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Dysphagia: implications for older people

Ranjit N Ratnaike

Reviews in Clinical Gerontology / Volume 12 / Issue 04 / November 2002, pp 283 - 294

DOI: 10.1017/S095925980201242X, Published online: 09 October 2003

Link to this article: http://journals.cambridge.org/abstract_S095925980201242X

How to cite this article:

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283-294 doi:10.1017/S095925980201242X

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Reviews in Clinical Gerontology 2002 12; 283–294
© 2002 Cambridge University Press Printed in the United Kingdom DOI:10.1017/S095925980201242X
Dysphagia: implications for older people
Ranjit N Ratnaike
Queens Elizabeth Hospital, University of Adelaide, Australia
Introduction
Dysphagia is defined as difficulty in swallowing
solids or liquids and is distinct from odynophagia,
which is pain on swallowing. Dysphagia occurs in
a range of conditions that affect the oral, pharyn-
geal and oesophageal phase of swallowing. The
problem of dysphagia assumes greater importance
in older persons. Some people may not be able to
communicate that a problem exists. In others the
lack of nutrition due to dysphagia compounds
existing undernutrition, a common problem in
institutionalized older persons. This paper discusses
dysphagia in the context of the older person and
outlines the normal mechanism of swallowing, the
important clinical distinction between oropharyn-
geal dysphagia and oesophageal dysphagia, the aeti-
ology of dysphagia and issues of management.
The swallowing process and aging
Anatomical structures involved in swallowing
The anatomical structures that are involved in
swallowing are the oral cavity and the tongue, the
pharynx (the common inlet to the respiratory and
digestive tracts) and the oesophagus. The pharynx
consists of the nasopharynx above the soft palate
and the oropharynx at the rear of the oral cavity.
The cricopharyngeal muscle forms the inferior
boundary of the oropharynx. This muscle func-
tions as the upper oesophageal sphincter.
The oesophagus is a narrow conduit about
20 cm long that connects the pharynx to the stom-
ach and transports solid and liquid nutrients from
mouth to stomach. The oesophagus is in a ‘col-
lapsed’ state, distending when liquid or food or air
is ingested. The oesophagus extends from the level
of the fifth to sixth cervical vertebra, descending
Address for correspondence: R Ratnaike, Department of
Medicine, University of Adelaide. The Queen Elizabeth
Hospital, Woodville, South Australia 5011, Australia.
through the posterior mediastinum and the
diaphragm into the stomach.
The cervical portion of the oesophagus consists
of voluntary striated muscle, and a mixture of
striated and smooth involuntary muscle forms the
upper thoracic portion. The distal half to one-
third contains only smooth muscle. The inner cir-
cular and outer longitudinal muscle layers effect
peristaltic movements to transport food through
the oesophagus to the stomach.
The upper oesophageal sphincter at the upper
end of the oesophagus is usually tonically con-
tracted. The lower oesophageal sphincter (LOS)
protects the oesophagus from acid gastric contents
regurgitating from the stomach and is therefore also
tonically contracted except when a peristaltic wave
reaches it. Parasympathetic innervation is by the
recurrent laryngeal nerve and the vagus. Sympa-
thetic innervation occurs from the thoracic sympa-
thetic chain of the splanchnic nerves and recurrent
sympathetic branches from the cervical plexus.
The blood supply to the cervical region is from
the inferior thyroid artery and the thoracic por-
tion is supplied by the oesophageal branches of the
aorta. The distal oesophagus receives blood from
the oesophageal branches of the inferior phrenic
and left gastric arteries.
The normal swallow and the influence of aging
The act of swallowing is complex, highly co-ordi-
nated and involves the synchrony of voluntary and
involuntary muscles: the tongue, palatal and pha-
ryngeal constrictors, the cricopharyngeus, and the
longitudinal and circular muscles of the oesopha-
gus. Swallowing also requires the coordinated
activity of neural regulatory mechanisms in the
medulla, the sensorimotor cortex and corticolim-
bic systems, mediated by cranial nerves V, VII, IX,
X and XII in the pons and medulla oblongata.
Three distinct phases occur during swallowing,
the oral phase, pharyngeal phase and the oeso-
phageal phase.
284 RN Ratnaike
The oral phase
Voluntary control determines the entry of food
into the oral cavity, lip closure, closure of the
anterior and lateral sulci, and mastication involv-
ing jaw movements and rotatory tongue move-
ments to mix the food with saliva. The anterior
bulging of the soft palate prevents premature
spillage of food from the oral cavity to the phar-
ynx. The tongue moves the food, masticated and
mixed with saliva, to the faucial arches.
The pharyngeal phase
The passage of the food bolus to the anterior
fauces stimulates the surface and deep receptors
within the faucial arches, pharynx and base of the
tongue. This triggers the involuntary pharyngeal
phase, and swallowing begins. Once this occurs,
involuntary activity ensues: the larynx is elevated,
the epiglottis is bent back and the vocal cords are
approximated. Thus the respiratory tract is pro-
tected. The upper oesophageal sphincter relaxes to
receive the bolus of food that is then transferred
to the oesophagus by the action of the superior
pharyngeal constrictor muscle.
The oesophageal phase
When food enters the upper oesophagus, a contin-
uation of the wave of peristalsis that occurred in
the pharynx continues. This propels the bolus to the
stomach through the lower oesophageal sphincter.
This phase lasts from between eight to 20 seconds.
The effect of age on swallowing
Dysphagia is not a consequence of aging. Aging
influences the structures involved in the swallow-
ing process and may alter the efficiency of the act
of swallowing. These changes are confined to the
oropharyngeal phases rather than the oesophageal
phase of swallowing. Salivary gland secretion is
reduced; mastication to prepare food is increased,
as is the time required to prepare the bolus. There
is a tendency to hold the prepared bolus on the
floor of mouth, reduced laryngeal and hyoid bone
elevation due to a drop in resting laryngeal posi-
tion, slowing of pharyngeal contractions, trigger-
ing of the pharyngeal phase more posteriorly and
delayed triggering of the pharyngeal phase of
swallowing.
Types of dysphagia
Dysphagia can be distinguished as two separate
entities: (1) oropharyngeal dysphagia, (2)
oesophageal dysphagia, based on distinctive clini-
cal features that reflect the different swallowing
mechanisms and structures involved. Other symp-
toms, in addition to dysphagia, common to both
types of dysphagia are odynophagia, a change in
eating habits and a rapid decline in nutritional sta-
tus. In both conditions the aetiology of dysphagia
is extensive and may occur from a localized prob-
lem or generalized disease process.
Oropharyngeal dysphagia
In oropharyngeal dysphagia the most distinctive
clinical feature is difficulty in initiating swallow-
ing. This is due to muscular incoordination dur-
ing the pharyngeal phase of swallowing. Other
prominent and distressing manifestations are
regurgitation, aspiration and as a consequence of
the latter, coughing. Dysphagia of pharyngeal ori-
gin may also be associated with speech difficulties
as muscles common to swallowing and speech
may be involved. Thus in addition to dysphagia,
dysphonia and or dysarthria may be present.
Localization of where food ‘sticks’ is not a use-
ful feature to distinguish oropharyngeal from
oesophageal dysphagia. In the former, patients
tend to point to the throat rather than a
retrosternal location.
Oesophageal dysphagia
Oesophageal dysphagia is not associated with dif-
ficulty initiating swallowing. The dominant com-
plaint is one of food ‘sticking’ once swallowing
has occurred. Localization of where food ‘sticks’
is not easy. Patients with oesophageal dysmotility
experience dysphagia with both liquids and solids.
In an obstructive anatomical lesion that is contin-
uing to encroach on the lumen increasing swal-
lowing difficulty occurs with solids rather than
liquids.
Aetiology of dysphagia
Despite its architectural-like simplicity of a tube,
the oesophagus is a structurally complex organ
vulnerable to a variety of disorders of its compo-
nent muscles, nerves and blood vessels. These
 Dysphagia: implications for older people 285

