Professional Documents
Culture Documents
By
Dr T Balasubramanian
Third (Final) M.B.B.S. Degree Examination Otolaryngology
September 2010
(2x15=30)
1. What is stridor? Enumerate the causes of stridor. Describe briefly the management modalities of
stridor.
Definition:
Stridor is defined as high pitched sound caused due to turbulent airflow in the upper airway due to
obstruction. This is actually an emergency and airway should be secured at the earliest in order to
save the patient.
Classification of stridor:
Inspiratory stridor – in case of airway obstruction above the level of vocal cords
Expiratory stridor – in case of obstruction at the level of bronchi (Bronchial asthma)
Biphasic stridor – stridor is present during both during inspiratory and expiratory phases. This is
classically caused due to tracheal obstruction. (Tracheomalacia is the classic example).
Causes for stridor in infants and adults are different and variable.
Causes of stridor:
Causes for stridor can be grossly classified into:
Laryngeal causes
Extralaryngeal causes
Laryngeal causes of stridor include varying disorders affecting laryngeal airway leading onto
obstructive airway pathology.
Congenital causes – These conditions cause stridor in infants. They include:
1. Infantile larynx – causing laryngomalacia
2. Laryngeal web / stenosis
3. Laryngomalacia
4. Congenital cysts / hemangioma
Neoplasms:
Includes both benign and malignant lesions.
Papillomas – two types juvenile and adults. Juvenile papilloma are multiple and their adult
counterpart is single. Juvenile papilloma has a high recurrence rate while adult papillomas after
removal are not known to recur.
Cysts – These are benign and can be surgically removed
Tumors – Benign / malignant. Malignant tumors involving larynx causes stridor due to
1. Obstruction to the airway
2. Paralysis of both vocal cords
3. Fixity of both arytenoids
4. Laryngeal oedema following irradiation
Figure showing the laryngeal causes of stridor
Inflammatory causes:
These include
Acute laryngitis – very rarely they cause stridor
Diptheria – Membrane dislodges and obstructs laryngeal inlet
Angioneurotic oedema – Steroids will help in these patients
Acute laryngotracheal bronchitis – common in children
Foreign bodies:
Aspiration of foreign bodies are rare causes of stridor. More common in children.
Neurological:
Vocal cord paralysis – Bilateral abductor paralysis will cause stridor. This can be caused due to
involvement of recurrent laryngeal nerve on both sides due to thyroid malignancy / or due to
injury following total thyroidectomy.
Hypocalcemic tetany can also lead to stridor in rare cases.
Management:
Priority should be given to securing the airway as early as possible.
Depending on the probable cause of stridor the management modality can be decided.
Attempting to oxygenate the patient: This is done on an immediate basis as a first aid procedure.
Oxygen can be administered either by nasal prongs / face mask. Nasal prongs are better tolerated
by patients.
Intubation- This is the easiest way to secure the airway on an immediate basis. This may not work if
stridor is caused due to tumors / oedema of larynx. Attempting to intubate these patients would do
more harm than good in these patients.
Contraindications for intubation:
1. Presence of hoarseness of voice in addition to stridor – This indicates coexistant malignancy.
Larynx of these patients should be examined before attempting intubation. This can be performed
by indirect laryngeal examination / video laryngoscopic examination.
2. Absence of laryngeal crepitus – This again indicates either the presence of foreign body at the
level of cricopharynx or growth at the level of cricopharynx. Intubation should not be attempted
in these patients.
3. Extralaryngeal causes of stridor is a contraindication for intubation.
Tracheostomy should be performed as a life saving procedure in these patients if intubation fails
or if it is contraindicated.
Before taking up the patient for tracheostomy the following investigations are a must:
Xray soft tissue neck lateral view to assess the adequacy of subglottic air column. For a
a successful tracheostomy a patient must have an adequate subglottic air column. This x ray
will also show any foreign body at the level of cricopharynx, retropharyngeal abscess etc.
