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442 PART V ORAL AND MAXILLOFACIAL SURGERY
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32. What is blue rubber bleb nevus syndrome?
Rare, sporadic disorder composed of cutaneous and gastrointestinal VMs. Skin lesions can occur
anywhere in body but have predilection for trunk, palms, and/or soles of feet. VMs are soft, blue, and
increase in size and number with age. Gastrointestinal lesions are most common in small bowel and
can cause bleeding, intussusception and volvulus.
33. What is Klippel-Trenaunay syndrome?
A sporadic capillary-lymphatic-venous malformation (CLVM) associated with soft tissue/skeletal
hypertrophy of a limb.
BiBliography
Abramowicz S, Padwa BL: Vascular anomalies in children, Oral MaxillofacSurg Clin North Am 24:443–455, 2012.
Chen MT, Yeong EK, Horng SY: Intralesional corticosteroid therapy in proliferating head and neck hemangiomas: a review of
155 cases, J Pediatr Surg 35:420–423, 2000.
Greene AG: Management of hemangiomas and other vascular tumors, Clin Plast Surg 38:45–63, 2011.
Greene AK, Orbach DB: Management of arteriovenous malformations, Clin Plast Surg 38:96–106, 2011.
Greene AK, Taber SF, Ball KL, et al.: Sturge-Weber syndrome: frequency and morbidity of facial overgrowth, J Craniofac
Surg 20:617–621, 2009.
Hogeling M, Adams S, Wargon O: A randomized controlled trial of propranolol for infantile hemangiomas, Pediatrics
128:e259–e266, 2011.
Kaban LB, Mulliken JB: Vascular anomalies of the maxillofacial region, J Oral Maxillofac Surg 44:203–213, 1986.
Marler JJ, Mulliken JB: Current management of hemangiomas and vascular malformations, Clin Plast Surg 32:99–116,
2005.
Mulliken JB, Fishman SJ, Burrows PE: Vascular anomalies, Curr Probl Surg 37:517–584, 2000.
Mulliken JB, Glowacki J: Hemangiomas and vascular malformations in infants and children: a classification based on
endothelial characteristics, Plast Reconstr Surg 69:412–422, 1982.
Padwa BL, Mulliken JB: Vascular anomalies of the oral and maxillofacial region. In Fonseca RJ, Marciani RD, Turvey T, edi-
tors: Oral and maxillofacial surgery, vol 2. St Louis, MO, 2008, Saunders, pp 577–591.
Sloan GM, Renisch JF, Nichter LS, et al.: Intralesional corticosteroid therapy for infantile hemangiomas, Plast Reconstr Surg
83:459–467, 1989.
OSTEORADIONECROSIS/
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OSTEONECROSIS OF THE JAWS
Regina Landesberg, Lisa Marie Di Pasquale
1. What is ORN?
Radiation plays a key role in the treatment of head and neck cancer. Due to the location of the tumor
or lymph node metastases, the salivary glands, oral cavity, and jaws are often included in the treatment radiation fields. As a result, these tissues often undergo changes secondary to radiation damage.
Osteoradionecrosis (ORN) is often defined as an area of exposed bone that persists for at least
3 months in bone that has been irradiated. This definition may be insufficient, as ORN can present
radiographically as a pathologic fracture with intact mucosa or skin.
2. What are the risk factors for ORN?
Multiple risk factors predispose to the development of ORN. Treatment-dependent factors include
cumulative radiotherapy doses to the bone, particularly those that exceed 5000 cGy. This is particularly
true of the molar region of the mandible. Other important predisposing factors include the anatomic
site of the primary tumor, tumor stage, proximity of the tumor to bone, external beam versus internal
radiation therapy, extent of surgery, and concomitant chemotherapy. Host factors that increase the
likelihood of developing ORN include the nutritional status of the patient, existing dental disease, oral
hygiene, and continued tobacco or alcohol use (Table 48-1).
3. What is the incidence of ORN?
The incidence of ORN ranges from 2% upward. The mandible is the most common site of radiation-
induced tissue damage following treatment of head and neck cancers.
