1. Radiation therapy for head and neck cancer can cause dysphagia both during and after treatment through damage to the muscles, nerves, and soft tissues involved in swallowing. During treatment, inflammation and edema can cause pain and difficulty swallowing food. 2. After treatment, fibrosis of the soft tissues is the main cause of long-term dysphagia. Excess transforming growth factor beta activates connective tissue growth factor, which causes unchecked scar tissue formation instead of normal wound healing. This results in stiff, non-functional tissues. 3. Symptoms of radiation-induced dysphagia include pain with swallowing, inability to swallow, coughing or choking during meals, weight loss,

1. DARS & DYSPHAGIA OPTIMIZED IMRT IN
HEAD & NECK SQUAMOUS CELL
CARCINOMA
PRESENTER: DR. VIVEK GHOSH
MODERATOR: PROF. DR. SUMAN BHASKER
31-10-2020

2. • Swallowing is a complex process that requires the precise coordination of
• Muscles : over 30 pairs of muscles in the oral cavity, pharynx, larynx, and esophagus
• Cranial nerves: 6 cranial nerves V, VII, IX sensory, IX motor, X and XII
• Neural control of swallowing, mediated by interactions between cortical centers in
both hemispheres, the “swallowing center” within the brainstem, cranial nerves and
pharyngeal receptors

3.  Dysphagia is a condition whereby a patient has difficulty with some or all parts of
the swallowing process.
 There are four stages to a normal swallow
1. Oral preparatory
2. Oral
3. Oropharyngeal
4. Oesophageal.

4. 1. ORAL PREPARATORY PHASE : food is ground and mixed
with saliva to form a food bolus in appropriate consistency for
safe swallow
1. ORAL PHASE:
• The bolus is then transported to the pharynx during the
oral phase
• Tongue presses the food bolus against the hard palate
and soft palate elevates
• The soft palate moves superior and posterior to close off
nasopharynx.
• Food bolus is moved backwards by the tongue

5. 3. PHARYNGEAL PHASE: The swallowing reflex is triggered,
resulting in
1. closure of the larynx to prevent aspiration
2. contraction of the pharyngeal constrictors from superior
to inferior
3. laryngeal elevation, epiglottic inversion
4. relaxation of the cricopharyngeus to allow the food
bolus to pass into the esophagus
4. ESOPHAGEAL PHASE: The peristalsis of the esophageal
muscles results in movement of the bolus into the stomach.

6.  Phases of Swallowing
 Voluntary Phase
 Mastication leads to a bolus of food being produced, during this stage the back of the tongue is elevated and the soft palate pulled anteriorly against it. This keeps the food within the oral cavity and allows the airway to remain open. The duration of this stage varies.
 Following this, inspiration is inhibited and the bolus of food is moved to the pharynx by the tongue. This leads to the stimulation of the swallowing reflex.
 Pharyngeal Phase
 Once the bolus has been moved to the pharynx, pressure receptors are activated in the palate and anterior pharynx. This signals the swallowing centre in the brain stem which:
• Inhibits respiration
• Raises the larynx
• Closes the glottis
• Opens the upper oesophageal sphincter
 The soft palate is elevated to close the nasopharynx to allow passage of food. In addition to this, the true vocal cords close to prevent aspiration.
 After this, the bolus is moved towards the oesophagus via peristalsis of the pharyngeal constrictor muscles. Gravity makes very little contribution to this process and the main factors affecting the speed of this are the viscosity and volume of the bolus.
 Oesophageal Phase
 The upper third of the oesophagus is voluntary skeletal muscle and the lower two thirds are involuntary smooth muscle. Further information on the anatomy of the oesophagus can be found here.
 At the beginning of this phase, the larynx lowers, returning to its normal position. The cricopharyngeus muscle then contracts to prevent reflux and respiration begins again.
 The bolus is moved down the oesophagus via peristalsis, which is coordinated by extrinsic nerves. Each area of muscle systematically relaxes to allow food through and contracts afterwards to propel it further. The bolus is propelled at a rate

7. • Dysphagia can be defined as a swallowing impairment and can result in penetration
or aspiration of food, drink or medication into the airway .
• ‘Penetration’ of food or drink means the passage of these materials into the larynx,
but not below the vocal fold
• Aspiration the material passes below the vocal folds and into the trachea.
• Aspiration can also be silent.

