Organic Voice Disorders Classification(signs and symptoms), Congenital conditions, infections and mass lesions of vocal folds
Voice disorders fall into three main categories: organic, functional, or a
combination of the two. A voice disorder is organic
if it is caused by structural or physiologic disease,
either a disease of the larynx
itself or by remote systemic or neurologic diseases that alter laryngeal structure or function.
Structural
lesions of the larynx can occur in any
of the tissues of the larynx and vocal folds. These lesions have a
wide variety of causes including congenital conditions, injury, systemic
diseases, infectious and inflammatory conditions, and phonotrauma. Lesions can
interfere with phonation. Some structural disorders interfere more with
respiration than with phonation and some affect both the functions. Feeding and
swallowing can also be affected.
Structural changes of the vocal folds at any age
produce one or more of the following pathologic changes:
§ Increase
or decrease the mass or bulk of the vocal folds or
immediately surrounding tissues
§ Alter
their shape
§ Restrict
their mobility
§ Change
their tension
§ Modify
the size or shape, or both, of the glottis, supraglottic or infraglottic
airway.
§ Prevent
the vocal folds from approximating partially or completely along the vibratory
edge
§ Result
in excessive tightness or irregularity of approximation
§ Result
in irregular chaotic vibrations
Laryngeal problem of a structural origin
may be either congenital or acquired. In either case, they result in a disorder
of pitch, loudness or quality.
The following are the classification of organic disorders of voice:
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Congenital:
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Inflammation:
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Neoplasms: (benign & malignant)
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Trauma:
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Others:
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Atresia
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Laryngitis
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Papilloma
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Contact ulcer
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Sulcus Vocalis
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Cri du chat
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Tuberculosis
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Chondroma
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Vocal nodule
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Presbylarynges
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Laryngomalacia
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Fungal laryngotracheal bronchitis
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Fibroma
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granuloma
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Metabolic disorders
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Stenosis
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Epiglottitis
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Cysts
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Vocal cord polyp
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Neurologic disorders
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Laryngeal web
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Diphtheritic laryngitis
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Malignant
neoplasms
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Reinke’s oedema
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Laryngeal cleft
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Keratosis/leukoplakia
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Laryngocele
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Rheumatoid arthritis
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Laryngeal cyst
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Systemic Lupus Erythematosus
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Subglottic hemangioma
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Relapsing Polychondritis
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Lymphangioma
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Congenital conditions of
larynx
1) Laryngeal atresia:-
Laryngeal atresia is the most rare and most devastating of the congenital anomalies of the larynx. Only
a few studies report documented survivors of such lesions. Failure of recanalization of the
laryngotracheal tube during the third month of gestation leads
to laryngeal atresia.
Clinical
presentation=
Laryngeal atresia
manifests as an acute airway obstruction in the newborn immediately after
clamping the umbilical cord. Examination reveals a neonate with severe
respiratory distress marked by strong respiratory efforts and inability to
inhale air or cry. Without immediate airway management with a tracheotomy
(intubation is unsuccessful), death is imminent. The exception is a child who
has a concurrent tracheoesophageal fistula of sufficient size to permit the
passage of air distal to the obstruction.
Management
The management of
laryngeal atresia involves immediate tracheotomy at birth. If the diagnosis is
anticipated, avoid clamping the umbilical cord until the tracheotomy is secured
to maximize oxygenation of the newborn.
2)
Cri du chat
Infants who are ill or who have
structural differences in the larynx, cry differently from normal infants, and
although certain types of cries are associated with specific illnesses in the
newborn, nonspecific distress cries are often produced at higher than normal
fundamental frequency ( Mallard and Daniloff, 1973). The syndrome of cri du
chat in neonates and children was so named because the voice has a distinctive
high pitched, plaintive wail resembling the cry of a cat, which is immediately
recognizable as different from other infants
3)
Laryngomalacia
It is common congenital laryngeal
disorder which is characterized by pathologically soft and flexible
supraglottic cartilages, particularly the epiglottis. Three structural
abnormalities are associated with this condition.
a)
The epiglottis tends to
be elongated and omega shaped,
rather than broad and flat.
b) The aryepiglottic folds are
unusually short, pulling the epiglottis towards the laryngeal lumen.
c)
The arytenoid cartilages may appear enlarged due to excessive amount of
overlying bulky tissue.
Because
the aryepiglottic folds do not have enough firmness to
withstand the negative pressures created by
inspiration, they are sucked inwards and collapse as the child inhales. This
causes the airway to be obstructed.
The etiology of laryngomalacia is uncertain.
The voices on exhalation, during crying, and during other types of phonation
may sound normal, but on forced exhalation and inhalation there is a low
pitched vibratory fluttering or a high- pitched crowing, more often
intermittent than constant. The primary symptom is inspiratory stridor. Other
symptoms may include wheezing, barking cough, frequent respiratory infections
and cyanotic episodes ( Rohde and Banner, 2006). The stridor is more common
when the infant is supine than prone. It is often when the child is around 6
months of age, and then gradually starts to improve.
While most cases of laryngomalacia do resolve
spontaneously, the condition occasionally persists to an older age particularly
in children with neuromuscular disorders such as cerebral palsy.
Evaluation and treatment
Flexible laryngoscopy is the best way to
diagnose and determine the degree of severity of laryngomalacia.in more severe
cases rigid laryngoscopy or bronchoscopy may be necessary ( Ritcher &
Thompson, 2008).
Until 1980’s , the standard procedure for severe laryngomalacia was
tracheostomy. Since that time a variety of techniques known collectively as
supraglottoplasty have been developed. It has been shown to be safe and
effective in relieving stridor and other airway symptoms. These are endoscopic
techniques that may involve fixating the epiglottis to prevent it from being
pulled inward( epiglottopexy) and / or removing excess tissue to enlarge the
airway.
4)
Subglottic Stenosis
Subglottic
stenosis is the third most common cause of stridor in the neonate after laryngomalacia
and vocal cord paralysis. Involves narrowing of the subglottic lumen in the
absence of trauma
(intubation). Arrested
embryonic development of the conus elasticus and maldevelopment of
cricoids cartilage will produce an obstructive narrowing of the airway from the
level of the vocal folds down to the cricoids area, the point of maximum
obstruction being 2 to 3 mm below the glottis. The voice will be stridorous
from birth, but sometimes it will be present only during respiratory
infections. The voice during cry is usually normal.
Etiology
I.
Congenital SGS
A.
Membranous
1. increased
fibrous connective tissue
2. hyperplastic
submucous glands
3. granulation
tissue
B.
Cartilaginous
1. cricoid
cartilage deformity
a. small cricoid
b. elliptical
cricoid
c. large anterior
lamina
d. large
posterior lamina
e. generalized
thickening
f. submucous
cleft
2. trapped first
tracheal ring
II. Acquired
SGS
A.
Intubation
B.
Laryngeal trauma
a. previous
airway surgery
- high
tracheotomy
-
cricothyroidotomy
- prior surgery
for respiratory papillomatosis
- prior laser
surgery for SGS
b. accidental
1. inhalational
(thermal or caustic)
2. trauma (blunt
or penetrating)
C.
Autoimmune
D.
Infection
E.
Gastroesophageal reflux (GER)
F.
Inflammatory diseases
a.
Anti-neutrophil Cytoplasmic Autoantibodies (C-ANCA)
b. sarcoidosis
c. Systemic
lupus erythematosis
G. Neoplasms
III.
Idiopathic SGS
There are two
types of congenital subglottic stenosis: membranous and cartilaginous.
Membranous is
usually circumferential, soft and dilatable, in contrast, the cartilaginous has
a
more variable
appearance. Mild-normal shape with narrowed lumen, or can have abnormal
shape of cricoid
cartilage with prominent lateral shelves giving an elliptical appearance to the
lumen.
Symptoms
Symptoms of
upper airway obstruction dominate, with inspiratory stridor, progressing to
biphasic as
obstruction worsens. Stridor is an important symptom of SGS as well as
many other causes of neonatal obstruction. The characteristics of stridor can
be a clue as to where the obstruction is occurring. Three distinct zones have
been identified, the supraglottic/supralaryngeal zone, the extrathoracic
tracheal zone which includes the glottis and subglottis, and the intrathoracic
trachea. Supraglottic stridor is high-pitched, and inspiratory.
Management
If the respiration is significantly
affected, surgical reconstruction is likely to be required, and there can be
long term consequences for voice. Stenosis involving soft tissues may resolve
spontaneously during childhood.
5)
Laryngeal Web
A web of tissue covering part or
all of glottis may be present at birth because of its failure to separate
during the 10th week of embryonic laryngeal development. Laryngeal web are often congenital,
about 75 % of them occuring at birth
(Blustone and stool, 1983). and are a result of incomplete maturation of the
developing larynx. Webs are often manifested as a sheet of tissue between the
vocal folds, usually at the anterior end. Webs can block upto 75 % of the
glottal airway in severe cases and the thickness can vary from very thin and
translucent to very thick.