problems may be intrinsic to the oesophagus or Oropharyngeal dysphagia

dysphagia may occur due to generalized systemic
Oral cavity Problems relating to the oral cavity
diseases involving these structures.
may not be adequately appreciated in older
patients with dysphagia and therefore are
Functional disorders neglected. Common problems relate to the mus-
cles of mastication and the tongue, poor dentition,
In the gastrointestinal tract, functional disorders
lesions of the tempero mandibular joint, and
are more common than organic illness but, espe-
xerostomia. These factors contribute to poor
cially in older persons, they are not often a cause
bolus preparation and its transfer to trigger the
of oropharyngeal or oesophageal dysphagia.
pharyngeal phase.
Globus hystericus refers to the sensation of a lump
in the throat causing dysphagia and persists even
Cerebrovascular accidents Older persons are at
when swallowing is not initiated. This condition
a significant risk of developing a cerebrovascular
attributed to psychosomatic causes is associated
accident (CVA). Silent aspiration occurs in about
with younger persons, but not exclusively so. In
two-thirds of patients after a CVA.1 Brain stem
older people, despite the presence of psychosocial
involvement affects the nerve supply to the mus-
problems, labelling dysphagia as due to globus
cles involved in the oral and pharyngeal phase, dis-
hystericus or of functional origin should be made
rupting the oropharyngeal phase. Importantly, vital
with extreme caution and certainly not as a sub-
airway protection is severely compromised and
stitute to a careful diagnostic evaluation.
may result in aspiration with its attendant respira-
tory complications. In 128 patients who were

