Transcript LARYNGEAL DISODERS

Laryngeal anatomy,
physiology and disorders
Prof. Alexander I. Yashan
Laryngeal Anatomy
• The larynx is the organ of
voice production
• It is a part of the
respiratory tract lying
between the trachea and
the pharynx, has a
framework of cartilages,
muscles and ligaments
• The entrance to the larynx
is guarded by a “U”shaped hyoid bone, which
is also the supportive
structure for the tongue
Laryngeal Structures
Muscles are cartilages support the
larygngeal framework, the key
structures are:
• Epiglottis - flexible, elastic, leaflike structure
• Thyroid - largest cartilages
• Corniculate - remnant in humans
• Arytenoid - on the border of
cricoid
• Extrinsic (supporting) and
intrinsic (influencing laryngeal
motion) muscles
Vocal Cords
• The true vocal cords project
into the laryngeal cavity
• paired vocal cords originate
from the thyroid cartilage, near
the thyroid notch
• They have a common anterior
attachment of the folds is
common (comissure)
• Medial borders are free to
vibrate
• The space between the vocal
folds - glottis – supraglottic /
subglottic regions
The Mucosal Wave
Vocal Cord Anatomy
• Thin layer of epithelium on
lamina propria
• Recent studies show a
delicate and complex
basement membrane
structure between epithelium
and the superficial layer of
lamina propria
• Strong connection between
basement membrane
attachment and healing of
vocal cord
Factors that effect phonation
•
•
•
•
•
•
•
Respiratory tract infection
Asthma
Smoking
Medication
Irritants: dust, fumes, smoke
Vocal abuse: singers
External Trauma
• Laryngeal injuries: prolonged
intubation
• Foreign bodies
• Degenerative disorders:
papilloma, granuloma, vocal
cord lesions etc.
• Sudden voice change may be
due to haemorrhage into the
vocal cords
• Hoarseness following upper
respiratory infection is due to
acute inflammation of the
larynx
Changes in Voice Production
• Change in airflow pressure
generated in the lower
respiratory tract
• Mass on the vocal cords
• Neurological control of vocal
cord movement
• Change in vocal cord tension
• Stiffness and vibration
• Stridor - indicates partial
obstruction of upper airway,
mostly in children
Congenital Abnormalities
• Laryngomalacia - softening of
laryngeal cartilage - surgery is
not usually required
• Atresia and Webs - lead to
opening of the airway by
surgical intervention
• Laryngoceles - air-sack, causing
a foreign body sensation in the
throat, can be removed
surgically
• Hemangioma - proliferation of a
blood vessel leading to a mass;
removed by laser surgery
Functional Disorders
• Abnormal vocal cord
position - surgical
intervention eg:
medialisation
• Recurrent laryngeal nerve
paralysis - all the internal
laryngeal musculature is
paralysed on the affected
side. If the case is
bilateral, the glottis is
widened with CO2 laser
surgery
Traumatic Injuries
• Vocal Abuse - often leads to
formation of polyps and
nodules which are removed
surgically
• Intubation Injury -formation of
heamatoma - usually heals
by itself - or granulomas
which can be surgically
removed
• Foreign Bodies
Inflammation
• Acute Laryngitis present
with red, swollen cords,
usually cured by antibiotics
• Specific Chronic Laryngitis
- eg: Tubercolosis,
Scleroma (granulation) in
the sub-glottic space
• Non-Specific Chronic
Laryngitis - usually caused
by smoking
Benign tumors of the Larynx
• Vocal Cord Polyps cause hoarseness and
attacks of coughing,
surgical removal
• Reinke’s Edema Reinke’s space is a
closed cleft under the
vocal cord epithelium the edema is always
almost bilateral and
usually affects smokers
Benign tumors of the
Larynx
• Papilloma - benign
epithelial tumor cause by
viral infection, usually
recurrent; causes
hoarseness and
respiratory obstruction
• Retention cysts - glazed,
white cysts derived from
the mucosal glands,
effect phonation
Summary
• Voice production is a
compley function requiring
fine neuromuscular
control and coordination
• Sound varies according to
mass, tension and lenght
of the vocal folds
• Minor changes in
anatomical structures as
well as disease and
pathology can greatly alter
phonation
LARYNGEAL DISODERS
The term "laryngitis" is frequently misused as a synonym for
hoarseness, but "laryngitis" refers to any acute or chronic,
infectious or noninfectious, localized or systemic inflammatory
process that involves the larynx. The clinic al presentation of
laryngitis depends on its underlying cause, the amount of tissue
swelling/edema, the region of the larynx primarily involved, and
the patient's age. Patients with laryngitis may present with one
or more symptoms:
dysphonia, odynophonia,
dysphagia, odynophagia,
cough,
dyspnea,
and/or stridor.
