PRIYANKO CHAKRABORTY

JUNIOR RESIDENT, M.S.Otolaryngology & Head and Neck SurgeryBanaras Hindu University , Varanasi

Introduction 11,000 new cases reported in U.S. every year

25% of head and neck cancer and 1% of all cancers

One-third of these patients die of their disease

Most prevalent in the 6th and 7th decades of life

4:1 male predilection

Downward shift from 15:1 post WWII

Increasing public acceptance of female smoking

More in lower socioeconomic class diagnosed at more advanced stages

Incidence 11K new cases of laryngeal cancer in U.S. annually

3,900 deaths annually

Gender Since 1950- M:F ratio 15:1 4:1 in 2004 women have equal place in the toxic work environment cigarette smoking

Risk factors: Tobacco

13-fold risk for laryngeal cancer for smokers risk increases with increasing tobacco use

Alcohol 34-fold risk for laryngeal cancer if consume >1.5 L wine/day

SubtypesGlottic Cancer: 59%

Supraglottic Cancer: 40%

Subglottic Cancer: 1%

Most subglottic masses are extension from glottic carcinomas

Risk FactorsProlonged use of tobacco and excessive alcohol use

primary risk factors

The two substances together have a synergistic effect on laryngeal tissues

90% of patients with laryngeal cancer have a history of both

Risk FactorsHuman Papilloma Virus 16 &18

Chronic Gastric Reflux

Occupational exposures

Prior history of head and neck irradiation

Genetics/ Risk factors Aneuploidy

Tumor suppressor gene inactivation Gene locus 17p13 : mutant p53 ………………………….DNA repair, apoptosis Gene locus 9p21 : mutant p16 …………………………. Cell cycle regulation

Proto-oncogene activation Proto-oncogene (11q13) amplifies cyclin D1………. Cell cycle regulation

Mutagen-induced chromosome breaks

HPV Types 16 and 18: E6 and E7 viral protein-mediated degradation of p53 Oropharyngeal malignancy

GERD Koufman: n=31 with glottic SCC, GERD documented in 84%; only 58% were smokers

Embryology Frazer (1909)

Supraglottis originates from the buccopharyngeal primordium while glottis develops from tracheobronchial primordium high risk of bilateral neck disease vs. glottic tumors - metastasize ipsilaterally

Pressman (1956) separate derivation from glottis- supraglottic tumors of substantial bulk

do not spread across the laryngeal ventricle to the vocal cord

Tucker and Smith (1982) Dye studies anatomically based confirmation : elastic tissue barriers

Formed basis of partial laryngeal surgery• Already advocated by Biller

Anatomy

SITE SUBSITE

Supraglottis Suprahyoid epiglottis

Infrahyoid epiglottis

Aryepiglottic folds

Arytenoids

Ventricular bands (false

vocal cords)

Glottis True vocal cords+ ant and

post. Commissure +rima

glottidis(slit)

Subglottis Subglottic space upto lower

border of cricoid

BARRIERS TO SPREAD Hyoid bone

Laryngeal cartilages

Hyoepiglottic ligament

Thyrohyoid membrane

Ventricle

Anterior commisure

Cricothyroid membrane

Conus elasticus

Quadrangular membrane

Anatomy

Fibroelastic membranes

Barriers to carcinoma spread

Quadrangular membrane Superior free edge= AE fold

Inferior free edge= False cord

Conus elasticus Supports vocal fold

Lateral attachment at cricoid

Medial attachment at anterior thyroid cartilage

Free edge forms vocal ligament

Pathways to spread Pre epiglottic space via multiple fenestrations in

epiglottis

Paraglottic space

Pre-epiglottic space & Para-glottic space

Pre-epiglottic space Anterior: thyrohyoid membrane &

thyroid cartilage Posterior: epiglottis elastic

cartilage Inferior: Petiole attachment to

thyroid cartilage Conduit :

elastic epiglottic cartilage has perforations -direct extension of infrahyoid supraglottic cancer into this fascia-bound space

Bilateral neck drainage

Paraglottic space quadrangular membrane inferiorly conus elasticus anteriorly and medially thyroid cartilage laterally

SubtypesGlottic Cancer: 59%

Supraglottic Cancer: 40%

Subglottic Cancer: 1%

Most subglottic masses are extension from glottic carcinomas

Transglottic tumors

Tumors crossing ventricle in vertical axis

Usually initiate as supraglottic or glottic cancers

McGravan (1961)

must cross three regions: false cords, ventricle, true cord

alters prognosis

Fail the compartmentalization hypothesis

direct mucosal extension

paraglottic space

.

