Steven H. Lin and Gopal K. Bajaj
What is the incidence of laryngeal cancer (LCX) in the U.S.?
~12,000 cases/yr of LCX (20% of all H&N cancers; 2008 data)
What are the risk factors for developing LCX?
Smoking, alcohol use, and voice abuse
What are the subsites of the larynx?
Supraglottic, glottic, and subglottic
What is the incidence/distribution of LCX according to subsite?
1. Glottic: 69%
2. Supraglottic: 30%
3. Subglottic: 1%
What % of premalignant lesions (leukoplakia/erythroplakia) progress to invasive laryngeal lesions?
20% of premalignant laryngeal lesions ultimately progress to invasive cancer (higher for erythroplakia than leukoplakia).
What is the most common LCX histology?
Squamous cell carcinoma (SCC) makes up >95% of LCX. Other histologies include verrucous carcinoma (1%–2%), adenocarcinoma, lymphoma, chondrosarcoma, melanoma, carcinoid tumor, and adenoid cystic carcinoma
What are the subdivisions of the supraglottic larynx?
Subdivisions of the supraglottic larynx include the epiglottis (suprahyoid and infrahyoid), aryepiglottic folds, arytenoids, and false vocal cords (FVCs)
What are the subdivisions of the glottic larynx?
Subdivisions of the glottic larynx include the ant/post commissures and the true vocal cords (TVCs)
What are the anatomic borders of the subglottic larynx?
The subglottic larynx lies 0.5 cm below the TVCs down to the 1st tracheal ring.
What are the nodal drainage pathways of the various laryngeal subsites?
1. Supraglottic: levels II–IV
2. Glottic: virtually no drainage
3. Subglottic: pretrachea and delphian (level VI)
What is the incidence of hypopharyngeal cancer (HPC) in the U.S.?
There are ~2,500 cases/yr of HPC in the U.S.
What is the median age at Dx for HPC?
The median age at Dx is 60–65 yrs for HPC.
What are the subsites of the hypopharynx (HPX)?
1. Pyriform sinus
2. Postcricoid area
3. Posterior pharyngeal wall
(Mnemonic: “3 P's”)
What are the anatomic boundaries of the HPX?
The HPX spans from C4-6 or from the hyoid bone to the inf edge of the cricoid cartilage.
What is the gender predilection for HPC based on the different subsites?
The gender predilection is predominantly male for pyriform sinus and post pharynx primaries, but predominantly female for postcricoid area tumors.
What are the classic risk factors for the development of HPC?
Smoking, alcohol, betel nut consumption, nutritional deficiency (vitamin C, Fe [Fe deficiency is associated with 70% of postcricoid cancers in northern European women]), and prior Hx of a H&N cancer
Is nodal involvement common with HPC?
Yes. Nodal involvement is common due to abundant submucosal lymphatic plexus drainage to the retropharyngeal nodes, cervical LNs, paratracheal LNs, paraesophageal nodes, and supraclavicular nodes.
What are the most commonly involved nodal stations in HPC?
Levels II, III, and V and the retropharyngeal nodes are most commonly involved in HPC.
What is the name for the most sup of the lat retropharyngeal nodes?
The most sup of the lat retropharyngeal nodes is the node of Rouviere.
What % of HPC pts have nodal involvement at Dx?
~75% overall have nodal involvement at Dx (~60% for T1; very high incidence, even at the earliest stages).
What is the typical histology seen in HPC?
The predominant histology is SCC (>95%) → adenoid cystic, lymphoma, and sarcoma.
What are the most common subsites of origin for HPC?
The pyriform sinus (70%–80%), post pharyngeal wall (15%–20%), and postcricoid (5%) are the most common subsites of origin.
At what cervical spine levels are the hyoid bone and the TVCs located?
The hyoid bone is at C3, whereas the TVCs are located near C5-6.
How do pts with LCX typically present?
Hoarseness, odynophagia/sore throat, otalgia (via the Arnold nerve, CN X), aspiration/choking, and neck mass
What is the typical workup for pts presenting with a possible laryngeal mass?
Possible laryngeal mass workup: H&P (voice change, habits, indirect/direct laryngoscopy), CXR, CT/MRI, PET, basic labs, EUA + triple endoscopy, and Bx of the primary +/− FNA of the neck mass
What does the loss of the laryngeal click on palpation of the thyroid cartilage indicate?
Loss of the laryngeal click on exam indicates postcricoid extension/involvement.
What does pain in the thyroid cartilage indicate on exam?