The diagnosis is usually based on the history and the laryngeal
examination, but it sometimes requires special diagnostic tests,
such as cultures, blood tests, skin tests, pH monitoring,
and/or rad iographs.
CHILDHOOD LARYNGITIS
• The smaller pediatric airway is much more
susceptible than the adult airway to obstruction
from edema. Equivalent amounts of mucosal
edema produce critical narrowing in children, but
cause minimal or no symptoms in adults. Table
48-2 shows the effects of1 mm of edema on the
airway of a neonate, a child, and an adult.
Laryngitis is therefore more often a lifethreatening illness requiring airway management
in infants and children than in adults.
Common Viral Laryngitis
• The most common cause of laryngitis is viral infection.
This type of nonobstructive laryngitis is clinically mild,
and is often associated with a viral upper respiratory
infection (URI). Patients may present with low-grade
fever, mild dysphonia, cough, or rhinitis. Rhinovirus,
parainfluenza, respiratorysyncytial virus, and adenovirus
have been implicated. Other viral illnesses causing
laryngitis include influenza, measles, mumps, pertussis,
and chicken pox.
• The diagnosis may be based on the history and
symptoms, so that examination of the larynx does not
always need to be performed. When examined, the
laryngeal mucosa is erythematous and edematous, with
normal vocal fold mobility and no evidence of airway
obstruction. Common viral laryngitis is usually selflimited, and treatment is aimed at providing hydration
and humidification, but antipyretics and decongestants
are frequently also prescribed.
Acute Laryngotracheitis (Croup)
• Acute laryngotracheitis1 (croup) is a common viral infection
which generally affects children younger than 5 years of age.
Typically, this illness lasts from 3 to 7 days and it is common in
the autumn and winter. Parainfluenza I is the most common
lyimplicated viral agent, but parainfluenza II, influenza A,
rhinovirus, and respiratory syncytial virus may also be
causative. The child first develops a febrile URI followed
dayslater by the classic "barky" or croupy cough; the cough is
usually nonproductive and worsens at night.
• Usually, croup is self-limited, but if significant edema develops,
progressive airway difficulty may ensue. Stridor with intercostal
and supraclavicular retractions becomes prominent as the child
struggles for air. In severe cases, with out treatment, the airway
obstruction may progress, exhaustion may ensue, and
complete airway obstruction may occur. Most often, the
diagnosis is based on the history and on lateral neck
radiographs, which usually reveal the classic "steeple sign,"
caused by subglottic narrowing due to edema.
Acute Laryngotracheitis (Croup)
• In laryngotracheitis, the subglottic larynx is the primary site of
inflammation and edema formation, although the trachea may also be
involved. In severe cases, epithelial sloughing, associated with
tenacious mucoid secretions, may accompany the inflammatory
process, and further compromise the airway. It should be noted that
the supraglottic larynx is usually unaffected in laryngotracheitis, and
this helps differentiate it from other causes of airway obstruction in
young children.
• Treatment is directed at reducing the edema, thinning the secretions,
and in severe cases, establishing an airway. Intensive humidification
and hydration are begun to help thin the secretions and soften the
crusts in the airway. If symptoms worsen, aerosolized epinephrine
treatments and high-dose corticosteroids are used to prevent further
progression of the edema.2,3,4 If impending airway obstruction
develops, intubation or tracheotomy is required to secure the airway
and permitadequate pulmonary toilet. Antibiotics are indicated for
secondary bacterial infection, which may be caused bystaphylococci,
streptococci, or pneumococci.