ORN can occur anywhere from a few months up to 30 years after irradiation. It may be related to
traumatic injuries such as pre- or post-radiation extractions, denture trauma, and other iatrogenic contributions. Additionally, ORN may occur spontaneously due to the progression of existing dental disease.
4. Why is the mandible a more common location for ORN than the maxilla?
In contrast to the relatively well-vascularized maxilla, the mandible consists primarily of cortical bone
that is essentially supported by a single arterial blood supply (inferior alveolar artery), thus making it
at increased risk of ischemic radionecrosis.
5. Does the mode of radiation delivery affect ORN incidence?
The different forms of radiation do not produce the same biologic effects. The initial delivered dose
of radiation becomes an effective dose with a biologic effect under the influence of three main
parameters: radiation type (type of atomic origin, level of energy), tissue type, and radiation schedule
(fractionation, dose per fraction, total cumulative dose). It has been shown that external beam radiation is more positively correlated with ORN incidence than internal implant radiation therapy. Total
radiation doses associated with increased risk of ORN are those higher than 5000 cGy, particularly
6000 to 7000 cGy.
6. What is the pathophysiology of ORN?
Four hypotheses have been described for the development of ORN. First described was a series of
local injury and infection following radiation exposure. Later, the “Triple H” hypothesis (hypocellular,
hypoxic, and hypovascular) was described where ORN was thought to occur as a result of microvascular damage resulting in a damaged blood supply. A more recent proposal implicates radiationinduced suppression of osteoclast-mediated bone turnover in the pathogenesis of ORN. Finally, a
fourth hypothesis is based on the histopathological features seen in ORN-proposed fibroatrophic
bone changes called radiation-induced fibrosis (RIF). The sum of these four hypotheses indicates that
irradiated bone has reduced cellular viability, obliteration of vessels, and compromised bone turnover
compared to healthy bone.
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Table 48-1. Risk Factors for Osteoradionecrosis
PATIENT-RELATED
FACTORS
Active dental disease
Oral hygiene
Pre-radiationoralcare
Alcohol and tobacco use
Table 48-2. Classification of Osteoradionecrosis and Recommended Therapy
1 < 2.5 cm length of bone affected (damaged or exposed); asymptomatic
Medical treatment only
2 > 2.5 cm length of bone; asymptomatic, including pathologic fracture or involvement of the
inferior alveolar nerve or both
Medical treatment only unless there is dental sepsis or obvious loose, necrotic bone
3 > 2.5 cm length of bone; symptomatic, but with no other features despite medical treatment
Consider debridement of loose or necrotic bone, and local pedicled flap
4 > 2.5 cm length of bone; pathologic fracture, involvement of the inferior alveolar nerve, orocu-
taneous fistula or a combination
Reconstruction with free flap if patient’s overall condition allows
From Lyons A, Osher J, Warner E et al., Osteoradionecrosis-A review of current concepts in defining the extent
of the disease and a new classification proposal, Br J Oral Maxillofac Surg 52:392-395, 2014.
TUMOR-RELATED
FACTORS
Anatomic location of the tumor
Clinical state of the tumor
Presenceoflymphnode
Metastasis
TREATMENT-RELATED
FACTORS
Field of radiation
Total radiation dose
Dose rate/day
Mode of radiation delivery
Tumor surgery
7. What are the clinical and radiographic features of ORN?
Diagnosis of ORN is primarily based on clinical findings and patient history. The clinical manifesta-
tions of ORN may present several years after irradiation. By definition, ORN occurs in patients with
a history of radiation and include one or several of the following that have failed to heal in at least
3 months:
• Nonhealingulcer
• Exposedbone
• Pain/dysesthesia/anesthesia
• Orocutaneousstula
• Pathologicfracture
Recently, Lyons et al. (Table 48-2) developed a new classification and recommendations for treatment
of ORN based on the extent of the condition.
8. What is included in radiographic criteria?
• Increaseddensity
• Periostealthickening
• Diffuseradiolucency
• Mottledareasofosteoporosis
• Sclerosis
• Sequestration
• CTscanorbonescintigraphycanalsobeusedtoevaluatetheextentoftheORN.
