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SECTION V — Diseases of Larynx and Trachea
4. Associated injuries. It is essential to examine for other
injuries like injury to head, cervical spine, chest, abdomen and extremities. X-ray chest for pneumothorax
and gastrograffin swallow for oesophageal tears may be
required.
TREATMENT
CONSERVATIVE
1. Patient should be hospitalized and observed for respiratory distress.
2. Voice rest is essential.
3. Humidification of inspired air is essential.
4. Steroid therapy should be started immediately and in
full dose. It helps to resolve oedema and haematoma
and prevent scarring and stenosis.
5. Antibiotics are given to prevent perichondritis and cartilage necrosis.
SURGICAL
1. Tracheostomy. Endotracheal intubation in cases of
laryngeal trauma may be difficult and hazardous. Tracheostomy is preferred in these cases.
2. Open reduction. Ideally, it is done 3–5 days after injury
and if possible should not be delayed beyond 10 days.
(a) Fractures of hyoid bone, thyroid or cricoid cartilage
can be wired and replaced in their anatomic positions. Miniplates made of titanium can be used for
immobilization of cartilaginous fragments.
(b) Mucosal lacerations are repaired with catgut and
any loose fragments of cartilage removed.
(c) Epiglottis is anchored in its normal position and if
already avulsed, may be excised.
(d) Arytenoid cartilages can be repositioned in their
normal position or may be removed if completely
avulsed.
(e) In laryngotracheal separation, end-to-end anasto-
mosis can be done.
(f) Internal splintage of laryngeal structures may be
required. It is done with a laryngeal stent, or silicone tube which may have to be left for 2–6 weeks
on an average.
(g) Webbing of anterior commissure can be prevented
by a silastic keel.
COMPLICATIONS
1. Laryngeal stenosis, which may be supraglottic, glottic
or subglottic.
2. Perichondritis and laryngeal abscess.
3. Vocal cord paralysis.
Chapter 58
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Acute and Chronic Inflammations
of Larynx
ACUTE LARYNGITIS
Acute laryngitis may be infectious or noninfectious.
AETIOLOGY
The infectious type is more common and usually follows
upper respiratory infection. To begin with, it is viral in
origin but soon bacterial invasion takes place with Strepto-
coccus pneumoniae, Haemophilus influenzae and haemolytic Streptococci or Staphylococcus aureus. Exanthematous
fevers like measles, chickenpox and whooping cough are
also associated with laryngitis.
The noninfectious type is due to vocal abuse, allergy,
thermal or chemical burns to larynx due to inhalation or
ingestion of various substances, or laryngeal trauma such
as endotracheal intubation.
CLINICAL FEATURES
Symptoms are usually abrupt in onset and consist of:
1. Hoarseness which may lead to complete loss of voice.
2. Discomfort or pain in throat, particularly after talking.
3. Dry, irritating cough which is usually worse at night.
4. General symptoms of head cold, rawness or dryness of
throat, malaise and fever if laryngitis has followed viral
infection of upper respiratory tract.
Laryngeal appearances vary with severity of disease. In
early stages, there is erythema and oedema of epiglottis,
aryepiglottic folds, arytenoids and ventricular bands, but
the vocal cords appear white and near normal and stand
out in contrast to surrounding mucosa, betraying the
degree of hoarseness patient has. Later, hyperaemia and
swelling increase. Vocal cords also become red and swollen. Subglottic region also gets involved. Sticky secretions
are seen between the cords and interarytenoid region. In
case of vocal abuse, submucosal haemorrhages may be
seen in the vocal cords.
TREATMENT
1. Vocal rest. This is the most important single factor.
Use of voice during acute laryngitis may lead to incom-
plete or delayed recovery.
2. Avoidance of smoking and alcohol.
3. Steam inhalations. It is done with Tr. Benzoin Co, oil
of eucalyptus or pine are soothing and loosen viscid
secretions.
4. Cough sedative. To suppress troublesome irritating
cough.
5. Antibiotics. When there is secondary infection with
fever and toxaemia or purulent expectoration.
6. Analgesics. To relieve local pain and discomfort.
7. Steroids. Useful in laryngitis following thermal or
chemical burns.
Acute membranous laryngitis. This condition is simi-
lar to acute membranous tonsillitis and is caused by pyogenic nonspecific organisms. It may begin in the larynx
or may be an extension from the pharynx. It should be
differentiated from laryngeal diphtheria.
ACUTE EPIGLOTTITIS (SYN.