Secondary Bacterial Laryngitis
• Some patients with laryngotracheitis progress to
develop secondary bacterial infection of the airway.
These patients present with various degrees of airway
obstruction, stridor, tachypnea, tachycardia, cough,
fever, and drooling. This condition is more serious and
it is usually attended by high fever and purulent
drainage. This condition has the potential to obstruct
the airway, and it requires prompt diagnosis
andtreatment.5 The organisms usually responsible are
Haemophilus influenzae, pneumococcus, and
hemolytic streptococci. Antibiotic therapy should be
directed at these organisms. When possible, culture
and gram stain of the exudate should be obtained.
Airway support is often needed in these patients.
Acute Supraglottitis
• Children between 2 and 4 years of age are most often affected, and
most cases of supraglottitis occur in the winter and spring. Acute
supraglottitis,6,7 also sometimes called "epiglottitis," is a lifethreatening infection of the larynx, most often caused by
Haemophilus influenzae type B. This condition is a medical
emergency, because airway obstruction and death can develop
rapidly. Typically, the illness begins and progresses rapidly, over 2 to
6 hours, with the onset of fever, sore throat, and inspiratory stridor.
The child's voice tends to be muffled, but a croupy cough is unusual.
As the supraglottic structures become increasingly edematous,
airway obstruction may develop. Affected children are frightened and
ill-appearing; often stridulous, and sitting upright in the "sniffing"
position. They often drool because swallowing is very painful.
Acute Supraglottitis
• A presumptive diagnosis of supraglottitis is based on the
history and clinical findings, but since laryngeal
examination in the emergency department may
precipitate airway obstruction, it is not recommended.
Lateral soft-tissue radiographs typically reveal the classic
"thumb" sign of the edematous epiglottis. In addition, the
entire supraglottis may be hazy and indistinct with a
dilated hypopharynx.
• When airway obstruction is severe, treatment should not
be delayed to obtain radiographs. If radiographs are
deemed necessary, the child should be constantly
attended by personnel capable of immediate intubation if
airway obstruction should occur.
Acute Supraglottitis
• Children with suspected supraglottitis should be taken to the
operating room immediately to establish the diagnosis and secure the
airway. The child is transported to the operating room by the parents,
an otolaryngologist, and an anesthesiologist. At the time of direct
laryngoscopy, the epiglottis usually appears veryswollen and cherry
red, as do the aryepiglottic folds and falsevocal cords. The true vocal
folds and subglottis usually appearvirtually normal.
• Treatment secures the airway and then provides antimicrobial and
supportive care. Drawing blood, starting intravenous lines, obtaining
a rectal temperature, and other necessary procedures are performed
after the airway is established. After controlled anesthesia and
diagnosis, the patient should be orally intubated. The oral
endotracheal tube can then be converted to a nasotracheal tube, with
direct visualization of the glottis as the orotracheal tube is removed,
or a tracheotomy may be performed. (Instruments necessary for rigid
bronchoscopy and tracheotomy must be ready in the operating room
in case the airway is lost before intubation). In some settings, such as
institutions without skilled pediatric intensive care staff available
around the clock, tracheotomy may be preferred to endotracheal
intubation, because it is easier to secure and maintain in the small
patient with a tenuous airway
Acute Supraglottitis
• Antimicrobial therapy is initiated against Haemophilus influenzae.
Extubation is usually possible after 48 to 72 hours, at which time the
edema has subsided sufficiently to allow an air leak around the
endotracheal tube. Direct laryngoscopy or fiberoptic laryngoscopy are
the most reliable techniques to ensure resolution of the inflammation
before extubation.
• Haemophilus influenzae type B polysaccharide vaccine has been
available since 1985 for children older than 18 months of age.Since
1988 conjugate vaccines have made possible the immunization of
children beginning at 2 months of age. Immunization has resulted in a
dramatic decrease in the incidence ofsupraglottitis.7 Although H.
Influenzae remains the leading cause of supraglottitis, beta-hemolytic
streptococci and staphylococcusmay also cause supraglottitis.