Presentation Hoarseness

Most common symptom

Small irregularities in the vocal fold result in voice changes

Changes of voice in patients with chronic hoarseness from tobacco and alcohol can be difficult to appreciate

Indirect mirror exam and/or flexible laryngoscope evaluation

Malignant lesions can appear as friable, fungating, ulcerative masses or be as subtle as changes in mucosal color

Videostrobe laryngoscopy may be needed to follow up these subtler lesions

PresentationOther symptoms include:

Dysphagia

Hemoptysis

Throat pain

Ear pain

Airway compromise

Aspiration

Neck mass

Pointers to disease extent Hemoptysis> supraglottic tumors

Dysphonia> TVC/glottic lesions

Airway Obstruction> insidious subglottic tumors

Aspiration> supraglottic (also with incompetent glottis)

Otalgia> Pyriform sinus and supraglottic (infiltration of musculature)

Dysphagia: any location, muscle, sensory, motor, joint

Neck mass: supraglottic tumors

PresentationGood neck exam looking for cervical

lymphadenopathy and broadening of the laryngeal prominence is required

The base of the tongue should be palpated for masses as well

Restricted laryngeal crepitus may be a sign of post cricoid or retropharyngeal invasion

Work upBiopsy is required for diagnosis

Performed in OT with patient under anesthesia

Other benign possibilities for laryngeal lesions include: Vocal cord nodules or polyps, papillomatosis, granulomas, granular cell neoplasms, sarcoidosis, Wegner’s granulomatosis

Diagnostic steps: Clinical

Careful evaluation of clinical records of prior diagnosis including staging, pathological slides, clinical examination, radiotherapy approach (technique, doses, courses).

Fiberoptic laryngoscopy

Direct layngoscopy under GA

In advanced case fiberoptic evaluation of the esophagus to R/O synchronous malignancy.

Video Stroboscopy

Diagnostic steps: Radiographic CT or MRI

Provide information regarding

primary tumor volume, cartilage

involvement, invasion of preepiglottic

space, extension beyond the larynx

and finally neck metastasis.

If cartilage invasion is suspected or imperative to be ruled out, MRI seems to be superior to CT.

.

Radiology• Tumor extent (limitations of endoscopy)• MRI:

• high-density tumor vs fat in the preepiglottic space• Soft tissue invasion• Nodal disease

• EXTRACAPSULAR SPREAD

• CT: thyroid cartilage destruction • presence mandates a total laryngectomy• Cartilage invasion

PET-CT:• Residual disease• Recurrence

Natural HistorySupraglottic tumors more aggressive:

Direct extension into pre-epiglottic space

Lymph node metastasis

Direct extension into lateral hypopharnyx, glossoepiglottic fold, and tongue base

Natural HistoryGlottic tumors grow slower and tend to metastasize

late owing to a paucity of lymphatic drainage

They tend to metastasize after they have invaded adjacent structures with better drainage

Extend superiorly into ventricular walls or inferiorly into subglottic space

Can cause vocal cord fixation

Natural HistoryTrue subglottic tumors are uncommon

Glottic spread to the subglottic space is a sign of poor prognosis

Increases chance of bilateral disease and mediastinal extension

Invasion of the subglottic space associated with high incidence of stomal reoccurrence following total laryngectomy (TL)

TNM DefinitionsAJCC 6th Ed. 2002 Primary tumor (T)

TX: Primary tumor cannot be assessed

T0: No evidence of primary tumor

Tis: Carcinoma in situ

Supraglottis

T1- Tumor limited to one subsite of supraglottis

or glottis with normal vocal cord mobility

T2- Tumor invades more than one subsite of supraglottis with normal/impaired vocal cord mobility

T3- Tumor limited to larynx with vocal cord fixation or invades postcricoid area, medial wall of pyriform sinus, or preepiglottictissues

T4a- Tumor invades through thyroid cartilage or extends to other tissues beyond the larynx (e.g., to oropharynx, soft tissues of neck)