Classification:
Type
1 glottic web
- Uniform
in thickness
- No
subglottic extension
- True
vocal cords clearly visible in web
- Although
there is usually no airway obstruction, voice dysfunction is common.
- Hoarseness is usually only slight.
Type
2 glottic web
·
Slightly thicker, with a significantly thicker anterior component.
·
True cords are usually visible within the web
·
Subglottic involvement is minimal.
·
The web restricts the airway by 35 to 50%
·
Usually causes little airway distress
·
The voice is usually husky.
Type
3 glottic web
- A
thick web that the anterior portion of the web is solid and extends into
the subglottis
- The
true vocal cords not well delineated.
- The
web restricts the airway by 50 to 75%, obstruction is moderately severe.
- Marked
vocal dysfunction, with a weak and whispery voice.
Type
4 glottic web
- The web is uniformly thick
- Extends
into the subglottic area with resulting subglottic stenosis.
- Occluding 75 to 90% of the airway.
- Respiratory obstruction is severe, and
the patient is almost always aphonic.
Supraglottic
webs
- Diaphragmatic growths of differing
thickness that partially occlude the supraglottic lumen.
- Symptoms depending on the size and
position of the web
- Voice changes and dyspnea.
Posterior
glottic web
- Rare but usually consists of a thin
membranous sheet between the posterior true vocal folds.
Perceptual signs and symptoms
Typically,
the major signs are hoarseness, and a high pitch. The web will interfere with
the normal vibratory movements resulting in hoarseness. The high pitch may be
due to shortening of the effective vibrating length of the vocal fold due to
the attachment of the web between the two vocal folds. The person may also have
difficulty in sustaining phonation, depending on the extend of the web.
Typical symptoms in the child include a weak
cry, difficulty breathing, and stridor. In the adult, the complaint is
hoarseness, high pitch, and perhaps, shortness of breath. Small webs at the
anterior commissure may present few
problems, whereas extensive webs could necessitate a tracheotomy.
Acoustic signs
Little
data exist on the acoustic signs of a laryngeal web. One would expect acoustic features
consistent with increased frequency and amplitude perturbation. If the patient
has a higher- than- normal pitch level, a higher than normal fundamental
frequency of phonation would be expected.
Measurable physiological signs
Since the
web would restrict the vibratory amplitude of the vocal folds, a decreased
airflow might be expected. Air pressure could be elevated if the patient is
trying to force vibration.
Observable physiological signs
Stroboscopically,
the patient with a web would show decreased amplitude of vibration and no
mucosal wave in the area of the web. If the voice is hoarse, the periodicity of
the vocal fold vibration will be affected. But the basic endoscopic procedures
will not be able to define the extent/thickness of the web. In order to
determine these parameters, direct laryngoscopy in the operating room and
bronchoscopy are necessary (Tewfik, 2006).
Pathophysiology
The
attachment of the tissue to the margins of the vocal folds would limit their
vibratory motions and produce instability. Moreover, the attachment of the web
would limit the vibrating length of the vocal folds producing a higher than
normal pitch. Often, voice symptoms take a back seat to establishing an airway,
thus making it easier for the patient to breathe.
Management
Treatment
typically consists of surgery to split the web, but, unless the surgery is
carefully performed, the possibility of a refusion of the web is very possible.
Management
of laryngeal webs involve resection of the web using either a knife or laser
procedure. A keel may be placed between the vocal fold edges to prevent
rescarring of the surgical site.
[a keel
is a stent designed to keep the anterior commissure area from closing. It is
typically made of silicone.]
6)
Laryngocele
Laryngeal ventricle is the space
between the true and false vocal folds and is filled with mucous and other
fluid producing glands. The anterior portion of the ventricle leads upwards
into a little pouch called the saccule. A laryngocele is the dialation or
herniation of the saccule extending upward within the false vocal fold. It is
usually filled with air, although mucous can also be present.
There are three types of laryngoceles:
Internal laryngoceles are those in
which the inflated tissue does not penetrate the thyrohyoid membrane, but
instead pushes against the false vocal folds and / or aryepiglottic folds,
which consequently looks swollen.
External laryngoceles
protrude through the thyrohyoid membrane , forming a bulge or swelling on the
side of the individual’s neck.
A combination laryngocele has features
of both internal and external types and has to be found to be the most common
type of laryngoceles ( Devesa et. Al, 2002).
The
cause of laryngoceles is mostly from excessive pressure within the larynx. This
is found in wind instrument players, weight lifting or habitual excessive
coughing due to asthma or smoking.
Symptoms include dyspnea, cough,
inspiratory stridor, dysphagia, globus etc.
Diagnosis and treatment:
The best way to diagnose laryngocele is by CT scan followed by
laryngoscopy. Depending upon the mass, and the patient’s symptoms, the disorder
may be left untreated except for periodic observation, or the laryngocele may
be aspirated or excised by means of endoscopic CO2 laser resection. In severe
cases tracheostomy may be recommended.
7)
Laryngo-tracheal cleft
Embryonic failure of fusion of the dorsal
cricoid lamina leaves an interarytenoid cleft and an open larynx posteriorly.
The cry is weak, feeble or aphonic. Feeding difficulties and survival initially
overshadow the voice disorder.
8)
Laryngeal cyst
Laryngeal cysts are uncommon congenital anomalies of the larynx.
Congenital saccular cysts represent 25% of all laryngeal cysts.
Etiology and pathogenesis
Obstruction of the laryngeal saccule orifice in the ventricle leads to
retention of mucus, which causes saccular cysts. Ductal cysts arise from
blockage of submucosal mucus glands. These cysts can occur in the vallecula,
subglottis, or vocal cords. They are common in the subglottis after prolonged
intubation because of irritation and blockage of submucosal glands.
Clinical presentation
Mild symptoms, varying degrees of airway obstruction, an inaudible or
muffled cry, or dysphagia can accompany laryngeal cysts.
In a small number of patients, the saccular swelling may cause an
external neck mass. Endoscopy reveals a bluish pink cystic lesion behind the
aryepiglottic fold (lateral cyst) or emanating from the ventricle and
protruding into the laryngeal lumen (anterior cyst).
Diagnosis
Endoscopy is the procedure of choice for aiding in the diagnosis of
laryngeal cysts.
Management
If emergent management of a saccular cyst is necessary, endotracheal
intubation is usually possible. Needle aspiration or incision of the lesion may
be performed as a temporary measure, but definitive management requires
endoscopic or open complete cyst excision to prevent recurrence. Forceps or
laser excision can remove ductal cysts if symptoms accompany the cysts.
9) Subglottic
hemangioma
Subglottic hemangiomas
account for 1.5% of all congenital anomalies of the larynx. Females are
affected twice as often as males.
Etiology and
pathogenesis
Subglottic hemangiomas develop as a result of a vascular malformation
derived from the mesenchymal rests of vasoactive tissue in the subglottis.
Clinical presentation
The child is usually asymptomatic at birth. As the lesion rapidly grows
from age 2-12 months, the child develops progressive respiratory distress that
is initially intermittent and then continuous. Symptoms are similar to those of
infectious croup, manifesting with biphasic stridor, barking cough, normal or
hoarse cry, and failure to thrive. Most patients develop airway obstruction
significant enough to necessitate intervention.
On examination, the child with a subglottic hemangioma may or may not be
in significant respiratory distress (nasal flaring, supraclavicular or
intercostal indrawing, cyanosis). Head and neck examination findings are
usually normal, although half of these patients may have cutaneous hemangiomas
of the head and neck. Flexible endoscopy does not demonstrate the lesion but is
a necessary procedure to exclude other laryngeal anomalies.
Diagnosis
Rigid bronchoscopy is necessary to establish a diagnosis of subglottic
hemangioma. The lesion is usually located posterolaterally in the submucosa in
the subglottis. It may be unilateral or bilateral, or it may be located in the
upper trachea. The lesion is pink-blue, sessile, and easily compressible (see
the image below).
When the diagnosis is unclear, perform biopsy of the lesion with caution
because of the risk of significant hemorrhage. Plain radiographs of the neck
may show an asymmetric narrowing of the subglottis, which may aid in
establishing the diagnosis prior to endoscopy.
Management
Observation usually suffices for small lesions, which do not cause
significant airway obstruction. Tracheotomy is typically necessary to secure
the airway until the lesion spontaneously regresses, usually by age 5 years.
Steroid injection , carbon dioxide laser ablation, cryosurgery,
intralesional interferon or sclerosing agent injection, and systemic steroids
etc are successful for the treatment. Open surgery has been used immediately
after diagnosis as primary intervention rather than after failure of other
therapies.
10) Laryngeal
Lymphangioma
Epidemiology
Laryngeal lymphangiomas are rare congenital anomalies of the larynx.
