
1N1M0.

Following surgical excision pathological evaluation the tumor margins in the above patient were clear and
the patient was staged as p 1N1M0. Would you per orm radiotherapy to either the primary or the neck?
No, unless there is presence o extracapsular spread.

What are the indications or postoperative radiotherapy to the neck?
More than one neck node involved or evidence o extracapsular nodal disease.

What type o head and neck cancer is associated with Epstein–Barr viral in ection?
Nasopharynx. Most commonly with a nonkeratinizing undi erentiated carcinoma. T ese tumors are rare in the
United States but endemic in East Asia and A rica. reatment is usually with chemotherapy and radiation with
surgery reserved or recurrent cancer.

An 18-year-old male presents with progressive bilateral nasal obstruction and recurrent epistaxis. Anterior
rhinoscopy demonstrates a so t, compressible purplish mass lling bilateral nasal cavities. What is the diagnosis?
Nasopharyngeal angio broma occurs most commonly in adolescent males with unilateral or bilateral nasal
obstruction and recurrent epistaxis. Advanced lesions can de orm the nose, ace, and orbits and may even erode
into the cranial cavity causing diplopia rom pressure on the optic chiasm.

CHAPTER 50 Head and Neck Cancer
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What is the treatment?
Preoperative embolization and estrogen hormonal therapy to limit intraoperative blood loss ollowed by surgical
resection. Postoperative radiation is usually given in cases with intracranial extension. T ese should never be
biopsied in the of ce due to risk o bleeding.

A patient requires segmental bony reconstruction o the mandible. T is can be achieved by which methods?
Reconstructive plate with no bone, reconstruction with nonvascularized bone, and reconstruction with
vascularized bone ( ree ap or pedicle ap).

When would you use a reconstruction plate?
For patients in whom no other reconstruction is possible, where good so t tissue exists, and/or when radiotherapy
has not been per ormed and is not planned.

What types o vascularized bone on a pedicle ap exist?
Clavicle on the sternocleidomastoid ap, rib on the pectoralis major muscle, and scapula on the trapezius muscle.

What types o vascularized bone as a ree ap would you consider?
Deep circum ex iliac artery (iliac crest) ap, radial orearm ap, ree bula ap, and ree scapula ap.

Which ree vascularized bone ap is most anatomically similar to a hemimandible?
Deep circum ex iliac artery (iliac crest) ap. ypically used or de ects less than 5 cm.

Which ree vascularized bone ap could you place osseointegrated implants into?
Fibula ap and deep circum ex iliac artery ap. Survival rate or osseointegrated dental implants in a
nonirradiated ree bular ap is 95%.

Which ree vascularized bone ap provides the longest length o bone?
Fibula ap. T is is important i you are per orming more than one osteotomy. Multiple osteotomies may be easily
per ormed without disrupting the blood supply to the bula given its segmental distribution.

A patient presents with a 2-cm mass in the parotid gland. Is the mass likely to be benign or malignant?
Benign. 80% o salivary tumors originate in the parotid, and 80% o parotid tumors are benign.

What actors rom the history in a patient with a parotid mass suggest malignancy?
Pain, obstruction, acial nerve involvement, invasion o other structures, and rapid progression.

What are the most common benign tumors o the parotid?
Pleomorphic adenoma (#1) and Warthin tumor (papillary cystadenoma lymphomatosum). Warthin tumors occur
primarily in males and are bilateral in 10%.

What are the most common malignant tumors o the parotid?
Mucoepidermoid (#1), adenoid cystic carcinoma, and malignant trans ormation o pleomorphic adenoma. Also
can have metastatic lesion rom squamous cell cancer or melanoma.

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Which surgical methods are available to remove parotid tumors?
Lumpectomy, super cial parotidectomy, and total parotidectomy. Super cial parotidectomy or benign lesion and
total parotidectomy or malignant lesions. Facial nerve should be taken in cases o nerve invasion.

A 45-year-old patient with parotid mass undergoes biopsy ollowed by total parotidectomy with acial nerve
preservation. T e nal pathology demonstrates a cribri orm (“Swiss cheese”) pattern o cells with perineural
invasion and residual microscopic disease at the deep margin. What is the type o cancer?
Adenoid cystic carcinoma has three subtypes: cribri orm (“Swiss cheese”), tubular, and solid. T is is the
second most common malignant tumor o salivary glands and most common malignant tumor o sublingual,
submandibular, and minor salivary glands.

What is the treatment plan?
T e patient should be treated with adjuvant radiation therapy or this stage III tumor ( 3N0M0). Surgical
reexcision o the margin should only be per ormed or gross disease either on postop physical examination or
imaging. T ere is no role or chemotherapy except in palliative cases.

What is Frey syndrome? How is it diagnosed? What is the treatment?
Gustatory sweating. Auriculotemporal secretomotor nerve bers disrupted during surgery reinnervate sweat glands
ollowing parotid surgery. Subsequent eating induces sweating in the distribution o the auriculotemporal nerve.
Frey syndrome can be diagnosed via the Minor’s starch iodine test. reatment typically involves the injection
o botulinum toxin A (Botox). Prevention can be accomplished by placing barrier (e.g., Alloderm, super cial
temporal artery acial ap) between the deep parotid lobe and the skin at time o surgery.

A patient has a biopsy-proven 1 oropharyngeal SCC. Which types o surgical access are possible?
ransorally or through pharyngotomy. Mandibulotomy/mandibular swings are used or larger tumors.

Which regions o the oropharynx are accessible transorally?
onsil, so t palate, and superior pharyngeal wall.

Which histological actors in the pathological report would in uence your decision in per orming
postoperative radiotherapy to the primary?
Close or positive margins, perineural or perivascular invasion, > 5 mm tumor depth, presence o a noncohesive
ront, degree o di erentiation, invasion o adjacent so t tissues, and subglottic extension.

A patient presents with a 3-week hoarseness o voice with a normal clinical examination. What is your
management?
C scan, laryngoscopy/biopsy.

How are laryngeal tumors classi ed anatomically?
Supraglottic, glottic, and subglottic.

What is the rate o nodal metastasis or a 1–2 glottic tumor?
Less than 10%; hence neck dissection rarely per ormed.

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What is the rate o nodal metastasis or a 1–2 supraglottic tumor?
Approximately 50%; hence bilateral neck dissections requently per ormed.

For advanced laryngeal tumors what are the treatment options?
Surgical excision, radiotherapy, chemotherapy, or a combination o all three. Organ preservation with
chemoradiotherapy has shown comparable local control rates to traditional surgery.

A 73-year-old man presents with recurrent laryngeal tumor 3 years a ter chemoradiation. He undergoes total
laryngopharyngectomy with the resultant de ect being rom the base o the tongue to 2 cm proximal to the
manubrium. What is the best single stage reconstructive option?
ubularized ree anterolateral thigh ree ap (skin orms the lining o the reconstructed GI tract). Restoration o
swallowing can be achieved in most patients.

A patient presents with mandibular pain and trismus. He has previously had an excision o a 2N0M0
oor o mouth SCC with close margins and postoperative radiotherapy 1 year ago. What is your dif erential
diagnosis?
Osteoradionecrosis, recurrence/another primary. Dental problems.

Biopsy in the patient above suggests osteoradionecrosis. What is your initial management?
Conservative—oral hygiene, antibiotics, analgesia.

When would you consider surgery or osteoradionecrosis?
Intractable pain, persistent bone exposure, stulas, pathological ractures.

Is there a role or hyperbaric oxygen in the management o osteoradionecrosis?
Yes.

Frequently, the involved mandible needs to be resected. How would you reconstruct the de ect?
With a ree vascularized bone ap.

A patient presents with postnasal drip, pain around the upper rst and second molar, and cheek numbness
on the le t side. A C scan shows a mass within the maxillary antrum and a biopsy con rms SCCa. Standard
maxillectomy is planned. What access skin incision is traditionally used?
Weber–Ferguson.

Does a neck dissection need to be per ormed in the above patient?
No. T e risk o metastasis rom maxillary tumors is rare.

A ter resection o the tumor the resultant de ect includes the le t orbital oor, hemipalate, maxillary sinus,
and nasal lining. How is the orbital oor reconstructed?
Usually with nonvascularized bone gra t, that is, rib or iliac crest.