Table 1. Aetiology of oropharyngeal dysphagia

Oral cavity
Muscular weakness
Poor dentition
Tempero mandibular joint lesions
Xerostomia

Central nervous system

Cerebrovascular accidents (especially involving the brainstem)
Alzheimer disease
Parkinson’s disease
Motor neuron disease
Progressive supranuclear palsy
Huntington’s chorea
Myasthenia gravis
Multiple sclerosis
Neoplasia
Head trauma
Guillain-Barré syndrome
Myopathies

Oropharyngeal causes
Infection
Diverticula
Webs
Therapeutic agents
• Haloperidol
• Trifluoperazine
• Loxapine
286 RN Ratnaike
examined clinically and by videofluoroscopy after
a CVA, dysphagia was diagnosed clinically in 51%
and by videofluoroscopy in 64%.2 Aspiration was
detected in 49% of patients clinically and in 22%
on videofluoroscopy. A particular hazard exists in
patients after a CVA who require to be fed but are
unable, because of a speech impediment, to com-
municate that swallowing problems exist.
Dysphagia may be a presenting symptom in
transient cerebral ischaemic attacks (TIA’s) involv-
ing the vertebrobasilar territory.
Alzheimer's disease The basis for dysphagia is
not certain in Alzheimer’s disease though it is a
frequent problem as the disease progresses. Dys-
phagia may manifest early in the disease. In mid-
stage Alzheimer’s disease, a pilot study on ‘eating
changes’ documented significantly prolonged
swallow ‘durations’ in the oral phase, pharyngeal
phase, and total swallow duration.3
Patients with severe cognitive impairment and
dysphagia are at risk, if unsupervised, of attempt-
ing to feed themselves and experiencing life-
threatening aspiration.
Parkinson’s disease Both oropharyngeal and
oesophageal dysphagia occur in Parkinson’s dis-
ease.4,5 Xerostomia affects bolus formation and
decreases lubrication for ‘easy’ swallowing. In the
oral cavity, repetitive tongue pumping delays the
movement of the bolus and diminishes triggering
the pharyngeal swallow. As Parkinsons’s disease
progresses, the voluntary components involved in
swallowing are also affected, leading to worsen-
ing oropharyngeal dysphagia. In a study of 75
patients with Parkinson’s disease, based on the
Hoehn and Yahr score which grades severity, the
frequency of swallowing abnormalities were:
Stage I, 58%; Stage II, 93%; Stage III, 91% and
94% of patients in stage IV.6
Motor neuron disease In motor neuron disease,
dysphagia is associated with dysphonia and
dysarthria. The oral phase is particularly affected
due to weakness of the tongue. Contributing to
the dysphagia are delayed triggering of the swal-
low response and decreased pharyngeal contrac-
ture. Muscle weakness prevents adequate closure
of the larynx. Other features of motor neuron dis-
ease are generalized muscular weakness, wasting,
fasciculation and brisk reflexes, though sensation
is intact.
Progressive supranuclear palsy This rare pro-
gressive extrapyramidal disease mimics Parkin-
son’s disease, but a tremor is absent. The
characteristic features are gaze palsy, decreased
movement and rigidity. Oropharyngeal dysphagia
occurs early in the disease and progressively wors-
ens, and is more common and severe than in
Parkinson’s disease. The mechanisms of dysphagia
based on videofluoroscopy are similar to those in
Parkinson’s disease.7,8
Huntington’s chorea Oropharyngeal dysphagia
is a major problem in Huntington’s chorea that is
characterized by involuntary choreiform move-
ments and progressive dementia. Videofluo-
roscopy distinguishes patients with Huntington’s
chorea as being either ‘hyperkinetic’ or ‘rigid
bradykinetic,’ based on their swallowing abnor-
malities.9 Aspiration pneumonia is a common
cause of death.
Myasthenia gravis This autoimmune disorder of
the neuromuscular junction affects voluntary mus-
cles and can occur in older males though it usu-
ally affects a younger age group. In a study of 153
patients, 32 patients (21%) were older than age
50, and some developed the first symptoms of
myasthenia gravis at age 80.10 Myasthenia gravis
may present with a variety of symptoms. Common
clinical features are ptosis, diplopia, dysarthria,
dysphonia and dysphagia, although the latter does
not always occur. Twenty per cent of patients pre-
sent with dysphagia.11 The oral phase of swallow-
ing may be affected due to diminished chewing
affecting bolus preparation and formation. The
major cause of dysphagia based on electrophysio-
logical studies is incoordination between a normal
cricopharyngeal muscle and abnormal function of
the striated muscles of the laryngeal elevators.12
Multiple sclerosis Multiple sclerosis is not com-
mon in older persons. Dysphagia may be one of
the many manifestations of this disease. A signifi-
cant number (p < .005) among 79 patients with
multiple sclerosis complained of abnormal swal-
lowing, of coughing upon eating, and of food
‘going down the wrong way’.13
Neoplasia and head trauma Dysphagia may
occur by invasion or compression of the brainstem
or by hemispheric lesions. Dysphagia is also asso-
ciated with injuries involving the brain or brain-