• Unfortunately, the mortality rate for supraglottitis today remains quite
significant despite advances in airway management.This is because
the diagnosis may be missed in the early stagesof the illness, (often
mistaken for croup) with rapid progression of airway obstruction.
Differentiating acute supraglottitis from laryngotracheitis is not always
easy, but this differentiation is essential.
Laryngeal Diphtheria
• Laryngeal diphtheria is very uncommon; however, outbreaks of
diphtheria have recently been reported in eastern Europe, believed to
be due to low immunization rates.8 It is caused by Corynebacterium
diphtheriae and generally affects individual solder than 6 years of
age. A febrile illness of slow onset associated with sore throat and
dysphonia is followed by progressive airway obstruction.
• The organism causes an exudative inflammatory response of the
mucous membranes, which results in a thick, gray-green, plaque-like
membranous exudate over the tonsils, pharynx, and larynx.
Characteristically, the exudate is difficult to dislodge, and it bleeds
when it is removed. Cultures and smears are obtained for
confirmation of the diagnosis.
• Treatment consists of establishing a safe airway, administrationof
diphtheria antitoxin, and erythromycin or penicillin toeradicate the
organism. Intubation is contraindicated because it may dislodge a
plaque and cause airway obstruction, thus, tracheotomy is often
performed. Mortality results largely from the neuropathic responses to
the diphtheria toxin. If the patienth as been previously immunized
against diphtheria, the disease may still occur, but tends to be mild.
Laryngopharyngeal Reflux
• Laryngopharyngeal reflux (LPR), the reflux of gastric contents
into the laryngopharynx, is ubiquitous in pediatric
otolaryngology, yet the diagnosis may be difficult to make. LPR
is associated with laryngomalacia, vocal nodules, polyps
,granulomas, laryngeal and tracheal stenosis, and
laryngospasm. LPR may also play a causal role in asthma,
sudden infant death syndrome, bronchopulmonary dysplasia,
and aspirationpneumonia.9,10
• A high index of suspicion is necessary for LPR tobe considered
in cases of laryngitis; unfortunately, the only reasonably
sensitive diagnostic test for this condition is ambulatory 24-hour
double-probe pH monitoring.9 Other tests, such as barium
esophagography, radionuclide scanning, and the lipid-laden
macrophage test, lack sufficient diagnostic sensitivity to be of
value in most cases.
Spasmodic Croup
• Spasmodic or false croup is a noninfectious form of
laryngeal inflammation, possibly related to allergy or
reflux laryngitis. It generally affects children 1 to 3
years of age. It is occasionally associated with an URI,
but not with a significant febrile illness. The child
usually wakes at night with a "barky“ cough, stridor,
and mild dyspnea. The coughing paroxysms may be
followed by vomiting, which may terminate the attack.
These episodes may occur as an isolated event or
recur over 2 to 3nights. The child is usually
asymptomatic during the day.
• Examination shows mildly erythematous laryngeal
mucosa, with subglottic edema. Humidification is
usually all that is required to alleviate the symptoms.
Spasmodic croup may be confused with
laryngotracheitis and with LPR-related laryngospasm.
Spasmodic Croup
Differential Diagnosis
• Inflammatory forms of laryngitis may result in airway
obstructionand should be diagnosed accurately and
promptly to provide appropriate treatment.5 The most
common causes of obstructive laryngitis in children
are laryngotracheitis, supraglottitis, and LPR.
However, in dealing with a child with dysphonia,
stridor, or airway obstruction, other diagnoses should
be considered. These include foreign bodies,
respiratory papillomas,laryngeal cysts and
hemangiomas, subglottic stenosis, bacterial
tracheitis, and retropharyngeal abscess. If the infant
or child develops laryngeal inflammation (with or
without airway obstruction), and there are no
definitive signs of infection, LPR should be
considered as the most likely diagnosis
ADULT LARYNGITIS
• Laryngitis in adults is usually less serious
than in childrenbecause the larger adult
larynx can accommodate swelling
withoutobstructing as readily. Most commonly,
adult laryngitis is causedby a viral URI,
smoking, or LPR. Unlike children, adults can
havechronic laryngitis that may go
unrecognized for many years, butlike
children, adults may occasionally develop
laryngotracheitisand supraglottitis.