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How is the maxillary de ect reconstructed?
A rectus abdominus ree ap is the best treatment o the above de ect. T e skin rom the abdomen can be used to
reline the maxillary sinus and repair the palatal de ect. Furthermore, the vascularized tissue obliterates the dead
space and provides a barrier rom the orbital oor reconstruction and the maxillary sinus or nasal cavity.

A patient presents with a 3-cm nodal mass in the posterior triangle ollowing radiotherapy to a
nasopharyngeal tumor 2 years previously. An FNA biopsy con rms SCCa. What type o neck dissection
would you per orm, comprehensive or selective?
raditionally a comprehensive neck dissection.

What is the dif erence between a selective and a comprehensive neck dissection?
A selective neck dissection only removes the nodal levels most likely to harbor metastases. A comprehensive neck
dissection removes lymph nodes rom all levels.

What dif erent types o comprehensive neck dissections exist?
Radical and modi ed radical neck dissections (MRNDs).

How many types o modi ed MRND are there?
T ree.

How do they dif er?
MRND type 1 preserves only the accessory nerve, MRND type 2 preserves both accessory and the internal
jugular, and MRND type 3 preserves accessory, internal jugular, and sternocleidomastoid.

A patient presents with a 2.4-mm malignant melanoma o the scalp clinically node negative. What is your
management plan?
For local control, a surgical excision o the malignant melanoma with a 2-cm margin. For staging o the clinically,
N0 neck sentinel node biopsy is recommended.

T e sentinel node biopsy shows metastases o 2 mm in level 2 in the neck. What is your management plan?
A staging C scan to determine any other disease—i negative, an MRND is recommended.

What i the sentinel node showed a micrometastases o 0.1 mm?
A staging C scan and, i negative, one should consider other pathological characteristics including whether
the micrometastases were con ned to the subcapsular sinus. For disease more than 0.1 mm, a completion
lymphadenectomy is recommended. Patients with disease under 0.1 mm have a long-term prognosis similar to
node-negative patients and can be spared completion lymphadenectomy.

T e neck dissection is clear o any urther disease. Does the patient require radiotherapy?
One should consult with an oncologist. Radiotherapy is usually unnecessary i only one node is involved with
micrometastasis without extracapsular spread. For more than one node or extracapsular spread, radiotherapy
should be considered.

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What about chemotherapy?
Yes, all stage 3 patients should be o ered chemotherapy in the context o a clinical trial.

A patient presents with a clinically apparent 2-cm morphoeic BCC on the tip o the nose. What are the
management options?
T e options are surgical and nonsurgical. For morphoeic BCCs, surgery would o er a better chance o local
control. In such a cosmetically sensitive position, Mohs surgery would be the ideal management option ollowed
by reconstruction.

What option would you use i the de ect included the nasal tip and dorsal sub units?
Forehead ap.

What i the nasal lining were involved, how would this be reconstructed?
One would place a skin gra t on the inner sur ace o the orehead ap and use the skin gra t as lining. I cartilage
was required, a second stage could be per ormed to insert the cartilage and thin the ap. A third stage would then
be used to inset the ap and divide the pedicle.

What i the donor site on the orehead does not close? How would you reconstruct?
Secondary intention healing on the orehead leaves a reasonable cosmetic result and can be superior to skin
gra ting. It is important to make sure that during ap harvest the periosteal layer is le t attached to the scalp. A
ew centimeters above the orbital rim, one can dissect under periosteum to protect the pedicle supply without
compromising closure.

An 85-year-old lady presents with a biopsy-proven radiorecurrent SCC o the temple. What is your
management?
C staging scan and, i negative, surgical excision.

What is your excision margin?
1 cm with rozen-section analysis.

T e patient develops local recurrence 18 months later and C scan shows involvement o temporalis but no
other disease, what is your management?
Excision o the mass and previous reconstruction with a 1-cm margin including temporalis. Reconstruction would
require a large scalp rotation ap or ree ap.

A 45-year-old male presents with a slowly growing mass o the mandible that is causing signi cant
distortion. Radiographically it is characterized as a multilocular mass with a “soap bubble” or “honeycomb”
appearance. What type o mass is this?
Ameloblastoma is derived rom odontogenic epithelium. reatment is typically with surgical resection and
immediate repair with vascularized bone (e.g., ree bula ap). T ese are not usually cancerous so wide margins are
not necessary, though rare cases o metastatic ameloblastic carcinoma have been reported, in which case the patient
should receive adjuvant radiation.

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A 3-year-old emale presents with a painless, slowly growing mass o the maxilla. An incisional biopsy is
per ormed that demonstrates sinonasal myxoma. Postoperative MRI demonstrates residual tumor. What is
the best course o treatment?
Resection o the mass until negative margins. umors are not o ten encapsulated so a rim o normal tissue should
be removed at the same time. Sinonasal myxoma most o ten present as slow growing masses in the maxilla or
mandible.
REFERENCES
Chrysomali E, Leventis M, itsinedes S, Kyriakopoulos V, Sklavounou A. Odontogenic tumors. J Craniofac Surg. 2013;24:1521–1522.
Cordeiro PG, Chen CM. A 15-year review o mid ace reconstruction a ter total and subtotal maxillectomy: part I. Algorithm and
outcomes. Plast Reconstr Surg. 2012;129:124–136.
Ettl , Schwarz-Furlan S, Gosau M, Reichert E. Salivary gland carcinomas. Oral Maxillofac Surg. 2012;16:267–283.
Futran ND, Parvathaneni U, Martins RG, et al. Malignant salivary gland tumors: part A: general principals and management. In:
Harrison LB, Sessions RB, Hong WK, eds. Head and Neck Cancer: A Multidisciplinary Approach. 3rd ed. Philadelphia, PA: Lippincott
Williams & Wilkins;2009:589–610.
Haddadin KJ, Soutar DS, Oliver RJ, Webster MH, Robertson AG, MacDonald DG. Improved survival or patients with clinically 1/
2, N0 tongue tumors undergoing a prophylactic neck dissection. Head Neck. 1999;21:517–525.
Leemans CR, iwari R, Nauta JJ, van der Waal I, Snow GB. Regional lymph node involvement and its signi cance in the development
o distant metastases in head and neck carcinoma. Cancer. 1993;71:452–456.
Leemans CR, iwari R, van der Waal I, Karim AB, Nauta JJ, Snow GB. T e ef cacy o comprehensive neck dissection with or without
postoperative radiotherapy in nodal metastases o squamous cell carcinoma o the upper respiratory and digestive tracts. Laryngoscope.
1990;100:1194–1198.
Li C, Yang X, Pan J, Shi Z, Li L. Gra t or prevention o Frey syndrome a ter parotidectomy: a systematic review and meta-analysis o
randomized controlled trials. J Oral Maxillofac Surg. 2013;71:419–427.
Mann WJ, Jecker P, Amedee RG. Juvenile angio bromas: changing surgical concept over the last 20 years. Laryngoscope. 2004;114:
291–293.
Neligan PC. Head and neck reconstruction. Plast Reconstr Surg. 2013;131:260e–269e.
Pillsbury HC 3rd, Clark M. A rationale or therapy o the N0 neck. Laryngoscope. 1997;107:1294–1315.
Robbins K . Classi cation o neck dissection: current concepts and uture considerations. Otolaryngol Clin North Am. 1998;31:
639–655.
Rotenberg BW, Daniel SJ, Nisha IA, Ngan BY, Forte V. Myxomatous lesions o the maxilla in children: a case series and review o
management. Int J Pediatr Otorhinolaryngol. 2004;68:1251–1256.
Shah JP. Patterns o cervical lymph node metastasis rom squamous carcinomas o the upper aerodigestive tract. Am J Surg. 1990;160:
405–409.
Spyropoulou GA, Lin PY, Chien CY, Kuo YR, Jeng SF. . Reconstruction o the hypopharynx with anterolateral thigh ap: de ect
classi cation, method, tips, and outcomes. Plast Reconstr Surg. 2011;127:161–172.
Van Akkooi AC, Nowecki ZI, Voit C, et al. Sentinel node tumor burden according to the Rotterdam criteria is the most important
prognostic actor or survival in melanoma patients: a multicenter study in 388 patients with positive sentinel nodes. Ann Surg.
2008;248:949–955.