Pain on palpation of the thyroid cartilage indicates tumor invasion into the thyroid cartilage.
What imaging device is best to assess for bony or cartilage erosion in pts with LCX?
CT scan is best for assessing bony/cartilage erosion.
What is the incidence of nodal involvement for T1, T2, and T3-T4 glottic cancer?
1. T1: 0%–2%
2. T2: 2%–7%
3. T3-T4: 15%–30%
What is the incidence of nodal involvement for supraglottic lesions according to T stage?
1. T1: 39%
2. T2: 42%
3. T3: 65%
4. T4: 59%
(Lindberg R et al., Cancer 1972)
What proportion of pts with supraglottic cancer present with unilat vs. bilat nodal Dz?
~55% of supraglottic cancer pts present with unilat nodal Dz, and 16% present with bilat nodal involvement. (Lindberg R et al., Cancer 1972)
What % of pts with subglottic cancer present with nodal involvement?
~20%–50% of subglottic pts present with nodal Dz (generally the prelaryngeal/delphian, lower jugular, pretracheal, or upper mediastinal nodes).
Describe the T staging for cancers of the supraglottic larynx.
1. T1: 1 subsite
2. T2: 1 adjacent subsite or outside supraglottis (base of tongue [BOT], vallecula, pyriform sinus) without fixation of larynx
3. T3: cord fixation and/or invasion of postcricoid area or pre-epiglottic tissue
4. T4a (resectable): through thyroid cartilage, trachea, soft tissue of neck, deep/intrinsic muscles of tongue, thyroid, esophagus
5. T4b: invasion of prevertebral space, mediastinum, carotid
Describe the T staging for cancers of the glottic larynx.
1. T1: limited to TVCs +/− ant/post commissure involvement with normal mobility (1a, 1 TVC; 1b, both cords)
2. T2: extends to supra- or subglottis with impaired vocal cord mobility
3. T3: fixed vocal cords
4. T4a-b: same as above/for supraglottic lesions
What is the T-staging breakdown for cancers of the subglottic larynx?
1. T1: tumor limited to subglottis
2. T2: extension to vocal cords, with normal or impaired mobility
3. T3: limited to larynx with vocal cord fixation
4. T4a-b: same as above
Describe the overall stage groupings for LCX.
1. Stages I–II: T1-2N0
2. Stage III: T3N0 or N1
3. Stage IVA: T4a or N2
4. Stage IVB: T4b or N3
5. Stage IVC: M1
With what stage of Dz do most pts with HPC present?
Most pts (>80%) present with stage III or IV Dz (lesions remain asymptomatic until the advanced stages).
What % of pts with HPC present with DMs?
~2%–4% of HPC pts present with DMs. ~20%–30% develop DMs within 2 yrs despite Tx.
With what Sx do most HPC pts present?
Neck mass, sore throat, dysphagia, hoarseness, and otalgia (Arnold nerve/CN X involvement)
What is the typical workup for pts who present with hoarseness?
Hoarseness workup: H&P (check for thyroid click), labs, CT/MRI, PET, neck FNA, EUA + triple endoscopy, and Bx of the primary mass
Describe the T staging of HPC.
1. T1: <2 cm or 1 subsite
2. T2: 2–4 cm or >1 subsite
3. T3: >4 cm or fixation of hemilarynx
4. T4a: invades thyroid/cricoid cartilage, hyoid bone, thyroid gland, esophagus, or central soft tissue
5. T4b: invades prevertebral fascia, carotid artery, or mediastinal structures
What is the nodal staging breakdown for HPC?
Same system as used for other H&N cancers (except for nasopharynx):
1. N1: single, ipsi, <3 cm
2. N2a: single, ipsi, 3–6 cm
3. N2b: multiple, ipsi, ≤6 cm
4. N2c: bilat or contralat ≤6 cm
5. N3: >6 cm
Describe the overall stage groupings for HPC.
1. Stages I–II: T1-2N0
2. Stage III: T3N0 or N1
3. Stage IVA: T4a or N2
4. Stage IVB: T4b or N3
5. Stage IVC: M1
What does total laryngectomy entail?
It entails the removal of the hyoid, thyroid and cricoid cartilage, epiglottis, and strap muscle with reconstruction of the pharynx as well as a permanent tracheostomy.
What structures are removed with a supraglottic laryngectomy?
A supraglottic laryngectomy sacrifices the FVCs, epiglottis, and aryepiglottic folds.