Surgically securing the airway can be performed by any of these following methods:
Percutaneous tracheostomy
Criothyroidotomy
Tracheostomy
The aim of all these procedures is to secure the airway by surgically bypassing the obstructing
airway lesion.
Uncinectomy:
Uncinate process is identified and medialized using a probe. It is completely removed using a
sickle knife / back biting forceps. It is important that the uncinate process is removed completely
including its inferior horizontal portion. Natural ostium of maxillary sinus can be seen when the
horizontal portion of inferior part of uncinate is removed. The natural ostium can be widened
using a back biting forceps.
Clearance of frontal recess area comes next. The frontal recess area can be widened after bulla
ethmoidalis is deroofed.
The horizontal portion of middle turbinate separates the anterior ethmoidal cells from the posterior
group. If the posterior group of ethmoidal cells are found to be involved then they can be accessed
after breaching the basal lamella. The idea is to remove the diseased mucosa, widening the
drainage channels of paranasal sinuses thereby allowing them to be ventilated normally. This
ensures faster regeneration of the ciliated columnar epithelium and restoration of normal ciliary
motility.
Complications of FESS:
1. Bleeding
2. CSF leak
3. Injury to orbit and its contents
4. Synechiae formation
b. Stapedial reflex:
Introduction:
Contraction of stapedial muscle occurs under normal conditions when a loud acoustic stimulus
is presented to the auditory system. This muscle contraction causes a stiffening of the
ossicular chain and decreases the compliance of the middle ear system. This change in the
middle ear compliance an be recorded by tympanometry. This reflex is binaural and simultaneously
occurs in both the ears. This reflex is activated in normal adults when the sound pressure levels
range between 70-105 dBHL.
Stapedial muscle contraction in response to intense sound signal occurs bilaterally because the
reflex pathway has both ipsilateral and contralateral projections. Acoustic reflex thresholds are
usually estimated in response to stimuli of 500, 1000, 2000, and 4000 Hz. For screening
purposes it is sufficient if recording is made at 1000 Hz.
Reflex pathway:
Any reflex pathway by definition should include:
1. Sensory limb - Input
2. Central integration
3. Motor limb – Output
This stapedial reflex is designed to be protective in nature that limits the damage caused by high
intensity sound. The sensory signals travel to the cochlear nuclei via the auditory component
of the 8th cranial nerve. From the cochlear nucleus signals travel to the superior olivary complex
bilaterally, and from there to the lower motor neurons in the facial nucleus which innervates
the stapedius muscle.
Indications:
1. Objective assessment of hearing – Range of acoustic reflex in persons with normal hearing
averages between 70-100dB sound pressure level. In conductive hearing losses, greater the loss
greater becomes the acoustic threshold reflex. Where as in sensorineural hearing loss the
acoustic reflex threshold may be within normal range, this is true in patients with mild to
moderate levels of sensorineural hearing losses with recruitment.
2. Can be used as a topognostic test in patients with facial nerve paralysis
3. Can be used in identifying deafness in infants
4. Acoustic neuroma dianosis
Contraindications:
1. In infants under the age of 7 months due to extreme pliability of external canal
2. In the presence of wax as the results may not be reliable
c. Scarlet fever:
Introduction:
Also known as scarlatina. It is an exotoxin mediated disease arising from group A Beta hemolytic
streptococcal infection. This condition usually evolves from tonsillar / pharyngeal focal infection.
Bacteriology:
Group A Betahemolytic streptococci are known to secrete a number of enzymes of toxins. One
such toxin is known as the erythrogenic toxin which is responsible for the pathognomonic rash
of scarlet fever. These organisms are known to survive extremes of temperature and are spread
via fomites.
During the 18th century scarlet fever was one of the most dreaded epidemics. With the advent of
excellent antibiotics this condition is not threatening anymore.
Incidence:
This condition frequently affects children between 4-8 years. This infection is rare in children under
the age of 2 because of the presence of maternal antibodies.