Half the cases are diagnosed in the neonatal period, and 75% are diagnosed by
age 1 year.
Etiology and pathogenesis
Lymphangiomas originate from lymphatic vessel malformations.
Clinical presentation
Individuals with laryngeal lymphangioma may be asymptomatic or may
present with significant airway obstruction when the lesions attain a large
size. Upper respiratory tract infections may precipitate symptoms by causing a
rapid increase in the size of these lesions.
Diagnosis
Endoscopy is the procedure of choice for aiding in the diagnosis of
laryngeal lymphangiomas.
Management
Tracheotomy is often necessary to establish an airway in patients with
laryngeal lymphangiomas. The large size and locally invasive nature of these
lesions often complicate excision. Laser ablation of these lesions is the
mainstay of current therapy.
Sclerosing agents are under investigation as a possible treatment
modality for laryngeal lymphangiomas.
Infectious conditions of larynx
Inflammation
is a regulatory process in which cellular and chemical reactions in blood
vessels and connective tissues in response to injury and defence against
harmful stimuli.
1.
Laryngitis
Laryngitis
is an inflammation of the vocal folds and larynx. It may result from exposure to noxious agents
(tobacco, alcohol, drugs), acidic gastric contents (GERD), environmental agents
(allergens, dust), or vocal abuse.
Laryngitis may also be the result of upper respiratory infections, which
have a generalized effect on the mucosa of the respiratory tract, including the
larynx. The problem may be acute or chronic.
Acute laryngitis resulting from bacterial infection is not directly
related to vocal abuse. However, it does
affect voice production and indirectly may be aggravated by abuse, as will be
described later. Chronic causes are more typical of adults (Koufman, 1996).
Chronic abuse of voice can lead to
chronic laryngitis with persistent inflammation and perhaps a thickening of the
vocal folds. Laryngitis may lead to
tissue changes, such as nodules, polyps, or hypertrophy of the laryngeal
epithelium.
Laryngitis can be acute or chronic
Acute Larngitis:
·
The nonspecific term ‘laryngitis’ is used
to describe an inflammation of the vocal fold mucosa, with mild to severe
dysphonia with lowered pitch and intermittent phonation breaks. The condition
is usually associated with upper respiratory inflammation due to bacterial,
viral or fungal infections or behavioural trauma ( e.g, vocal abuse)The condition
usually begins abruptly, and typically the infection is self- limiting, lasting
upto around 10 days ( Koufman, 1996). It
can be of two types:
·
Infective:
It is usually viral and occurs in
association with an upper respiratory tract infection. In most cases, it is
self limiting and resolves spontaneously, but in some cases secondary
infections compound the primary problem. Laryngeal infections commonly acute
mucosal inflammation which is sometimes accompanied by oedema. The degree to
which the condition affects voice is generally proportional to the severity of
the condition, with voice problems ranging from aphonia to slight hoarseness.
·
Non-
infective: An acute inflammation of the
laryngeal mucosa can also be caused by a range of laryngeal irritants from an
episode of laryngeal abuse, such as shouting at a football game, to exposure to
a polluted atmosphere. The voice will be hoarse and aphonia may occur. The
condition usually improves after 2 or 3 days if the voice is rested and not
subjected to further abuse.
Symptoms
·
Odynophonia( pain while
talking)
·
Dysphagia
·
Odynophagia (painful
swallowing)
·
Dyspnea.
Perceptual
Signs and Symptoms
The
symptoms of laryngitis include marked roughness or hoarseness of the voice with
accompanying sensations of discomfort and dryness in the throat. When secondary to infection, the hoarseness
may persist for some time after the infection has been controlled. Continued heavy use of the voice during this
time may contribute to the laryngitis and the continued hoarseness. The pitch level of the voice may appear to be
either higher or lower than normal, and it will be difficult to speak in a loud
voice.
Evaluation:
Laryngitic larynges in the acute stage
show a marked redness; small, dilated blood vessels may be visible on the
inflamed folds. Chronic laryngitis may
not be marked by inflammation, but rather by thickened epithelium.
The vocal folds may show increased
asymmetry and aperiodicity, with reduced mucosal waves and reduced amplitude.
While most types of
acute laryngeal infections are relatively benign, some are more dangerous,
particularly in the case of infants and very young children. Acute
laryngotracheitis, commonly called as croup, is a disease affecting young
children. The subglottal area tends to be more severly inflamated, and the
child develops the characteristic ‘barky’ cough, as well as hoarsness and
inspiratory stridor. The disease can be life threatening depending on how
severly the airway is obstructed.
Another serious form of
laryngitis is acute supraglottitis( epiglottitis). Both adults and children can
be affected. But it is more commonly seen in children. Epiglottis may be life
threatening if the epiglottis becomes sufficiently enlarged to result in airway
obstruction. Emergency treatment may be
required. Antibiotics may be used to
control the infection or steroids may be used to reduce the inflammation
(Sataloff, 1987).
Treatment
The most effective treatments for acute laryngitis include external and
internal hydration, antibiotics, if prescribed and rest. Mucolytics such as
guaifenesin may be helpful in thinning and clearing secreations. Occasionally a
cough suppressant may be prescribed to limit additional damage to the vocal
folds.
Chronic Laryngitis
Laryngitis that lasts for more than 3 weeks is classified as chronic (
Shah & Shapshay, 2006). The ongoing inflammatory process may damage the vocal
fold epithelium resulting in hyperkeratosis ( thickening of the mucosal
membrane), fibrosis and scarring. Chronic laryngitis id the result of excessive
smoking, alcohol, environmental pollutants, toxic products, vocal abuse etc.
Stroboscopic examination
reveales a jerk-like movement of the mucosal wave, in which the wave appears to
travel along part of the surface at one speed, then changes its speed for the
remainder of its travel. The movement
may also be called biphasic (Woo, personal communication, 1988). There is a stiff, jerky quality to this
movement.
Pathophysiology
Laryngitis
affects the cover of the vocal folds by increasing its stiffness, with little
effect on the mass of the vocal folds.
Chronic
laryngitis, if allowed to continue untreated, may result in serious
complications, including laryngitits sicca, which is characterized by marked
atrophy of the mucosa of the larynx. The
major abnormality is the lack of vocal fold lubrication due to the reduction or
absence of glandular secretions. The
vocal folds will become dry and sticky, and a chronic cough may be present as
the system attempts to remove the thick secretions on the vocal folds. On occasion, laryngeal crusting may result,
requiring surgical removal.
Other
forms of laryngitis result from diphtheria, tuberculosis, and syphilis, all of
which are extremely rare.
2) Tuberculous Laryngitis:
Tubercles
appear on the swollen mucosa of the epiglottis and arytenoids, which break down
and form greyish ulcer. Severe pain is usually present. It is almost always
secondary to the pulmonary lesion. It may be: Sputogenic., hematogenic Or carried by lymph stream.
Pathology:
With sputogenic type of infection the
tubercle bacillus can infect the intact laryngeal mucosa, the submucosal layer
become infected and small round cell infiltration occur. One or more surface
nodules soon appear which caseate and leads to ulceration and later on there
will be formation of granulation tissue and cellular swellings which is called
pseudo-edema.
Clinical
features:
Weakness of voice with periods of aphonia.
Hoarseness
Cough is a prominent symptom.
Pain on swallowing if the laryngeal inlet is
involved.
Referred otalgia is common.
Dyspnea rarely.
Localized tenderness is rare unless perichondritis
is present.
Laryngoscopic
appearance:
- Slight impairment of
adduction.
- Ulceration of the edge
of the cord (mouse-nibbled)
- Granulation in the
interarytenoid region or on the vocal process of the arytenoid cartilage.
- Edema of the mucosa of
the ventricle.
- Pseudo-edema of the
epiglottis and arytenoids (turban larynx) of a pale sausage-like
appearance, with occasional small bluish superficial ulcers.
- Vocal cord paralysis
may occur from apical pulmonary disease, this affect the right side more
commonly than the left.
Treatment is that of the general infection.
3) Cricoartenoid and cricothyroid Arthritis
Rheumatoid arthritis is a chronic
immunologic and inflammatory disorder that disrupts the normal structure and
function of synovial joints, including cricoarytenoid and cricothyroid joints.
Vocal fold inflammation and edema may accompany arytenoids mucosal erythema.
During
symptomatic periods, laryngeal function for both respiration and voice
production may be compromised by pain, swelling and in most severe form,
mechanical fixation or ankylosis ( fusion) of the cricoarytenoi joints.