What is the preferred surgical option for dysplastic lesions on the glottic larynx?
Mucosal stripping is typically curative for dysplastic lesions. Close follow-up is needed.
What are the Tx options for Tis lesions of the glottic larynx?
Cord stripping/laser excision (need close follow-up; cannot r/o microinvasive Dz) or definitive RT
What are the ~5-yr LC rates for glottic CIS with the use of stripping vs. laser vs. RT?
1. Stripping: 72%
2. Laser: 83%
3. RT: 88%–92% (all >95% after salvage)
What are the Tx options for T1-T2 glottic cancer?
Cordectomy (CO2 laser)/partial laryngectomy, definitive RT alone, or surgery + CRT for +margin, and ECE (based on postop H&N data)
What are the 5-yr control and survival rates after hemilaryngectomy for T1-T2 glottic cancer?
After hemilaryngectomy, the ~5-yr LC is 83% and the DFS is 88% for T1-T2 glottic cancer. (Scola B et al., Laryngology 1999)
What is the salvage Tx of choice for glottic lesions after RT failure?
The salvage Tx of choice is total laryngectomy +/− neck dissection.
What is the ~5-yr CSS for T1 glottic cancers treated with definitive RT?
The 5-yr CSS with RT is >90% (95% with salvage; organ preservation rate is >90%).
What are the advantages and disadvantages of using RT for early glottic cancer?
1. Advantages: better voice quality, noninvasive, organ preservation
2. Disadvantages: long Tx duration, RT changes could obscure post-Tx surveillance
What is the voice quality preservation rate for early glottic tumors/pts treated with laser vs. RT?
The Johns Hopkins Hospital data (Epstein BE et al., Radiology 1990) suggests better voice quality after RT (laser: 31%, RT: 74%, p = 0.012).
What are the initial and ultimate (after salvage) LC rates for T2 glottic lesions?
Initial LC is ~70%–90% and ~50%–70% after salvage for T2 glottic lesions.
What are the currently accepted dose fractionation and total dose Rx for CIS and T1 glottic lesions?
The currently accepted RT doses are 56.25 Gy for CIS and 63 Gy for T1, at 2.25 Gy/fx.
What is the typical RT dose used for T2 glottic lesions?
The typical RT dose for T2 lesions is 70 Gy at 2 Gy/fx or 65.25 Gy at 2.25 Gy/fx.
What randomized data/trial highlighted the importance of hypofractionation for early glottic cancers?
Japanese data (Yamazaki H et al., IJROBP 2006): 180 pts, 2 fractionations: 2 Gy/fx (60–66 Gy) vs. 2.25 Gy/fx (56.25–63 Gy). 5-yr LC rate was better with 2.25 Gy/fx (92% vs. 72%). The greater toxicity for the hypofractionation regimen was acute skin erythema (83% vs. 63%).
What RT field sizes/spans are employed for Tis/T1 glottic cancers?
5 × 5 cm opposed lat fields are typically employed (from the upper thyroid notch to the lower border of the cricoid, post border at the ant edge of the vertebral body, and flash skin at the ant border).
What RT planning technique can be used when treating T1 glottic lesions with ant commissure involvement?
Generally, for T1 glottic lesions, wedges are used (heel anteriorly, usually 15 degrees) to reduce ant hotspots due to curvature of the neck. However, if there is ant commissure Dz, the wedges can be removed to add hotspots to this region. Alternatively, a bolus/beam spoiler can be added for additional coverage.
What structures must be encompassed by the 95% IDL when irradiating T1 glottic cancer?
The 95% IDL must encompass the TVCs, the FVCs, and the sup subglottis.
What RT fields are used for T2 glottic lesions?
This is controversial and may depend upon degree of supraglottic/subglottic extension. Most advocate using 6 × 6 cm opposed lat fields; others advocate covering level II–III nodes (2 cm above the angle of the mandible, splitting vertebral body, down to the bottom of the cricoid) to 54 Gy, with CD to the 5 × 5 cm box covering the larynx to 70 Gy.
What are the Tx options for early-stage supraglottic LCX?
Supraglottic laryngectomy, transoral laser resection, or definitive RT
What are the 5-yr LC and OS rates for early supraglottic cancers treated with surgery and LND?
The 5-yr LC rate is ~85%, whereas the 5-yr OS is ~100% for T1 and ~80% for T2 supraglottic lesions.
What are the LC rates for early-stage supraglottic cancers after definitive RT alone?