Clinical features:
Scarlet fever has an incubation period ranging from 1-4days. Evolution and presentation of this
disease is usually dramatic. These patients complain of:
Sudden onset fever
Throat pain
Malaise
Myalgia
Characteristic skin rash appears within 12 – 48 hours after the onset of fever.
If these patients are untreated the fever peaks by 48 hours.
Condition abates within a couple of days after starting treatment with appropriate antibiotics.
On examination:
Exudative tonsillitis usually precede this condition.
Tonsillar infections are usually accompanied by erythematous oral mucous membrane along with
petechiae / punctate red macules over hard palate/soft palate/uvula. These spots are known as
Forchheimer's spots. The tongue appears coated and reddish “raspberry tongue”.
Features of skin rash:
1. Rash generally appears within 12 – 48 hours after the onset of fever. In the beginning it appears
as erythematous patches below the pinna, chest and axilla. Dissemination to the trunk and
extremities occur within the first day.
2. The rashes typically consist of scarlet macules over generalized erythema (Boiled lobster
appearance).
3. The skin lesion later evolves to become more diffuse, and later turn punctate resembling
sunburn / goose pimples.
4. Fragile capillaries under the skin ruptures displaying arrays of petechiae known as (Pastia
lines).
5. Circumoral pallor is another distinguishing feature seen in these patients.
6. Peeling of skin occurs in the skin of axilla, groin, and toes.
Blood count – shows predominant leucocytosis. Eosinophilia develops during the first week of
infection.
Throat culture is diagnostic. It also helps in deciding the sensitivity of the organism to the specific
antibiotic.
Management:
The goals in managing this disease are
1. Prevention of acute rheumatic fever
2. Reducing the spread of infections
3. Prevention of suppurative complications
4. Shortening the course of ailment
Antibiotics:
Penicillin is the drug of choice. Could be administered either orally / parenterally. Amoxycillin
has gradually replaced penicillin as the first choice antibiotic in these patients.
d. Septal hematoma
Introduction:
Septal hematoma is defined as collection of blood between the perichondrium of nasal septum and
the septal cartilage. Since nose is the most prominent part of the face it is more prone to injuries
which could lead to septal hematoma formation.
Pathophysiology:
The submucosal blood vessels present under the mucosal lining of nasal septum may be damaged
due to sharp buckling forces to which nasal septum could be subjected to in case of trauma. If the
mucosa is intact then blood will collect under the perichondrium leading on to hematoma formation.
This will strip the muco perichondrial layer away from the septal cartilage causing a bulge which
could be seen in the nasal septal area. If the trauma is severe enough to cause fracture of nasal
septal cartilage then blood may seep to the opposite side also stripping the muco perichondrial
layer on the opposite side also. This condition can be identified by the presence of bilateral
septal swelling. This bilateral septal hematoma is really critical because it can compromise the
nourishment of the septal cartilage which occurs only when the perichondrium is in contact with it.
This nutritional compromise can lead to liquifaction necrosis of the septal cartilage leading on to
pig snout deformity. Cartilage resorption starts to occur from the third day of vascular compromise.
If the septal hematoma is unilateral and small it may cause localized necrosis of cartilage leading
on to fibrosis and thickening of cartilage in that area.
e. CROUP:
Synonyms: Acute laryngotracheal bronchitis, Viral laryngotracheal bronchitis
Introduction:
This clinical syndrome is characterized by:
a. Hoarseness of voice
b. Stridor which could be inspiratory or biphasic
c. Barking cough
d. Fever
e. Malaise
Pathophysiology:
This condition is usually caused by mucosal oedema of larynx and trachea. The lining mucosa of
larynx and trachea is pretty lax in infants, and hence can swell up rapidly causing airway
compromise. Inflammation and oedema occurs in the subglottic area and trachea commonly.
Children of age between 6 months and 3 years are affected commonly. Peak age of occurrence
happens to be 2 years.