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Alex Senchenkov, MD, FCAS

What are the histological eatures o salivary glands and how are they related to oncogenesis?
T e parenchyma o the salivary glands is ormed rom the acini that lead to the sequence o ducts. While origin o
the salivary tumors is poorly understood, there may be a correlation between the salivary neoplasms and the cells
orming salivary units. T is unit consists o acinus, intercalated, striated, and excretory ducts. able 51-1 illustrates
the correlation between normal structure and tumor cells.
Salivary Gland Tumors
CHAPTER 51

Which salivary gland is the most common site or salivary tumors?
Parotid gland harbors 70% to 85% o all salivary tumors.
Table 51-1 Histogenic Scheme of Salivary Gland Neoplasms
Norm al Structure Cell of Origin

Neoplasm
Excretory duct

Excretory duct reserve cells

Squamous cell Ca
Mucoepidermoid Ca
Acinus

Intercalated duct reserve cells

Acinic cell carcinoma
Mixed tumor
Monomorphic adenoma
Myoepithelioma
Intercalated duct

Adenoid cystic Ca
Myoepithelium

Adenocarcinoma
Striated duct

Oncocytic tumors
Data from Regezi JA, Batsakis, JG. Histogenesis of salivary gland neoplasms. Otol Clin N Am.
1977;10:298.

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What is the incidence o malignancy in di erent salivary glands?
Benign (%) Malignant (%)
Parotid

80

20
Submandibular

50

50
Minor salivary

20

80

umors o which salivary gland are most requently malignant?
Sublingual gland.
Starting with lowest to the highest chance o malignancy the sequence is as ollows:
Parotid < submandibular < minor salivary < sublingual gland

Overall, what salivary gland harbors the most o the malignant tumors?
Parotid gland. Although about 80% o parotid tumors are benign, the remaining 20% are malignant, and
since tumors in the parotid are much more requent than in all other salivary glands combined, the majority o
malignant salivary glands tumors occur in the parotid gland.

What is the most common benign salivary neoplasm or all salivary glands?
Pleomorphic adenoma (benign mixed tumor) is both the most common benign parotid neoplasm and the most
common benign salivary neoplasm overall, comprising about 60% o all salivary tumors and about 80% o benign
tumors. Mixed tumor is derived rom dual epithelial (granular cells) and myoepithelial (mesenchymal) origin.
T e latter connective tissue (stromal) component o ten exhibits myxo broid and cartilaginous di erentiation.
It has histologic appearance o stellate and spindle cells with a myxoid background. Pleomorphic adenoma has a
potential or malignant trans ormation.

T e patient who was diagnosed with pleomorphic adenoma o the parotid (mixed parotid tumor) has
another tumor in the same parotid gland. What is histology o the second primary parotid tumor most
likely to be?
Warthin’s tumor (papillary cystadenoma lymphomatosum) has a reputation o the most common second primary
parotid tumor. T e tumor histologically characterized by papillary cysts with mucoid uid and the presence o
lymphoid tissue (T ink o intercalated parotid lymph nodes); Warthin’s is highly unusual outside the parotid gland
and periparotid lymph nodes.

Do any o the parotid tumors have propensity to be bilateral?
Warthin’s tumors are bilateral in 10% o patients.

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A patient who has a symptomatic Warthin’s tumor in the parotid gland is ound to have an occult contralat-
eral parotid tumor on the C scan. What would you do about it?
In the patients with bilateral Warthin’s tumors, the symptomatic side should be treated operatively, whereas
you may observe an asymptomatic contralateral tumor. When it becomes symptomatic, you would remove it.
Warthin’s tumor is known or being bilateral and multicentric (Fig. 51-1).
Figure 51-1 MRI o a bilateral and multicentric recurrence o Warthin’s tumor a ter incomplete super cial parotidectomy.

Why are oncocytomas requently ound on the c-99 scans and what do you do with them?
T eir origin is thought to correlate with striated ducts. T is striation is related to the presence o large number o
mitochondria. c-99 is pre erentially picked up by tissues rich in mitochondria (gastric mucosa in the Meckel’s
diverticulum lights up on c-99 Meckel’s scan). When oncocytoma is ound on the scan and is not symptomatic,
it may be observed initially.

What is the most common malignant tumor o the parotid gland?
Mucoepidermoid carcinoma is the most common malignancy o the parotid. Histologically, it contains two major
components o mucin-producing cells and epidermoid epithelial cells hence its name. Low-grade tumor is more
common and greater mucin-secreting component. High-grade, poorly di erentiated variant is largely solid with
paucity o mucin-producing elements with the loss o di erentiation.

What is the most common malignant tumor o the salivary gland outside the parotid?
Adenoid cystic carcinoma (cylindroma) is the most common submandibular, sublingual, and minor salivary
gland malignancy. T ere are three histologic types: the cribri orm (“Swiss cheese” appearance), the tubular
(resembles glandular architecture), and solid or basaloid pattern (solid sheets o cells without luminal or glandular
appearance).

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What is the most common malignant tumor o the salivary glands overall?
Mucoepidermoid carcinoma. Low-grade variant is more common and is predominantly cystic, whereas high-grade
tumors are solid with small amount o mucin.

How do salivary malignancies spread?
Lymphatic, hematogenous, direct invasion o the surrounding structures, as well as perineurally.

Which head and neck malignancies are notorious or perineural spread?
Adenoid cystic carcinoma is a classic example. Malignant mixed tumor, melanoma, and squamous cell carcinoma
also demonstrate perineural invasion.

What are peculiar eatures o adenoid cystic carcinomas?
Lack a tumor capsule, direct invasion o the surrounding tissues, and very high propensity or perineural invasion.
T ese three eatures make it very challenging to achieve negative resection margins. T is tumor has hematogenous
route o spread, which leads to the lung, liver, and bone metastases. It has excellent 5-year survival (75%), but
poor 10-year survival, and even worse 20-year survival (13%); it tends to recur late.

What are the important clinical eatures o acinic carcinoma?
While the majority o the acinic carcinomas are curable, about 10% can mani est very aggressively and be
tenacious with a tendency to recur.

What is an important consideration in planning the removal o malignant mixed tumors?
Malignant mixed tumors (or carcinoma-ex-pleomorphic adenoma) are locally destructive and require wide
resection and requently, microvascular ap reconstruction.

What is the most common parotid tumor o young children?
Hemangioma.

What are other common pediatric parotid tumors?
Most common benign epithelial tumor is pleomorphic adenoma. Most common malignant tumor is
mucoepidermoid carcinoma, similarly or adults.

Does the ratio 80:20 between benign and malignant parotid tumors apply to children?
No. Pediatric parotid tumors are much more likely to be malignant. In act, an older child with a parotid mass has
50% chance o harboring malignancy.

What is the most common presentation o parotid tumors?
It is a mass below the angle o the mandible and not in ront o the ear. T e clinician needs to be aware that most
parotid tumor present as upper cervical masses.

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Do you always eel parotid tumor on palpation?
No. Sometimes the presentation is subtle. I the tumor is in the deep lobe, only di use enlargement o the gland
can be appreciated, and you have to rely on imaging to demonstrate the tumor.

What about the size o the tumor? I the tumor is large, is it more likely to be malignant?
Not necessarily. You can have a large pleomorphic adenoma that has grown over past 20 years to be very large, yet
still benign.

A patient presents to you with a parotid mass, when should you think about malignancy?
Start with history and physical examination. Patient’s age, history o head and neck radiation, and history o
previous malignancies and symptoms are important. umors in children and older individuals are more likely
to be malignant. Pain and rapid growth are very suspicious or malignancy as are tumors that are adherent to
surrounding structures on physical examination and have regional adenopathy. Facial nerve paralysis and eruption
through the skin are rare even in advanced malignancy and are grave prognostic signs.

A mass with acial nerve paralysis is a bad prognostic sign. What would be a benign condition that could
have a similar presentation?
Sarcoidosis is the most common cause or nonneoplastic parotid mass with acial nerve paralysis.

What is importance o cystic parotid mass in an HIV patient?
A benign lymphoepithelial cyst is a cystic degeneration o salivary gland inclusions within intercalated lymph
nodes. T e cyst is lined with lymphocytes. It is mani estation o progression to AIDS. reatment is repeat
aspiration and care ul use o a sclerosing agent.