9. What are the preventive methods of management of ORN?
The decision to extract symptomatic and asymptomatic teeth before radiation therapy has tra-
ditionally been based on empirically designed protocols and not on “evidence-based” dentistry.
Consideration is given to the preexisting condition of the teeth in the radiation field and to
teeththatmightcausepost-irradiationcomplicationsifleftinplace.Pre-radiationextractionis
indicated for teeth with advanced or symptomatic periodontal disease, advanced carious decay,
pulpal involvement, mobility with root furcation, periapical pathology, and residual root tips
CHAPTER 48 OSTEORADIONECROSIS/OSTEONECROSIS OF THE JAWS 445
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not covered by alveolar bone. Critical to the decision-making process is the patient’s previous
history of good oral hygiene and commitment to routine and ongoing professional dental visits.
For optimum healing after extractions, 3 weeks prior to the initiation of radiotherapy is desirable;
however, in most situations this is not feasible. An atraumatic approach should be employed
in the pre-radiation extraction procedure with care taken to remove all sharp bony edges. If
possible,anattempttoachieveprimaryclosureismade.Patientsundergoingradiationtherapy
ideally should be treated with a fluoride regimen of 1.1% NaF (5000 parts per million) gel and
fluoridetrays.Frequentsurveillanceandcarebydentalprovidersisessentialbothduringand
after radiation therapy.
10. What are the conservative methods of management of ORN?
In the early stages of ORN, there is typically only a small nonhealing lesion present. Conservation
management, commonly pain relief, and antibiotic therapy can be considered. Superficial debride-
ment,orsequestrectomy,hasbeenshowntopromotesofttissuecoverage.Irrigationandexcellent
oral hygiene are essential. Over half of these early stage lesions can be cured in this manner. Hyper-
baricoxygentherapyhasalsobeenusedinconservativemanagementofORN.Earlystudy(PhaseII),
based on the hypothesis of radiation-induced fibrosis, has shown promising results with a cocktail
regimenofpentoxifylline-tocopherol-clodronate(PENTOCLO).
11. What is hyperbaric oxygen (HBO) therapy? What are the uses of HBO in ORN?
HBO therapy is another nonsurgical treatment modality for ORN. The use of HBO therapy is based on
the Triple H theory (previously described). HBO is thought to increase the blood-tissue oxygen gradient, improving the diffusion of oxygen in hypoxic tissues, which promotes angiogenesis by increasing
growth factors such as vascular endothelial growth factor (VEGF), as well as stimulating osteogenesis.
HBO has been used therapeutically to treat ORN or prophylactically in irradiated bone prior to
surgical intervention. Additionally, HBO is used in treatment of necrotizing skin infections, gas gangrene, and refractory osteomyelitis.
12. What is the HBO protocol?
Therapeutic HBO treatment consists of 30 HBO dives to 2.4 atm for 90 minutes. If the wound shows
definitive clinical improvement, additional dives may be added. Dives are typically once a day, 5 days a
week.
Although surgery is contraindicated in heavily irradiated fields, when it cannot be avoided HBO
hasbeenusedinanattempttoavoidthedevelopmentofORN.Patientsusuallyreceive20dives
preoperatively, followed by 10 dives postoperatively.
Although HBO therapy seemed to be effective in early investigations using animal models, more
recent studies have failed to conclusively show its benefit. A recent systematic review of the literature
by Fitz et al. failed to identify any reliable evidence to support or refute the efficacy of HBO in the
prevention of postextraction ORN in irradiated patients.
13. What are surgical treatment options for ORN?
In the more advanced stages of ORN and in cases where conservative measures failed, surgical
treatment,withorwithoutHBO,isrequired.First,apossiblelocalrecurrenceofamalignancyshould
be excluded via biopsy. As previously described in Table 48-1, management may be medical and/or
surgical depending on the extent of the lesion.
14. What is osteonecrosis of the jaws (ONJ)?
Osteonecrosis of the jaws (ONJ), also known as medication-related osteonecrosis of the jaws (MRONJ)
and antiresorptive osteonecrosis of the jaws (ARONJ), is a clinical entity with the diagnostic characteristics defined by a number of medical and dental professional societies (AAOMS, ASBMR, ADA).