T4b- Tumor invades prevertebral space, encases the carotid artery, or invades the mediastinal structures

Glottis

T1- Tumor limited to vocal cord(s) (may involve anterior or posterior commissures) with normal mobility

T2- Tumor extends to supraglottis or subglottis, or with impaired vocal cord mobility

T3- Tumor limited to the larynx with vocal cord fixation and/or paraglottic space involvement or minor thyroid cartilage invasion (inner cortex)

T4a- Tumor invades through thyroid cartilage or extends to other tissues beyond the larynx, (e.g., to oropharynx, soft tissues of neck)

T4b- Tumor invades prevertebral space, encases the carotid artery, or invades the mediastinal structures

SubglottisT1- Tumor limited to the subglottis

T2- Tumor extends to vocal cord(s) with normal or impaired mobility

T3- Tumor limited to the larynx with vocal cord fixation

T4a- Tumor invades through cricoid or thyroid cartilage or extends to other tissues beyond the larynx (e.g., to oropharynx, soft tissues of neck)

T4b- Tumor invades prevertebral space, encases the carotid artery, or invades the medistinal structures

Regional lymph nodes (N)

NX: Regional lymph nodes cannot be assessed

N0: No regional lymph node metastasis

N1: Metastasis in a single ipsilateral lymph

N2: Metastasis in a single ipsilateral lymph node > 3 cm but ≤ 6 cm, or in multiple ipsilateral lymph nodes ≤ 6 cm, or in bilateral or contralateral lymph nodes ≤ 6 cm.

N2a: Metastasis in a single ipsilateral node > 3 cm but ≤ 6 cm N2b: Metastasis in multiple ipsilateral nodes ≤ 6 cm N2c: Metastasis in bilateral or contralateral nodes ≤ 6 cm

N3: Metastasis in a lymph node > 6 cm

Distant metastasis (M)

MX- Distant metastasis cannot be assessed

M0- No distant metastasis

M1- Distant metastasis

AJCC Stage Groupings Stage 0

Tis, N0, M0

Stage I

T1, N0, M0

Stage II

T2, N0, M0

Stage III

T3, N0, M0

T1, N1, M0

T2, N1, M0

T3, N1, M0

Stage IVA

T4a, N0, M0

T4a, N1, M0

T1, N2, M0

T2, N2, M0

T3, N2, M0

T4a, N2, M0

Stage IVB

T4b, any N, M0

Any T, N3, M0

Stage IVC

Any T, any N, M1

Histology >95% SCC

Variations : verrucous carcinoma, spindle cell carcinoma, basaloid SCC, and papillary

SCC

Other types of carcinoma: neuroendocrine carcinoma lymphepitheliomatous carcinoma adenocarcinoma others (sarcomas, lymphomas) adenoid cystic (trachea more than subglottis)

Underlying: hyperplasia, dysplasia, CIS

Overlying: surface keratinization may be present.

Histology Mucosa: 5-7 cell layers

stratified squamous epithelium, (eg, ventricle, false cord, and subglottis)

Mitotic figures: present in the basal layer should be absent above this second layer

CIS: full-thickness atypia of the squamous cells

Atypia is characterized by the cell architecture: mitoses count per hpf, high NC ratio, large nucleoli

Differentiation is characterizes by the tissue architecture: well, moderately, or poorly differentiated

Points to ponder Patients with glottic tumors are seen early because of hoarseness….

Biopsy !!!!!

D/D fungal laryngitis, sarcoidosis, tuberculosis, or Wegener's granulomatosis ,

pseudoepitheliomatous hyperplasia (granular cell myoblastoma)

Premalignant lesions Most cancers of larynx are Carcinomas- often develop

from premalignant lesions

Dysplasia Carcinoma in situ Invasive carcinoma

Lesions:

Chronic laryngitis

Keratosis

Leucoplakia

Erythroplakia

Erythroleukoplakia

Hyperplastic dysplastic lesions

Leucoplakia Hyperkeratosis

Pathology: Premalignant lesions The five categories of laryngeal squamous cell

abnormality (from benign to clearly malignant): hyperkeratosis hyperkeratosis with atypia carcinoma in situ (CIS) superficially invasive carcinoma invasive carcinoma