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Figure 51-2 Le t parotid mass in a patient with a long-standing Sjögren’s syndrome. See Color insert.

T e patient presents with xerostomia dry eyes and history o long-standing periodic cheek swelling.
On physical examination the patient has a unilateral ill-de ned parotid mass. What clinical entity should be
considered?
Clinical presentation o keratoconjunctivitis sicca and xerostomia is typical or Sjögren’s syndrome, a chronic
progressive autoimmune disorder resulting rom lymphocyte-mediated destruction o lacrimal and salivary glands.
As the disease progresses, a sizable parotid mass may develop (Fig. 51-2). It may mani est as an isolated (primary)
or associated with other autoimmune disorders (secondary) orms. A biopsy o a minor salivary gland, usually
orm the lower lip under local anesthetic in the of ce is a valuable diagnostic tool. Representative serologies, such
as rheumatoid actor, ANA, SS-A, and SS-B are also requently obtained. T e risk o primary non-Hodgkin’s
lymphoma o the parotid is increased.
T e treatment is medical. Parotidectomy plays a very limited role in the case o Sjögren’s syndrome patients and is
reserved or parotitis re ractory to medical management, gross dis gurement, and diagnostic concerns o parotid
lymphoma.

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Figure 51-3 Large pleomorphic adenoma involving deep and super cial lobes o the right parotid. See Color insert.
B
A
Figure 51-4 Surgeon-per ormed diagnostic ultrasound o the parotid tumor. AP and lateral images demonstrate the size o the tumor.
A

B
Ultrasound is a versatile and important tool in the hands o an experienced practitioner. Some head and neck
surgeons may choose to per orm parotid and neck of ce ultrasound and an ultrasound-guided ne-needle
aspiration (FNA) biopsy o the parotid mass and suspicions lymph nodes as the only preoperative imaging study
and a biopsy (Fig. 51-4). I the tumor does not extend outside the parotid on ultrasound and FNA cytology is
benign, MRI or C may be avoided and the patient may proceed to the operative treatment.

How do you workup a parotid mass?
A ter thorough history and physical examination (Fig. 51-3A), MRI is the best study; however, a good quality
head and neck C is acceptable (Fig. 51-3B). T ese will evaluate local and regional extent o the disease. C
imaging o the tumors o deep lobes and parapharyngeal space is undermined by scattering rom petrous pyramids
and MRI is the study o choice or those locations.

How good is FNA or salivary tumors?
It accurately diagnoses more than 95% o pleomorphic adenomas. It is very good in diagnosing malignancy, but
may not tell you the type.

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How do you best per orm FNA o a parotid mass?
Routine use o ultrasound allows precise needle placement. Usually 21- to 25-gauge needle is used. Keeping the
bevel o the needle up acilitates continuous sonographic visualization o the needle tip (Figure 51-5). One places
the needle into the mass and per orms several passes back and orth with continuous aspiration. It is very help ul
to have a cytology technician on stand by to con rm that the rst aspirate is suf cient. T is may obviate the need
or per orming multiple aspirates. It is a common practice to irrigate the syringe with saline or CytoLyt® solution
and send it or cell block preparation.
Figure 51-5 Surgeon-per ormed ultrasound guided FNA o the parotid mass. Note: bright echogenic re ection o the needle tip and the
ultrasound waves re ected o the bevel o the needle turned upward.

What about core needle biopsy used or breast masses? It gives histological, not cytological diagnosis. Would
it help to establish the type o parotid malignancy preoperatively?
Core needle biopsy or breast masses is per ormed with 14- and 11-gauge needles. Its use is contraindicated or the
parotid masses because o the danger o transection o the acial nerve branch.

You have a young patient with a small mobile mass that is very super cial in the parotid lobe. You per ormed
an FNA and it is a pleomorphic adenoma. You explained to her that although it is a benign tumor it needs to
be removed. She is asking i you can do “minimally invasive surgery” and just take out the lump.
Enucleation or local excision o the adenoma is not a good option. T e minimal operation or the parotid tumor is
a super cial parotidectomy. Partial parotid resection have high rate o complications and should not be done.

Some surgeons advocate not doing FNA, but just taking the patient with a parotid mass to the OR,
per orming super cial parotidectomy with rozen section, and having that be the biopsy. Why is it
important to know whether the tumor is malignant preoperatively?
T is approach is also valid. However, knowing preoperatively that the patient has a malignant parotid tumor will
allow better planning o the operation. While treatment o benign tumors is straight orward, a malignancy may
require radical parotidectomy with resection o the mandible, neck dissection, acial nerve gra ting, microvascular
mandibular, and so t-tissue reconstruction and postoperative XR . T e patient and the amily will have better
understanding o what these all entail to make an in ormed consent.

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What are the clinical implications o perineural spread?
Perineural spread is an important pathologic actor described in the majority o head and neck tumors. T is
process is a major cause o local ailure and ultimately tumor-related mortality. High level o suspicion should be
maintained in diagnostic and treatment e orts. Most o the time, it is clinically silent, but as the process becomes
more advanced, the patient may present with ormication ( eeing o ants crawling) and eventual with loss o nerve
unction (numbness or the sensory or paralysis o the motor nerve). T ickening o the named nerves on MRI and
changes in the skull oramina on C is ound in late cases. Certain tumor histologies (adenoid cystic carcinoma),
suggestive locations o the tumors (areas o major nerves), perineural invasion identi ed on the diagnostic
biopsies or excised tumor specimens are all actored into a complex clinical decision to sacri ce a named nerve
or histologic evaluation. Ideally, negative margins on the involved nerves should be attained. T ese e orts are
requently limited by the advanced nature o the process (adenoid cystic carcinoma) and highly debilitating nature
o these resections (Fig. 51-6).
Figure 51-6 Adenoid cystic carcinoma o the le t submandibular gland (size 2 cm physical examination) treated with composite resection,
total parotidectomy with resection o lower division o the le t acial nerve, ree bula (A and B), specimen (C) static sling, and postoperative
radiation. Appearance o the patient without evidence o disease at 6 years (D). See Color insert.
A
C

D
B

How do you stage parotid malignancies?
NM staging. (primary tumor): 1: < 2 cm, 2: 2 to 4 cm, 3: 4 to 6 cm, 4: > 6 cm; a—no local extension,
b—local extension
• Stage I: 1a or 2a/N0;
• Stage II: 1b, 2b, 3a/N0;
• Stage III: 3b, 4a or any (except 4b) with N1,
• Stage IV: 4bN0 or Any with N2–3 or M1

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T e patient presents to you with pleural malignant e usion and multiple bilateral lung metastases. He had a
1.5-cm high-grade mucoepidermoid carcinoma o the parotid removed 2.5 years ago. He did not have neck
dissection at that time because the neck was clinically negative and distant workup did not show metastasis.
What is his stage now?
Stage 1( 1N0M0)
A cancer patient is staged only once around the time his initial diagnosis and treatment based on anatomic extent
o the tumor. T is staging can be clinical c NM or histologic p NM, and this stage remains unchanged. Stage
is predictor o prognosis drawn rom retrospective analysis o outcomes. One cannot “restage” or “downstage”
the cancer patient when he presents with a recurrence. In the setting o neoadjuvant chemotherapy or radiation
therapy and prior to surgical resection, the change in the tumor extent is indicated by pre x y, or example,
yc NM or yp NM.

What is the surgical treatment or parotid tumors?
Enucleation or lumpectomy is not an adequate treatment o the parotid tumors. Wide local excision with negative
margins in conjunction with appropriate surgical treatment o the neck and durable reconstruction that would
allow timely delivery o adjuvant radiation therapy i clinically indicated.
Benign tumor o the super cial lobe:

Super cial parotidectomy with acial nerve preservation
Benign tumor o the deep lobe:

otal parotidectomy with acial nerve preservation
Malignant parotid tumor:

Without nerve involvement:

otal parotidectomy with acial nerve preservation

With nerve involvement:

Radical parotidectomy (involved branch, division, or trunk o
the acial nerve is sacri ced)

What is the di erence between total and radical parotidectomy?
In total parotidectomy, the acial nerve is preserved. T e operation starts with super cial parotidectomy, then the
acial nerve is dissected ree o the deep lobe and the deep lobe is removed rom underneath the nerve. In radical
parotidectomy, the involved trunk o the acial nerve is removed en bloc with both lobes o parotid.