SUPRAGLOTTIC LARYNGITIS)
It is an acute inflammatory condition confined to supraglottic structures, i.e. epiglottis, aryepiglottic folds and
arytenoids. There is marked oedema of these structures
which may obstruct the airway.
AETIOLOGY
It is a serious condition and affects children of 2–7 years of
age but can also affect adults. H. influenzae B is the most common organism responsible for this condition in children.
CLINICAL FEATURES
1. Onset of symptoms is abrupt with rapid progression.
2. Sore throat and dysphagia are the common presenting
symptoms in adults.
3. Dyspnoea and stridor are the common presenting
symptoms in children. They are rapidly progressive
and may prove fatal unless relieved.
4. Fever may go up to 40 °C. It is due to septicaemia. Patient’s condition may rapidly deteriorate.
EXAMINATION
1. Depressing the tongue with a tongue depressor may
show red and swollen epiglottis. Indirect laryngoscopy
may show oedema and congestion of supraglottic structure. This examination is avoided for fear of precipitating complete obstruction. It is better done in operation
theatre where facilities for intubation are available.
2. Lateral soft tissue X-ray of neck may show swollen epiglottis (thumb sign).
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SECTION V — Diseases of Larynx and Trachea
TREATMENT
1. Hospitalisation. Essential because of the danger of respiratory obstruction.
2. Antibiotics. Ampicillin or third generation cephalosporin are effective against H. influenzae and are given
by parenteral route (i.m. or i.v.) without waiting for
results of throat swab and blood culture.
3. Steroids. Hydrocortisone or dexamethasone is given
in appropriate doses i.m. or i.v. They relieve oedema
and may obviate need for tracheostomy.
4. Adequate hydration. Patient may require parenteral
fluids.
5. Humidification and oxygen. Patient may require
mist tent or a croupette.
6. Intubation or tracheostomy. May be required for res-
piratory obstruction.
ACUTE LARYNGO-TRACHEO-BRONCHITIS
It is an inflammatory condition of the larynx, trachea
and bronchi; more common than acute epiglottitis.
AETIOLOGY
Mostly, it is viral infection (parainfluenza type I and II)
affecting children between 6 months and 3 years of age.
Male children are more often affected. Secondary bac-
terial infection by Gram-positive cocci soon supervenes.
suprasternal and intercostal recession. Differences between acute epiglottitis and acute laryngo-tracheo-bronchitis are given in Table 58.1.
TREATMENT
1. Hospitalisation is often essential because of the increasing difficulty in breathing. Any manipulation of
the patient can precipitate acute respiratory distress.
Administer inhalation anaesthesia (sevoflurane) and
oxygen to the patient, secure i.v. line and then perform
laryngoscopy to make the diagnosis. Take laryngeal
swabs for culture and sensitivity tests and intubate the
patient. Most of the patients recover with antibiotics,
steroids and intubation within 48 h.
2. Antibiotics like ampicillin 50 mg/kg/day in divided
doses are effective against secondary infections due to
Gram-positive cocci and H. influenzae.
3. Humidification helps to soften crusts and tenacious
secretions which block tracheobronchial tree.
4. Parenteral fluids are essential to combat dehydration.
5. Steroids, e.g. hydrocortisone 100 mg i.v. may be useful
to relieve oedema.
6. Adrenaline, racemic adrenaline administered via a respirator is a bronchodilator and may relieve dyspnoea
and avert tracheostomy.
7. Intubation/tracheostomy is done, should respiratory
obstruction increase in spite of the above measures.
Tracheostomy is done if intubation is required beyond
72 h. Assisted ventilation may be required.
PATHOLOGY
The loose areolar tissue in the subglottic region swells
up and causes respiratory obstruction and stridor. This,
coupled with thick tenacious secretions and crusts, may
completely occlude the airway.
SYMPTOMATOLOGY
Disease starts as upper respiratory infection with hoarseness and croupy cough. There is fever of 39–40 °C. This
may be followed by difficulty in breathing and inspiratory type of stridor. Respiratory difficulty may gradually increase with signs of upper airway obstruction, i.e.