H, H+A, CIS hyperkeratosis +/- atypia and CIS

conservative management: stripping of VC

5%–30% with future invasive cancer

follow-up and possible re-biopsy 6 - 12 weeks

Superficially invasive vs. Invasive SCC

•Optical coherence tomography : New diagnostic modality •Can be used intra –op to look for microinvasion

•Results similar to histology. Uses Infra-red technology

Management of precancerous lesions

Radiotherapy failure (10%) no future option for XRT T1 / T2

Surgery Generous stripping Informed consent for multiple treatments Good compliance (years) Supravital staining with toluidine blue Rapid or frequent recurrence

Smoking cessation program must be part of management!!!!

Early glottic carcinoma T1 glottic cancer:

Options – EBRT

Open partial laryngectomy

Transoral endoscopic CO2 laser resection

Dey et al published a systematic review comparing RT,open surgery and endoscopic excision (with or without CO2) for early glottic cancer.

They all confer similar survival advantages with endoscopic excision becoming more common now.

T1 Glottic ca

Mid cord T1a

• RT

• Endoscopic laser resection

• Laryngofissure and cordectomy

Ant commissure(T1a)

Cord + AC (T1b)

• Frontal /frontolaterallaryngectomy

• Endoscopic laser resection

• RT

Posterior cord (T1a)

• Endoscopic laser resection

• Laryngofissure & cordectomy

• RT

Surgical options for small T1 lesions

CO2 laser: Transoral endoscopic CO2 laser cordectomy

Cure rates are uniformly above 90%

Quality of voice depends on extend of resection

CO2 laser Indications : Tumor limited to the glottis (T1/T2)

normal vocal cord mobility

localised residual /recurrent disease following failure of RT for early cancer

debulking of tumour for stridor

Laryngofissure and cordectomy.. rarely used now When endoscopic exposure is very poor

Surgical optionsfor small T1 lesions

CO2 laser

T1a mid cord cancer Surgery alternative to RT in:

young patients where it is best to avoid radiotherapy

For verruccous cancer since it responds poorly to radiotherapy

In patients who desire a short treatment time and are willing to accept some compromise in voice

surgical options are

Anterior commisure(T1a)/Cord lesion into ant commisure (T1b) Surgery is prefered option.

Vertical partial laryngectomy(frontal laryngectomy/fronto lateral laryngectomy preferred options

Cure rates >90%

Failure rates with RT and Endoscopic CO2 excision are more due to understaging at this site (direct attachment to thyroid cartilage by broyle’s tendon witout intervening inner perichondrium.)

Surgical options in T2 and advanced glottic lesion :

Surgical options :

SCPL-CHEP Supracricoid partial laryngectomy-cricohyoidoepiglottopexy

VPL Vertical partial laryngectomy

Transoral endoscopic CO2 laser resection.

Surgical options in advanced glottic

lesion : SCPL-CHEP offers superior cure rates preferred over

VPL

But problems of aspiration with SCPL-CHEP reserves this procedure for very fit patients

Feasible in those T3 lesions with fixed vocal cords but not hemilarynx and minimal subglottic extention

Preserves voice and nasal respiration

Surgical options in advanced glotticlesion : Vertical partial laryngectomy: (hemilaryngectomy or

frontolateral laryngectomy) Cord fixed & minimal subglottic extention

Arytenoids mobile

b/l No cartilage erosion

Near total laryngectomy: Preserves speech and swallowing but not nasal respiration

Done in Subglottic extention and fixed hemilarynx

Procedure is oncologically safe and physiologically acceptable even in elderly because incidence of aspiration is very low(<1%

T2a glottic cancerfreely mobile cords

Mid cord glotto -supraglotic

• RT

• Endoscopic laser resection

• VPL/SCPL-CHEP

Anterior glottosupraglottic

• SCPL-CHEP

• Endoscopic laser resection

• RT

Posterior glottosupraglottic

• Endoscopic laser resection

• Extended hemilaryngectomy

• SCPL-CHEP

• RT

Glottosubglottic

• VPL/SCPL-CHEP

• Endoscopic laser resection

• RT

T2b glottic cancer(impaired cord mobility)

• VPL(hemilarynx)

• SCPL-CHEP

• Chemo RT

• RT

Lateralisedlesion

• SCPL-CHEP

• VPL(fronto lateral)