Retrospective series demonstrate LC rates of 73%–100% for T1 and 60%–89% for T2 lesions (e.g., University of Florida and Italian data).
Describe the standard RT fields used in treating supraglottic cancers.
Since 20%–50% of T1-T2 supraglottic cancers have +LNs (occult), necks need to be covered for all pts (levels II–IV). This requires an off-cord CD after 45 Gy and a boost to the post neck to 50 Gy with electron fields.
What definitive RT doses are typically recommended for early-stage supraglottic cancers?
1. T1 dose: 70 Gy in 2 Gy/fx
2. T2 dose: hyperfractionated dosing to 76.8 Gy in 1.2 Gy/fx or with concomitant boost techniques to 72 Gy (1.8 Gy in am × 30 fx to 54 Gy to areas of subclinical Dz, and 1.5 Gy in pm for the last 12 days of Tx to boost GTV + 1.5 − 2 cm to 72 Gy)
What data supports the use of re-irradiation for previously treated early-stage LCX pts?
Massachusetts General Hospital data (Wang CC et al., IJROBP 1993): 20 pts treated with 1.6 Gy bid to 65 Gy. 5-yr OS was 93%, and LC was 61% after re-irradiation.
What are the Tx options for pts with advanced LCX?
Total laryngectomy (with adj RT or CRT for +margin, +ECE) or organ preservation with definitive CRT (RTOG 91-11) or RT alone (altered fractionation)
What are the Tx options for pts with advanced HPC?
Induction chemo → RT or surgery depending on response for T1-3N + Dz; total laryngectomy/laryngoesophagectomy (with CRT for + margin, + ECE) for T4 Dz
Describe the standard RT fields used to treat advanced LCX/HPC.
1. Opposed lateral fields: superiorly to the base of skull to cover the retropharyngeal nodes, anteriorly with 1-cm flash, posteriorly behind the spinous process, inferiorly to the shoulders
2. Low anterior neck: superiorly match with lat fields (may use half beam block), laterally at two thirds of the clavicular length, inferiorly 1 cm below clavicle (include the stoma, if present)
What is the preferred position of the stoma when utilizing the 3-field technique in the adj setting?
If using a monoisocentric 3-field technique for the postop setting, the isocenter is set above the stoma if the stoma is not being boosted; the stoma will be treated in the low ant neck field. Alternatively, the isocenter is set below the stoma if the stoma is to be boosted (generally to >60 Gy).
What techniques can be employed if the shoulders get in the way of the opposed lat fields when boosting an area of concern in the postop setting?
In this scenario, one can employ either the caudal tilt technique (both the couch is tilted away from the gantry by 10 degrees and the gantry is angulated 10 degrees above the horizontal plane) or IMRT
What are the typical RT doses used to treat advanced LCX/HPC?
Off-cord at 40–44 Gy, boost with electrons posteriorly to 50 Gy; subclinical Dz to 50–54 Gy; primary tumor to 70 Gy (in 2 Gy/fx)
What are the 3 indications for boosting the stoma with PORT?
Indications for boosting the stoma with PORT:
1. Emergency tracheostomy
2. Subglottic extension
3. Ant soft tissue extension
What are some indications for performing an elective neck dissection after definitive RT?
This is controversial, but elective neck dissection should be done for persistent Dz and can be considered with >N2 Dz.
What randomized data/study compared preop RT to PORT for (predominantly) HPC?
RTOG 73-03 (Tupchong L et al., IJROBP 1991): 354 pts, 50 Gy preop vs. 60 Gy postop; 69% of pts had advanced supraglottic or HPC. LC was better with PORT but not OS.
What are the 2 randomized phase III trials that demonstrated a benefit with postop CRT vs. PORT alone for high-risk H&N pts?
EORTC 22931 (Bernier J et al., NEJM 2004): 334 pts randomized to PORT 66 Gy vs. PORT + cisplatin 100 mg/m2 on days 1, 22, and 43. Eligibility: ECE, + margin, PNI, LVI, and level 4–5 + N from oral cavity cancer (OCC)/oropharyngeal cancer (OPC). There was better OS, DFS, and 5-yr LC with CRT but ↑ grade 3–4 toxicity.
RTOG 95-01 (Cooper JS et al., NEJM 2004): 459 pts randomized to 60–66 PORT vs. PORT + cisplatin 100 mg/m2 on days 1, 22, and 43. Eligibility: >2 LNs, ECE, +margin. There was better DFS (43% vs. 54%) and 2-yr LRC (72% vs. 82%) with CRT but only a trend to improvement in OS (57% vs. 63%).