Mechanical fixation or ankylosis cannot be determined visually, due to possible
confounds with paralysis, rather diagnosis may be through direct palpation. The
fixation may occur unilaterally or bilaterally and at any point along the
cricoid rim, from midline to laterally abducted positions. Thus resulting
airway and voice complications cold include aspiration risk and breathy aphonic
voice quality in cases of bilateral lateral fixation. In rare cases of
bilateral arytenoids midline fixation, the airway obstruction requires a
tracheostomy or unilateral arytenoidectomy to re- establish adequate
ventilation. Unilateral arytenoids fixation at midline creates stridor and
dysphonia that can usually be managed with anti-inflammatory and corticosteroid
medications, to relieve the exacerbation.
4) Chemical sensitivity/
Irritable Larynx Syndrome
Some individuals appear to develop
consistent and repeated sensitivity to airborne chemical exposures that trigger
abnormal airway and voice changes, including dysphonia, weak voice quality and
vocal fatigue. These responses are highly individualized and impossible to
predict on the basis of patient or chemical features.
ILS
is the term given to the cluster of symptoms reported commonly including one or
more of the following: dysphonia following exposure, airway distress, globus,
chronic cough, throat pain or dryness and reflux. Symptoms may exacerbate,
plateau or recede, some lasting only brief periods of time, while others
persist for years. Treatment typically includes anti- reflux medications and
reasonable precautions against repeated exposure to chemical stimulants, if
known.
5) Laryngo- Tracheal Bronchitis (Croup)
It is an acute inflammatory
disease of the larynx and lower respiratory tract predominantly involving
subglottis, trachea and tracheobronchial tree.
Etiology:
It is seen in children below 5 years.Causative agent is Myovirus/
Para- influenza virus type A and B with Secondary bacterial invasion (Hemophilus influenzae,
pneumococcus, hemophilytic streptococci).
Clinical
features:
Initial
presentation of URTI with Acute,
rapidly progressive symptoms, Restlessness and refusal to take food,
Marked fever, toxic with increased pulse rate,
Cry may be weak, Croupy cough – “Seal’s bark” is most
prominent at night, Inspiratory/
biphasic stridor, Air
hunger, hypoxia and cyanosis may be present in severe stridor.
6)
Epiglottitis:
It is an acute inflammatory condition involving the supraglottis, caused by Haemophilus
influenzae type B, which is common in children, and may lead to fatal
respiratory obstruction. Most
cases are seen between 1 and 6 years of age, with a peak incidence between ages 3 and 4
Causative agent: Hemophilus
influenzae-type B.
Clinical Features:
Rapidly progressive
symptoms starting with an URTI,
High fever and Sore throat, Dysphagia/ Odynophagia,
Muffled voice/ hot potato voice,
Inspiratory stridor,
Pharynx congested and pooling of saliva,
Cherry red epiglottis
7) Larygeal diphtheria:
Laryngeal
diphtheria is often seen secondary to faucial diphtheria. Primary laryngeal
diphtheria is rare. Causative agent: Corynebacterium diphtheria.
Children below ten years are commonly affected.
The incidence has been drastically reduced following
immunization
Clinical
features:
Onset
is insidious. Hoarseness
of voice is the first symptom, Croupy cough (hoarse) is the initial feature ,Stridor is the prominent feature which is inspiratory
and is often accompanied by cyanosis and recession of chest wall,
Membrane can be
seen over the vocal cords and laryngeal vestibule.,
Cervical lymphadenitis is usually present in
association with faucial diphtheria. Examination of throat shows characteristic grey
membrane in oropharynx which may spread to larynx,
Enlarged tender cervical lymph nodes are also seen.
Inflammatory Autoimmune
diseases:
1) Systemic
Lupus Erythematosus
It is a progressive disorder that damages
connective tissues, blood vessels and mucous membranes (Ozcan et al., 2007).
Symptoms include inflammation, infection, subglottic stenosis and epiglottitis.
Cricoarytenoid arthritis occurs relatively commonly in conjunction with SLE,
and recurrent laryngeal nerve damage with resulting vocal fold paralysis.
Laryngeal symptoms range in severity from mildhoarsness to life threatening
airway obstruction. Treatment is usually administration of systemic corticosteroids
to reduce laryngeal symptoms.
2) Relapsing
Polychondritis
It is characterized by recurring episodes
of inflammation of connective tissues, particularly affecting the cartilages of
the ears , nose, larynx, trachea, blood vessels etc. this disorder occurs in
conjunction with rheumatoid arthritis and other connective tissue diseases.
When the larynx, trachea and bronchi are involved, the disease can be very
serious, because the supporting cartilages of these structures collapse,
causing respiratory problems. RP is more prevalent in females and its peak
onset is in the middle years.symptoms include hoarsness, aphonia, tenderness
and swelling over the thyroid cartilage, cough, dyspnea, wheezing and choking.
The most serious aspect of the disease is airway obstruction, which can result
due to subglottic edema, laryngeal and tracheal ring collapse or tacheomalacia.
Treatment is typically corticosteroids and immune system suppressants ( Bandi
et al., 2002).
Mass Lesions of Larynx
- Vocal nodules (singers’/screamers’
nodules)
Appearance and site: vocal nodules are
non-malignant minute neoplasms seldom exceeding 1.5 mm in diameter. They are
symmetrical, bilateral lesions usually occurring at the junction of the
anterior and middle thirds of the vocal folds, the midpoint of the membranous
vocal folds.
VF nodules occur, therefore, at the site
of greatest vibratory amplitude and maximum impact.
Occasionally, diagnosis of unilateral
nodule is made and in these cases some reddening or slight sweeling will
commonly be apparent on the contralateral vocal fold, caused by the irritative
action of the node.
Specific aetiology:
Titze (1994a) uses the analogy of hands
clapping to illustrate the impact of the vocal fold surfaces across the
glottis: the force of the impact is greater when the free edges of the VFs are
far apart at the onset of closure. Jiang and Titze (1994) report that, after
the impact phase of VF adduction, there is a pre-open phase during which
intraglottal pressure increases as the result of subglottal pressure being
applied to the tissue, starting from the inferior surface and ending at the top
lip of the vocal fold.
Vocal nodules tend to occur more
frequently when voices are loud and high pitched.
Starting with local inflammation and
oedema, the nodules appear initially as soft red swellings on the free edges of
the fold. At this stage, nodules are either oedematous or telangiectatic, if
the trauma has been sufficiently violent to injure microvessels (Remacle,
Degols and Delos, 1996). It is possible to reverse the changes at this stage
with voice therapy. If there is no intervention, the swellings gradually
fibrose and harden as connective tissue proliferates and chronic nodules, white
in colour and conical in shape, become established.
Incidence:
®
vocal nodules are the
most commonly occurring vocal fold lesions caused by hyperfunction. They occur
more commonly in children and more frequently in boys than girls under the age
of 20 years (Heaver, 1958).
®
After adolescence, the
incidence decreases in males and increases in females and the highest incidence
appears to in young to middle-aged women.
®
Fritzell (1996)
postulated that women have a greater need to speak than men and female voice is
less able to cope with the demands made upon it.
Perceptual signs and symptoms
®
Hoarseness and
breathiness are the major perceptual signs of nodules.
®
Some individuals complain
of soreness or pain in the neck lateral to the larynx that may radiate upward
to the ear or downward to the upper chest.
®
Some have the sensation
of something in the “throat” that they need to try to clear.
®
Difficulty in producing
pitches in the upper third of the range is a complaint especially true for
singers.
®
The degree of hoarseness
and breathiness present may be related to the size and firmnesss of the nodules
and may vary from slight to moderately severe.
®
Specific sensory
features: Before vocal nodules become fibrosed, the patient may complain of
episodes of marked laryngeal soreness after vigorous voice use, in addition to
the sensory feature associated generally with MTD. With increasing fibrosis of
the nodules, soreness usually disappears.
Laryngoscopic findings:
Bilateral nodules in the classic position
at the midpoint of each membraneous vocal fold (i.e. at the junction of the
anterior third and posterior 2/3rd of each VF) create an
hour-glass-shaped glottis chink.
The area surrounding the nodules might be
inflamed and oedematous.
On stroboscopy, the mucosal waves will be
reduced throughout the fold and absent in the area of each nodule when the
nodules are fibrosed and hard, but can be seen to travel over soft, oedematous
nodule.
Advanced, white, fibrosed nodules obstruct
VF approximation.
Differential diagnosis:
®
A submucosal cyst and the
traumatised area on the contralateral VF have a similar superficial appearance
to bilateral VF nodules is easily made in children where a hoarse voice and
vigorous vocal use are seen so frequently.
®
An abnormal voice since
birth is a common feature of the history of a cyst, although careful
Laryngoscopic examination frequently reveals that lesions are of significantly
different sizes.
®
On stroboscopy, the cyst
might be distinguished from the traumatised area on the opposing fold by
differences in the mucosal wave.
Expected vocal profile:
®
The voice is hoarse with
elements of roughness and breathiness. These features arise in part from the
glottal insufficiency that occurs as the nodules meet.
®
Impaired mucosal waves
contribute further to the rough vocal quality.