TABLE 58.1 DIFFERENCES BETWEEN ACUTE EPIGLOTTITIS AND ACUTE LARYNGO-TRACHEO-BRONCHITIS IN
CHILDREN
Acute epiglottitis Acute laryngo-tracheo-bronchitis (or group)
Causative organism Haemophilus influenzae type B Parainfluenza virus type I and II
Age 2–7 years 3 months to 3 years
Pathology Supraglottic larynx Subglottic area
Prodromal symptoms Absent Present
Onset Sudden Slow
Fever High Low grade or no fever
Patient’s look Toxic Nontoxic
Cough Usually absent Present (barking seal-like)
Stridor Present and may be marked Present
Odynophagia Present, with drooling of secretions Usually absent
Radiology
Treatment Humidified oxygen, third generation
a
Examination of larynx and radiographs are avoided lest complete obstruction is precipitated. Examination is done in the operation theatre where im-
mediate intubation can be done.
a
Thumb sign on lateral view Steeple sign on anteroposterior view of neck
cephalosporin (ceftriaxone) or amoxicillin
LARYNGEAL DIPHTHERIA
AETIOLOGY
Mostly, it is secondary to faucial diphtheria affecting children below 10 years of age. Incidence of diphtheria in general is declining due to widespread use of immunization.
PATHOLOGY
Effects of laryngeal diphtheria are due to:
1. Formation of a tough pseudomembrane over the larynx
and trachea which may completely obstruct the airway.
Humidified O2 tent, steroids
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2. Exotoxin liberated by bacteria leading to myocarditis
and various neurological complications.
CLINICAL FEATURES
• General symptoms. Onset is insidious with low-grade
fever (100–101 °F), sore throat and malaise but patient
is very toxaemic with tachycardia and thready pulse.
• Laryngeal symptoms. Hoarse voice, croupy cough,
inspiratory stridor, increasing dyspnoea with marked
upper airway obstruction.
• Membrane. Greyish white membrane is seen on the
tonsil, pharynx and soft palate. It is adherent and its
removal leaves a bleeding surface. Similar membrane is
seen over the larynx and trachea.
• Cervical lymphadenopathy. Characteristic “bull-
neck” may be seen.
DIAGNOSIS
Laryngeal diphtheria is mostly secondary to faucial diphtheria. Diagnosis is always clinical but confirmed by
smear and culture of Corynebacterium diphtheriae. Treatment is started on clinical suspicion.
TREATMENT
1. Diphtheria antitoxin. Dose depends on clinical severity and duration of illness, and varies from 20,000 to
100,000 units i.v. route as saline infusion after a test
dose. It neutralizes free toxin circulating in the blood.
2. Antibacterials. Benzylpenicillin, 500,000 units i.m.
every 6 h for 6 days, is effective against diphtheria bacilli. Erythromycin can be given to those who are allergic to penicillin.
3. Maintenance of airway. Tracheostomy may become
essential. Direct laryngoscopy, removal of diphtheritic
membrane and intubation can be done. Intubation
relieves respiratory obstruction and can make subsequent tracheostomy easy.
4. Complete bed rest. Complete bed rest for 2–4 weeks is
essential to guard against effects of myocarditis.
(b) Infection in neighbourhood, e.g. peritonsillar ab-
scess, retropharyngeal abscess and Ludwig’s angina.
2. Trauma. Surgery of tongue, floor of mouth, laryngeal
trauma, foreign body, endoscopy especially in children, intubation, thermal or caustic burns or inhalation or irritant gases or fumes.
3. Neoplasms. Cancer of larynx or laryngopharynx often
associated with deep ulceration.
4. Allergy. Angioneurotic oedema or anaphylaxis.
5. Radiation. For cancer of larynx or pharynx.
6. Systemic diseases. Nephritis, heart failure or myxoedema.
SYMPTOMS AND SIGNS
1. Airway obstruction. Degree of respiratory distress varies. Tracheostomy may become essential.
2. Inspiratory stridor.
3. Indirect laryngoscopy. It shows oedema of supraglot-
tic or subglottic region. Children may require direct
laryngoscopy.
TREATMENT
If there is airway obstruction, intubation of larynx or tracheostomy will be immediately required. Less severe cases
are treated conservatively and treatment will depend on
the cause. An injection of adrenaline (1:1000) 0.3–0.5ml
i.m., repeated in 15 min if necessary, is useful in allergic
or angioneurotic oedema. Steroids are useful in epiglottitis, laryngo-tracheo-bronchitis or oedema due to traumatic allergic or postradiation causes.
CHRONIC LARYNGITIS
A. CHRONIC LARYNGITIS WITHOUT
HYPERPLASIA (Chronic Hyperaemic
Laryngitis)
It is a diffuse inflammatory condition symmetrically
involving the whole larynx, i.e. true cords, ventricular
bands, interarytenoid region and root of the epiglottis.