How do you decide whether to per orm total or radical parotidectomy?
Direct invasion o the nerve is what determines the choice o the operation. I the patient’s acial nerve is paralyzed
preoperatively, radical parotidectomy is per ormed. I the nerve is not paralyzed, operation starts with super cial
parotidectomy. I dissection plane between the tumor and the nerve branch cannot be established, that nerve or
branch is resected with rozen-section evaluation. I the acial nerve cannot be dissected ree, the branch, division,
or trunk is sacri ced accordingly.

You have mentioned super cial and deep lobes o the parotid. Could you de ne these terms?
Division between the lobes o parotid is purely arti cial. T e parotid is one gland; however, during embryologic
development acial nerve was trapped in the gland and the plane o the acial nerve branches de nes the border
between the lobes. Super cial lobe is much larger and encompasses approximately 80% to 90% o parotid
parenchyma.

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Figure 51-7 Positioning o parotidectomy patient on a shoulder roll and donut head rest. NIM acial nerve monitor or at least zygomatic
(blue) and marginal mandibular (red) branches o the acial nerve as well as grounding electrodes (white and green) are placed. Both modi ed
Blair and aceli t incisions are outlined and lidocaine with epinephrine is injected prior to the prep. See Color insert.

Describe the steps o parotidectomy.
A ter induction o general anesthesia with a short-acting paralysis, the patient is positioned with a shoulder roll
and “donut” head rest with operated hal o the ace prepped in the eld. T e skin is injected with lidocaine with
epinephrine, and a modi ed Blair or aceli t incision is used (Fig. 51-7). SMAS is adherent or parotomasseteric
ascia (parotid capsule) in the preauricular region; there ore, the sub-SMAS plane needs to be entered sharply. I
oncologically sa e, the dissection is per ormed between the SMAS and parotomasseteric ascia. With the index
nger in the external auditory canal and double-prone skin hook placed in the canal’s cartilage, subperichondrial
dissection to the level o the tragal pointer i per ormed. Next, the plane between the sternocleidomastoid muscle
and the tail o parotid is developed and the posterior belly o the digastric muscle is visualized. T e tissue between
this level and dissection and the tragal pointer is sa ely divided as the acial nerve is quite deep in this location
(Fig. 51-8A). Once that is done, the trunk o the nerve is ound under the thin layer o the ascia and at just deep
to the superior border o the posterior belly o the digastric (Fig. 51-8B). A split o the parotid tissue is created to
visualize the upper and lower divisions, and only then, either superior or in erior mobilization o the gland can
be sa ely per ormed without the risk o mistaking the acial nerve trunk or a division and risking the injury. T e
branches o the nerve then sequentially dissected (Fig. 51-8C). In the case o total parotidectomy, the acial nerve
is dissected and elevated and the deep lobe is removed (Fig. 51-8D).

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What recent technological advances that may improve ef ciency o parotidectomy?
Harmonic Focus® scalpel (Ethicon, Cincinnati, OH) utilizes ultrasound technology to achieve e ective
seal o the blood vessels and lymphatics. It was designed to optimize ergonomics o head and neck procedures
(thyroidectomy, parotidectomy, and neck dissections). It has enhanced precision and decreased heat dissipation in
the tissues, which makes it exceedingly e ective in working around the cranial nerves.
Intraoperative acial nerve monitoring (Fig. 51-7) utilizes EMG technology. It assists in identi ying acial
nerve, recording intraoperative injurious potential, and con rming intact electrophysiologic unction o the acial
nerve. Although clear evidence o reduction o acial nerve injuries during parotidectomy is still not available,
the technique does provide additional assurance, and is particularly use ul in the cases with excessive acial nerve
manipulation, or example, malignant tumors, deep lobe tumors, and parapharyngeal space procedures.

T e most critical part o the parotidectomy is nding o the acial nerve. How do you do that?
(1) ragal pointer is the medial end o the tragal cartilage. T e dissection is carried out in the subperichondrial
plane to expose the tragal pointer. T e acial nerve trunk is 0.5 to 1 cm deep and in erior to the pointer. (2) T e
Posterior belly o digastric muscle is identi ed and ollowed superiorly to the digastric groove. T e acial nerve
is deep to cephalad border o the muscle. It is surrounded with small amount o at that is incased in thin ascial
envelop. (3) ympanomastoid suture is the most constant landmark that can be palpated. T e acial nerve is 6 to
8 mm deep to the in erior end o the suture line. (4) As a last resort, alternative method is retrograde dissection
o the branches o the acial nerve.
A

B
C

D
Figure 51-8 A ter sub-SMAS and external auditory canal dissection and separation o the parotid tail rom the sternocleidomastoid muscle the
deep points o dissection are connected by dividing the tissue between these points (A). T e nerve trunk (B) and divisions are identi ed and the
branches are sequentially dissected (C). In the case o total parotidectomy the nerve is dissected o the deep lobe, which is then removed (D).
See Color insert.

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You have been called by your senior partner to give him a hand in the OR with a parotidectomy that he
started 3 hours ago. He does not believe in preoperative FNA. T e patient has a tumor o the super cial
lobe o the parotid that was close to the nerve, but does not directly involve it. T e pathologist is having a
dif cult time to determine the nature o the tumor on rozen section. How would you handle this situation?
Some o the salivary malignancies are dif cult to call on rozen section. In this case, sample upper cervical nodes
(level 2) even they are not enlarged and send them or rozen section. I tumor is present in the nodes, per orm
total parotidectomy with neck dissection. I there is no tumor present in the nodes, per orm total parotidectomy i
suspicious or malignancy. In the worst case, add postoperative radiation i the tumor is malignant on permanent
section. It is very important to avoid going back or completion parotidectomy in the previously operated eld.
Reoperative parotid surgery adds next level o complexity and risk to the acial nerve that can be avoided by
per orming initial total parotidectomy.

How do you reconstruct total or radical parotidectomy de ect?
Unreconstructed total parotidectomy de ect results in signi cant acial asymmetry. T is problem is dif cult
to correct secondarily i there is a unctional acial nerve present. T ese operations can be particularly dif cult
ollowing adjuvant radiation therapy. T ere ore, such reconstruction is best per ormed in the immediate setting.
I the skin overlying the parotid has not been removed, the ace and neck is delaminated in the manner similar
to aceli t technique. T e most distal portion o this cervico acial f ap is tucked in, marked, and deepithelialized.
T e ap is secured with a mastoid stitch and sutured in place. T e deepithelialized end o the ap usually provides
suf cient volume to make the de ormity less pronounced (Fig. 51-9).
A

B
Figure 51-9 Cervico acial ap reconstruction o the total parotidectomy de ect. See Color insert.
Microvascular tissue trans er should be considered i the skin overlying the parotid is missing or the so t-tissue
de cit is too great. Anterolateral thigh ap (AL ) has three advantages: (1) the ascia lata in the ap that will
protect the acial nerve or acial nerve gra ts during the uture debulking procedures (Fig. 51-10); (2) the ascial
lata rom the AL donor site is readily accessible or the construction o the static sling; (3) brunches o the
emoral nerve can be used as acial nerve gra ts (Fig. 51-11).

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A

B
C

D
Figure 51-10 Metastatic squamous cell carcinoma o the temporal region with removal o the rontal branch o the acial nerve treated with
total parotidectomy, neck dissection, and ree AL ap, ollowed by radiation, staged debulking, endoscopic browli t and upper blepharoplasty.
See Color insert.

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When do you per orm neck dissection or the parotid tumors?
T erapeutic neck dissection should be per ormed or all patients with clinically positive neck (N+ ). T e
patients with high-grade, high-stage, or requiring entrance o the neck or a ree ap should undergo an elective
(prophylactic) neck dissection with is usually selective, which implies removal o less than ve lymph node levels.
A

B
C

D
E

F
Figure 51-11 Metastatic malignant melanoma o the scalp requiring radical parotidectomy with neck dissection (A). T e thigh was used as a
donor site or AL ree ap, ascia lata gra t (B) or static sling (C), and emoral nerve gra ts (D). Both acial nerve gra t reconstruction (E) and
static sling (C and F) were per ormed in addition to AL ree ap (F). See Color insert.