8. DYSPHAGIA: CAUSES
Mechanical Congenital abormalities, head & neck tumours,
oral pathology, stenosis, diverticula,
xerostomia
Infection Inflammation, ulceration, neurological
dysfunction
Iatrogenic Post-surgery, Medications, Radiation induced
Neurological Decreased consciousness, dementia, CVA,
trauma, CNS tumours
Neuromuscular Ageing, myasthenia gravis, critical illness,
sepsis, myopathies

9. DYSPHAGIA IN HEAD & NECK CANCER
 Pretreatment:
- 14-18% of HNC pts.(Molen et al, BMC Ear, Nose and Throat Disorders 2009)
1. Obstruction by tumour volume
2. Infiltration of structures involved in swallowing
3. Prior Sx: extirpation of strs. a/w swallowing

10. RADIATION INDUCED DYSPHAGIA
 Radiation Therapy (RT)- pivotal role in the definitive,
postoperative and palliative treatment of HNC
 80% of all HNC patients will receive RT at least once
during the course of their disease
 RT affects both tumor cells and uninvolved normal cells;
the former to the benefit and the later to the detriment
of patients
 Goal- balancing between these two is an art and a
science of radiation oncology

11. RADIATION ASSOCIATED DYSPHAGIA
 Acute and long-term complication
 Nearly 50 % of patients identifying it as a distressing symptom
following radiation treatment (J.W.G. Roe et al. / Oral Oncology 50
(2014) 1182–1187)
 Greater in those treated for curative purposes
 Acute dysphagia tends to resolve shortly after treatment
 Severity of late dysphagia has been reported to decrease in 32 %, to
remain unchanged in 48 % and to worsen in 20 % , even years after
therapy(Nguyen et al., Oral Oncology (2006) 42, 374–380)
 Pathophysiology:
 Radiation Induced soft tissue fibrosis
 Radiation Necrosis
 Vascular Changes

12. In brief, early radiation-induced treatment effects are evident
in the epidermis and mucosa. This is mainly due to
cell depletion, inflammation, and hypoplasia that can lead
to mucositis and desquamation accompanied by edema and
erythema (Table 1) [16]. Often acute injuries are transient
and resolve within a few months after treatment; however,
early injuries can sometimes persist, producing chronic
changes that lead to consequential late effects (discussed
below). In contrast, there may not be any significant correlations
between the severity of acute and chronic radiation-
induced injuries. For example, a patient may develop
severe fibrosis post-radiation treatment despite only suffering
a low-grade acute reaction, or a patient with severe
acute mucositis (grade 3 or 4) may ultimately experience
minimal treatment-related effect 6–9 months later.

14. Factors predictive of dysphagia
T and N stage, primary site, type of treatment, extension of
treated region (volume of tissue and anatomic structures), patient
characteristics (baseline swallowing function, performance
status [PS], smoking and alcohol abuse, age, lean mass, gender)
predict the risk of acute and late dysphagia.
All treatment modalities, whether involving surgery or organ
sparing protocols, and CRT result in swallowing problems along
with aspiration. Therefore, we can classify factors predictive of
dysphagia as patient-related, tumor-related, and treatment-related
[18,25]. Patient characteristics such as baseline swallowing
function, PS, smoking and alcohol abuse, age, lean mass, and
gender predict the risk of dysphagia [13]. Advanced T and N
stage are associated with worst swallowing impairment [22].