®
As a result of increased
mass of the VFs, which then vibrate at a lower frequency than normal and thus,
vocal pitch is lowered.
®
When vocal nodules are
soft, the clarity of the vocal note can be considerably improved by increased
hyperadduction.
Acoustic analysis profile:
reduced speaking Fundamental frequency, reduced harmonics-to-noise ratio and
reduced intensity when nodules well established are the common features.
Summary:- vocal fold nodule profile
|
Pathology
|
VF nodules (singers’/screamers’ nodules)
|
|
Aetiology
|
Trauma to the VF mucosa resulting from
hyperfunctional phonation
|
|
Signs & symptoms
|
Gradual onset of hoarseness, initially episodic but
eventually constant, effortful phonation and vocal tract discomfort
|
|
Laryngoscpic findings
|
B/l mass lesions at the junction of the anterior
third and posterior 2/3rd of the VFs
Soft or fibrosed: soft nodules may range from minute
to large; fibrosed nodules re small, hard, white and horn-shaped
Typical hour-glass glottis chink
Reduced Vf vibration
Mucosal wave may travel across soft nodules
Mucosal wave absent in region of fibrosed nodules
Supraglottic activity.
|
|
Expected vocal profile
|
Breathy/ rough vocal note
Voiceless segments
Low pitch and reduced pitch range
Voice deteriorates with use
|
|
Acoustic analysis
|
Reduced speaking F0
reduced harmonics-to-noise ratio
reduced intensity when nodules well established
|
|
Airflow and volume measures
|
Usually, high transglottal airflow
In some cases of soft nodules, the VFs are
hyperadducted so that subglottal air pressure is high.
|
|
Medicosurgical decisions
|
Voice therapy is the treatment of choice in most
cases
Phonosurgery may be required in cases of fibrosed
nodules, but voice therapy is essential inorder to change vocal behaviour and
prevent recurrence.
|
Medicosurgical decisions
®
Voice therapy is the
preferred course of treatment for nodules, however large, while they are soft
and while fibrosis is absent or minimal.
®
Surgical intervention
should be avoided if at all possible, inorder to minimize the risk of damage to
the layers of lamina propria. When nodules are removed by laser and although
the vocal folds look normal on indirect laryngoscopy, stroboscopic examination reveals reduced or absent mucosal
waves at the site of the excised lesions.
®
If there are doubts
concerning the appropriate intervention route,
atrial programme of voice therapy should be instigated initially.
®
Fibrosed nodules require
surgical removel but surgery should be preceded by voice therapy inorder to
reduce inflammation and surrounding oedema and to give the patient insight into
prevailing vocal behaviours.
®
Microsurgery should
always be preceded by advice from a SLP and followed by voice therapy as soon
as possible.
®
Postoperatively, the
voice should not be used until re-epithelialisation of the VFs has taken place,
usually a period of approx 3 days. During this period forced whispering can
cause damage; to produce a forced whisper, the anterior 2/3rds of the VFs are tightly
adducted and air passes through the triangular posterior glottis chink under
pressure.
- Polyps
Appearance
and site:
VF polyps are either pedunculated or
sessile. A pedunculated polyp is attached at its base and has no stalk. The
typical site is 3mm behind the anterior commissure on the free edge or the
subglottic surface of the VF. According to Jackson (1941), a polyp is larger
and more vascular, edematous and inflammatory than a nodule.they may also
involve almost the entire length of the VFs.
Polyps usually occur in Reinke’s space
(superficial layer of lamina propria) and may consist of dilated blood vessels,
fibrotic tissue and small haemorrhages.
Specific aetiology
®
Polyps tend to be the
result of acute trauma to the VF mucosa, in combination with infection,
allergy, pollution or endocrine disorders (Remacle, Degols and Delos, 1996).
®
Histologically, there are
several types of polyp which appears as a soft, translucent structure. If small
blood vessels have been affected by the vocal trauma, submucosal bleeding in
combination with connective forms a haemorrhagic polyp.
®
The majority of polyps
occur singly (one at a time). In a series of 100 operated cases, Kleinsasser
found that 79% were single and 21% presented with two or more polyps.
®
It is generally accepted
that hyperfunctional VF adduction is the chief cause of VF polyps (Luchsinger
and Arnold, 1965; Morrison, Nbichol and Rammage, 1986).
®
Luchsinger and Arnold
(1965) consider that polyps and nodules have the same etiology and differ only
in degree. Polyps can result from a period of vocal abuse and can even occur as
a result of a single traumatic incident, e.g. yelling at a basketball game.
Incidence
VF polyps are the 2nd or 3rd
most frequently occurring lesions resulting from vocal abuse.
Polyps were frequent in middle aged males
and females (Nagata. K et al, 1983).
Perceptual signs & symptoms
®
In addition to various
elements of vocal tract discomfort experienced by many with hyperfunctional
dysphonia, patients with polyps, frequently report a sensation of ‘something in
the throat’.
®
Patients have difficulty
in clearing mucus secretion from the larynx. As a result, throat clearing is
vigorous and frequent.
®
Typical perceptual signs
of polyp include hoarseness or breathiness.
Laryngoscopic findings
®
Polyps often can be
visualized with standard laryngoscopy. They appear as rather large masses on
one VF, sometimes witha very broad base, sometimes attached to a stalk.
®
Polyps range in size from
the equivalent of a small ‘blood blister’ to a large pedunculated mass. When
the polyp is on the free edge of the VF, it is easily visualised, but some
large polyps that hang into the subglottis are only fully visualised as they are
blown superiorly into the glottis during phonation.
®
All polyps affect glottis
competency on VF adduction; the size and shape of the glottis chink depend on
the size and position of the polyp.
®
On stroboscopy, the polyp
inhibits mucosal waves on both the VF site of the lesion and the contralateral
VF. Amplitude of VF movement will be decreased.
Differential diagnosis
®
If the lesion is diffuse,
it may cover one-half to two-thirds of the ntire length of the VF and is
usually referred as polypoid degeneration or Reinke’s edema. The distinction
between polyp and polypoid degeneration is sometimes confusing.
®
Small sessile polyps can
present as unilateral VF nodules and as stated by Remacle, Degols and Delos
(1996), the clinician feels difficult to diagnose if he/she relies on
histopathology to confirm Laryngoscopic diagnosis.
Expected voice profile
®
The vocal features are
similar to that of vocal nodules, although polyps generally occur singly.
®
The increase in mass of
one VF tends to lower vocal pitch and to restrict pitch range.
®
The vocal note is rough
and breathy, partly because VF approximation is incomplete as a result of
obstruction by the polyp and also because VF vibratory patterns are
asymmetrical.
®
The severity of voice
disorder generally reflects the extent of lesion.
Acoustic
analysis profile
®
Speaking F0 is reduced.
This reduction correlates with the size of lesion.
®
Frequency range is
reduced because frequencies in the upper part of the normal vocal range cannot
be achieved due to increased VF mass and reduced ability to thin the VF.
®
Shows increased jitter
and shimmer measures because the polyps tend to lag behind the VF vibration and
have its own vibratory pattern, the successive vibrations of which are often
aperiodic (Hirano and Bless, 1993).
®
The incompetent VF
adduction allows air to leak, causing an increase in noise which is reflected
as reduced harmonics-to-noise ratio.
®
Poor VF closure may also
result in reduced intensity as the potential to increase subglottal air
pressure is reduced.
Airflow
and volume measures
Transglottic airflow measures are raised
according to the size of the lesion and the extent to which it prevents
competent VF approximation.
Medicosurgical decisions
®
Voice therapy is a
possible course of intervention when a sessile polyp is small, but in most
instances microsurgery is required to remeve the lesion.
®
The patient should be
seen by the voice therapist preoperatively for voice conservation and vocal
hygiene advice.
®
In some cases, a short
course of preoperative voice therapy is helpful inorder to reduce inflammatory
changes.
®
Surgery should be
followed by voice therapy inorder to reduce the possibility of recurrence.
Summary:
vocal fold polyp profile
|
Pathology
|
Vocal fold polyps (sessile or pedunculated)
Usually occur singly.
|
|
Aetiology
|
Acute trauma to the VF mucosa, often in combination
with other factors.
|
|
Signs and symptoms
|
Hoarseness, vocal tract discomfort as in other
hyperfunctional voice disorders.
Reported sensation of ‘something’ in the throat
which cannot be cleared.
|
|
Laryngoscopic findings
|
Small or extremely large mass on or attached to VF
Pedunculated polyp may hang into subglottis and be
visible only on phonation.