• CRT

• RT

Lesion across ant

commissure

T3 glottic ca(cord fixed arytenoid mobile)

• SCPL-CHEP

• Concurrent CTRT

Performance status good

• VPL

• Neoadjuvant CTRT

• RT

Performance status poor

T3 glottic ca fixed hemilarynx

• Concurrent CTRT

• Near total laryngectomy(lat disease)

• Total laryngectomy

Performance status good

• Near total laryngectomy

• Total laryngectomy

• Neo adjuvant CT RT

Performance status poor

T4 LESION

T4a resectable lesion –

A) Total laryngectomy followed by RT

• Non surgical option CTRT not effective once cartilage or gross soft tissue invasion is there.

B) Near total laryngectomy

when lesion is well lateralised with uninvolved arytenoid region and2/3 of contralateral cord

Supraglottic Preferentially spreads in upward direction above

ventricle, lately involves larynx below ventricle.

epiglottic tumours

Tumours of false cord

Tumour of ventricle

Tumour of arytenoids and AE folds

T1-T2 supraglotticEndoscopic laser resection +ND(N+)

IF NOT FEASIBLE

Supraglotticlaryngectomy/SCPL-

CHP+ND(N+)

IN

1.Infrahyoid supraglottic cancer

2.T2 rather than T1bulky nodal disease

3.Fit patient no COPD

4.Young patient

RT to Primary + ND

IN

1.Lesions at marginal zone

2.Smaller lesions

3.Minimal neck disease

4.Poor pulmonary reserve

Local control rates T1/T2 supraglottic cancer with endoscopic laser excision – 80-100%

T 2 3year disease free intervall rates with RT is reported to be 50%-80%.

Two types of open partial laryngectomy are possible for supraglottic cancer.

Horizontal SGPL T1/ small T2

For bulkyT 2 tumours SCPL –CHEP ensures better and yields superior rates

T3 Supraglottic capreepiglottic space invasion,cords mobile

Options

CTRT

Endoscopic CO2 laser resection if the epiglottic space invasion is limited

Supraglottic partial laryngectomy (for small volume disease) SCPL-CHP (if growth is bulky or encroaching the glottis)in patients who are fit and have no significant chest problem

Near total laryngectomy if none of above is possible

T3 Supraglottic ca cord fixity;arytenoids mobile

Options

CTRT

SCPL-CHP if chemo rad is refused or response to neoadjuvant chemotherapy is poor

NTL if SCPL-CHP not feasible

total laryngectomy if not rest

T3 Supraglottic ca fixed hemilarynx

Options CTRT

Near total /total laryngectomy

T4 Supraglottic ca Wide field total laryngectomy +post operative RT

Wide field NTL + post operative RT(for lateraliseddisease)

SCPL-CHP (for minimal cartilage erosion;no gross soft tissue invasion minimal subglottic disease)

Subglottic cancer Primary subglottic is very are unsuitable for voice

preservation surgeries

Total laryngectomy necessary as laryngeal cartilage involvement often present

Ipsilateral thyroidectomy with Paratracheal lymph node dissection done.

Treatment based on stage

Subglottic cancer-STAGE I/II Lesions can be treated successfully by radiation

therapy alone with preservation of normal voice.

Surgery is reserved for failure of radiation therapy or for patients who cannot be easily assessed for radiation therapy.

Subglottic cancer-STAGE III Laryngectomy plus isolated thyroidectomy and

tracheoesophageal node dissection usually followed by postoperative radiation therapy.

Extended tracheal resection may be necessary

Treatment by radiation therapy alone is indicated for patients who are not candidates for surgery. Patients should be closely followed, and surgical salvage should be planned for recurrences that are local or in the neck.

Subglottic cancer-STAGE IV Laryngectomy plus total thyroidectomy and bilateral

tracheoesophageal node dissection usually followed by postoperative radiation therapy.

Treatment by radiation therapy alone is indicated for patients who are not candidates for surgery

Voice conservation surgery Organ preservation surgery done:

Young patients when one prefers avoiding RT

I. Horizontal partial laryngectomy: T 3 pre-epiglotticspace with free vocal cords and fit -withstand aspiration

II. SCPL-CHEP: T3 supraglottic ca cord fixed but arytenoidmobile or glotto-supraglottic

III. Three quarter laryngectomy : T3 supraglottic ca extended to glottic & spilling over to pyriform fossa, one arytenoid should be mobile. Disease should be lateralised .