15. Radiation therapy may also result in significant acute and
late effect dysphagia, but the etiology of the underlying
tissue
damage differs. Acutely, radiation therapy results in
damage
to the mucosa and soft tissue within the radiation
treatment
volume.15 This results in an inflammatory reaction and the
production of reactive oxygen species.16 Clinically, the pa-
tients develop mucositis, radiation dermatitis, and edema of
the soft tissues. Pain, thickened and more viscous mucous
production, xerostomia, and tissue swelling contribute to
acute dysphagia.17 By 3 months after treatment, clinical acute
effects have largely resolved, and swallowing function begins
to return for most patients. Nonetheless, a “continuing cascade
of cytokines” results in ongoing effects on tissue secondary
to radiation. Tissues become fibrotic and rigid with resultant
loss of function. It is hypothesized that ongoing
hypoxia and chronic oxidative stress may perpetuate tissue
damage long after treatment has been completed,18,19 thus
explaining why some patients develop dysphagia years after
therapy has been completed. Late-effect lymphedema and
radiation-induced damage to neural structures may also contribute
to dysphagia.

16. It may be hypothesized that increased acute inflammation
may increase late-effect fibrosis and lymphedema resulting in
increased dysphagia. Acute tissue damage heals in 2 distinct
phases: a regenerative phase and a fibrosis phase. During the
regenerative phase, tissues repair and are replaced by similar
cell types. During the fibrotic phase, the normal cells are
replaced by connective tissue.28 It may be hypothesized that
when the acute reaction is protracted or over exuberant, the
repair process transitions from being beneficial to becoming
harmful. The use of chemotherapy concurrently with radiation
therapy clearly increases the rate of grade 3 and 4 mucositis.
29 Does the increase in acute mucositis result in increased
fibrosis and late-effect dysphagia? Clinical experience would
support this hypothesis; however, well-conducted studies to
prove this are lacking.18 One study comparing concurrent regimens
found no difference in swallowing function.22
An additional factor that may contribute to acute and late
swallowing abnormalities is the use of feeding tubes. There is
considerable variability in practice patterns regarding the use
of feeding tubes.

17.  What are the symptoms of radiation-induced dysphagia?
• Pain while swallowing (odynophagia)
• Inability to swallow
• Sensation of food sticking in the throat or chest
• Drooling
• Regurgitation (bringing food back up)
• Frequent heartburn
• Food or stomach acid backs up into the throat
• Unexpected weight loss
• Coughing or gagging when swallowing
• Avoidance of certain foods that cause trouble swallowing
 Frequent episodes of liquids/solids going into the airway may lead to pneu

18. INDICATORS OF DYSPHAGIA
it is essential to know what signs to look out for to identify patients who may be struggling with
swallowing safely.
patients with, or at risk of, developing dysphagia.
dysphagia Swallowing difficulties can lead to aspiration and reduced oral intake, which in turn can
lead to more serious complications such as pneumonia, malnutrition and dehydration
The obvious signs that can be identified include:
■ ■Difficult or painful chewing or swallowing
■ ■Drooling
■ ■Hoarse voice
■ ■Unintentional weight loss
■ ■Coughing and choking before, during or after a swallow
The less obvious signs can include:
■ ■‘Wet’ voice quality
■ ■Change in respiratory patterns

20. Although the precise mechanisms of radiation injury of
muscles are incompletely defined, acute microvascular
injury and muscle edema are commonly implicated
pathogenic mechanisms, with vessel and myofilament
atrophy, collagen deposition, and characteristic late
myofilament and vascular lesions appearing after many
months (3). The resulting ischemic and inflammatory
changes are postulated to promote fibrogenic cytokine
signaling and myofibroblast activity, eventually resulting
in clinically significant fibrosis (3). Peripheral nerve injury
is similarly mediated by microvascular damage that
produces early Schwann cell loss and microvascular
fibrosis and necrosis, followed by demyelination, axonal
degeneration, and nerve fiber loss (3). Secondary
demyelination resulting from nerve entrapment by
perineural fibrosis has also been proposed. Radiation
injury in both skeletal muscles and peripheral nerves is
observed more frequently and after shorter latency
periods with larger fraction sizes, consistent with the
radiobiology of late-responding tissues