Glottis chink anterior and posterior to polyp
Asymmetrical VF vibration
Polyp inhibits vibration of the affected VF and the contralateral VF
Polyp may vibrate separately and slightly after the
VF on each cycle.
|
|
Expected vocal profile
|
Breathy/rough vocal note
Lowered pitch and reduced pitch range
Voice deteriorates with use.
|
|
Acoustic analysis
|
Reduced speaking F0
Reduced Harmonics-to-noise ratio
Increased measures of jitter and shimmer
Reduced intensity.
|
|
Airflow and volume measures
|
Slightly increased transglottal airflow
Subglottal air pressure almost normal.
|
|
Medicosurgical decisions
|
Trial voice therapy initially for small sessile
polyps, before considering phonosurgery.
Large sessile and pedunculated polyos require
surgical intervention, preceded and followed by voice therapy.
|
- Contact ulcers
Appearance and site
Contact ulcers occur on the posterior part
of the VF which overlies the vocal process of the arytenoids cartilage.
They consist of crater-like forms with
highly thickened squamous epithelium piled up over connective tissue, with some
oedema. In the early stages, the arytenoids (cartilaginous) portions of the VFs
may simply appear oedematous and reddened.
The anterior 2/3rd of folds may
not appear healthy and exhibit some thickening of epithelial cover.
A glottis chink b/w folds anteriorly is
often observable. Ulcer may be confined to one arytenoids region or both may be
involved.
Specific aetiology
Contact ulcers are the result of an
extreme form of vocal abuse typified by the speaker’s excessively low speaking
F0, high levels of vocal creak and effortful phonation.
The aetiology of ulceration of the folds
in the arytenoids region was first related to vocal abuse by Jackson &
Jackson (1935). They gave the condition its now accepted name ‘contact ulcer’,
on account of the trauma of ‘hammer and anvil’ with which arytenoids strike
each other.
In deep throaty voice, prolonged
approximation of arytenoids surfaces occurs in the in the region of vocal
processes is the cause of the Contact ulcer.
Laryngeal intubation (placement of a tube
in your airway to help you breathe) injury following surgery or for long term
airway ventilation.
Associated with persistent voice misuse,
especially the use of a pressed, low-pitched voice quality.
In addition to phonatory patterns, gastric
reflux also contributes to the problem. Peptic reflux while the patient is
asleep can seep into the posterior larynx and cause inflammation and
ulceration.
Incidence
Mostly occur in males. Vibration of the
arytenoids occurs naturally in the pulse register (glottal fry) and contact
ulcer develops in people with deep voices.
Women do not employ similar methods of
voice producton and do not develop contact ulcers.
High incidence of contact ulcers in USA
than Britain as American men is using a lower part of pitch range than British
men (Giles & Powesland, 1975).
Signs and symptoms
®
The primary symptoms are
constant throat clearing and vocal fatigue.
®
There may be breathy
voice with some hoarseness, accompanied by discomfort or even severe stabbing
pain. The pain is usually unilateral and located in the area of the greater
horn of thyroid. The pain may radiate to ear.
®
The arytenoids are seen
to approximate forcefully in phonation and the pars respiratus is closed,
providing a ‘posterior air shunt’ (Proctor, 1974).
®
There is constant feeling
of something in the throat results in continuous throat clearing.
Laryngoscopic findings
®
CU will be visible as a
build up of pink or pinkish-white tissue on one of the vocal processes of the
arytenoids.
®
On the contralateral
process, there may be injection of mucosa or a depression. This has been
described as the “cup and saucer” appearance because the two processes fit
together in that way.
®
Inflammation of the
arytenoids and the posterior pharyngeal wall may be seen.
®
The VFs approximate
forcefully and are hyperadducted, particularly in the area of arytenoids
cartilages, so that there is a prolonged closed phase in each vibratory cycle.
®
Extreme inflammation in
the posterior larynx suggests the effects of gastric reflex.
Differential diagnosis
®
Bulky inflamed tissue on
the arytenoids cartilages is a classic presentation of contact ulcers that is
easily recognised.
®
Pachydermia laryngis,
which appears within the interarytenoid space, differs in its formation and
site.
Expected vocal profile
®
Habitual pitch is low and
pitch range is restricted to the loer part of the speaker’s range.
®
The voice is harsh, with
high levels of vocal creak and a rough vocal note.
®
Effortful for the speaker
to increase loudness and further discomfort or pain will occur.
®
Speakers are able to use
base pitch but unable to initiate high pitch.
Acoustic analysis
®
The harmonic to noise
ratio is reduced and jitter is increased.
®
Low F0 and limited pitch
range.
Airflow and volume measures
®
As a result of firm VF
adduction, the transglottal airflow is reduced.
®
Increased air pressure
might be expected due to the tendency to use higher than normal forces when
speaking.
Medicosurgical decisions
®
CU should not be operated but treated with voice
conservation and vocal hygiene measures followed by a programme of vocal
re-education.
®
Gastric reflux medication
may be prescribed..
®
Myerson (1952) claimed
that removal of specific irritants could result in immediate alleviation of
symptoms, if at a mildly oedematous stage. He reported that heavy smokers had
lost their ulcers within 24 hours of ceasing to smoke.
®
With established CU,
surgery is necessary. Absolute voice rest is advisable after surgery until
healing is complete.
®
Voice therapy is
essential.
4. Reinke’s
oedema (or polypoidal degeneration/polypoid
cordites/polypoid laryngitis/chronic hypertrophic laryngitis/polypoid fringe)
Appearance and site
®
It involves the
superficial layer of the lamina propria (Reinke’s space), which fills with
fluid and becomes oedematous and distended , primarly on the superior surface
of VF.
®
The oedematous swelling
is usually b/l and symmetrical , but in some cases there is a marked difference
in the size of the oedematous folds.
®
Zeitels et al (1997) have
proposed grading system for this condition based on severity and extent of VF
abnormality:
Grade I: VF contact is confined to the
anterior third of musculomembraneus VFs.
Grade II: contact is confined to anterior
2/3rd.
Grade III: contact is extended to the
entire length of VF.
Specific aetiology
Prolonged smoking is accepted as the
primary cause of Reinke’s oedema (Remacle, Degols and Delos, 1996). The
resulting chronic glottal mucositis may then be further compounded by gastric
reflux.
Zeitels et al (1997) suggest that primary
irritants render the VFs more susceptible to trauma, which finally results in
the lesion.
Bishop and Lumpkin (1987) from their
study, reported that smoking was the major factor and only 25% of the patients
with Reinke’s oedema exhibited vocal abuse.
Vocal abuse is an inevitable secondary
feature that exacerbates the initial changes in Reinke’s space.
Incidence
Women over the age of 40 years are the
most common group presenting with Reinke’s oedema (Kleinsasser, 1968).
Although this condition is also seen in
men, hormonal effects predispose women to the condition.
Signs and symptoms
®
Typical symptoms of edema
include a lower than normal pitch level and hoarseness.
®
If the condition is
particularly severe, the patient may complain of shortness of breath because
the oedematous VFs may partially block the airway.
®
In some cases of oedema,
patients c/o loss of pitch range and increased effort required to produce
voice.
Laryngoscopic and stroboscopy
findings
®
During laryngoscopy, Have
the appearance of enlarged of enlarged fluid-filled boggy structures. They do
not appear firm or solid.
®
Oedema usually involves
the full length of VFs bilaterally.
®
In some aspects, RO gives
the appearance of a broad based polyp occupying the full length of VF.
®
Stroboscopic features of
RO are expected to show greater than normal excursion of mucosal wave and
complete glottal closure.
®
Colton et al (1995)
showed that the mucosal wave was slightly decreased but glottal closure was
complete in case of 4 patients with RO. Both amplitude and mucosal wave may be
decreased.
Differential diagnosis
Well established, b/l cases of RO are
distinctive, but early, u/l presentations bear some resemblance to a sessile
polyp.
Expected vocal profile
®
As a result of increased
mass of VFs, pitch is extremely low and correlates with the severity of
condition.
®
Bishop & Lumpkin (1987) found that not only was
the speaking F0 much lower than normal, but it was even lower than in cases of
laryngeal carcinoma.
®
Extremes of pitch range
are affected, with both the upper and lower limits significantly lowered.
®
Loudness is also reduced
as the oedema reduces the potential for increasing VF tension.
Acoustic analysis
Speaking F0 is significantly lower than
normal and pitch range reduced.
Jitter and shimmer measures are raised and
intensity is low.
Airflow and volume measures
Correlate with the extent of oedema. When
there is complete VF contact throughout the length of VFs, Subglottal air
pressure may be high.
Greater than normal and peak airflows.
Medicosurgical decisions
Microsurgery is the primary treatment
route together with a programme of voice therapy. Voice therapy alone does not
resolve oedema.
Fritzell et al (1982) describe a patient
who does not receive voice therapy post operatively and subsequently developed
VF nodules.
It is important to reduce laryngeal
irritants particularly, smoking should be eliminated.
The aim of the surgery is to reduce the
volume of superficial layer of lamina propria while preserving its
characteristics and to ensure that deep layers of mucosa remain intact.
5.