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Plastic & Reconstructive Surgery Board Review

When is postoperative radiation therapy indicated?
Grossly positive margins are treated with surgical resection when possible. Adjuvant radiation therapy is a
treatment modality that aims to treat known or unknown local and regional microscopic disease that the surgeon
le t behind and thus enhance local and regional control o the tumor.
umors with close or microscopically positive margins that cannot be e ectively re-resected; tumors in proximity
to the acial nerve and the deep lobe, where margins are notoriously close and dif cult to re-excise; tumors with
presence or propensity or perineural spread; and tumors with lymphovascular invasion and cervical metastases
should be considered or adjuvant radiation therapy.

Is there any benign tumor that may bene t rom postoperative radiation therapy?
Recurrent pleomorphic adenoma.

When ast neutron radiation can be considered?
Adenoid cystic carcinoma and recurrent acinic carcinoma.

You mentioned earlier that history o previous malignancies is important. Can you explain why?
Parotid is a common site or metastases, both regional and distal.

Why is the parotid a common site o regional metastases?
Because o the embryologic delay o ormation o the parotid capsule, lymph nodes became incorporated
into the parotid. T ese intercalated nodes serve as regional lymph nodes or the area o skin between line over
temporozygomatic arch to labial attachment o the nose in eriorly, sagittal line rom the base o the nose to
the vertex medially, and imaginary line rom the vertex to the temporozygomatic arch posteriorly. In addition,
it drains the external auditory canal, part o external ear including tragus, helical root, and superior helix,
conjunctival sac, orbital content, posterior oral cavity, part o the pharynx, and the parotid gland itsel .

What is the most common metastatic tumor o the parotid?
Malignant melanoma (40%) is the most common and squamous cell carcinoma is the next most common.
In management o these tumors, the parotid is considered not as a gland, but rather as an additional cervical
lymph node level; there ore, the decision to per orm parotidectomy is guided by usual lymphadenectomy
indications.
Sentinel node biopsy procedure allowed limiting elective parotidectomy and neck dissections in some low-risk
patients.

What tumors have propensity or hematogenous spread to the parotid?
For the reasons that are not well understood, hematogenous metastases o the breast, lung, kidney, prostate, and
gastrointestinal carcinomas have af nity or parotid tissues.

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What is gustatory sweating and how it relates to the parotid innervation?
Postsynaptic sympathetic bers arrive to the parotid in the adventitia o the branches o the external carotid
artery. Preganglionic parasympathetic bers travel within the glossopharyngeal nerve (cranial nerve IX) and then
in tympanic branch (nerve o Jacobson) entering tympanic cavity, where it orms the tympanic plexus. T e bers
leave the tympanic cavity through lesser super cial petrosal nerve entering middle cranial ossa. T e nerve leaves
the cranium via its own bony canal or the oramen ovale and terminates in the otic ganglion located on the medial
sur ace o mandibular nerve (V3). T e postganglionic bers join the auriculotemporal nerve (brunch o V3), which
in turn gives o the parotid branches to the gland.
Gustatory sweating or Frey’s syndrome occurs ollowing parotidectomy or rhytidectomy. It is caused by
dys unction o the auriculotemporal nerve. T e pathways o this nerve are disrupted during the operation, and
they regenerate incorrectly. Cross innervation o cholinergic postganglionic parasympathetic bers rom the otic
ganglion and the cholinergic postganglionic sympathetic bers innervating sweat glands o the skin. T is results
in parasympathetic innervation o the cholinergic postganglionic sympathetic bers. A ected patients have acial
sweating and ushing in response to gustatory stimulation.

How do you manage it?
Most patients with Frey’s syndrome can be simply observed because the symptoms are usually mild. Injection o
botulinum toxin (Botox) and operative placement o AlloDerm, dermis, or ascia gra t under the a ected skin to
prevent improper nerve regeneration.

What is the parapharyngeal space?
It is an upside-down pyramid: superior border is skull base; in erior is lesser horn o the hyoid; medial is superior
constrictor, tonsil, and eustachian tube; and lateral is ramus o the mandible. It is important that the lateral wall
structures are rigid and the medial wall structures are pliable; tumors o the parapharyngeal space will present as a
bulging tonsil.

What does the parapharyngeal space have to do with salivary tumors?
umors o parapharyngeal space are requently o salivary gland origin. T ey can be tumors extending rom the
deep lobe o the parotid or tumors o accessory salivary gland rest.

You have suspected that the patient has a parapharyngeal tumor, how do you work it up?
Do not biopsy—some o the parapharyngeal tumors can be highly vascular and orientation o the tumor and the
carotid artery cannot be determined on physical examination. Workup is largely based on imaging—get a C scan
with contrast.

What in particular you look or on the C scan?
Axial cuts o the C will show relation o the tumor to the styloid.
Prestyloid tumors are salivary in origin with the rare exception o connective tissue neoplasms.
Poststyloid tumors are neurogenic (CN IX, X, XI, and sympathetic chain), vascular (paragangliomas), or lymph
node (metastases) in origin.

Overall, what is the most common tumor o the parapharyngeal space?
Metastatic lesions are the most common. T e most common primary tumor is pleomorphic adenoma (50%).

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What are the lymph nodes in the parapharyngeal space?
Nodes o Rouviere drain the nasopharynx.

What is Vernet syndrome?
Enlargement o the nodes extending to the jugular oramen that causes compression o CN IX, X, XI, and
paralysis o their motor components.

Does radical surgery or parotid tumors and radiation therapy signi cantly a ect long-term survival?
No. T ey do improve local and regional control, but do not change long-term survival. Un ortunately, outcome o
parotid malignancies is largely predetermined by the histology o the tumor.
REFERENCES
AJCC Cancer Staging Manual, 7th ed. New York, NY: Springer; 2010.
Batsakis JG. umors o the head and neck: clinical and pathological considerations. 2nd ed. Baltimore, MD: Williams Wilkins; 1979.
Close LG, Larson DL, Shah JP. Essentials o head and neck oncology. 1st ed. New York, NY: T ieme Medical Publishers, Inc.; 1998.
Jan aza P, Nadol JB, Galla RJ, Fabian RL, Montgomery WW. Surgical Anatomy o the Head and Neck. 1st ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 2001.
Medina JE. Clinical Practice Guidelines or the Diagnosis and Management o Cancer o the Head and Neck. American Head and Neck
Society; 2002.
Regezi JA, Batsakis JG. Histogenesis o salivary gland neoplasms. Otol Clin N Am. 1977;10:297–307.
Salivary Gland Tumors, NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®), Version 2.2014, National Comprehensive
Cancer Network®; 2015.
Shah JP. Head and neck surgery. 2nd ed. London: Mosby-Wol e; 1996.
Spiro RH. Salivary neoplasms: overview o a 35-year experience with 2,807 patients. Head Neck Surg. 1986;8(3):177–184.
Woods JE. Parotidectomy versus limited resection or benign parotid masses. Am J Surg. 1985;149(6):749–750.

509
Pieter G.L. Koolen, MD,
John B. Hijjawi, MD, FACS, and
Samuel J. Lin, MD, MBA, FACS

Which muscles close the mouth?
• Masseter
• emporalis
• Medial pterygoid

Which muscles open the mouth?
• Digastric muscles
• Mylohyoid muscles
• Geniohyoid muscles
• Genioglossus muscles

Which muscles protract the mandible?
• Lateral pterygoid muscles
• Digastric muscles
• Mylohyoid muscles

What are the goals o mandible reconstruction?
• Restore shape o the lower third o the ace.
• Preserve occlusion (i dentition).
• Allow or potential dental implants.
• Heal in a timely ashion—do not delay adjuvant therapy.
Head and Neck
Reconstruction
CHAPTER 52

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Plastic & Reconstructive Surgery Board Review

When can nonvascularized bone gra ts be used in mandible reconstruction?
• Isolated small de ects in avorable locations or so t-tissue coverage (ramus, body).
• No radiation history or plan or radiation therapy.

In the medically compromised patient, what can be done to reconstruct a segmental de ect at the time o
mandibular resection?
• Reconstruction plate and regional tissue (pectoralis major, latissimus dorsi).
• Avoid plate reconstruction with anterior de ects.