21.  Radiation therapy affects people differently. During the typical 6-week course of RT, some patients have only a mild inflammation and complaint of sore throat. Other
patients experience severe pain in the mouth and throat, so much so that a PEG is required to ensure adequate nutrition. Laryngoscopy reveals the inflammatory response
to the tissue, with edema and erythema visible. In most patients, the inflammation and discomfort begins to diminish soon after completion of the 6-week RT program.
Some patients recover rapidly; in fact, 4-6 weeks after radiation therapy, some patients report swallowing is back to normal. There is another group of patients, however,
that do not recover well from radiation therapy. Sometimes patients develop significant ―late-effect‖ complications, generally understood to begin 3 months after the
completion of RT. Anywhere from 3-12 months after treatment, they complain that they cannot eat their usual diet. Occasionally, patients will report that they swallowed
adequately for a few years, but then began to experience a decline. Instrumental examination shows these patients are unable to swallow normally. The major reason for
long-term dysphagia after RT seems to be fibrosis, which is the abnormal accumulation of scar-like tissue. This fibrotic tissue seems to accumulate almost everywhere:
under the skin, in the connective tissue layers, around muscles, and even between muscle fibers (Gauldie, Bonniaud, Sime, Ask, & Kolb, 2007; Gervaz, Morel, & Vozenin-
Brotons, 2009; Gramley et al., 2009). HNC patients can present with either progressive or spontaneous fibrotic onset. In some patients, edematous tissue seen during RT
progressively will be replaced with stiffer fibrotic tissue. Alternatively, other patients who resolved nicely after RT can experience a sudden onset of fibrotic accumulation,
at times years after treatment. So what triggers this fibrotic mechanism? Normal wound healing involves a plethora of inflammatory and cell signaling mediators. One of
these mediators, transforming growth factor beta (TGF-β), instructs cells involved in the wound healing process to fix damaged tissue. These cells then make new tissue
and stitch it all together—just like fixing a cut on your finger. This process stops when appropriate, because there are many checks and balances that regulate it (Ask et al.,
2008; Bourgier et al., 2005; Gauldie et al., 2007; Okunieff, Chen, Maguire, & Huser, 2008; Pohlers et al., 2009). In radiation induced fibrosis, this normal wound healing
process has gone awry. Too much TGF-β is created, and the checks and balances are overwhelmed. This leads to the activation of another potent mediator called
―connective tissue growth‖ factor (CTGF), which is usually inhibited during normal wound healing. CTGF tells the cells to keep making scar tissue and does not allow any
of that tissue to be degraded. Turning CTGF off becomes almost impossible, because it is self-inducing, so it chronically makes more of itself. Both CTGF and TGF-β then
can activate other cells to do the same thing, thereby spreading the fibrosis within the confines of an anatomical structure (Bourgier et al., 2005; Gauldie et al., 2007;
Gervaz et al., 2009; Gramley et al., 2009; Haydont, Riser, Aigueperse, & Vozenin-Brotons, 2008; Pohlers et al., 2009). A critical threshold amount of TGF-β appears to be
required to trigger this process. Some people may have higher or lower thresholds, based on genetics and co-morbidities (Rodningen, Borresen-Dale, Alsner, Hastie, &
Overgaard, 2008). Accordingly, people who experience a progressive onset of fibrosis probably reach that threshold during or soon after radiation therapy. Alternatively,
those who experience a sudden (later) onset may have had an experience (trauma or surgery, addition of co-morbidity, exhaustion of compensatory mechanisms) that
resulted in the addition of extra TGF-β, or a suppression of that threshold, thereby triggering the aberrant wound healing process

22. Soft tissue fibrosis, Muscle atrophy,
Lymphedema, Neuropathy
LATE EFFECT
ACUTE EFFECT
Radiation induced inflammatory damage
Mucosal damage & edema in pharynx

24. COMPLICATIONS OF DYSPHAGIA
 Aspiration
 Aspiration Pneumonia
 Dietary modifications
 Nutritional deficiencies
 Prolonged feeding tube dependence
 Poor social interactions & lifestyle alterations
 Degradation in QOL

25. The first step required is to identify the anatomic structures whose damage or
malfunction after intensive therapy caused dysphagia and aspiration.
It is necessary to identify the most important structures whose damage causes
dysphagia and aspiration, and group them into OAR that can easily sparing by
IMRT.