Although there are slight differences in the various definitions of ONJ, a breach in the oral mucosa
leading to exposed bone that fails to heal in 6 to 8 weeks is a mandatory element in the diagnosis of
this condition. Additionally, patients must have a history of receiving antiresorptive therapy and no
previous head and neck radiation. While the occurrence rate of ONJ in oncology patients ranges from
1.5% to 15%, patients treated for benign conditions (most commonly osteoporosis) appear to have a
much lower incidence of ONJ (1/10,000 to 1/100,000).
15. What causes ONJ?
Whilemanyquestionsregardingtheincidence,pathoetiology,andnaturalhistoryofthiscondition
still need to be answered, it appears this disorder is multifactorial in nature. There seems to be a
strong association between antiresorptive therapy (bisphosphonates, anti-RANK ligand) and ONJ;
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Table 48-3. Antiresorptives
BENIGN MALIGNANT
Antiresorptive Route Antiresorptive Route
Bisphosphonate Bisphosphonate
Alendronate (Fosamax) PO Pamidronate(Aredia) IV
Risedronate (Actonel) PO
Ibandronate (Boniva) PO
Zoledronate (Reclast) IV Zometa (Reclast) IV
Monoclonal
antibody
however, a definitive cause-and-effect relationship between the two has not been established.
Development of ONJ is often preceded by a traumatic event, most commonly an extraction. The
fact that many of ONJ are immunosuppressed by medications (steroids, chemotherapy) or disease
(diabetes, rheumatoid arthritis, cancer) suggests that an alteration in wound healing may play a
signicantroleinthedevelopmentofONJ.Furthermore,theuniquemicrobialenvironmentand
thehighsusceptibilityoftheoralcavitytofrequenttraumaticeventsmayexplainwhyONJlesions
show a preference for the craniofacial region.
16. What are bisphosphonates?
Bisphosphonates(BPs)areawidelyusedclassofdrugsindicatedforthepreventionandtreatment
ofpostmenopausalandsteroid-inducedosteoporosis,Paget’sdiseaseofbone,hypercalcemiaof
malignancy, multiple myeloma, and bone metastases associated with breast, prostate, lung, and other
soft tissue tumors (Table 48-3).
17. What is denosumab?
Denosumab (Dmab), a receptor activator of NF-kappa Bligand (RANKL) inhibitor, has recently been
approvedforsimilarindicationstoBPs,andithasalsobeenstronglyassociatedwithONJ(see
Table 48-3).
18. What is the staging system for ONJ?
The ONJ staging system, originally described in 2009 by a special committee of the AAOMS, has been
largely accepted by both the medical and dental professions. This system has essentially remained
unchanged in the most recent AAOMS 2014 update on MRONJ. The stage of disease is based on the
severity of clinical symptoms as well as radiographic findings. Of note is the inclusion of a Stage 0
category where only nonspecific radiographic findings are identified in a patient receiving antiresorptive therapy (Table 48-4).
19. How is ONJ treated?
Several studies have shown that patients who have a screening examination and appropriate
treatment of dental disease prior to the initiation of antiresorptive therapy have a significant
decrease in the risk of developing ONJ. The present recommendations by both the ADA and
AAOMSdonotincludeadrugholidayorCTX(C-terminaltelopeptide)testinginpatientsrequiring
oral surgical procedures who are on antiresorptive therapy for benign conditions. In contrast,
surgical procedures in individuals who have cancer and are receiving antiresorptive therapy
should be avoided if at all possible. Nonsurgical therapies, such as endodontic treatment, are
preferred in these patients.
The management of patients with ONJ has traditionally been conservative, with the recommendation that surgical intervention only be performed in the most severe cases (Stage 3) where
the patients have significant symptomatology. See Table 4. It should be noted, however, that Carlson
as well as others have recently reported success rates of greater than 90% when using aggressive
surgical resections to treat ONJ.