COMPLICATIONS
1. Asphyxia and death due to airway obstruction.
2. Toxic myocarditis and circulatory failure.
3. Palatal paralysis with nasal regurgitation.
4. Laryngeal and pharyngeal paralysis.
OEDEMA OF LARYNX
Often termed “oedema glottidis” in the past, it involves
the supraglottic and subglottic region where laryngeal
mucosa is loose. Oedema of the vocal cords occurs rarely
because of the sparse subepithelial connective tissue.
AETIOLOGY
1. Infections
(a) Acute epiglottitis, laryngo-tracheo-bronchitis, tu-
berculosis or syphilis of larynx.
Aetiology
1. It may follow incompletely resolved acute simple laryngitis or its recurrent attacks.
2. Presence of chronic infection in paranasal sinuses,
teeth and tonsils and the chest are important contributory causes.
3. Occupational factors, e.g. exposure to dust and fumes
such as in miners, strokers, gold or iron smiths and
workers in chemical industries.
4. Smoking and alcohol.
5. Persistent trauma of cough as in chronic lung diseases.
6. Vocal abuse.
Clinical Features
1. Hoarseness. This is the commonest complaint. Voice
becomes easily tired and patient becomes aphonic by
the end of the day.
2. Constant hawking. There is dryness and intermittent
tickling in the throat and patient is compelled to clear
the throat repeatedly.
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3. Discomfort in the throat.
4. Cough. It is dry and irritating.
Laryngeal examination. There is hyperaemia of laryngeal structures. Vocal cords appear dull red and rounded.
Flecks of viscid mucus are seen on the vocal cords and
interarytenoid region.
Treatment
1. Eliminate infection of upper or lower respiratory
tract. Infection in the sinuses, tonsils, teeth or chronic
chest infection (bronchitis, bronchiectasis, tuberculo-
sis, etc.) should be treated.
2. Avoidance of irritating factors. E.g. smoking, alcohol
or polluted environment, dust and fumes.
3. Voice rest and speech therapy. Voice rest has to be
prolonged for weeks or months. Patient should receive
training in proper use of voice.
4. Steam inhalations. They help to loosen secretions
and give relief.
5. Expectorants. They help to loosen viscid secretions
and give relief from hawking.
B. CHRONIC HYPERTROPHIC LARYNGITIS
(SYN. CHRONIC HYPERPLASTIC
LARYNGITIS)
It may be either a diffuse and symmetrical process or a
localized one, the latter appearing like a tumour of the
larynx. Localized variety presents as dysphonia plica ventricularis, vocal nodules, vocal polyp, Reinke’s oedema
and contact ulcer. (They have been described in the relevant sections.)
Aetiology
Same as discussed under chronic laryngitis without
hyperplasia.
Pathology
Pathological changes start in the glottic region and later
may extend to ventricular bands, base of epiglottis and even
subglottis. Mucosa, submucosa, mucous glands and in later
stages intrinsic laryngeal muscles and joints may be affected.
Initially, there is hyperaemia, oedema and cellular infiltration in the submucosa. The pseudostratified ciliated
epithelium of respiratory mucosa changes to squamous
type, and squamous epithelium of the vocal cords to hyperplasia and keratinization. The mucous glands suffer
hypertrophy at first but later undergo atrophy with diminished secretion and dryness of larynx.
Clinical Features
This disease mostly affects males (8:1) in the age group of
30–50 years.
Hoarseness, constant desire to clear the throat, dry
cough, tiredness of voice and discomfort in throat when
the voice has been used for an extended period of time
are the common presenting symptoms.
Examination. On examination, changes are often diffuse and symmetrical.
1. Laryngeal mucosa, in general, is dusky red and thickened.
2. Vocal cords appear red and swollen. Their edges lose
sharp demarcation and appear rounded. In late stages,
cords become bulky and irregular giving nodular
appearance.
3. Ventricular bands appear red and swollen and may be
mistaken for prolapse or eversion of the ventricle.
4. Mobility of cords gets impaired due to oedema and
infiltration, and later due to muscular atrophy or
arthritis of the cricoarytenoid joint.
Treatment
1. conserVatiVe. Same as for chronic laryngitis without
hyperplasia.
2. surgical. Stripping of vocal cords, removing the hy-
perplastic and oedematous mucosa, may be done in selected cases. Damage to underlying vocal ligament should
be carefully avoided. One cord is operated at a time.
POLYPOID DEGENERATION OF VOCAL
CORDS (REINKE’S OEDEMA)
It is bilateral symmetrical swelling of the whole of membranous part of the vocal cords, most often seen in middle-aged men and women. This is due to oedema of the
subepithelial space (Reinke’s space) of the vocal cords.