Causative organism:
Viruses have been implicated as the common cause. They include:
Parainfluenza type I virus, Parainfluenza type II virus, Respiratory syncitial virus and Influenza
type A and type B viruses.
Management:
Since it is a self limiting disease reassurance and supportive therapy may be all that is needed. The
Child usually improves dramatically within the first 24 hours and complete recovery occurs within
4 days even without treatment.
If the affected child has acute airway obstruction then hospitalization is a must. Coexistent
measles infections and bronchopneumonia may complicate the issue.
Croup scores:
Grading croup will help us in deciding the optimal management modality of these patients:
Commonly used grading system is the Westley scale.
Westley scale:
This scoring system helps the examiner in assessing the degree of respiratory compromise.
Usually the following five factors are taken in to consideration in this scoring system:
Inspiratory stridor:
None – 0 points
Upon agitation – 1 point
At rest – 2 points
Chest retractions:
Mild – 1 point
Moderate – 2 points
Severe – 3 points
Air entry:
Normal – 0 points
Mild decrease – 1 point
Marked decrease – 2 points
Cyanosis:
None – 0 points
Upon agitation – 4 points
At rest – 5 points
Level of consiousness:
Normal – 0 point
Depressed – 5 points
g. Atrophic rhinitis
Definition:
Atrophic rhinitis is defined as a chronic nasal disease characterized by progressive atrophy of nasal
mucosa along with the underlying bones of turbinates. There is also presence of viscid secretions
which gets dried up leading on to the formation of foul smelling crusts. The characteristic foetid
odour emanating from these crusts is known as ozaena. The nasal cavity in these patients appear
to be abnormally patent. The patients with this condition are fortunately unaware of this condition
because of the coexisting presence of anosmia (Merciful anosmia).
Etiology:
Still remains obscure. Numerous pathogens have been implicated. The most important of them are:
a. Coccobacillus
b. Bacillus mucosus
c. Coccobacillus foetidis ozenae
d. Diptheroid bacilli
e. Klebsiella ozenae
Even though these organisms have been repeatedly isolated from the nasal cavity of these patients
they have not been categorically proved to be the cause.
Other predisposing causative factors include:
a. Chronic sinusitis
b. Excessive destruction of nasal mucosa and turbinates (overzealous nasal surgeries)
c. Nutritional deficiencies
d. Syphilis
e. Endocrine imbalances (This disease is known to worsen with pregnancy)
f. Hereditary
g. Autoimmune mechanisms – According to Faud these patients have altered cellular immunity
leading on to intolerance to nasal tissues. This immune intolerance can be caused by viral
infections.
Fraenkel triad:
Dr Bernhard Fraenkel described a classic triad of symptoms seen in these patients. According to
Fraenkel the presence of this triad is a must for the diagnosis of atrophic rhinitis. This triad include:
1. Fetor
2. Crusting
3. Atrophy
Age of onset – This disorder commonly occurs at puberty.
Females are more commonly affected than males
Bernat postulated that iron deficiency could probably cause this condition.
Histopathology:
1. Metaplasia of ciliated columnar epithelium into squamous epithelium
2. There is a decrease in the number and size of nasal compound alveolar glands
3. Dilated capillaries can be seen
Pathologically atrophic rhinitis has been divided into two types:
Type I – This is characterized by the presence of endarteritis and periarteritis of terminal arterioles.
Usually this type could be caused by chronic infections. These patients benefit from the
vasodilator effects of oestrogen. Majority of these patients belong to this categoty.
Type II – This type is characterised by vasodilatation of capillaries and these patients are likely to
worsen with oestrogen therapy. The endothelial cells of these capillaries contain more cytoplasm
than those of normal capillaries. These cells also show active reaction for alkaline phosphatase
indicating rapid bone destruction.
Clinical classification of atrophic rhinitis:
Clinically atrophic rhinitis can be classified into primary and secondary types.