What are the disadvantages o plate reconstruction?
• Plate atigue and racture
• Screw loosening
• Plate exposure—beware with anterior de ects and/or radiation therapy
• Osteoradionecrosis

What common microvascular aps are available or mandible reconstruction?
• Fibula ap
• Iliac crest ap
• Scapula ap
• Radial orearm osseous ap

What is the blood supply to the iliac crest ree ap?
Deep circum ex iliac artery.

What are the advantages o the iliac crest ree ap?
• Good length o bone.
• all bone stock—good or implants. Abundant so t tissue—good or large-volume de ects.

What are the disadvantages o the iliac crest ree ap?
• Short pedicle, small vessels.
• Poor skin paddle mobility.
• Protracted gait pain, risk o abdominal hernia.
• Potential or meralgia paresthetica (lateral emoral cutaneous nerve injury/entrapment).

What are the advantages o the bula ree ap?
• Reliable skin paddle or closure/monitoring.
• Long, sturdy bone.
• Long pedicle, large caliber vessels.
• Supports osseointegrated implants.
• Allows or simultaneous dissection while tumor is being resected.
• Can make two skin islands based on separate per orators and include a portion o soleus muscle.

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What are the disadvantages o the bula ree ap?
• Contraindicated with severe peripheral vascular disease.
• Donor-site healing can be di cult and prolonged in some patients.

What options exist or reconstruction o the mandibular condyle?
• Reinsert condylar process as a nonvascularized bone gra t i disease ree—viability may be unpredictable,
especially with radiation therapy.
• Neocondyle—rounding o o the f bula ap trans er.
• Prosthetic reconstruction—not recommended i postoperative radiotherapy is planned.
• No reconstruction—mandible will rotate obliquely with opening.

What is the typical dose to a tumor bed a ter resection o an oral cavity tumor?
ypical dose is between 60 and 80 Gy.

What ef ect does radiation therapy have on normal tissue?
• Acute: dermatitis, mucositis, dysphagia, odynophagia, xerostomia, altered taste, atigue.
• Late: xerostomia, hyperpigmentation, dental decay, osteoradionecrosis, dysphagia, strictures, cataracts,
sensorineural hearing loss, so t-tissue f brosis, neck lymphedema.

What are the implications o xerostomia on oral unction?
• Accelerated tooth decay.
• Chewing, swallowing di culties.
• Speech problems.

Why is the mandible vulnerable to osteoradionecrosis?
• Radiation therapy–induced obliteration o in erior alveolar artery without adequate redundant blood supply is
believed to contribute.
• Histologically, scarcity o osteoblasts leads to ragile bone, susceptible to minimal injury.

When does osteoradionecrosis mani est?
• 1 to 3 years a ter radiation therapy, with an overall risk o 3% with current radiation techniques.
• Risk is present or the patient’s entire li e.

How does radiation therapy complicate dental extractions?
• T e incidence o osteoradionecrosis increases signif cantly i dental extraction is per ormed after radiotherapy.
T ere ore, it should be done be ore radiotherapy.
• Should wait 10 to 14 days between extractions and radiation therapy.
• Atraumatic extraction with minimal mucoperiosteal ap undermining should be practiced i extraction is
unavoidable.
• Hyperbaric oxygen and empiric antibiotic therapy have to be employed to minimize risk.

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Plastic & Reconstructive Surgery Board Review

What common reconstructive options are available or buccal de ects?
Any option employed should avoid intraoral contractures and avoid bulky aps.
• Primary closure.
• Split-thickness skin gra t—contracts 50% to 75%.
• FAMM ap—ensure acial artery patency, no more than 2 cm wide.
• Radial orearm ap—workhorse.
• Anterolateral thigh ap—may be too thick in some patients. Good option or large and through-and-through
de ects.
• Lateral arm ap—may be too thick in some patients.

How do you minimize the risk o a stula with oral cavity reconstruction?
With an incidence o 5% to 15%, this can progress to microvascular ailure.
• Ensure proper closure with nice mucosa–skin edge eversion. Avoid tight running or tight horizontal mattress
sutures that may compromise the mucosal/skin edge blood supply.
• Obliterate dead space—this is the single most important measure. Include an appropriate amount o muscle to
f ll the submandibular dead space. With a good muscle f lling, you really do not have to have watertight closure
that is impossible in most cases. ight closure should actually be avoided since it may cause ischemia o ap/
mucosa edges.
• Proper postoperative oral care.

What are the tenets o ap choice and design or tongue and oor o mouth reconstruction?
• Sealed communication between oral cavity and dissected neck. Some muscle f lling is desirable.
• Overcorrect volume or total or subtotal glossectomy reconstruction, especially i XR is planned so that the
neotongue can touch the palate or better speech reproduction. It will also create a trough or gutter to route
secretions posteriorly to minimize the risk o aspiration.
• For isolated oor o mouth or partial glossectomy de ects, the ap should be thin to preserve the mobility o the
remaining tongue.
• Design the ap to optimize protrusion o the residual tongue tip by recreating the ventral sulcus.
• A sensate ap may achieve better patient satis action and possibly better swallowing unction.

What are the common ap options or tongue and oor o mouth reconstruction a ter hemiglossectomy or
total glossectomy?
• T in anterolateral thigh ap: good or FOM and hemiglossectomy reconstruction.
• T ick anterolateral thigh ap: good or total or subtotal glossectomy reconstruction.
• Radial orearm ap: good or FOM and hemiglossectomy reconstruction but not enough bulk or total
glossectomy.
• Rectus abdominis/DIEP ap: good or total or subtotal glossectomy reconstruction, way too thick or
hemiglossectomy or FOM reconstruction.
• Latissimus ap: good or total or subtotal glossectomy reconstruction.

What is an “in-continuity” neck dissection?
Removal o the lymphatic drainage pathways between the primary tumor and adjacent nodes that lie in proximity
to the primary. T is does present the possibility o f stula ormation in oor o mouth/tongue tumors due to the
potential communication between the oral de ect and the neck.

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Is it necessary to innervate a ree ap or partial or total tongue reconstruction?
• Anastomosis o a sensory nerve o the trans erred ap is advantageous.
• T e pre erred recipient sensory nerve is the lingual nerve.
• Sensory recovery can be nearly complete.
• Motor reinnervation o a muscle ap by anastomosing the motor nerve to the hypoglossal nerve is poor at best.

What de ects may exist a ter resection o an oral cancer o the tongue?
• Wedge resection.
• Hemiglossectomy—may extend to oor o mouth and tonsillar pillar.
• Near-total glossectomy—entire tip o tongue and up to hal o the tongue base.
• otal glossectomy—entire tip and tongue base. No unctional residual tongue.

What are the common complications o pharyngoesophageal reconstruction?
• Pharyngocutaneous f stula—1 to 4 weeks postoperation, mani ests as a leakage o saliva or as a neck in ection.
• Anastomotic stricture—occurs months to years a ter reconstruction, usually at the distal anastomosis;
minimized by converting a circum erential repair with a staggered anastomosis.
• Neck in ection—should rule out the possibility o anastomotic leakage.
• Medical complications—usually respiratory or cardiac.

Which ree ap is least tolerant o ischemia and there ore microanastomosis should precede insetting?
Jejunum ap.

What are the common aps used or partial or total pharyngoesophageal de ects?
• Anterolateral thigh ap
• Radial orearm ap
• Jejunum ap
• Pectoralis major ap

What are the options or speech rehabilitation a ter pharyngolaryngectomy?
• racheoesophageal puncture ( EP) and insertion o voice prosthesis
• Voice tube using trans erred ileum, jejunum, or ileocecal valve
• Electrolarynx
• Esophageal speech

What recipient vessels are commonly utilized or head and neck ree ap reconstruction?
• Arteries: lingual artery, acial artery, superior thyroid artery, external carotid artery, superf cial temporal artery.
• Veins: common acial vein, internal jugular vein, superf cial temporal vein, external jugular vein.

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Which recipient vessels can be considered in the radiated and previously operated neck?
• ransverse cervical artery o the thyrocervical trunk
• Contralateral neck-vein gra ts are usually needed
• T oracoacromial artery
• Arteriovenous loop o the subclavian artery (cephalic vein ideal)
• Internal mammary vessels

What is a “ rozen neck”?
Severe so t-tissue f brosis o the neck as a result o neck dissection and radiation therapy. T ere is absence o
surgical planes, as well as limitation o passive motion at the neck, making exposure potentially challenging.