stem and in one study occurred in 71% of 23
patients with brain injury due to trauma. 14
Guillain-Barré syndrome Dysphagia occurs due
to cranial nerve involvement, a feature in many
patients with the Guillain-Barré syndrome. Since
tongue weakness is a major problem, the oral
phase is especially affected.15
Myopathies Most myopathies manifest as mus-
cle weakness and atrophy and dysphagia. The
aetiology is diverse, with implications for
older persons and includes infections, immune
processes and endocrine causes, for example,
hypothyroidism, hyperthyroidism, hyperadrenal-
ism, hyperparathyroidism and hyperpituitarism.
Oculopharyngeal muscular dystrophy is a rare
genetic condition affecting the striated muscles of
the head and neck. Since the striated pharyngeal
muscles are involved, oropharyngeal dysphagia is
common in this disease.16
Infections In infections such as pharyngitis and
tonsillitis, odynophagia is the cause of dysphagia.
An abscess in the retropharyngeal space causes
dysphagia and acute neck pain and the optimal
diagnostic tool is magnetic resonance imaging.17
Diverticula Diverticulae increase with aging and
may cause oropharyngeal and oesophageal dys-
phagia.
Zenker’s diverticulum Zenker’s diverticulum is
an outpouching of a weak posterior pharyngeal
wall above the cricopharyngeal muscle and
extending inferiorly downwards. The symptoms
reflect the size of the diverticulum. The cause of
dysphagia is oesophageal compression by the
food-fluid filled diverticulum. Other features are
fullness in the throat, a gurgling noise, halitosis,
regurgitation, and aspiration. The treatment
options are cricopharyngeal myotomy and diver-
ticulopexy or endoscopic diverticulectomy. 18,19
Webs A cricopharyngeal web is associated with
the Paterson-Kelly syndrome (also called the Plum-
mer-Vinson syndrome). Other features in this con-
dition that are more common in females, are iron
deficiency anaemia, glossitis, and koilonychia.
Therapeutic agents A variety of drugs can cause
or contribute to oropharyngeal dysphagia and
Dysphagia: implications for older people 287
include those that cause xerostomia. Neuroleptic
drugs such as haloperidol, trifluoperazine and
loxapine, frequently prescribed to older persons,
decrease production of saliva and affect neuro-
transmitter function that disrupts extrapyramidal
activity and impairs swallowing.20
Oesophageal dysphagia
Dysphagia occurs from lesions occluding the
lumen or affecting the function of the posterior
mediastinum, and is particularly vulnerable to dis-
eases affecting other structures with which it is
contiguous.
Motility disorders Dysphagia due to a motility
disorder of the oesophagus has distinguishing
diagnostic features that can be elicited from the
history. Dysphagia occurs with both solids and liq-
uids. Dysphagia is eased by repeated swallowing,
postural change adopting an erect posture or lift-
ing the head. The commonest motor disorders are
achalasia and diffuse oesophageal spasm.
Although a relationship exists between stress and
dysphagia in that stress worsens dysphagia, it
should not be attributed to psychosomatic factors.
Achalasia Dysphagia is due to degeneration of
the ganglion cells in Auerbach’s plexus (the myen-
teric plexus) resulting in disruption of co-ordi-
nated oesophageal activity in the mid- and
especially lower oesophagus, and this causes
absent or ineffectual peristalsis, a high-resting
LOS pressure and incomplete LOS relaxation. The
majority affected are in middle age but the onset
may be in later life. Patients complain mainly of
dysphagia, though symptoms of reflux and chest
pain also are reported.21 In severe achalasia, food
accumulates and causes regurgitation. Features of
achalasia may also occur from a gastric malig-
nancy encroaching on the gastroesophageal junc-
tion22 or by malignant infiltration of Auerbach’s
plexus.23
Diagnostic features on a barium swallow are a
dilated oesophagus, absent peristalsis in the lower
two-thirds, a smooth bird-beak-like tapering of
the distal portion of the oesophagus, and failure
of the LOS to relax. In a chest radiograph, the
dilated food and fluid-filled oesophagus may be
seen as a mediastinal mass. Manometry confirms
the failure of the LOS to relax on swallowing.
Endoscopy is helpful in detecting a malignancy of
288 RN Ratnaike