Primary atrophic rhinitis:
This is the classic form of atrophic rhinitis and is supposed to arise denovo. Diagnosis of this type
of atrophic rhinitis is by the process of exclusion. All the known causes of atrophic rhinitis should
be ruled out before branding the patient to be suffering from primary atrophic rhinitis. The
causative organisms in these patients are usually klebsiella ozenae.
Secondary atrophic rhinitis:
This is the most common form of atrophic rhinitis seen in developed countries. The most common
causes of this form of atrophic rhinitis include:
1. Extensive destruction of nasal mucosa and turbinates during nasal surgery
2. Following irradiation
3. Following granulomatous infections like syphilis, leprosy and tuberculosis
Clinical features:
1. Nasal obstruction
2. Epistaxis
3. Anosmia (Merciful)
4. Foul smelling greenish yellow crust can be seen inside the nasal cavity
5. Roomy nasal cavity due to atrophy of nasal mucosa and turbinate bones
6. These patients are psychologically depressed because of the foul smelling crusts in the nose
Reason for nasal obstruction despite the presence of roomy nasal cavity:
The nasal cavity is filled with sensory nerve endings close to the nasal valve area.
These receptors sense the flow of air through this area thus giving a sense of freeness in
the nasal cavity. These nerve endings are destroyed in patients with atrophic rhinitis
thus depriving the patient of this sensation. In the absence of these sensation the nose
feels blocked.
Radiographic findings:
This is more or less the same for both type I and type II atrophic rhinitis. Plain x-rays paranasal
sinuses show:
1. Lateral bowing of nasal walls
2. Thin / absent turbinates
3. Hypoplastic maxillary sinuses
CT scan findings:
1. Mucoperiosteal thickening of paranasal sinuses
2. Loss of definition of osteomeatal complex due to destruction of bulla
3. Hypoplastic maxillary sinuses
4. Enlargement of nasal cavity with erosion of lateral nasal wall
5. Atrophy of inferior and middle turbinates
Management:
Conservative:
Nasal douching – Patient is encouraged to douch the nasal cavity at least twice a day with solution
prepared with:
1. Sodabicarb – 28.4 g
2. Sodium diborate – 28.4 g
3. Sodium chloride – 56.7 g
mixed in 280 ml of luke warm water.
The greenish yellow crusts can be removed by suction or by teasing with forceps.
Glucose glycerine drops:
25% glucose dissolved in glycerine can be administered into the nasal cavity. Glycerine is an
hygroscopic agent hence moistens the nasal cavity thereby softening the crusts. 25% glucose
inhibits proteolytic organisms which are commonly present in the nasal cavity of these patients.
Patients with histological type I atrophic rhinitis could benefit from nasal topical administration of
oestradiol in arachis oil in concentrations of 10,000 units / ml.
Another topical medication that could benefit these patients is Kemecitine antiozena solution.
Kemecitine antiozena solution contains:
1. Chloramphenicol – 90 mg
2. Oestradiol dipropionate – 0.64 mg
3. Vitamin D2 – 900 IU
4. Propylene glycol
5. Isotonic saline 1 ml
Oral administration of potassium iodide has been tried in an effort to increase nasal secretions
with varying degrees of success.
Systemic administration of placental extracts have also been attempted in these patients.
Surgical management:
Submucous injection of paraffin - This happens to be one of the procedures that displaces the
lateral nasal wall medially. Various materials are being used for this procedure. This medialization
procedure is also known as “Lautenslauger's operation”. Recently teflon strips / autogenous
cartilages are being inserted after elevating the flaps in the lateral wall and floor of the nasal cavity.
Wilson's operation: Submucosal injection of 50% teflon in glycerine paste. This not only narrows
the nasal cavity but also helps in dislodging the crusts.
Stellate ganglion blocks: This helps to some extent in increasing the glandular secretions of the
nasal cavity. Sometimes this process may need to be repeated more than once for optimal
benefit.