What are the problems associated with per orming reconstruction in the rozen neck?
• Risk o carotid artery rupture.
• Lack o recipient vessels or ree tissue trans er.
• Neck skin def cit—may be signif cant.

How does the surgeon avoid morbidity and mortality in reconstructing the pharyngoesophagus in the
rozen neck?
• Avoid dissection o the great vessels.
• Use alternative recipient vessels: transverse cervical vessels, internal mammary vessels, thoracoacromial trunk.
• Provide abundant skin coverage with ap trans er.

When is a pectoralis ap used or pharyngoesophageal reconstruction?
• Partial de ects, male patients
• High-risk patients
• Failed ree ap

What happens i the patient has ap loss or is too ragile or reconstruction a ter pharyngectomy?
• Create spit f stula at upper neck.
• Use pectoralis major ap or latissimus dorsi ap to protect neck vessels and divert saliva away rom
tracheostomy.

I a patient has a hemipalatectomy or maxillectomy de ect with intact contralateral maxillary dentition,
what is the reconstruction o choice?
Palatal obturator with denture is an acceptable option. T e maxillectomy wound or the maxillary sinus can be skin
gra ted and the obturator separates the oral cavity rom the nasal cavity to prevent VPI and nasal regurgitation. T is
is a quick and simple option, particularly use ul or high-risk patients who are not ree ap candidates. Postoperative
radiation may cause skin-gra t loss and bone exposure. For most patients with planned radiotherapy or with previous
radiation, a so t-tissue ap reconstruction is the most popular option. For younger and more unctional patients,
especially with benign diseases, vascularized bone reconstruction with osteointegrated dental implants provides the
best possible aesthetic and unctional outcomes when the maxillectomy de ect extends beyond the anterior midline
to the contralateral side, vascularized bone reconstruction becomes the pre erred choice.

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What are common ree aps or mid ace reconstruction o bony and so t-tissue de ects?
Bone aps
• Fibula osteocutaneous ree ap
• Iliac crest osteocutaneous ap
• Scapula osteocutaneous ree ap
• So t-tissue ree ap with bone gra ts
So t-tissue aps
• Anterolateral thigh ap
• Radial orearm ap
• Rectus abdominis myocutaneous ap
• Latissimus dorsi with bone gra t

What general principles guide skull base reconstruction?
• Seal the dura rom the aerodigestive tract.
• ight seal o violated dura to prevent cerebrospinal uid leak—muscle is desirable to eliminate dead space.

What is Jackson and Hyde’s classi cation o skull base reconstruction?
1
2
3
Figure 52-1 Regions o the skull base.

What aps are available or region 1 skull base de ects?
• Galea- rontalis ap (midline)
• Pericranial ap (midline)
• emporalis ap (lateral de ect)
• emporoparietal ascial ap (lateral de ects)

What aps are available or region 2 or region 3 skull base de ects?
• emporalis ap
• emporoparietal ascial ap
• Free ap (rectus abdominis or other muscle ap)

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Plastic & Reconstructive Surgery Board Review

What are the basic tenets to minimize ap pedicle and anastomotic problems besides meticulous
anastomotic techniques?
• Interrogate the recipient vessels or adequate in ow, venous out ow obstruction (valves, thrombus).
• Pedicle artery and vein should be parallel i possible. I this is not possible due to location o the respective
recipient artery and vein, then the ap pedicle should be dissected and anastomosed so one should not
compromise the other (long enough dissection to avoid kinking).
• Minimize redundancy—may cause kinking and twisting o pedicle.
• Minimize tension—vein gra ts may be necessary.
• Avoid compression—especially an issue in the irradiated neck, never underestimate swelling at the end o the
case or the need or a large ap skin paddle to close the de ect. Flap insetting should not be tight. Some skin
redundancy can be easily revised at a later stage. rying to achieve the “best aesthetic result” by insetting the ap
tight may cause pedicle (especially per orator) compression.
• Study and test the pedicle by moving the head back and orth. Be ore closing the neck incision, the head should
return to a neutral position ( rom a turned away position) and the neck return rom a hyperextended position.
T e pedicle position should then be care ully inspected again and any kinking or twisting should be corrected.
• T e most common cause o venous occlusion (80%) is mechanical obstruction such as twisting, kinking, and
compression. T ere ore, great care should be taken to avoid these problems.

What are the common ree aps or scalp reconstruction?
• Latissimus dorsi muscle with skin gra ting or large de ects.
• Radial orearm or lateral arm aps or smaller de ects.
• Rectus abdominis muscle with or without skin components.
• Vastus lateralis muscle/anterolateral thigh ap.
• Scapular, parascapular aps.

What is the most common recipient vessel or scalp reconstruction and what are the potential problems with
these vessels?
T e superf cial temporal vessels are most commonly used as recipient vessels or scalp reconstruction due to their
proximity to the de ect. However, the superf cial temporal vessels have a bad reputation o being prone to spasm
and having higher ailure rates. T e key to avoid such problems is to use the very proximal part o the superf cial
temporal vessels near the zygomatic arch, to a point that they cannot be dissected any more. At this level, the
diameter and ow are much greater and there ore most reliable. Only use the most proximal 1 cm o superf cial
temporal vessels or anastomosis.
REFERENCES
Coleman JJ. Reconstruction o the mid ace with vascularized bone and so t tissue. Semin Plastic Surg. 2003;17:291–303.
Cordeiro PG, Santamaria E. A classif cation system and algorithm or reconstruction o maxillectomy and mid acial de ects. Plast
Reconstr Surg. 2000;105:2347–2348.
Jackson I , Hide A. A systematic approach to tumors o the base o the skull. J Maxillofac Surg. 1982;10:92–98.
Neligan PC, Wei F-C, eds. Microsurgical Reconstruction of the Head and Neck. St Louis, MO: Quality Medical Publishing; 2010.

Figure 51-3 A: Large pleomorphic adenoma involving deep and
super cial lobes o the right parotid.
Figure 51-2 Le t parotid mass in a patient with a
long-standing Sjögren’s syndrome.
COLOR INSERT

A
C

D
B
Figure 51-6 Adenoid cystic carcinoma o the le t submandibular gland (size 2 cm physical examination) treated
with composite resection, total parotidectomy with resection o lower division o the le t acial nerve, ree bula
(A and B), specimen (C) static sling, and postoperative radiation. Appearance o the patient without evidence o
disease at 6 years (D).
Figure 51-7 Positioning o parotidectomy patient on a shoulder roll and donut head rest. NIM acial nerve
monitor or at least zygomatic (blue) and marginal mandibular (red) branches o the acial nerve as well as
grounding electrodes (white and green) are placed. Both modi ed Blair and aceli t incisions are outlined and
lidocaine with epinephrine is injected prior to the prep.

A

B
C

D
Figure 51-8 A ter sub-SMAS and external auditory canal dissection and separation o the parotid tail rom the sternocleidomastoid muscle the deep
points o dissection are connected by dividing the tissue between these points (A). T e nerve trunk (B) and divisions are identi ed and the branches
are sequentially dissected (C). In the case o total parotidectomy the nerve is dissected o the deep lobe, which is then removed (D).
A

B
Figure 51-9 A, B: Cervico acial f ap reconstruction o the total parotidectomy de ect.

A

B
C

D
Figure 51-10 A –D: Metastatic squamous cell carcinoma o the temporal region with removal o the rontal branch o the acial nerve
treated with total parotidectomy, neck dissection, and ree AL f ap, ollowed by radiation, staged debulking, endoscopic browli t and
upper blepharoplasty.

A

B
C

D
E

F
Figure 51-11 Metastatic malignant melanoma o the scalp requiring radical parotidectomy with neck dissection (A). T e thigh was
used as a donor site or AL ree f ap, ascia lata gra t (B) or static sling (C), and emoral nerve gra ts (D). Both acial nerve gra t
reconstruction (E) and static sling (C and F) were per ormed in addition to AL ree f ap (F).
Figure 54-6 C: Dental crossbite.
Figure 54-6 D: Anterior openbite.