Table 2. Aetiology of oesophageal dysphagia

Motility disorders
Achalasia
Diffuse oesophageal spasm
Therapeutic agents
• Anticholinergics
• Tricyclic antidepressants
• Theophylline
• Calcium channel blockers
• Alcohol

Oesophagitis
Gastroesophageal reflux disease (GERD)
Infectious causes:
• Candida albicans
• Clostridium botulinum
Therapeutic agents
• Alendronate
• Aspirin
• Non-steroidal anti-inflammatory drugs (NSAIDs)
• Vitamin C
• Potassium chloride
• Quinidine
Radiation injury

Strictures
Diverticula
Webs and rings
Systemic conditions
• Scleroderma
• Amyloidosis
• CREST syndrome
• Myasthenia gravis
• Mixed connective tissue disorders
• Diabetes mellitus
• Parkinson’s disease

Neoplasia
Extraoesophageal causes
• Aberrant right subclavian artery
• Massive thoracic aortic aneurism
• Mediastinal masses
• Left atrial enlargement

the stomach extending to the oesophagus or the
rare complication of malignancy complicating
achalasia and eliminating a stricture mimicking
achalasia.
The goal of treatment is to reduce LOS pres-
sure. Rigiflex fixed diameter balloon dilation pro-
vides a positive response in about 90% of
patients24 and is successful even in a massively
dilated oesophagus.25 Heller’s myotomy can be
performed laparoscopically, when pneumatic
dilatation has failed. An alternative to dilatation
or surgery in patients who are unsuitable for these