IV. Transoral endoscopic resection with CO2 laser: vocal cords mobile

Non surgical voice preservation in advanced laryngeal cancer

Advanced stage laryngeal cancer traditionally has been treated with surgery, most often total laryngectomy, and post-operative radiation therapy (PORT)

In Past two decades there has been change in objective of non surgical treatment approach.

Several randomized trials have demonstrated the feasibility of organ preservation in patients with advanced laryngeal.

Management of neck in laryngeal cancer Status of lymph node is an important factor

influencing survival in laryngeal cancer

Appropriate treatment of neck is as important as primary cancer(level II/III/IV/VI)

Supraglottic ( 23-50%) present with cervical lymph node even T1/T2 lesions have significant nodal metastasis

Glottic cancer less common –lack of submucosallymphatics in this area is responsible(1-4% in T1/T2)( 15-42% in T3/T4)

Delphian node (also known as midline anterior metastatic node or poirer’s prelaryngeal ganglia node is rarely associated with T3/T4 tumors with significant subglottic extention.

Larynx is midline organ b/l neck involvement is high

N0 neck ipsilateral risk of contalateral neck is very low vice versa

Management of neck Depends on site of primary

T stage of primary

Clinical N stage

Choice of treatment modality for the primary

N0 neck in supraglottic cancerPrimary treatment plan

RT(B/L neck irradiation)

Surgery1. Endoscopic CO2 laser resection ( vigilant f/u of neck)

2. Near total /total laryngectomy ( ipsilateral clearance of levels II,III,IV,VI & contralateral clearance of levels II,III,IV)

3. Open partial laryngectomy

sampling of lymph nodes level II,III U/L for lateralisedlesion & B/L for midline lesion

If frozen section positive for metastasis ( selective infrahyoid neck dissection)

otherwise follow up

N+ neck in supraglottic cancer Primary treatment with

CTRT /RT- Neck dissection prior to radiation or post radiation salvage surgery for residual neck nodes

Endoscopic laser resection – interval neck dissection after 4-5 days

Open surgery -– if unilateralo N1/N2a (ipsilateral level 1 sparing neck dissection & contalateral II,III,IV

clearance

o N2b/N3 ( ipsilateral RND and contralateral clearance of level II,III,IV)

--If B/L (b/l ND preserving atleast one IJV)

Neck in glottic cancer Clinically N0 NECK T1/T2 : no treatment of neck T3/T4 : treatment plan surgery then b/l ND

treatment plan RT then b/s incl. RT N+ NECK Surgery --- level I sparing neck dissection on ipsilateral side clearance of levels II,III,IV on C/L side with B/L level VI

clearance RT/CTRT ----N1 neck include in field surgery reserved for salvage N2/N3 neck dissection prior to RT or salvage neck dissection

after RT

Radiation therapy :

Radiation therapy :Cure rates with radiation therapy ranges from 80% -95%.(wide variation RTOG )

Conventional radiotherapy consists of :

Once daily treatment delivering 2 Gray/day.

5 doses/week to total dose of 70 Gy over period of 7 weeks.

Attempts to improve outcome of RT schedules ..focus upon modification of radiotherapy fractionation schedules.

Two altered fractionation schedule:• Hyperfractionation

• Accelerated fractionation

Hyperfractionation Delivers a higher total dose over the same 7 week

treatment period using multiple smaller fractions of radiotherapy per day.

The lower dose per fraction results in preferential sparing of late responding tissues thus reducing the incidence of late normal tissue effects.

Accelerated fractionation: Delivers the same total dose over a shorter overall

treatment time

Aimed at overcoming treatment failures caused by tumour cell repopulation during longer courses of treatment.