Denosumab(Prolia) SQ
Monoclonal
antibody
Denosumab (Xgeva) SQ
CHAPTER 48 OSTEORADIONECROSIS/OSTEONECROSIS OF THE JAWS 447
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Table 48-4. ONJ Staging System
STAGING TREATMENT
At-risk category: No apparent necrotic bone in
patients who have been treated with either
• Notreatmentindicated
• Patienteducation
oral or IV bisphosphonates
Stage 0: No clinical evidence of necrotic bone,
but nonspecific clinical findings, radiographic
• Systemicmanagement,includingtheuse
of pain medication and antibiotics
changes, and symptoms
Stage 1: Exposed and necrotic bone, or fistulae that
probe to bone, in patients who are asymptomatic
and have no evidence of infection
• Antibacterialmouthrinse
• Clinicalfollow-uponaquarterlybasis
• Patienteducationandreviewofindications
for continued bisphosphonate therapy
Stage 2: Exposed and necrotic bone, or fistulae
that probe to bone, associated with infection
as evidenced by pain and erythema in the region
of the exposed bone with or without purulent
drainage
Stage 3: Exposed and necrotic bone or a fistula that
probes to bone in patients with pain, infection,
and one or more of the following: exposed and
necrotic bone extending beyond the region of
• Symptomatictreatmentwithoralantibiotics
• Oralantibacterialmouthrinse
• Paincontrol
• Debridementtorelievesofttissueirritation
and infection control
• Antibacterialmouthrinse
• Antibiotictherapyandpaincontrol
• Surgicaldebridement/resectionforlonger
term palliation of infection and pain
alveolar bone (i.e., inferior border and ramus in
the mandible, maxillary sinus and zygoma in the
maxilla) resulting in pathologic fracture, extraoral
fistula, oroantral and oronasal communication, or
osteolysis extending to the inferior border of the
mandible or sinus floor
From Ruggiero SL, Dodson TB, Fantasia J, et al.: American Association of Oral and Maxillofacial Surgeons
Position Paper on Medication-Related Osteonecrosis of the Jaw-2014 Update. J Oral Maxillofac Surg, 72(10):
1938–1965, 2014.
BiBliography
Assael LA: New foundations in understanding osteonecrosis of the jaws, J Oral Maxillofac Surg 62(2):125–126, 2004.
Carlson ER: Management of antiresorptive osteonecrosis of the jaws with primary surgical resection, J Oral Maxillofac Surg
72(4):655–657, 2014.
Delanian S, Chatel C,PorcherR, Depondt J, Lefaix JL: Complete restoration of refractory mandibular osteoradionecrosis by
prolongedtreatmentwithapentoxifylline-tocopherol-clodronatecombination(PENTOCLO):aphaseIItrial,Int J Radiat
Oncol Biol Phys 80(3):832–839, 2011.
Dimopoulos MA, Kastritis E, Bamia C, Melakopoulos I, Gika D, Roussou M, Migkou M,Eleftherakis-PapaiakovouE, Christou-
las D, Terpos E, Bamias A: Reduction of osteonecrosis of the jaw (ONJ) after implementation of preventive measures in
patients with multiple myeloma treated with zoledronic acid, Ann Oncol 20(1):117–120, 2009.
Edwards BJ, Hellstein JW,JacobsenPL, et al., and the American Dental Association Council on Scientific Affairs Expert
PanelonBisphosphonate-AssociatedOsteonecrosis:Updatedrecommendationsformanagingthecareofpatientsreceiving oral bisphosphonate therapy: an advisory statement from the American Dental Association Council on Scientific
Affairs, J Am Dent Assoc 139(12):1674–1677, 2008.
Fritz GW, Gunsolley JC, Abubaker O, Laskin DM: Efficacy of pre- and postirradiation hyperbaric oxygen therapy in the
prevention of postextraction osteoradionecrosis: a systematic review, J Oral Maxillofac Surg 68(11):2653–2660, 2010.