26. FUNCTIONAL SWALLOWING UNITS (FSUS)
 Defined as groups of swallowing muscles sharing their function, that are in close proximity to
each other.
 Seven FSUs involved in HLE, TBR and tongue motion were identified:
1. floor of mouth,
2. thyrohyoid muscles,
3. posterior digastric/stylohyoid muscles complex,
4. longitudinal pharyngeal muscles,
5. hyoglossus/styloglossus muscles complex,
6. genioglossus muscles,
7. intrinsic tongue muscles.
Gawryszuk et al., Radiotherapy and Oncology 130 (2019)

27. SWALLOWING ANATOMY
Complex behaviors including both volitional & reflexive activities involving more than 30 nerves
and muscles
 Pharyngeal musculature
- circular constrictors (superior, middle & inferior PCM)
- longitudinal muscles (stylopharyngeal, salpingopharyngeal & palatopharyngeal muscles)
 Base of tongue
 Glottic adductor muscles (thyroarytenoid, lateral cricoarytenoid & transverse arytenoid
muscles)
 Supraglottic adductors (oblique arytenoids & aryepiglottic muscles)
 Upper esophageal sphincter (Cricopharyngeus)

28.  Dysphagia aspiration structures(DARSs)
 Anatomical structures that are critical to the swallowing function
 Radiation dose delivery to these structures (DARSs), shown to predict swallowing
outcome
 Dysphagia-optimized IMRT (Do-IMRT)
 Preferential sparing of key swallowing structures implicated in post-radiation
dysfunction without compromising locoregional control & survival outcomes.

29. DYSHPAGIA/ ASPIRATION RELATED
STRUCTURES (DARS)

31. Complications of Dysphagia
Disordered swallowing may
result in aspiration, pneumonia, and chronic bronchial inflammation.
Aspiration is defined as the passage of materials
below the true vocal cord. Aspiration may occur at different
phases of swallowing: (1) before the pharyngeal phase because
of the loss of control of the tongue or delayed reflexive
swallowing, (2) during the pharyngeal phase because of inadequate
airway closure, and (3) after the pharyngeal phase
because of retained materials in the pharynx.36 Aspiration
usually manifests itself by cough or clearing of the throat
before, during, or after swallowing.
Unfortunately, silent aspiration is frequent in irradiated
HNC patients.37 Furthermore, the cough reflex is ineffective
or absent in almost half of patients.38 Although some degree
of aspiration may be tolerated by patients, particularly if they
have an intact cough reflex, it is critical to identify patients
with clinically significant aspiration.
A second common complication of late-effect dysphagia is
permanent or long-term feeding tube dependence. Although
patients may receive adequate nutrition via a feeding tube,
there are many negative aspects of tube feeding that impact
on patients and their families; tube feedings are expensive
and may not be covered by insurance, feedings are time intensive
and may require disruptions in the patients’ activity,
and minor complications are frequent.