What are the presumed reasons why EORTC 22931 showed an OS benefit while RTOG 9501 did not?
The EORTC trial included more margin+ pts (28% vs. 18%), pts with worse tumor differentiation (19% vs. 7%), more HPX cases (20% vs. 10%), and more pts who started RT 6 wks or later after surgery (32%).
What randomized trials demonstrated a benefit with altered fractionation RT in advanced H&N cancer?
EORTC 22851 (Horiot JC et al., Radiother Oncol 1997): 512 pts (all H&N except the HPX) randomized to conventional RT to 70 Gy (7 wks) or 1.6 Gy tid to 72 Gy (5 wks). There was better 5-yr LRC with tid RT (59% vs. 46%) but not OS.
RTOG 9003 (Fu KK et al., IJROBP 2000): 1,073 pts (all H&N sites) randomized to (a) standard fx 70 Gy/2 qd; (b) 81.6 Gy/1.2 bid; (c) accelerated with split 67.2 Gy/1.6 bid; and (d) accelerated with concomitant boost 72 Gy/1.8 qd × 17 → 1.8 Gy am + 1.5 Gy pm × 33 fx. All altered fx schemes were better than conventional RT in terms of LRC (54% vs. 46%) but not OS.
What studies investigated induction CRT for organ preservation in pts with LCX?
Department of Veterans Affairs (VA) larynx study (Wolf GT et al., NEJM 1991): stage III–IV resectable LCX; 332 pts randomized to total laryngectomy + PORT vs. induction CRT. If after induction chemo × 2 cycles the tumor had <PR, salvage surgery + PORT was the next step. If there was a CR or >PR, 1 more cycle was added, then RT was initiated if there was no progression. 2-yr larynx preservation rate was 64%. There was no OS difference (there were less DMs but more local relapses in the chemo arm).
GETTEC (Richard JM et al., Oral Oncol 1998): early closure due to poor accrual; only 68 pts, mostly T3N0, design similar to the VA study. There was poorer 2-yr survival for the chemo group (69% vs. 84%). 3-yr laryngectomyfree survival was 20%.
What is the only randomized study that investigated organ preservation for advanced HPC with induction CRT?
EORTC 24891 (Lefebvre JL et al., JNCI 1996): 194 pts randomized to surgery + PORT vs. induction chemo (5-FU/cisplatin) + RT; if NR to induction chemo, then salvage laryngectomy + PORT. 5-yr larynx preservation rate was 35%. At 3 yrs, OS was better, but there was no difference at 5 yrs (DMs were less in the chemo arm; no difference in LRF).
What are the key studies demonstrating a benefit with concurrent CRT over RT alone for resectable LCX?
Cleveland Clinic (Adelstein DJ et al., Cancer 2000): randomized phase III, 100 pts with stage III–IV H&N cancer (50% larynx/HPX); RT alone vs. chemo (platinum/5-FU) + RT. 5-yr larynx preservation rate was 77% vs. 45%, 5-yr laryngectomyfree survival was 42% vs. 34% (no OS difference).
RTOG 91-11 (Forastiere AA et al., NEJM 2003): 547 pts, T2-T4 (excluded T4 with thyroid cartilage invasion or >1-cm BOT invasion) randomized to (a) CRT (platinum 100 mg/m2 on days 1, 22, and 43), (b) induction chemo → RT (like the VA study), and (c) RT alone (all to 70 Gy). There was a better rate of laryngeal preservation at 3.8 yrs with concurrent CRT (84% vs. 72% vs. 67%); better 2-yr LRC (78% vs. 61% vs. 56%); and better DM rate with any chemo arm than with RT alone. There was no OS benefit. There was ↑ acute grade 3–4 toxicity but no ↑ late toxicity with concurrent CRT.
What are the survival/LC numbers based on the latest update of RTOG 91-11?
At the latest update of RTOG 91-11 with a median follow-up of 3.8 yrs, the 5-yr laryngectomyfree survival was 47% (CRT), 45% (chemo → RT), and 34% (RT); 5-yr LRC was 69% (CRT), 55% (chemo → RT), and 51% (RT). The 5-yr OS was the same (54%, 55%, and 56%, respectively).
What is the only randomized study that compared total laryngectomy + RT to CRT in advanced LCX?