Hellstein JW, Adler RA, Edwards B,etal.,andtheAmericanDentalAssociationCouncilonScienticAffairsExpertPanel
on Antiresorptive Agents: Managing the care of patients receiving antiresorptive therapy for prevention and treatment
of osteoporosis: executive summary of recommendations from the American Dental Association Council on Scientific
Affairs, J Am Dent Assoc 142(11):1243–1251, 2011.
Khosla S, Burr D, Cauley J, et al.: American Society for, and R. Mineral, Bisphosphonate-associated osteonecrosis of the jaw:
report of a task force of the American Society for Bone and Mineral Research, J Bone Miner Res 22(10):1479–1491, 2007.
Landesberg R, Woo V, Cremers S,etal.:Potentialpathophysiologicalmechanismsinosteonecrosisofthejaw,Ann N Y
Acad Sci 1218:62–79, 2011.
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Lyons A, Osher J, Warner E, et al.: Osteoradionecrosis–a review of current concepts in defining the extent of the disease
and a new classification proposal, Br J Oral Maxillofac Surg 52(5):392–395, 2014.
Marx RE: A new concept in the treatment of osteoradionecrosis, J Oral Maxillofac Surg 41(6):351–357, 1983.
Marx RE, Tursun R: Suppurative osteomyelitis, bisphosphonate induced osteonecrosis, osteoradionecrosis: a blinded
histopathologic comparison and its implications for the mechanism of each disease, Int J Oral Maxillofac Surg
41(3):283–289, 2012.
McCaul JA:Pharmacologicmodalitiesinthetreatmentofosteoradionecrosisofthejaw,Oral Maxillofac Surg Clin North Am
26(2):247–252, 2014.
Oh HK, Chambers MS, Garden AS,WongPF, Martin JW: Risk of osteoradionecrosis after extraction of impacted third molars
in irradiated head and neck cancer patients, J Oral Maxillofac Surg 62(2):139–144, 2004.
Ripamonti CI, Maniezzo M, Campa T et al.: Decreased occurrence of osteonecrosis of the jaw after implementation of den-
tal preventive measures in solid tumour patients with bone metastases treated with bisphosphonates. The experience of
the National Cancer Institute of Milan, Ann Oncol 20(1):137–145, 2009.
Ruggiero SL, Dodson TB, Assael LA et al.: Task Force on Bisphosphonate-Related Osteonecrosis of the Jaws, American
Association of Oral and Maxillofacial Surgeons position paper on bisphosphonate-related osteonecrosis of the
jaw - 2009 update, Aust Endod J 35(3):119–130, 2009.
Ruggiero SL, Dodson TB, Fantasia J,etal.:AmericanAssociationofOralandMaxillofacialSurgeonsPositionPaperon
Medication-Related Osteonecrosis of the Jaw-2014 Update, J Oral Maxillofac Surg 72(10):1938–1956, 2014.
Sulaiman F, Huryn JM, Zlotolow IM: Dental extractions in the irradiated head and neck patient: a retrospective analysis of
Memorial Sloan-Kettering Cancer Center protocols, criteria, and end results, J Oral Maxillofac Surg 61(10):1123–1131,
2003.
NECKMASS
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HuiShan Ong, Tong Ji, Chen Ping Zhang
1. What are the main categories of neck masses?
Congenital, infectious/inflammatory, and neoplastic (benign/malignant)
2. What can the age of a patient tell you?
The patient’s age should be a prime consideration in differential diagnosis. Three main age groups are
taken into consideration: pediatric (≤15 years), young adult (16 to 40 years), and adult (>40 years). See
Table 49-1.
3. How do you establish a differential diagnosis based on the average duration of
the patient’s symptoms?
Rule of 7:
• Swellingfrominflammationwillhaveexistedfor7 days.
• Swellingfromneoplasmwillhaveexistedfor7 months.
• Swellingfromcongenital deformitywillhaveexistedfor7 years.
4. How do you establish differential diagnoses for a neck mass in an adult?
Rule of 80s after age of 40:
• 80% of all nonthyroidneckmasseswillbeneoplastic.
• 80% of neoplastic masses are malignant.
• 80% of malignant mass are metastatic.
• 80%ofmetastasesarefromprimarysitesabovetheleveloftheclavicle.