Dose Fractionation :

RTOG (radiation therapy oncology group) carried out a phase III study comparing four fractionation schedules:

Conventional fractionation:

Hyperfractionation:(1.2Gy 2D /Td 81.6Gy){ 8% at 5 yr}

Acclerated radiotherapy(1.8Gy 1D, 5d/week with second fraction of 1.5Gy 1D, during final 12 days /TD 72Gy{2% at 5 yr} 1.6 Gy 2D with a 2 week break to deliver TD 67.2 Gy.{1.7% at 5 yr}

Radiotherapy for T1/T2 glotticcarcinoma : Radiotherapy for T1/T2 glottic carcinoma

Local control rate

approximating 90% for T1

70 to 80% for T2

5 year local control- T1a 94% T1b 93% T2a 80% T2b

72% (Spriano, 1997; Fletcher 1994, Mendenhall, 2001)

Voice quality after radiotherapy tend to be less when

compared to pre-radiotherapy but almost normal 2-3 years

after treatment

(Verdonck,1999;Hirano,1994;Heeneman,1994)

Transoral Laser Surgery

Transoral Laser Surgery: Inclusion Criteria

Complete endoscopic visualization of the carcinoma

Tumor extension to the contralateral VC < 3mm

Absence of arytenoid involvement (except vocal process)

Subglottic extension < 5mm

Supraglottic extension no further than lateral extension of ventricle

Mobile vocal folds

No cartilage involvement

Strict correlation between recurrent lesion and 1° lesion before radiation.

Transoral Laser Surgery: Reported advantages

Good voice quality

Good swallowing

Lower complications rates

Lower costs

Shorter hospitalization

Tracheostomy and NG tubes not routinely required

Transoral Laser Surgery: Operative considerations

Increased difficulty in identification of recurrent carcinoma in irradiated tissue leads to routine use of frozen section

All margins to be confirmed by permanent section post-op

Strict follow-up with fibroscopic examination and serial imaging allowing early detection of recurrence

The use of CO2 laser excision after radiation failure does not preclude its use for persistent or multiple recurrent disease.

Transoral Laser Surgery: Complications

Complication rates are <5% and from most to least common include:

Granuloma formation

Laryngeal edema

Laryngeal stenosis

Chondronecrosis

Vertical Partial Laryngectomy

Vertical Partial Laryngectomy TYPES

Hemilaryngectomy

Frontal laryngectomy

Frontolateral laryngectomy

Extended Hemilaryngectomy

Vertical Partial Laryngectomy

Vertical Partial Laryngectomy:

Removal of:

One vocal fold - from anterior commissure to vocal process

½ of opposite vocal fold may also be removed if involved

Ipsilateral false vocal cord

Ventricle

Paraglottic space (and overlying thyroid cartilage)

Vertical Partial Laryngectomy:Contraindications

Large T3 or any T4 lesion More than 1/3 rd of contralateral VC.

Intrarytenoid or cricoarytenoid joint involvement

Bilateral arytenoid cartilage involvement or bilaterally diminished vocal cord mobility

Thyroid cartilage penetration

Supraglottic extension exceeding 10mm at the anterior commissureor 5mm at the vocal process of the arytenoid

Poor pulmonary function

Vertical Partial Laryngectomy:Operative Considerations

The use of intraoperative frozen sections is imperative for maximal local control

All margins should be confirmed with permanent section postoperatively

In the event of failure of salvage VPL total laryngectomy remains an option and this will not ultimately affect local control.

The use of bipedicled flaps of strap muscles to replace excised intralarygeal soft tissue may facilitate post-op rehabilitation

.

Vertical Partial Laryngectomy:Outcomes

Meta-analysis performed in the same study showed:

Local control rate 50-100% (mean 78%)

Approximately 15% of patients require completion laryngectomy for second recurrence

Vertical Partial Laryngectomy: Complications

Early - generally tracheostomy related

Infection

Aspiration and dysphonia (should not persist for > 3 weeks)

Late Aspiration

Chondritis

Laryngeal stenosis (Must rule out local recurrence)

Severe hoarseness

Granulation tissue (CO2 laser and keel)

Tumor recurrence

Supracricoid LaryngectomyRemoval of: Entire thyroid cartilage

Bilateral true and false vocal cords

Ventricles

Paraglottic and Preepiglottic spaces

Epiglottis

Hyoid bone

One arytenoid (may spare both if not involved)

- At least one arytenoid must be spared to preserve phonation and sphincter functions

Supracricoid partial laryngectomy with cricohyoidoepiglottopexy

Supracricoid partial laryngectomy with cricohyoidopexy—exposure of malignancy. 1, Arytenoid; 2, external thyroid perichondrium; 3, vocal process; 4, thyroid cartilage; 5, epiglottis; 6, false and true cord.