Intracordal
Cysts:
Primary Voice Symptom: Hoarseness
Description
and Etiology
Intracordal
cysts appear as small spheres on the margins of the vocal folds and sometimes
on the superior surface. They may be
mistaken for early nodules because small nodule-like growths may appear on one
cord but not the other. Cysts are
predominantly unilateral. Cysts may also
occur in association with vocal nodules (Monday, 1983).
Intracordal
cysts may be caused by blockage of a glandular duct in which there is retention
of mucus (Monday, 1983). Because there
is no way for the mucus to escape, a cyst may, with time, grow larger. Another type of cyst, usually smaller than a
retention cyst, is the epidermoid cyst.
Epidermoid cysts of the vocal folds have a strong similarity to
epidermal cysts of the skin.
Most
patients with intracordal cysts are young adult women (Bouchayer, Cornut,
Witzig, Loire, Roch, & Bastian, 1985; Monday, 1983). Cysts often occur in professional voice
users.
Perceptual
Signs and Symptoms
Typical
signs of a cyst include hoarseness and a lowered pitch. The patient may report a “tired” voice.
Acoustic Signs:
Data
are not available on the acoustic characteristics of the voices of patients
with cysts. We might expect data similar
to those for nodules, since the effect on the vocal folds appears to be
similar.
Measurable
Physiological Signs
Again,
there are few physiological data available on patients with cysts. However, higher than normal average airflows
might be expected as a result of elevated offset flows and higher than normal
peak flows. The closing phase of the
vocal folds, as seen in an electroglottogram, may also be slower than normal.
Observable
Physiological Signs
Laryngoscopy
Identification
of a cyst can be very difficult.
Bouchayer et al. (1985) report that in only 10% of their cases was a
cyst obvious on initial examination.
However, the appearance of fullness of the vocal fold and dilated
capillaries raised the suspicion of a cyst in 55% of cases. Endoscopicllaly, cysts are sometimes
highlighted by a persistent light reflection from the slightly raised area of
the cyst.
Stroboscopy
Stroboscopy
has been found to be very helpful in the diagnosis of a cyst because there is
an absence of mucosal wave in the area over the cyst. Other signs include greater aperiodicity and
reduced glottal closure (Kitzing, 1985). Colton, Woo, Brewer, Griffin &
Casper 1995, have found that the vibration of the two folds is often
asymmetric, especially over the area of the cyst. Amplitude of the affected
side, in particular, will be reduced.
Pathophysiology
A
cyst originates in the superficial layer of the lamina propria (Hirano,
1981a) as it grows, it increases the
distance between the cover and the lamina propria but usually does not extend
into the layers. A cyst increases the
mass and stiffness of the cover, whereas the transition layers and the body are
unaffected.
Management:
surgical removal of the cyst followed by
voice therapy is recommended
6. Submucosal
vocal fold haemorrhage
Appearance and site
Haemorrhages on the surface of VFs can
range from isolated blood vessels to involvement of surface of an entire VF.
Specific aetiology
VF haemorrhages are the reult of rupture
of a varicose vain on the superior surface of the VF.
Sataloff (1991) notes that this condition
in professional voice users is commonly seen in pre-menstrual women who are
using aspirin products.
Any type of trauma involving forceful VF
adducton, particularly when there is a coexisting upper respiratory tract
infection or acute laryngitis, exacerbates these vascular events.
Incidence
More frequently seen in females than in
males. VF Haemorrhages can occur in isolation or coexist with other laryngeal
pathology.
Signs and symptoms
Patients do not generally experience any
discomfort but may c/o pain particularly at the time of precipitating event.
Dryness, vocal fatigue and loss of upper
range and sign of hoarseness present.
Depending on the severity of bleed, the
voice may be intermittently aphonic and require added effort for voicing to be
produced.
Laryngosopic and stroboscopic
findings
Small telangiectatic blood vessels can be seen
on the superior surface of the VF and in case of extensive haemorrhage, entire
VFs appear dark red.
Although VF adduction is usually
unaffected, the movement of mucosal wave can be impaired by haemorrhagic area.
Under stroboscopic observation, stiffness
of haemorrhagic VF is apparent with reduced amplitude of involved fold and
absence of mucosal wave in the area of haemorrhage.
Differential diagnosis
It is necessary to clarify whether the
haemorrhage is an isolated event or whether other factors have increased the
susceptibility of VF mucosa to this damage.
Stroboscopy is an important tool in making
these judgements.
Expected voice profile
Mostly, vocal note is slightly rough
because of altered oscillations of VFs.
Pitch breaks also occur due to increased
tension as a result of compensatory behaviours.
Acoustic analysis profile
Speaking F0 can be relatively unaffected,
although notes in the upper part of the range might be impaired
NHR is reduced and jitter and shimmer
measures tend to be increased.
Airflow and volume measures
Usually within normal limits. Sometimes
shows increased SGP due to effortful phonation and increased airflow due to
stiffness of haemorrhagic cord.
Medicosurgical decisions
®
In cases of simple
trauma, even when the haemorrhage is extensive, voice therapy facilitates the
spontaneous resolution of the vascular damage.
®
Surgery might be
necessary when VF structural abnormalities like; cysts, nodules and polyps have
been the basis of trauma.
®
Postoperative voice
therapy is needed.
Sataloff (1991) advised that, when recurrent VF
haemorrhage is clearly related to menstrual cycle, hormonal adjustments should
be considered with an endocrinologist
7.
Keratosis
Keratosis
refers to epithelial lesions in which there is abnormal tissue growth on the
vocal folds. This usually originates in
epithelium but may enter the superficial layer of the lamina propria. Other terms may be used to describe this condition,
including leukoplakia, hyperkeratosis, Keratosis with cellular atypia and
dyskeratosis. Two kinds of lesions may
be seen: flat, white, plaque like lesions (leukoplakia) or irregular growth of
epithelium that results in a warty lesion (papillary keratosis).
Smoking, environmental pollutants, and
other factors have been implicated in the development of keratotic epithelium
on the vocal folds. These lesions tend
to occur more often in males than females.
Recently, gastro esophageal reflux disease (GERD) has also been
implicated as an etiology of these tissue changes (Koufman, 1991). The lesions may be unilateral or bilateral
but are usually asymmetric in appearance.
The glottal edge is often rough.
Perceptual
signs and symptoms
The primary symptom is hoarseness or
roughness in the voice.
Acoustic
signs
There are few data available on the
acoustic characteristics of patients with keratosis of the vocal folds. Due to the growths on the vocal folds,
greater than normal frequency and amplitude perturbation as well as greater
than normal spectral noise would be expected.
Measurable
physiological signs
Minimal measurable physiological data
exist on patients with keratosis of the vocal folds, Iwata, von Leden, and
Williams (1972) reported a mean airflow rate of 227 ml/sec for patients with
leukoplakia of the vocal folds. Lesions
that might have a similar effect (papilloma, epithelial hyperplasia) also show
greater than normal airflow (Hirano, 1981b).
Observable
physiological signs
In patients with leukoplakia, there will
be whitish plaque like lesions on the mucosal surface of the vocal folds. These may be limited in extent or may cover
almost the entire vocal fold. Ballenger
(1985) reports that another form of this lesion, papillary Keratosis, may show a
piling up of small, reddish epithelium or an irregular mucosa covered by Keratin.
Because
these lesions can be so variable in extent and in location on the folds, their
stroboscopic appearance will vary. Vocal
fold edges may be rough and result in an irregularly shaped glottic chink on
vocal fold closure. There will be
asymmetric behavior and aperiodicity. In extensive lesions, diminished
amplitude of lateral vocal fold excursion and limited mucosal wave, especially
over the sites occupied by the lesion, are seen. In instances of early and superficial
hyperkeratosis, it is possible to observe a fairly normal mucosal wave. This stroboscopic feature may help to
distinguish keratosis from cancer.
Deeper invasion of the underlying structures occurs in carcinoma
limiting vibratory behavior to a greater extent.
Pathophysiology
Keratotic type lesions, for the most part,
affect the cover, increasing its mass and stiffness.
8.
Granulomas
Granulomas most commonly are a
complication of intubations. Their
development may be an early complication occurring at some point between
intubation and extubation, or a late complication, the morbid sequelae of extubation
(Balestrieri and Watson 1982). The passing of an intubation tube between the
vocal processes may be necessary in order to provide access to the airway for
purposes of delivering anesthesia and maintaining appropriate oxygenation
during a surgical procedure. Intubation
may also be necessary in nonsurgical situations to maintain adequate oxygen
supply for persons in need of respiratory assistance. Contact between the tube and the vocal
processes may occur at the time of intubation or with the tube in situ. During such contact the mucosal perichondrium
of the vocal processes may be traumatized, causing a small ulcer to appear on
the vocal process. The bare process will
eventually be covered by granulation tissue, which will become epithelialized
and present as granuloma.