Chronic irritation of vocal cords due to misuse of voice,
heavy smoking, chronic sinusitis and laryngopharyngeal
reflex are the probable aetiological factors. It can also occur in myxoedema.
CLINICAL FEATURES
Hoarseness is the common symptom. Patient uses false
cords for voice production and this gives him a lowpitched and rough voice.
On indirect laryngoscopy, vocal cords appear as fusi-
form swellings with pale translucent look. Ventricular
bands may appear hyperaemic and hypertrophic and
may hide the view of the true cords.
TREATMENT
1. Decortication of the vocal cords, i.e. removal of strip
of epithelium, is done first on one side and 3–4 weeks
later on the other.
2. Voice rest.
3. Speech therapy for proper voice production.
PACHYDERMIA LARYNGIS
It is a form of chronic hypertrophic laryngitis affecting
posterior part of larynx in the region of interarytenoid
and posterior part of the vocal cords.
Clinically, patient presents with hoarseness or husky
voice and irritation in the throat. Indirect laryngoscopy
reveals heaping up of red or grey granulation tissue in the
interarytenoid region and posterior thirds of vocal cords;
the latter sometimes showing ulceration due to constant
hammering of vocal processes as in talking, forming
what is called “contact ulcer.” The condition is bilateral
and symmetrical. It does not undergo malignant change.
However, biopsy of the lesion is essential to differentiate
Chapter 58 — Acute and Chronic Inflammations of Larynx
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331
the lesion from carcinoma and tuberculosis. Aetiology is
uncertain. It is mostly seen in men who indulge in excessive alcohol and smoking. Other factors are excessive
forceful talking and gastro-oesophageal reflux disease
where posterior part of larynx is being constantly bathed
with acid juices from the stomach.
Treatment is removal of granulation tissue under operating microscope which may require repetition, control
of acid reflux and speech therapy.
ATROPHIC LARYNGITIS
(LARYNGITIS SICCA)
It is characterized by atrophy of laryngeal mucosa and
crust formation. Condition is often seen in women and is
associated with atrophic rhinitis and pharyngitis.
Common symptoms include hoarseness of voice
which temporarily improves on coughing and removal
of crusts. Dry irritating cough and sometimes dyspnoea is
due to obstructing crusts.
Examination shows atrophic mucosa covered with
foul-smelling crusts. When crusts have been expelled,
mucosa may show excoriation and bleeding. Crusting
may also be seen in the trachea.
Treatment is elimination of the causative factor and
humidification. Laryngeal sprays with glucose in glycerine or oil of pine are comforting and help to loosen the
crusts. Associated nasal and pharyngeal conditions will
require attention. Expectorants containing ammonium
chloride or iodides also help to loosen the crusts.
LARYNGEAL EXAMINATION
1. Hyperaemia of the vocal cord in its whole extent or
confined to posterior part with impairment of adduction is the first sign.
2. Swelling in the interarytenoid region giving a mamillated appearance.
3. Ulceration of vocal cord giving mouse-nibbled appearance.
4. Superficial ragged ulceration on the arytenoids and interarytenoid region.
5. Granulation tissue in interarytenoid region or vocal
process of arytenoid.
6. Pseudoedema of the epiglottis “turban epiglottis.”
7. Swelling of ventricular bands and aryepiglottic
folds.
8. Marked pallor of surrounding mucosa.
DIAGNOSIS
In addition to X-ray chest and sputum examination, biopsy of laryngeal lesion is essential to exclude carcinoma
and differentiate it from other condition.
TREATMENT
Treatment is the same as for pulmonary tuberculosis.
Voice rest is important.
LUPUS OF THE LARYNX
TUBERCULOSIS OF LARYNX
AETIOLOGY
It is almost always secondary to pulmonary tuberculosis,
mostly affecting males in middle age group. Tubercle bacilli
reach the larynx by bronchogenic or haematogenous routes.
PATHOLOGY
Disease affects posterior part of larynx more than anterior. Parts affected are: (i) interarytenoid fold, (ii) ventricular bands, (iii) vocal cords and (iv) epiglottis, in that
order.
Tubercle bacilli, carried by sputum from the bronchi,
settle and penetrate the intact laryngeal mucosa particularly in the interarytenoid region (bronchogenic spread).
This leads to formation of submucosal tubercles which
may later caseate and ulcerate. Laryngeal mucosa appears
red and swollen due to cellular infiltration (pseudoedema). Stages of perichondritis and cartilage necrosis are
not commonly seen these days.
SYMPTOMS AND SIGNS
They would greatly depend on the stage of tuberculosis.