Singapore study (Soo KC et al., Br J Cancer 2005): 119 pts, the majority with bulky T4 (56%) or stage IVA (78%) Dz; closed early due to poor accrual; nonstandard chemo (platinum 20 mg/m2; 5-FU 1,000 mg/m2), nonstandard RT (66 Gy). There was no difference in 3-yr DFS, with a larynx preservation rate of 45%. Pts with LCX or HPC had higher organ preservation rates (68% vs. 30%).
What study demonstrated an OS and DFS benefit with CRT over RT alone for unresectable H&N cancers?
Cleveland Clinic (Adelstein DJ et al., JCO 2003): 295 pts with unresectable stage III–IV H&N cancers (15% oral cavity [OC], 55% oropharynx [OPX], 20% HPX), RT alone vs. CRT with cisplatin 100 mg q3wks × 3. 3-yr OS (37% vs. 23%) and DFS (51% vs. 33%) were better with CRT.
What study demonstrated improvement in OS with the addition of cetuximab (C225) to RT in H&N cancers?
Bonner et al. (NEJM 2006): 424 pts with stage III–IV SCC of the OPX, larynx, or HPX randomized to RT vs. RT + C225; RT options were conventional to 70 Gy, 1.2 bid to 72–76.8 Gy, or concomitant boost to 72 Gy. There was better 3-yr LRC (47% vs. 34%) and OS (55% vs. 45%) with RT + C225. Subset analysis showed improvement mostly in OPC and in the altered fractionation RT arms (~50% with altered fractionation).
What 2 randomized studies demonstrated a benefit with induction taxane/platinum/5-FU (TPF) chemo → by RT or CRT in pts with unresectable H&N cancers?
TAX 324 study (induction chemo → CRT) (Posner MR et al., NEJM 2007): 501 pts, unresectable stage III–IV H&N cancers (52% OPX; ~13%–18% OC, larynx, HPX) randomized to induction platinum + 5-FU or TPF → CRT with carboplatin. There was better 3-yr OS (62% vs. 48%), MS (71 mos vs. 30 mos), and LRC (70% vs. 62%) in the TPF arm. Pts in the TPF arm had fewer Tx delays than those who rcv platinum/5-FU despite higher myelotoxicity in the TPF arm (98% rcv planned Tx in TPF vs. 90% in the platinum/5-FU arm).
TAX 323 study (induction chemo → RT) (Vermorken JB et al., NEJM 2007): 358 pts, unresectable stage III–IV H&N cancers (46% OPX, 18% OC, 29% HPX, 7% larynx) randomized to induction platinum + 5-FU or TPF → RT alone. TPF resulted in better median PFS (11 mos vs. 8.2 mos), MS (18.8 mos vs. 14.5 mos), with a HR of 0.73. The rate of toxic deaths was greater in the platinum/5-FU group (5.5% vs. 2.3%). There was also more grade 3–4 thrombocytopenia, anemia, stomatitis, n/v, diarrhea, and hearing loss in the platinum/5-FU arm. Neutropenia, leukopenia, and alopecia were more common in the TPF arm.
What are some acute and late toxicities with RT in the Tx of LCX?
1. Acute: hoarseness, sore throat, odynophagia, skin irritation
2. Late: laryngeal edema, glottic stenosis, hypothyroidism, xerostomia, L–hermitte syndrome, myelitis, laryngeal necrosis
What are the main late toxicities after organ preservation with concurrent CRT for LCX?
Moderate speech impairment, dysphagia (25% of pts; <5% cannot swallow), and xerostomia (advanced cases)
What are some approximate RT dose constraints for laryngeal edema?
Recent data suggests that the incidence of laryngeal edema ↑ significantly with mean doses ≥44 Gy. (Sanguineti G et al., IJROBP 2007)
What is the QOL impact of larynx preservation when compared to laryngectomy in the Tx of LCX?
1. VA data demonstrated better social, emotional, and mental health function with larynx preservation (swallowing and speech function were similar), which suggests that better QOL is not due to preservation of speech but due to freedom from pain, emotional well-being, and less depression.
2. Hanna et al. demonstrated that pts had worse social functioning, greater sensory disturbance, more use of pain meds, and coughing after total laryngectomy than those treated with CRT. (Arch Otolaryngol H&N Surg 2004)
What is the follow-up paradigm for LCX pts?
LCX follow-up paradigm: H&P + laryngoscopy (q1–3mos for yr 1, q2–4mos for yr 2, q4–6mos for yrs 3–5, q6–12 mos if >5 yrs), imaging (for signs/Sx), TSH (if neck is irradiated), speech/hearing evaluation, and smoking cessation