• 80% of metastatic lymph nodes (LNs) in adults are SCC.
5. How do you diagnose a neck mass?
Adiagnosiscandevelopfrompatient’schiefcomplaint,patient’sage,location,onsetandduration,
size,pain,drainage/exudates,characteristicsandprogressionofaneckmass,andpastmedicalhistoryincludingpreviousheadnecksurgery.
6. What are the clinical investigations in evaluating the cervical mass?
• Ultrasound
• Contrast-enhancedCT
• Fineneedleaspirationcytology(FNAC)
• PET-CT
• MRI
• Clinicalpalpation
7. What is a normal LN?
ClinicallypalpablenormalLNisabout1cminsize(atarangeof0.5to2cm),relativelysoftinconsis-
tency,andmobile.Tenderuponpalpationdoesnotdifferentiatebetweennormalandcancerous.But
thesizeoftheLNcanbevariousamongdifferentagegroups.SeeTable 49-2.
Therefore,anynodegreaterthan2cmbeyondthesenormalhyperplasticzonesshallbeevalu-
atedwithcaution.
8. In what circumstances should you be particularly concerned about a
neck mass?
• Hard or fixed mass
• Obstructiveairway/breathingdifculty
• Elderly patient
• Medicallycompromisedpatient
• Presenceoforopharyngeal masswhensimplepharyngitisordentalinfectionhasbeenruledout
• Signsofcachexia
• Ahistoryofpersistenthoarseness of voice or complaining of dysphagia
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Table 49-1. Patient’s Age and How It Relates to Differential Diagnosis
Pediatric: Inammatory>congenital>malignant>benign
Youngadult: Inammatory>congenital>benign>malignant
Adult: Malignant>benign>inammatory>congenital
Table 49-2. Size of LN According to Different Age Groups
Infant: SmallpalpableLNsaremorereadilypalpatedintheposteriorcervical
Pediatric: SmallpalpableLNsarepalpableoverthesubmandibularregion>anterior
9. How does a contrast-enhanced CT compare to MRI in evaluation of neck mass?
CTimagescansignicantlymanifestanenhancedrimwithcenterliquefactionlymphnodetoindicatea
regionalmetastasis.SignalintensityonMRIwithintravenousgadoliniumadministrationisstillineffectiveindemonstratingametastaticlymphnode;MRIlymphnodeassessmentreliesmoreonanalysisof
enhancementkinetics(peakandwashouttimingslope)afterbolusadministrationofgadoliniumchelate
agentsthataretechnicallydependent.Furthermore,anMRIcannotidentifyanintranodalcalcication,
whichisaparticularconcernformetastaticpredictioninpapillarycarcinomaofthethyroidgland.
10. How do you evaluate a neck mass with a minimally invasive approach?
FNAC.Itisacytologicalstudyofaspiratedcells.
11. What are the limitations in FNAC?
Itdoesnotallowevaluationofcellularmorphology.Sometimes,accuratediagnosiscannotbeestab-
lished due to sampling error, handling, and processing errors or reading errors. A repeated aspiration
oranexcisionalbiopsyshouldbeconsideredifthecytologyresultdidnotcorrespondtoclinical
presentation.
12. How can aspirated content help to provide diagnostic information?
Fluid content aspiration.Detectionofuidcontentcanaidinprimitivediagnosisestablishment.
Color and consistency of fluid content:
• Plugging ranula: Clear fluid, viscous fluidenrichedwithamylaseandtotalproteincontent
• Cystic hygroma:Cleartoyellowishuid,serous fluid
• Vascular malformation: Hemorrhagic content (blood)whenbloodvesselwasnot being punctured
• Dermoid/epidermoid cyst: Clear contentuidwithsomedebris, serousuid.Occasionally,no
uidcanbeaspiratedastheentirecontentwaslledwithdebris(cheesyandsemisolid).
13. What is the most common congenital mass in the lateral neck?
Branchialcleftcyst.