Supracricoid partial laryngectomy with cricohyoidopexy—laryngoplasty using three circumferential cricoid, hyoid, and tongue base stitches.

Supracricoid partial laryngectomywith cricohyoidoepiglottopexy

Supracricoid Laryngectomy: Contraindications Infiltration of both aryntenoid cartilages

Infiltration of cricoarytenoid joint or inter-arytenoid region

Subglottic extension >1cm below the vocal fold

Extension to the glossoepiglottic valecula

Major preepiglottic space invasion

Hyoid bone invasion

Invasion of outer perchondrium of thyroid cartilage

Extra-laryngeal spread

Supracricoid Laryngectomy: Complications Swallowing disorders are the most common in the

short term

Voice quality is hoarse, rough, breathy but with acceptable intelligibility.

Aspiration Pneumonia is the most frequent complication (17.5%)

Neo-laryngeal edema

Supraglottic laryngectomy T1,2, or 3 if only by

preepiglottic space invasion

Mobile cords

No anterior commissure involvement

FEV1 >50%

No tongue base disease past circumvallate papillae

Apex of pyriform sinus not invloved

Supraglottic laryngectomy Laryngoplasty

performed with three closure stitches circumferentially around the inferior half of the thyroid cartilage and submucosally into the tongue base, as is done in the supracricoidpartial laryngectomies.

Near total laryngectomy INDICATIONS:

T3/T4 laterlised transglottic lesions with no extension to arytenoids

T3/T4 laterlised lesions of PFS with involvement of apex and causing fixity of hemilarynx

Near total laryngectomy

Total Larygectomy Indications:

T3 or T4 unfit for partial

Extensive involvement of thyroid and cricoidcartilages

Invasion of neck soft tissues

Tongue base involvement beyond circumvallate papillae

Recurrence following RT/Residual disease

Incision optionsA, Long apron flap without separate incision for tracheostomy from mastoid tip to mastoid tip intersecting the midline at approximately the level of the

cricoid cartilage, usually about 2 cm above the sternal notch in the midline. B, Short apron flap with separate tracheostome incision 2 to 3 cm inferior to the flap incision. A U-shaped incision (not shown) is rarely used, but feasible when

neck dissection is not performed

Skeletonisation of larynx and hyoidA, Division of the strap musculature after elevation of a subplatysmal flap

. B, Division of suprahyoidmusculature

Division of constrictor musculature along the lateral aspect of the thyroid cartilage and dissection of the thyroid.

Entry into larynx A, Use of a Freer elevator to

mobilize the pyriform sinus and internal perichondrium from the thyroid cartilage. This should not be performed if the pyriformsinus is likely to be involved by the tumor. B,

The trachea is transected, and the ligamentous attachments are divided permitting dissection of the trachea away from the upper esophagus up to the level of the posterior cricoarytenoid musculature. C, Dissection follows the hyoepiglottic ligament to the epiglottis and vallecula to avoid entry into the preepiglottic space. D, If

clinically uninvolved, the vallecula is entered on the nontumor side

A, Closure of pharynx with detail of suturing technique. B, T-closure. C, Vertical closure. D, Horizontal closure.

Conclusions More patients with advanced disease can enjoy

organ preservation

Work is ongoing to define the ideal protocols for organ preservation

More work needs to be done to define which patients are acceptable for aggressive organ preservation and what quality of life and functional outcomes they can expect

Role of the surgeon is changing

Medical oncologist should come to tumor board

Conclusion “I conclude by saying that many things have changed in the surgical

management of supraglottic cancer, but changes concern the techniques and not the principles of cancer surgery, that is, the necessity of being radical in both the primary and the neck. Supraglottic laryngectomycombined with functional elective or curative neck dissection is fully in line with those principles and it represents a priceless contribution to saving lives while sparing mutilation…I am persuaded that the solution to the problem of supraglottic cancer in its entirety is still in the surgeon’s hands, provided that we remember that we are waging a war against cancer in the larynx and in the lymph nodes of the neck, and not against the larynx and the neck.”

Ettore Bocca

Ann Otol Rhinol Laryngol, 1991; 100: pp261-267.