32. Anatomical Changes after XRT
Early – edema; can persist for 1+ yrs
Later – fibrosis replaces normal mucosa;
appearance = ‘thick’
infiltrates connective tissue, muscle, cartilage
Can invade nerves, bone
Formation of webs, strictures

33. Motility problems after XRT
Reduced range of movement of all structures
Tongue base retraction
Pharyngeal wall squeeze
Hyolaryngeal elevation
Airway closure
UES opening
Vocal folds often spared so glottic closure
may be intact at that level

34. Pro-fibrotic cell “priming” theory
XRT results in just enough TGF-β1 to induce
pro-fibrotic cell differentiation but
not enough to overwhelm cell’s compensatory
ability
Subsequent stressor increases TGF-β1
concentration just enough to reach a
threshold level overwhelming cell’s
compensatory ability leading to fibrotic
cascade.
Explains delayed onset these people would
have a higher or lower
threshold or better/worse compensatory
mechanisms
People may have co-variables that affect this
threshold (Delanian 2004)

35. Variables affecting XRT induced Dysphagia?
What variables in implicated in a patient’s
reaction to XRT, especially swallow status?
Pre-treatment variables
Treatment variables
Post treatment variables
Pre Treatment Variables that may
affect outcome/ swallowing
Age
Comorbidites (DM, others)
Weight
Weight loss before XRT
Smoking
Drinking
FT placed prophylactically
Social support
Prior radiation therapy or surgery to H&N
Treatment variables that may affect
outcome/ swallowing
Location, stage of cancer
XRT Treatment (type, dose, etc)
Additional surgery
Chemotherapy (type, dose)
Smoking during XRT
Drinking during XRT
Weight loss during XRT
FT placed during XRT

36. Patient Predictors: Social
Patients’ Body Mass Index (BMI)
Normal/Under weight <25Kg/m2
4.13X more likely to have a PEG tube (McRacken. et al)
1.3X more likely per unit below 25Kg/m2
PEG tube dependence and duration (late morbidity)
Obesity and dysphagia protection
Protective adipose tissue, nutritional status able to
withstand treatment
Patient Predictors:
Cancer Location & Severity
Defining tumor location
May vary-Dependant on study design
Need for standard reporting
Oropharynx, hypopharynx (Machtay. et al.,)
May cause dysphagia before treatment
Advanced tumor stage (T3/4)
Less likely to cure
Treated with more invasive therapies
Increased adverse swallowing outcomes (Machtay et al)
May cause dysphagia before treatment.
Patient Predictors: Social
Smoking habits during radiotherapy
Heavy smokers and Radiotherapy
1 pack/day (20 cig/day) (Mangar. et al)
PEG and Nasogastric tube placed during treatment.
Increased dysphagia related morbidities
– mucositis, xerostomia
Smoking during treatment, low (WHO) PS score
and advanced T stage(3/4)
>75% chance of needing enteral nutrition

37. Treatment predictors:
Chemoradiotherapy
CRT increases local regional control
increasing survival rate.
Downside to increasing the toxicity profile
Mucositis 39%(RT) vs. 71%(CRT) (grade 3-4)
Xerostomia 37%(RT) vs. 92%(CRT)(Grade 2-3)
Feeding tube 15%(RT vs. 36%(RT) (Nuyts et al,.)

38. Different Categorization Schemes:
Cancer Location
Langendijk. et al., (2009)
Oral Cavity vs. Nasopharynx vs. Oropharynx vs. Larynx vs.
Hypopharynx
Caudell. Et al., (2008)
Tonsil, Soft Palate, Oral Cavity, Nasoalcavity, Nasopharynx vs.
Larynx, Hypopharynx, Base of Tongue, Pharyngeal Wall
Machtay. et al., (2008)
Oral Cavity/Oropharynx vs. Larynx/Hypopharynx
Cheng, S. et al., (2006)
Oral Cavity vs. Larynx vs. Oropharynx/Hypopharynx
Bold Indicates Significance

39. Fibrotic Onset
What we do know…
XRT causes inflammation which produces pro-fibrotic
mediators
Pro-fibrotic mediators cause “acute” & normal clinical
reactions to XRT burning
Erythema, pain, edema
Following acute rxn some people return to normal
What we’re still confused about
Edema may be replaced by progressive fibrosis
Normal inflammatory response turns into uncontrolled
fibrotic
response.
Fibrosis can occurs spontaneously in the future
Fibrosis not related to inflammatory responseOverproduction of TGF-β1
Latent activation
Cellular production
Self-induction
Addition of CTGF overproduction
Activation of synergistic pathway
Negative feedback loops inhibited
Cellular compensation
overwhelmed
Receptor downregulation
Reduces collagen degradation
Downregulation of proteases