The condition is surprisingly uncommon in
light of the frequency with which intubation is required, and spontaneous
resolution occurs within a few weeks in most cases. The incidence of granuloma is dependent on
factors such as duration of intubation, the method of intubation, the patient’s
age and general condition, nursing techniques, and other factors. All reported cases have occurred in patients
15 years or older and women are more prone to develop an intubation granuloma
because of small laryngeal size and a thinner mucosal layer covering the vocal
processes (Snow Marano, and Balogh 1966).
Endotracheal
intubation is being accepted for longer and longer periods of time. Although it is not a benign procedure,
morality and morbidity rates, when compared to the option of tracheotomy, are
much lower.
Perceptual
signs and symptoms
The symptoms of granuloma are breathiness
and hoarseness; some may not affect phonation due to their location
Acoustic
signs
There are no data on the acoustic
characteristics of patients with granulomas.
Greater than normal frequency and amplitude perturbation would be
expected, and depending on the severity of the hoarseness, greater than normal
spectral noise could be present.
Measurable
physiological signs
Normal airflow rates have been reported in
patients with contact granulomas (Hirano, 1981b).
Observable
physiological signs
Granulomas manifest themselves
laryngoscopically as irregularly shaped masses of tissue either at the site of
the vocal processes of the arytenoids (if an intubation granuloma) or elsewhere
on the vocal folds or larynx (Friedman, 1973)
The
vocal folds will show normal stroboscopic signs unless the granuloma appears on
the vocal fold margins. In that case,
glottic closure may be incomplete and we would expect to see reduced amplitude
of lateral excursion of the affected vocal fold(s) and some degree of
disturbance of the mucosal wave.
Pathophysiology
Intubation granulomas primarily affect the
mucosa of the vocal processes of the arytenoids.
9.
LARYNGEAL
PAPILLOMA
Papilloma is a rather common benign tumor
that starts in the epithelium and is thought to be caused by a virus, probably
of the papovavirus group. it occurs in
both children and adults. In children it
is referred to as juvenile papilloma, and it is very resistant to
eradication. Surgical excision is
required, as papillomas tend to proliferate and can obstruct the airway. It is not uncommon for children with this
problem to require multiple surgical excisions before the condition runs its
course. If juvenile papilloma persists
or begins in adulthood, it continues to be a condition that is highly resistant
to treatment. The papilloma may occur in
various parts of the larynx: subglottally, at the level of the vocal folds, and
supraglottally. It is sometimes necessary for children with aggressive
papilloma growth to undergo tracheotomy.
When the papillomas have ceased recurring, or perhaps between episodes
of recurrence, voice therapy may be appropriate in order to maintain or restore
the best possible voice production. The
prognosis will depend largely on the state of the vocal fold mucosa.
Perceptual
signs and symptoms
Hoarseness
is the primary symptom and sign of the
voice disorder caused by this condition.
Because of the sometimes extensive involvement of the true vocal folds,
a low pitch level might also be evident, although there are no data to support
this hypothesis.
Physiological
signs
We know of no measurable physiological
data reported for individuals with papillomas of the vocal folds. However, because of the increased stiffness
of the cords we might expect greater expiratory air pressures.
Laryngoscopy
A Papilloma will typically present as a
whitish cluster of tissue, somewhat comparable in texture to a raspberry.
Stroboscopy
Papillomas will often interfere with
glottal closure. To what extent this is
true will depend on the extent of the lesion.
The increased stiffness created by the lesion will impede horizontal
excursion of the folds and mucosal wave will be absent in the area of the
lesions. When multiple surgical
excisions have been required for vocal fold papilloma, the membranous cover of
the vocal folds may have been sufficiently damaged to interfere with amplitude
and vibratory behavior.
Pathophysiology
Papillomas affect vocal fold vibration by
increasing the mass and the stiffness of the vocal folds and altering the
biomechanical characteristics of the mucosa.
Although they can be removed surgically the lesions tend to recur,
especially in children (Bastian 1986).
Treatment with interferon has been tried but with inconclusive results
(Benjamin, Gatenby, Kitchen, Harrison, Cameron and Basten 1988).
Management
Surgery is usually the treatment of choice
and includes traditional knife surgery as well as CO2 laser (Simpson and
Strong, 1983). Various other treatments have been tried, including interferon
(Benjamin et, al., 1988; Leventhal, Kashima& Mounts, 1991), photodynamic
therapy and various drugs.
10) Chondroma:
It arises from cricoid
cartilage and may be present in subglottic area causing dyspnea.
May grow outward posterior plate of cricoid and cause
sense of lump in the throat and dysphagia.
Mostly affect men in age group 40-60 years.
Pathophysiology: most commonly arise
from internal posterior cricoid cartilage (hyaline cartilage), may also
arise from thyroid, arytenoid, epiglottic cartilage (fibroelastic)
Symptoms:
Insidious
hoarseness from vocal fold restriction, dyspnea for subglottic lesions,
dysphagia for posterior cricoid lesions, globus sensation
Treatment:
complete excision
11) Fibroma:
They are small pedunculated lesions that
usually arise from the true vocal cords.They
are probably not true neoplasm but rather a representation of localized fibrous overgrowth of the tissue.
Symptoms: Hoarseness
is the only symptom.On indirect laryngoscopy they appear as a small
pedunculated nodular mass seen commonly in the anterior one thirds of the
larynx.
Treatment:
is microlaryngoscopic excicion.
Others:
Sulcus Vocalis:
Sulcus
vocalis refers to a condition in which a furrow along the upper medial edge of
the vocal folds is observed. Bastian
(1986) describes it as an “epithelial-lined furrow or pocket whose lips
parallel the free edge of the cords” (p. 1974).
In a cross-section of the vocal folds, the furrow appears as a pocketed
ledge on the medial surface of the vocal folds.
The longitudinal extent of the furrow is variable, as is its depth. If very deep, it seems to divide the cord in
half. According to Arnold (1980), sulcus
vocalis may be associated with other laryngeal or oral asymmetries.
Ford et. al has classified Sulcus Vocalis
into 3 groups:
Type 1: epithelial invagination limited to lamina propria; Normal voice
Type 2a: epithelial invagination along the vocal fold: some dysphonia
Type 2b: epithelial invagination into the vocalis muscle; severe dysphonia
Type 2a and 2b are considered pathologic
The
etiology of sulcus vocalis is uncertain, although Bastian (1986) attributes it
to vocal misuse and abuse. Luchsinger
and Arnold (1965) in their review of the literature summarized the possible
etiological factors as being congenital, developmental, or traumatic. Bouchayer et al. (1985) argued for a
congenital etiology. The disorder is
rather rare, at least in Europe and the United States (Luchsinger & Arnold,
1965); it may be more prevalent in Japan (Hirano, 1981b). according to Hirano and Bless (1993), sulcus
vocalis is either congenital or the result of repeated chronic inflammatory
processes.
Perceptual
Signs and Symptoms
Symptoms
include a breathy, hoarse voice quality that apparently is due to incomplete
closure of the vocal folds and disturbed vibratory behavior. The pitch of the voice may be lower than
normal, and the loudness may be reduced.
Acoustic
Signs
Phonational and intensity ranges would be expected to be
reduced, although there are no data available to support this expectation. There may be elevated levels of spectral noise
in the voice. We might also find greater
than normal frequency and amplitude perturbation, although of small magnitude.
Measurable
Physiological Signs
Airflows
may be slightly elevated (Shigemori, 1977), We would expect vibratory flows, to
show greater than normal perturbation and slightly greater than normal airflow
leakage (offset flow).
Electroglottographic recordings should show increased perturbation with
the possibility of short closed times.
Observable
Physiological Signs
Laryngoscopy
Laryngoscopically,
a sulcus will be seen as a depression or line along the upper medial edge of
the vocal fold. The depression may
extend the entire length of the vocal fold and may vary in depth from shallow
to very deep.
Stroboscopy
We
have found diminished amplitudes of vocal fold movement with little continuity
of the mucosal wave across the sulcus. A
mucosal wave can usually be seen across the uninvolved superior surface of the
vocal fold. A narrow, spindle-shapled
glottal chink closure configuration with bowed vocal fold edges is described by
Hirano and Bless (1993).
Pathophysiology
The
sulcus is located in the superficial layer of the lamina propria, which
decreases the mass of the cover but may increase its stiffness. The body and
the transition layers are normal.
References
·
Stemple. J.C. (2000)
Clinical voice pathology: Theory and Management- 3rd edition.
·
Matheison. L. (2001). Greene
& Matheison‘s The voice and its disorders ( 6th edn). London: Whurr
Publishers
·
Aronson, E.A., and Bless,
M.D. (2010). Clinical Voice Disorders, 4th edition. New York: Thieme.
·
Prater, R. J., Swift, R. W. (1984). Manual of Voice
Therapy.
·
Ferrand.T.(2012), Voice Disorders Scope of theory and
practice.
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