Weakness of voice is the earliest symptom followed by
hoarseness. Ulceration in the larynx gives rise to severe
pain which may radiate to the ears. Swallowing is painful
with marked dysphagia in later stages.
It is an indolent tubercular infection associated with lupus
of nose and pharynx. Unlike tuberculosis of larynx which
mostly affects posterior parts, lupus involves the anterior part of larynx. Epiglottis is involved first and may be
completely destroyed by the disease. The lesion spreads
to aryepiglottic folds and sometimes to ventricular bands.
Lupus of larynx is a painless and often an asymptomatic
condition and may be discovered on routine laryngeal
examination in cases of lupus of nose. There is no pulmonary tuberculosis. Treatment is antitubercular drugs.
Prognosis is good.
SYPHILIS OF THE LARYNX
It is a rare condition now. Only gumma of tertiary stage
is sometimes seen. It may occur in any part of the larynx and present as a smooth swelling which may later
ulcerate. Diagnosis is only on biopsy and serological tests.
Laryngeal stenosis is a frequent complication.
LEPROSY OF THE LARYNX
It is a rare condition and is often associated with leprosy
of the skin and nose. It presents as diffuse nodular infiltration of epiglottis, aryepiglottic folds and arytenoids.
Lesions may ulcerate. It is associated with nasal leprosy.
Diagnosis is made on biopsy from the lesion. Deformity
of the laryngeal inlet and stenosis are the end results of
this disease after healing.
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SCLEROMA OF THE LARYNX
It is a chronic inflammatory condition caused by
Klebsiella rhinoscleromatis. Nasal involvement is very
common in India. Laryngeal involvement may be seen
occasionally with or without a nasal lesion. Typically,
it presents as a smooth red swelling in the subglottic
region. Hoarseness of voice, wheezing and dyspnoea
may be the presenting symptoms in addition to the
nasal lesion. Diagnosis is made on biopsy. Treatment
is by streptomycin or tetracycline, often combined
with steroids to prevent fibrosis. Subglottic stenosis is a frequent complication requiring subsequent
reconstructive surgery.
LARYNGEAL MYCOSIS
Fungal infections such as candidiasis, histoplasmosis and
blastomycosis may rarely affect the larynx. Diagnosis is
usually made on biopsy and on finding a similar lesion in
other parts of the body.
Chapter 59
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Congenital Lesions of Larynx
and Stridor
CONGENITAL LESIONS OF LARYNX
• Laryngomalacia (congenital laryngeal stridor)
• Congenital vocal cord paralysis
• Congenital subglottic stenosis
• Laryngeal web
• Subglottic haemangioma
• Laryngo-oesophageal cleft
• Laryngocele
• Laryngeal cyst
1. LaryngoMaLacia (congenitaL LaryngeaL StriDor).
It is the most common congenital abnormality of the
larynx. It is characterized by excessive flaccidity of supraglottic larynx which is sucked in during inspiration producing stridor and sometimes cyanosis. Stridor is increased
on crying but subsides on placing the child in prone position; cry is normal. The condition manifests at birth or
soon after, and usually disappears by 2 years of age. Direct
laryngoscopy shows elongated epiglottis, curled upon itself
(omega-shaped Ω), floppy aryepiglottic folds and prominent arytenoids. Flexible laryngoscope is very useful to
make the diagnosis. Laryngomalacia cannot be diagnosed
in a paralyzed patient. Mostly, treatment is conservative.
Tracheostomy may be required for some cases of severe respiratory obstruction (Figure 59.1). Supraglottoplasty is required in cases of severe laryngomalacia.
2. congenitaL vocaL corD ParaLySiS. It results from
birth trauma when recurrent laryngeal nerve is stretched
during breech or forceps delivery or can result from
anomalies of the central nervous system.
3. congenitaL SuBgLottic StenoSiS. It is due to ab-
normal thickening of cricoid cartilage or fibrous tissue
seen below the vocal cords. Child may remain asymptomatic till upper respiratory infection causes dyspnoea and
stridor. Cry is normal as in laryngomalacia. Diagnosis is
made when subglottic diameter is less than 4 mm in fullterm neonate (normal 4.5-5.5 mm) or 3 mm in premature
neonate (normal 3.5 mm). Many cases of congenital stenosis improve as the larynx grows but some may require
surgery.