Viral Laryngitis
• Infectious laryngitis in adults is most commonly
associated with a viral URI. Patients present with a
generalized viral syndrome and dysphonia that is
characterized by voice breaks, episodic aphonia,
hoarse cough, and a lowering of the vocal pitch.
• Rhinoviruses are the most common causative agents.
Characteristically, the laryngeal mucosa is
erythematous and edematous, especially over the true
vocal folds. The disease is self-limited and is treated
symptomatically with humidification, voice rest,
hydration, smoking cessation, cough suppressants,
and expectorants. Antibiotics are indicated only for
secondary bacterial infection.
Bacterial Laryngitis
• Supraglottitis is manifested by fever, sore throat, a muffled
voice, odynophagia, and dyspnea. The diagnosis is usually
made by observing the swollen, red supraglottic structures
by fiberopticlaryngoscopy or by detecting the swollen
epiglottis/supraglottison a lateral neck radiograph.
Haemophilus influenzae is the most common organism, but
Streptococcus pneumoniae, Staphylococcus aureus, and
hemolytic streptococci are also found. Close observation of
the adult patient with serial fiberoptic examinations is
appropriate, with intubation or tracheotomy reserved for
progressive airway obstruction. Patients whose symptoms
progress rapidly over less than 24 hours are at high risk for
airway compromise.11,12 Conservative measures include
humidification, hydration, corticosteroids, and intravenous
antibiotics. Epiglottic abscess is an uncommon complication
of bacterial laryngitis, and it occurs more commonly in adults
than in children. Tracheotomy followed by drainage is the
treatment of choice.
NONINFECTIOUS LARYNGITIS IN
ADULTS
• Laryngopharyngeal Reflux (LPR)
• Of all the causes of laryngitis in adults, LPR is probably the
most common. It has been estimated that reflux affects 50
million Americans, and that as many as 50% of patients with
laryngeal complaints have reflux-related causes.13,14 LPR
may be associated with an acute, chronic, or intermittent
pattern of laryngitis, with or without granuloma formation. LPR
has also been implicated in the development of laryngeal
carcinoma and stenosis, recurrent laryngospasm, crico
arytenoid fixation, and many other conditions, including globus
pharyngeus, cervical dysphagia, bronchiectasis, asthma, and
chronic cough.15,16 The highest reported association (92%)
is with subglottic stenosis (inchildren and adults).13
Laryngopharyngeal Reflux (LPR)
• Gastroenterologists consider reflux patients who denygastrointestinal
symptoms to be "atypical refluxers," but they are quite typical of the
patients encountered in an otolaryngology practice. Otolaryngology
patients with LPR are probably under-diagnosed and under-treated,
because the signs, symptoms, and mechanisms of LPR are quite
different than those seen in gastroenterology patients, who
characteristically have heartburn, regurgitation, and esophagitis. In
addition, when compared to esophagitis patients, LPR patients have
up rightreflux, normal esophageal acid clearance, and normal
esophagography. Consequently, LPR patients usually present with
symptoms of dysphonia, cough, and frequent throat clearing, butoften
deny having symptoms of heartburn.(Table 48-4)
• Examination of the larynx may reveal a variety of findings. Posterior
laryngitis, demonstrating red arytenoids with interarytenoid mucosal
hypertrophy, is commonly seen with LPR. Subglottic edema forming a
"pseudo-sulcus vocalis" is alsofrequently seen. The larynx may instead
show diffuse edema, Reinke's space edema, or mucosal thickening
without significant erythema. This may cause ventricular effacement.
Diffuse erythema with granular, friable mucosa, and vocal process
granuloma(s), with or without associated laryngeal edema and
erythema are also seen. Although granulomas of the vocal process
may be caused by vocal abuse and endotracheal intubation, available
data indicate that LPR plays a role in most cases
Laryngopharyngeal Reflux (LPR)
• Ambulatory 24-hour double-probe pH monitoring is the
current "gold standard" for the diagnosis of LPR. (The second
probe is placed in the hypopharynx, behind the laryngeal
inlet). This technique is highly sensitive and specific for LPR
and also delineates each patient's reflux pattern, allowing
treatment to be somewhat individualized.17
• The treatment of LPR includes dietary and life style
modifications, and antireflux medication, such as an H2blocker or proton pump inhibitor (PPI), such as omeprazole.