procedures is intrasphincteric botulinum toxin
injection of the LOS. This is a safe and effective
option but the benefits are of short duration and
treatment is expensive.26
Diffuse oesophageal spasm Diffuse oesophageal
spasm is associated with gastroesophageal reflux
disease (GERD), discussed below. Prominent
symptoms are dysphagia and on occasion, central
chest pain.27 The latter may suggest myocardial
ischaemia due to the severity and radiation to the
neck and jaw (though infrequently to the arms).
Exercise can induce reflux and spasm of the
oesophagus and cause chest pain. Manometry
shows non-peristaltic, repetitive, high-amplitude,
simultaneous, and multiphasic contractions.
Barium studies may be normal or, if spasm occurs
during the study, may show a ‘corkscrew’ oesoph-
agus.
Oesophageal spasm is treated with nitrates
and/or calcium-channel blockers and with treat-
ment directed to GERD. Antidepressant therapy
in patients with severe oesophageal spasm and
major psychiatric disorders has provided dramatic
relief.28 Dramatic resolution of symptoms is
reported after low plasma magnesium was replen-
ished.29 Both these therapeutic successes need fur-
ther confirmation.
Therapeutic agents Some drugs affect oeso-
phageal peristalsis, thus causing dysphagia. These
agents include anticholinergics, tricyclic antide-
pressants, theophylline, calcium-channel blockers
and alcohol.30
Oesophagitis
Gastroesophageal Reflux Disease (GERD) In
older persons, the increased incidence of a hiatus
hernia may increase the occurrence of GERD.
GERD is a consequence of decreased LOS,
enabling the reflux of gastric contents to enter and
damage the oesophageal mucosa. The severity
depends on the frequency and duration of reflux
and the acidity of the gastric contents. LOS tone
is decreased by calcium antagonists, beta-block-
ers, prostaglandins, progesterone, diazepam,
tobacco, alcohol, and caffeine.
Patients complain of retrosternal burning or
discomfort, acid regurgitation into the mouth and
in severe disease due to oesophageal spasm, dys-
phagia and odynophagia and chest pain. In per-
Dysphagia: implications for older people 289
sistent, severe GERD, inflammation and fibrosis
result in stricture formation and severe dysphagia.
Management includes patient education such as
weight loss if needed; the avoidance of highly
spiced foods, alcohol, and caffeine; consuming
minimum fluid with meals (a period of acid secre-
tion); and avoiding tight clothing around the
waist. Acid regurgitation during sleep can be
decreased by not drinking fluids or eating a meal
immediately before going to bed, and by elevating
the head end of the bed with two bricks.
Initial therapy is with an H2 receptor antago-
nist. If this fails, an endoscopy is indicated to eval-
uate if oesophagitis is present. The indications for
protein pump inhibitors (PPIs) are when symp-
toms persist or if endoscopy and biopsy show
severe oesophagitis. If severe chest discomfort is a
symptom (and if myocardial ischaemia is
excluded) an eight-week course of PPIs are indi-
cated but a longer 12-week course may be neces-
sary. The indications for surgery are failed medical
therapy, and evidence of oesophageal ulceration or
strictures.
A complication of chronic GERD is Barrett’s
oesophagus, a premalignant condition, in which
metaplastic columnar epithelial cells replace nor-
mal squamous epithelium in the lower oesopha-
gus. Barrett’s oesophagus is associated with an
increased risk for adenocarcinoma of the oesoph-
agus and the gastric cardia. The extra-oesophageal
complications of severe GERD due to aspiration
are bronchial asthma, chronic cough due to aspi-
ration and bouts of pneumonia, and hoarseness
due to posterior laryngitis.
Infectious causes Older persons who are
immunocompromised by disease or therapeutic
agents such as cytotoxic agents are more suscep-
tible to an infection resulting in oesophagitis. Can-
dida albicans is the most common infectious
agent. Clostridium botulinum causes dysphagia,
blurred vision, and dysarthria by its neurotoxin
affecting the cranial nerves.31 Temporary dyspha-
gia occurs in a small number of patients treated
with botulinum toxin type A for neurologic and
ophthalmologic disorders.32
Therapeutic agents causing dysphagia Some
therapeutic agents commonly prescribed for older
people have the potential to cause oesophageal
injury. Examples are shown in Table 2. Dysphagia
results from drug-induced mucosal irritation, and
290 RN Ratnaike
even ulceration may occur if there is prolonged