4. LaryngeaL weB (Figure 59.2). It is due to incom-
plete recanalization of larynx. Mostly, the web is seen
between the vocal cords and has a concave posterior margin. Presenting features are airway obstruction, weak cry
or aphonia dating from birth. Treatment depends on the
thickness of the web. Thin webs can be cut with a knife
or CO2 laser. Thick ones may require excision via laryngofissure and placement of a silicon keel and subsequent
dilatations.
5. SuBgLottic haeMangioMa. Though congenital,
patient is asymptomatic till 3-6 months of age when
haemangioma begins to increase in size. About 50% of
the children have associated cutaneous haemangiomas.
Patient may present with stridor but has a normal cry.
Agitation of the patient or crying may increase airway
obstruction due to venous filling. Direct laryngoscopy shows reddish-blue mass below the vocal cords.
Biopsy is sometimes, not always, associated with haemorrhage. Some patients have associated mediastinal
haemangioma.
Depending on individual case, the treatment is:
(a) Tracheostomy and observation, as many haemangio-
mas involute spontaneously.
(b) Steroid therapy. Dexamethasone 1 mg/kg/day for
1 week and then prednisolone 3 mg/kg in divided
doses for 1 year.
(c) CO2 laser excision, if lesion is small.
6. Laryngo-oeSoPhageaL cLeFt. It is due to failure of
the fusion of cricoid lamina. Patient presents with repeated aspiration and pneumonitis. Coughing, choking and
cyanosis are present at the time of feeding.
7. LaryngoceLe. It is dilatation of laryngeal saccule
and extends between thyroid cartilage and the ventricle.
It may be internal, external or combined. Treatment is
endoscopic or external excision.
8. LaryngeaL cySt. It arises in the aryepiglottic fold
and appears as bluish, fluid-filled smooth swelling in the
supraglottic larynx. Respiratory obstruction may necessitate tracheostomy. Needle aspiration or incision and
drainage of cyst provide an emergency airway. Treatment
is deroofing the cyst or excision with CO2 laser.
STRIDOR
Stridor is noisy respiration produced by turbulent airflow
through the narrowed air passages. It may be heard during inspiration, expiration or both (Figure 59.3).
• Inspiratory stridor is often produced in obstructive le-
sions of supraglottis or pharynx, e.g. laryngomalacia or
retropharyngeal abscess.
• Expiratory stridor is produced in lesions of thoracic tra-
chea, primary and secondary bronchi, e.g. bronchial
foreign body, and tracheal stenosis.
• Biphasic stridor is seen in lesions of glottis, subglottis
and cervical trachea, e.g. laryngeal papillomas, vocal
cord paralysis and subglottis stenosis.
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SECTION V — Diseases of Larynx and Trachea
Figure 59.1. Laryngomalacia. Note: epiglottis is folded longitudinally forming an omega.
Figure 59.2. Laryngeal web.
AETIOLOGY
Stridor may arise from lesions of nose, tongue, mandible,
pharynx, larynx or trachea and bronchi. Common causes
of stridor in infants and children are given below:
Figure 59.3. Types of stridor and their site of origin.
5. Larynx.
(a) Congenital. Laryngeal web, laryngomalacia, cysts,
vocal cord paralysis, subglottic stenosis.
(b) Inflammatory. Epiglottitis, laryngotracheitis, diph-
theria, tuberculosis.
(c) Neoplastic. Haemangioma and juvenile multiple
papillomas, carcinoma in adults.
(d) Traumatic. Injuries of larynx, foreign bodies, oede-
ma following endoscopy, or prolonged intubation.
(e) Neurogenic. Laryngeal paralysis due to acquired
lesions.
(f) Miscellaneous. Tetanus, tetany, laryngismus stridulus.
6. Trachea and bronchi
(a) Congenital. Atresia, stenosis, tracheomalacia.
(b) Inflammatory. Tracheobronchitis.
(c) Neoplastic. Tumours of trachea.
(d) Traumatic. Foreign body, stenosis trachea (e.g.
following prolonged intubation or tracheostomy).
7. Lesions outside respiratory tract
(a) Congenital. Vascular rings (cause stridor and dys-
phagia), oesophageal atresia, tracheo-oesophageal
fistula, congenital goitre, cystic hygroma.
(b) Inflammatory. Retropharyngeal and retro-oesopha-
geal abscess.
(c) Traumatic. FB oesophagus (secondary tracheal
compression).
(d) Tumours. Masses in neck.
1. Nose. Choanal atresia in newborn.
2. Tongue. Macroglossia due to cretinism, haemangioma
or lymphangioma, dermoid at base of tongue, lingual
thyroid.
3. Mandible. Micrognathia, Pierre-Robin syndrome. In
these cases, stridor is due to falling back of tongue.