PPIs are the most effective antireflux medicine available,
because unlike theH2-blockers, they can achieve total
suppression of gastric acidproduction. With H2-blockers,
treatment fails in approximately one-third of LPR patients.
Patients who fail medical anti-refluxtherapy may require a
surgical anti-reflux procedure, such as fundoplication
Traumatic Laryngitis
• "Traumatic laryngitis" is commonly caused by vocal abuse, such as
excessive shouting or yelling, but it can also result from persistent
coughing, muscle tension dysphonia, or direct endolaryngeal injury.
Such patients present with various degrees of dysphonia and
odynophonia. The mucosa of the true vocal folds is hyperemic from
dilated vessels on the vocal fold surface. Edema within Reinke's
space develops, and submucosal hemorrhage may occur. This form
of laryngitis is self-limited and subsides within a few days when
treated with voice conservation and humidification.
• Thermal Injury
• Laryngitis due to thermal damage to the larynx is well recognized.
Patients complain of dysphonia, odynophagia, andodynophonia.
Exposure of the larynx to steam, smoke, very hot liquids or food
(particularly if microwaved) leads tosupraglottic edema and
erythema. It is more common in children. Laryngeal edema due to
exposure to free-base cocaine may also present a diagnostic
dilemma. Treatment of such injuries is with humidification,
corticosteroids, and airway observation or intubation if the larynx is
severely edematous.
Angioedema
• Acquired angioedema is an inflammatory reaction characterized by
vascular dilation and increased vascular permeability. This can be
caused by a variety of substances particularly angiotensinconverting enzyme (ACE) inhibitor medications and is potentially
life-threatening if the larynx is involved.
• Hereditary angioedema is an autosomally dominant deficiency of
C1esterase inhibitor that leads to recurrent attacks of
mucocutaneous edema. Diagnosis is based primarily on the history,
although the offending agent may not be readily apparent. Patients
present with edema that may involve the face, oral cavity,
oropharynx, or larynx. The onset is rapid and may be associated
with pruritus. Dysphonia is common with laryngeal involvement.
• Treatment must be aggressive. Supplemental oxygen, epinephrine,
corticosteroids, antihistamines, and aminophylline are the
mainstays of therapy. However, ACE inhibitor related angioedemais
not believed to be IgE mediated and therefore such patients may be
refractory to this therapy. If progressive airway obstruction
develops, intubation or tracheotomy may be required. Chronic
"pretreatment" of hereditary angioedema with danazol appears to
elevate levels of functional C1 esterase inhibitorand may help to
prevent recurrent episodes.
Allergic Laryngitis
• Allergy-mediated inflammation involving the larynx is controversial.
It may be responsible for symptoms of chronic and recurrent
dysphonia in some patients. Anaphylaxis is well known and will not
be re viewed here. Laryngeal chemical sensitivity and delayed food
allergies are less well known. Examination may reveal glottic edema
and erythema as well as muscular tension dysphonia. The most
common triggering substances are insecticides, phenol, and
petroleum- based compounds. Diagnosis is based on the history,
ruling out more common causes such as LPR, a standard allergy
evaluation, and challenge testing with the suspected triggering
agent(s).
• The contribution of vocal abuse, misuse, LPR, and secondary gain
after exposure(s) to such compounds is unknown. Treatment begins
with optimizing vocal hygiene with hydration, conservative voice
use, and treating LPR, if it is present. Training with as peechlanguage pathologist and avoidance of the incitingsubstances are
also critical.
Relapsing Polychondritis
• Relapsing polychondritis is characterized by
episodes of inflammation and fibrosis with
subsequent destruction of the cartilage of the
ears, nose, larynx, and tracheo-bronchial tree.
Laryngeal disease occurs in more than half the
cases and is manifested by dysphonia,
dysphagia, and throat pain. Airway involvement
leads to the high mortality seen with this
disease. Treatment includes dapsone,
corticosteroids and other immunosuppressive
drugs. Tracheotomy may be necessary.