14. What is a branchial cleft cyst?
Itisacongenitalmassfrequentlyfoundinchildrenoryoungadults.Itismanifestedasadeveloping
massordrainingtractanywherebetweenthepreauricularregionandsupraclavicularfossawithinthe
anterior triangle depending on branchial arch origin (Table 49-3). The etiology of the cyst is related to
incompleteinvolutionofbranchialcleftduringdevelopment.
15. What is the treatment option for a branchial cleft cyst?
Surgicalexcisionistheprimarymanagementforbranchialcleftcyst.Aninfectedcystneedstobe
treatedwithanantibioticbeforedenitivemanagement.Astula,sinustract,orpreviousdissected
plane/pathmightharboranepithelialremnant;therebytheyshallbecompletelyresectedtogether
withtheunderlyingcyst.
16. What is a thyroglossal duct cyst (TGDC)?
Itisthemostcommoncongenitalmassfoundinthemidlineoftheneck.Itcanpresentanywhere
betweenthebaseofthetongueandthesuperioraspectofthethyroidgland.Itmovesinavertical
plane,especiallyduringswallowingandtongueprotrusion.Itistypicallypainless,butitcanalsocause
exacerbatedpainwheninfected.
region.
cervicalchain>posteriorcervicalregion.
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Table 49-3. Comparison of different types of branchial cleft cyst
BRANCHIAL
ARCH REMNANT
ASSOCIATED
LOCATION
SINUS
TRACT PRECAUTION
First Preauricularregion Externalauditorycanal Facialnerve
Second Superior one-third and
beneathtoSCM,
part of the lesion
extendedanteriorly
toSCM
Extendedsuperiormedially
runningbetweenInternal
CarotidArtery(ICA)and
ExternalCarotidArteryECA
and running superiomedially beneath the posterior
belly of digastric muscle to
Marginalmandibular
nerve,spinal
accessorynerve,
and hypoglossal
nerve
Carotid sheath superior
laryngealnerve
enter tonsil fossa
ThirdandFourth Middleone-thirdto
mediastinal
ICA, Internal Carotid Artery; ECA, External Carotid Artery
Piriformfossa Recurrent laryngeal
nerve
17. How do you manage a TGDC?
First,ensurethepresenceofafunctioningorthotopicthyroidglandpriortosurgicalresection.TGDC
requiresaSistrunkprocedureduringsurgicalexcision,asthehyoidbone(arisesfromthesecondbranchialarch)startstodevelopafterthedescentofthethyroidgland,whichresultsinthethyroglossalduct
locatedposteriorlytohyoidbone.Fusionofthesecondbranchialarchatmidlinewillcauseanentrapmentofthethyroglossalductoverthehyoidbone.Therefore,Sistrunkresectionrequiresaremovalof
the middle third of hyoid bone. A center cuff of muscles (mylohyoid raphe, part of genioglossus and
hyoglossus muscle) around the tract is circumcised at a 45° angle posterosuperiorly up to the foramen
cecum.Theoverlyingtonguebasemucosalcanbekeptintactorviolated.Lastly, passing a 3-0 suture in
a“gure8”toensureawatertightclosureandpreventpostoperativeseepageorsurgicalsiteinfection.
18. Why should you suspect a neck mass in an adult might be a malignancy instead
of a second branchial cleft cyst?
Bothofthemsharethesameanatomicregion.Thesecondbranchialcleftcystismorecommonlyfound
inchildrenthanadults;radioimagesareimportanttosupportadifferentialdiagnosis.Branchialcleft
cyststypicallyappearasawell-denedandhomogeneousnonenhancingmassofuidattenuationatthe
characteristic location [second branchial cleft cyst: immediately anterior or beneath upper one-third of
sternocleidomastoidmuscle(SCM)].Ontheotherhand,aradiopaque-enhancedrimwithcentralnecrosis.
Intralesionalsolidcomponentsorirregularouterbordershallpromptadiagnosisofmetastaticcancer.
19. Why do cervical lymph nodes need to be assessed?
Evaluationofnodalstatusandthestagingoflymphnodesisessentialfordetermininganappropriate
therapeuticoption(surgicalresectionwithneckdissectionandpostoperativeradiation,chemotherapy,
and prognosis prediction).
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