4. Pharynx. Congenital dermoid, adenotonsillar hypertrophy, retropharyngeal abscess, tumours.
MANAGEMENT
History
Stridor is a physical sign and not a disease. Attempt
should always be made to discover the cause. It is important to elicit:
1. Time of onset. To find whether cause is congenital or
acquired.
2. Mode of onset. Sudden onset (foreign body, oedema),
gradual and progressive (laryngomalacia, subglottic
haemangioma, juvenile papillomas).
3. Duration. Short (foreign body, oedema, infections),
long (laryngomalacia, laryngeal stenosis, subglottic
haemangioma, anomalies of tongue and jaw).
4. Relation to feeding. Aspiration in laryngeal paralysis,
oesophageal atresia, laryngeal cleft, vascular ring, foreign body oesophagus.
Chapter 59 — Congenital Lesions of Larynx and Stridor
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5. Cyanotic spells. Indicate need for airway maintenance.
6. Aspiration or ingestion of a foreign body.
7. Laryngeal trauma. Blunt injuries to larynx, intubation, endoscopy.
Physical Examination
1. Stridor is always associated with respiratory distress.
There may be recession in suprasternal notch, sternum, intercostal spaces and epigastrium during inspiratory efforts.
2. Note whether stridor is inspiratory, expiratory
or biphasic which indicates the probable site of
obstruction.
3. Note associated characteristics of stridor.
(a) Snoring or snorting sound-nasal or nasopharyn-
geal cause.
(b) Gurgling sound and muffled voice-pharyngeal
cause.
(c) Hoarse cry or voice-laryngeal cause at vocal cords.
Cry is normal in laryngomalacia and subglottic
stenosis.
(d) Expiratory wheeze-bronchial obstruction.
4. Associated fever indicates infective condition, e.g.
acute laryngitis, epiglottitis, laryngo-tracheo-bronchitis or diphtheria.
5. Stridor of laryngomalacia, micrognathia, macroglossia
and innominate artery compression disappears when
baby lies in prone position.
6. Sequential auscultation with unaided ear and with
stethoscope over the nose, open mouth, neck and the
chest helps to localize the probable site of origin of
stridor.
7. Examination of nose, tongue, jaw and pharynx and
larynx can exclude local pathology in these areas.
In adults, indirect laryngoscopy can be done easily
while infants and children require flexible fibreoptic
laryngoscopy.
FLexiBLe FiBreoPtic LaryngoScoPy. It can be done
under topical anaesthesia as an outdoor procedure and
allows examination of nose, nasopharynx and larynx.
It helps in the diagnosis of laryngomalacia, vocal cord
paralysis, laryngeal papillomas, laryngeal cysts and
congenital anomalies of larynx, e.g. laryngeal web or
clefts.
INVESTIGATIONS
History and clinical examination will dictate the type of
tests required.
1. Soft tissue lateral and PA view of neck and X-ray chest
in PA and lateral view help in diagnosing the foreign
bodies of the airway.
2. X-ray chest in inspiratory and expiratory phases or a
fluoroscopy of chest help to diagnose radiolucent foreign bodies.
3. CT scan with contrast is helpful for mediastinal mass
and other congenital vascular anomalies compressing
the trachea or bronchi, e.g. anomalous innominate artery, double aortic arch or an anomalous left pulmonary artery forming a sling around the trachea.
4. Angiography may be needed for above vascular anomalies before operation.
5. Oesophagogram with contrast may be needed for tracheobronchial fistula or aberrant vessels or oesophageal atresia.
Direct laryngoscopy
Microlaryngoscopy and bronchoscopy under general anaesthesia. This procedure is done in operation theatre with
full preparation for resuscitative measures to deal with
respiratory distress. Patient is monitored for oxygen saturation, pulse, blood pressure and electrocardiography.
Services of an expert anaesthetist are essential. Anaesthesia is induced with insufflation and i.v. route established.
Patient is kept on spontaneous respiration.
After a quick and short direct laryngoscopy, broncho-
scope is inserted to examine the air passage from the subglottis to bronchi for any obstruction. Secretions can be
collected for culture and sensitivity, crusts and foreign
body if any removed. After bronchoscopy, child is intubated and examination of larynx or oesophagus can be done.
Microlaryngoscopy can be done without intubation with
patient on spontaneous breathing and oxygen and gases being delivered through a catheter via the laryngoscope. Magnification can be provided with telescope or microscope.
TREATMENT
Once the diagnosis has been made, treatment of exact
cause can be planned.
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