oesophageal contact. Tablets should not be swal-
lowed in the semi-supine or supine position,
and/or sufficient fluid should be taken with large
tablets. Older persons should avoid lying down
immediately after medication to prevent possible
oesophageal injury that some drugs may cause.
When alendronate is taken (for osteoporosis) the
manufacturer recommends that the patient not lie
supine for at least 30 minutes.
Radiation injury Radiation injury from therapy
for malignancies of the head, neck, or oesophagus
can cause oesophagitis.
Strictures Strictures are the commonest oeso-
phageal cause of dysphagia due to longstanding
GERD. Stricture formation is frequent after ingest-
ing caustic chemicals such as strong acids or alka-
lis. Other causes are mechanical oesophageal
injury, radiation therapy and, rarely, Crohn’s dis-
ease. Diagnosis is made by radiology. Endoscopy
with biopsy is essential to exclude a malignancy.
Endoscopic dilatation is the treatment of choice
for a benign stricture, though a more recent tech-
nique is endoscopic mucosal injection of cortico-
steroid.
Diverticula Diverticula are not common in the
oesophagus. Traction diverticula are asympto-
matic and located in the mid-oesophagus. Pulsion
diverticula (epiphrenic diverticula) in the mid-
oesophagus are associated with abnormal motor
activity or a structural abnormality and may occa-
sionally cause dysphagia. In instances of signifi-
cant dysphagia, the treatment is diverticulectomy
and surgical myotomy or dilatation.
Webs and rings Webs and rings are associated
with dysphagia in older rather than younger peo-
ple. Webs are very thin luminal protrusions a few
millimetres thick, usually in the upper one third of
the oesophagus.
A Schatzki’s ring is a band-like constriction at
the gastroesophageal junction and is one of the
most common and best known causes of dyspha-
gia.33 In one study of 300 patients with dyspha-
gia, Schatzki’s ring was the second most common
cause (124 patients) after peptic stricture (160
patients),34 though an incidence as low as 3.8%
has been reported.35 Soft foods and well-chewed
foods are swallowed more easily, as are liquids.
Bread and meat are particularly difficult to swal-
low. The problem often occurs while eating steak,
which has led to the term ‘steakhouse syndrome.’
In time patients learn that chewing food well, eat-
ing small quantities and swallowing food with
plenty of liquid eases the dysphagia. Impaction of
food is an important and alarming feature36 and
triggers prolonged oesophageal peristalsis and
spasm and chest pain suggestive of myocardial
ischaemia. Impacted food requires endoscopic
removal.
In some instances, a Schatzki’s ring is not rec-
ognized as the cause of dysphagia for long periods
of time. This is because symptoms of dysphagia
may be intermittent. This lack of consistency of
symptoms confuses both patient and doctor and
psychosomatic issues are attributed or sought to
explain the dysphagia. Diagnosis of a web or a
ring is by radiology and solid bolus challenge,
since endoscopy may not detect either. Treatment
is by dilatation or by surgery.
Systemic conditions In up to 75% of patients
with scleroderma, the oesophagus is sufficiently
affected to result in dysphagia.37 This may precede
skin changes by many years.38 Dysphagia is mul-
tifactorial, due to smooth muscle atrophy and
fibrosis causing decreased oesophageal con-
tractibility and poor LOS tone that culminates in
GERD, chronic oesophagitis, and oesophageal
stricture formation. A management priority is to
control GERD. If a stricture is present, dilatation
is necessary.
Dysphagia is a component of the CREST syn-
drome that consists of calcinosis, Raynaud’s phe-
nomena, oesophageal dysmotility, sclerodactyly
and telangiectasia. In myasthenia gravis, dyspha-
gia may be a presenting problem.
In mixed connective tissue disorders, the
oesophagus is more vulnerable than the rest of the
gastrointestinal tract, resulting in dysphagia.39 In
patients with diabetes mellitus complicated by
amyloidosis and autonomic neuropathy, dyspha-
gia is associated with abnormal oesophageal peri-
stalsis and decreased LOS pressure.40,41
In Parkinson’s disease, oesophageal dysphagia
(in addition to oropharyngeal dysphagia) occurs
due to motor abnormalities. The majority of
patients with Parkinson’s disease have symptoms
of dysphagia, acid regurgitation and heartburn
and in 50% of the patients, noncardiac chest
pain and manometric abnormalities occur.42