40. Aspiration Common
(but pneumonia uncommon)
Early post- treatment: 13-65% aspirated –
Eisbruch 02 & 07; Feng 07; Smith 00)
Late post-treatment: 44-62% aspirated
Campbell ’04; Eisbruch, ’02
Silent Aspiration
About 50% (Eisbruch 02; Smith 99)

41. Treatment Predictors:
Altered fractionation
Hyperfractionation controls tumor growth…
Increase in radiation dose/day (Many smaller
Fractions)
Decreased total radiation dose
Less likely for tumor to repopulation (Citrin)
Acute Adverse Effects
Early onset of mucositis and xerostomia
compared to Conventional fractionation.
Increased dependence of feeding tube (Leborgne
et al.)

42. RTOG ACUTE RADIATION TOXICITY
Grade 1 2 3 4
Pharynx
&
esophagu
s
Mild dysphagia or
odynophagia /
may require
topical anesthetic
or non-narcotic
analgesics / may
require soft diet
Moderate
dysphagia or
odynophagia /
may require
narcotic
analgesics /
may require
puree or liquid
diet
Severe
dysphagia or
odynophagia
with
dehydration or
weight loss >
15% from
pretreatment
baseline
requiring NG
feeding tube, IV
fluids, or
hyperalimentati
on
Complete
obstruction,
ulceration,
perforation,
fistula

43. EVALUATION OF THE SWALLOWING MECHANISM
A. Objective
Evaluation:
Instrumental
Assessment
1. Videofluoroscopy (VFS)
2. Modified barium swallow (MBS)
3. Fiber-optic endoscopic evaluation of
swallowing(FEES)
4. Manometry
B. Objective
Evaluation:
Observer-
Assessed
1. CTACE
2. RTOG/ EORTC criteria
3. SOMA scale
C. Subjective
Evaluation:
Patient-Reported
Quality of Life
1. UWQOL
2. MDADI-HN
3. EORTC-QLQ H&N
4. PSS-H&N
5. QOL-RTI/H&N
6. FACT-H&N

44. ETIOLOGY
 Number of factors identified that may correlate with the development of acute or late dysphagia
 Radiation dose delivery to dysphagia–aspiration-related structures (DARSs), those“anatomical”
structures that are critical to the swallowing function shown to predict swallowing outcome

45. PREDICTION:
 Langendijk et al.- 5 independent prognostic factors
predicting G2–G4 swallowing dysfunction
(RTOG/EORTC) at 6months after treatment
(SWALL6 months):
1. advanced T stage (T3–T4)
2. oropharyngeal and nasopharyngeal tumour site
3. primary and bilateral neck irradiation
4. weight loss at baseline
5. treatment modality (accelerated RT or
concomitant CT–RT)

46. EVALUATING DYSPHAGIA
 Commonly used techniques:
1. Fiber-optic endoscopic evaluation of
swallowing(FEES)
2. Videofluoroscopy
3. Modified barium swallow
 Patient-reported instruments:
1. RTOG and EORTC Radiation Morbidity Scoring Criteria
2. Late Effects of Normal Tissue Subjective, Objective,
Management, and Analytic(LENT SOMA) scale
3. Common Terminology Criteria for Adverse Events
(CTCAE)
4. EORTC Quality of Life Questionnaire C30
5. MD Anderson Dysphagia Inventory (MDADI)

47.  What are the complications of radiation-induced dysphagia?
 Dysphagia can take the joy out of eating and drinking and can lead to more severe complications such
as malnutrition, weight-loss, and dehydration. In addition, patients who aspirate liquids or solids (breathe
them into the airway while swallowing) can develop respiratory problems such as pneumonia, bronchitis,
or other upper respiratory infections.