Videofluoroscopy shows (in addition to abnor-
malities in the oropharyngeal phase) multiple
oesophageal abnormalities, such as delayed trans-
port, stasis, bolus redirection, tertiary contrac-
tions, and abnormal function of the LOS leading
to GERD.43
Neoplasia Most oesophageal neoplasms are
squamous cell carcinoma located in the lower
third of the oesophagus. Dysphagia may also
occur from direct oesophageal invasion from
malignancies of the stomach, hypopharynx, thy-
roid, and tracheobronchial tree, and from
metastatic carcinoma of malignancies of the lung
and breast, the pancreas, testis, eye, prostate,
bone, cervix, and endometrium. The goal of man-
agement, apart from quality of life priorities, is to
maintain a patent oesophageal lumen by dilata-
tion, by surgical resection, chemotherapy and/or
radiotherapy, endoscopic laser therapy, bipolar
electrocautery, or self-expanding stents.
Extraoesophageal causes Extraoesophageal com-
pression leading to dysphagia occurs infrequently
due to the elasticity and relative mobility of the
oesophagus. Therefore dysphagia occurs only with
significant external compression. Dysphagia luso-
ria is a condition in which a congenital aberrant
right subclavian artery from the thoracic aorta
undergoes atherosclerosis and increased arterial
rigidity and indents the oesophagus. Surgical recon-
struction of the artery relieves the dysphagia. Other
causes of oesophageal compression are a thoracic
aortic aneurysm, a mediastinal mass due to lym-
phadenopathy, lymphoma or left atrial enlarge-
ment, where the mobility of the oesophagus is
restricted by the aorta and is compressed against
the spine.44,45
Management
The optimal management of dysphagia requires
making a rapid diagnosis, based on the history, the
physical examination and appropriate investiga-
tions to confirm the diagnosis and treatment. The
urgency of establishing a diagnosis to effect treat-
ment is especially important in older patients, who
are often malnourished and have concomitant
chronic illnesses. The speech pathologist is an
invaluable member of the team to assist in both
diagnosis and management.
History-taking to determine if dysphagia is pre-
Dysphagia: implications for older people 291
sent and, if so, whether it is oropharyngeal or
oesophageal may not be possible in patients who
have difficulty communicating due to physical ill-
ness or cognitive impairment. This barrier to
obtain a history does not warrant ordering a bat-
tery of investigations. Carers and other witnesses
who have observed the patient at meal times are
a valuable source of information. The observation
that the patient is not eating should not be attrib-
uted to anorexia due to drug therapy or to severe
depression, unless dysphagia is ruled out.
Both carers and patients report (if asked) that
liquids and certain foods are avoided, attempts are
made by the patient to modify the consistency of
food or to eat only foods that are easy to swal-
low, and that meal times are significantly pro-
longed. Rapid weight loss and nutritional
deficiencies are invariable consequences. Evidence
that the patient experiences recurrent bouts of
pneumonia is an important clue to aspiration that
may be silent, as a result of dysphagia. If dyspha-
gia is present, the history aims to establish (among
other issues of onset, severity and complications)
if it is oropharyngeal or oesophageal. If it is
oesophageal, is it due to a motor disorder or due
to luminal constriction?
The history should also include a detailed
review of systems to determine if dysphagia is part
of generalized systemic disease. A complete drug
history, including all over-the-counter medications
must be sought and it is a useful practice for the
clinician to visually inspect all the medications.
The oral cavity should be routinely examined
for conditions that could compromise the oropha-
ryngeal phase. Correcting problems of dentition or
addressing oral pathology may be all that is nec-
essary to resolve the problem of the ‘patient not
eating.’ Careful local examination of the orophar-
ynx and a thorough systemic examination should
be carried out to establish if a neurological prob-
lem or musculoskeletal disease is present. Evidence
of a malignancy such as lymphadenopathy, should
also be sought.
A simple though valuable step at the bedside is
to ask the patient to swallow a small quantity of
liquid and to eat a small portion of food. This may
suggest the type of dysphagia. It is essential to
document and monitor the nutritional status of
the patient. The ‘daily weight’ in the hospital
should not be the sole indicator of nutritional sta-
tus. Any nutritional deficiencies, of protein, vita-
mins or minerals require urgent replenishment.
292 RN Ratnaike
The working diagnosis should be confirmed by
a minimum of investigations. The speech patholo-
gist has an essential role in the diagnosis and sub-
sequent management of dysphagia. An initial
assessment is made of sensory and motor function
of the swallowing mechanisms, airways protec-
tion, phonation, volitional cough and the cough
reflex. A determination of whether the patient is
aspirating should be made. The speech pathologist
directly visualizes the pharyngeal phase, utilizing
endoscopic assessment of swallowing (EAS), a
procedure performed routinely in Australia. EAS
is a convenient bedside investigation enabling
inspection of the hypopharynx and laryngophar-
ynx. Apart from its diagnostic value, EAS is also
invaluable in the management of dysphagia, pro-
viding visual feedback of the patient’s response to
swallowing, information on the response to
manoeuvres to improve swallowing and other
therapeutic interventions. Videofluoroscopy uses a
modified barium swallow to record the dynamic
radiographic examination of the oropharyngeal
phase of swallowing and is recorded on tape for
detailed analysis. Swallowing is assessed using a
variety of graduated food and fluid consistencies.
In requesting radiology, it is important for the
radiologist to be aware of the clinician’s opinion
of the type and possible aetiology of the dyspha-
gia. A barium study is incomplete if the stomach
is not clearly visualized, to exclude lesions
encroaching on the oesophagus. Endoscopy is
essential if an obstructive lesion is suspected. In
addition to direct visualization, a mucosal biopsy
is easy to obtain. In patients with possible motor
abnormalities, manometric studies are necessary.
Once a diagnosis has been reached and defini-
tive treatment decided upon, an important aspect
of management is to maintain optimal nutrition
and hydration and to ensure that the nutritional
support is safe and aspiration is not occurring.
Percutaneous endoscopic gastrostomy (PEG) feed-
ing is preferred to oral or nasogastric feeding if
long-term nutrition is necessary; if nutritional
requirements are not being met; if aspiration is a
problem, or in instances of patient discomfort or
persistent removal of the nasogastric tube by the
patient. Although PEG feeding has major benefits,
it is not without complications, such as aspiration,
re-hospitalization, skin breakdown at the insertion
site and increased morbidity.46 Factors that are
associated with an increased mortality after PEG
are hospitalization with an acute illness, advanced
age, reduced serum albumin concentration, disori-
entation, a higher Charlson co-morbidity score,
and malignancy.47,48,49,50 The Charlson co-morbid-
ity score is a composite score of measures to assess
longitudinal health outcomes.51
The presence of dysphagia should be routinely
sought for in the care of older patients. Carers are
often able to provide useful information on prob-
lems with eating solids and drinking fluids and
avoidance of certain solids, and liquids or other
changes in eating habits. The aetiology of dys-
phagia is extensive. If resources are available, a
team approach involving a speech pathologist is
the best management strategy. The management
priorities are directed to resolving as far as possi-
ble the problem of dysphagia, correcting existing
nutritional deficiencies and providing safe and
optimal ongoing nutrition.
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