48.  How is radiation-induced dysphagia diagnosed?
 To diagnose oropharyngeal dysphagia doctors will likely probably perform two or more of the following tests:
• Videostroboscopy: In this test doctors use a camera called an endoscope to visualize the larynx. Using a flexible endoscope, a small
flexible camera, they can look up through the nose and over the back of the throat. Using a rigid endoscope, a slightly larger, but still
small, firm camera, they can examine the via the mouth. Both endoscopes use light sources called strobe lights that allow the
physicians to view the larynx, and both tests take only a few minutes to complete.
• Esophageal Manometry: An esophageal manometry measures the rhythmic muscle contractions, and the coordination and force
exerted by the muscles, that occur in the esophagus when a person swallows. During this test, a thin, flexible tube (catheter) that
contains sensors is passed through the nose, down the esophagus, and into the stomach. (The throat and nose are numbed for this
test.) Patients will be asked to take small sips of water and swallow on command during the test.
• Modified Barium Swallow Study (MBS): During this test patients are asked to swallow a variety of substances that are coated with
barium, a whitish paste that lights up during an X-ray, enabling the examiner to determine how well these substances are moving
through the mouth, pharynx, and esophagus. The test will show if the upper esophageal sphincter is not relaxing or if foods or liquids
are blocked as they pass through the esophagus.
• Flexible Endoscopic Evaluation of Swallowing (FEES): FEES is an instrumental examination of swallowing that allows the
examiner to view food and liquid as it passes through the throat. Doctors pass a small flexible fiberoptic scope through the nose and
hold it above the larynx to view the swallow.

49. PREDICTION:
 5 independent prognostic factors predicting
G2–G4 swallowing dysfunction (RTOG/EORTC)
at 6months after treatment (SWALL6 months):
1. advanced T stage (T3–T4)
2. oropharyngeal and nasopharyngeal tumour
site
3. primary and bilateral neck irradiation
4. weight loss at baseline
5. treatment modality (accelerated RT or
concomitant CT–RT)
Langendijk et al, J Clin Oncol 26:3770-
3776

50. INTENSITY MODULATED RADIATION
THERAPY (IMRT)
 Optimizes the radiation delivery to irregularly-shaped volumes
 Simultaneously deliver different radiation doses to the different
CTVs
 Greater sparing of normal structures such as salivary glands,
esophagus, optic nerves, brain stem, and spinal cord
 Treatment delivery in a single phase
 Higher radiation doses to regions of hypoxia within the GTV to
further increase LR control
 Re-irradiation of recurrent disease to tumoricidal doses

51. IMPROVING RT IN HNC
1. Three-Dimensional Conformal Radiation
2. Acceleration of Radiation Dose
3. Intensity Modulated Radiation Therapy
4. Radiosensitizers
5. Radiation Protectors

52. DELINEATION GUIDELINES FOR DARS AS OARS

53. RADIATION ASSOCIATED DYSPHAGIA
 Acute and long-term complication
 Nearly 50 % of patients identifying it as a distressing symptom following
radiation treatment
 Greater in those treated for curative purposes
 Acute dysphagia tends to resolve shortly after treatment
 Severity of late dysphagia has been reported to decrease in 32 %, to remain
unchanged in 48 % and to worsen in 20 % , even years after therapy
Pathophysiology:
 Radiation Induced soft tissue fibrosis
 Radiation Necrosis
 Vascular Changes

55.  Do-IMRT
Aim : To spare the PCM lying outside the high dose CTV.
For oropharyngeal primaries,
mandatory mean dose constraints of <50 Gy to the volume of SMPCM lying outside CTV
optimal mean dose constraint of <20 Gy to the volume of IPCM lying outside CTV_6500
Hypopharyngeal tumours,
mandatory mean dose constraints of <50 Gy set for IPCM and
optimal mean dose <40 Gy have been set for SMPCM.

56. O
R
O
P
H
A
R
Y
N
X

57. H
Y
P
O
P
H
A
R
Y
N
X