Young's operation:
This procedure aims at closing the nasal cavity by raising mucocutaneous flaps. In this method
mucocutaneous flaps are raised all around inside the nasal cavity. This flap is then sutured in
such a way that the whole nasal cavity is obliterated. The nasal cavity is kept blocked for a period
of 9 months during which time the nasal mucosa would have regenerated. After 9 months the
nasal mucosa can be assessed by performing a post nasal examination. If it had regenerated
then the sutured flaps can be released and the nasal cavity reopened. This procedure should
be performed on one side first, then after opening up the nasal cavity after 9 months the other side
should be attempted.
Modified young's operation:
In this procedure a small hole measuring 3 mm is left while the flaps are being sutured. This hole
helps the patient to breath normally through the nasal cavity. The healing process can also be
monitored by performing periodical nasal endoscopic examination via the opening.
h. Physiology of hearing
In the study of physiology of hearing the role played by external ear, middle ear and internal ear
should be discussed separately.
Role played by external ear:
Because of its funnel shape the external ear helps in capturing sound waves and focuses it
on the ear drum. The portions of external ear which play an important role in sound conduction
are: Pinna, concha and external auditory meatus.
Functions of external ear:
1. By acting as an resonator it increases the pressure of sound at the level of ear drum in a frequency
specific manner. It is known to resonate better in the frequency range of 2-5 Khz.
2. It helps in sound localization
3. The pinna conchal system acts like a trumpet focussing the sound to the ear drum for transmission
Bone conduction audiometry: is usually performed by using a bone vibrator which is placed over
the mastoid process. The opposite ear should be masked by using appropriate masking
stimulus. Auditory thresholds are estimated as done for air conduction audiometry. Usually
air conduction values should be better than bone conduction ones. If bone conduction value
is better than air conduction then the patient should be suffering from conductive deafness. In
sensorineural hearing losses both air and bone conduction curves will take a dip. This dip
will be pronounced for high frequencies.
j. Leukoplakia
Introduction:
This is a clinical term used to indicate patches of keratosis seen over the mucous membrane
of oral cavity, palate, tongue etc. On gross appearance it is seen as adherent white patches
over the mucous membrane. It is considered to be a premalignant condition. Common in cigarette
smokers.
Causative factors:
1. Tobacco chewing
2. Smoking
3. Ill fitting dentures
4. UV radiation
5. Presence of torus palatinus
6. Alcoholism
Gross appearance:
Leukoplakia begin as gray or grayish white plaques. They may appear somewhat translucent,
wrinkled, typically flat. Usually they are soft on palpation. Their borders are usually sharply
demarcated, sometimes gradually blending with the surrounding mucosa. When a leukoplakic
patch becomes red it is known as “erythroplakia” which is definitely a premalignant lesion.
Histology:
Histologically it is a thickened surface layer of parakeratin and sometimes orthokeratin. Basilar cells
and keratinocytes show no evidence of dysplasia. There may be mild basilar hyperplasia. If the
basilar cells and keratinocytes show evidence of dysplasia then it should be considered to be a
premalignant lesion.
Staging of leukoplakia:
Phase I leukoplakia – In this phase the leukoplakic patch appears rather thin. It is so thin that
the underlying mucosa can be clearly seen through it. This stage leukoplakia can undergo
spontaneous regression if the offending cause is removed.
Phase II leukoplakia – These patches are homogeneous, thick and sometimes fissured. A
leukoplakia can remain in this stage for ever or may progress to phase III.
Phase III leukoplakia – These patches are thick and have surface irregularities which could
be nodular. Hence it is also known as Nodular leukoplakia. Leukoplakia belonging to this phase
may turn dysplastic and become invasive.
Phase IV leukoplakia – This type is rather inhomogeneous. When it is reddish in color it is known as
erythroplakia. It also goes by the name speckled leukoplakia. This lesion may undergo malignant
transformation.
Short answer questions: 10x2=20
a. Leukoplakia
b. Erythroplakia
3. Mention any two clinical findings in nasal cavity of a patient suffering from allergic rhinitis
a. Pale boggy nasal mucosa
b. Mulberry shaped hypertrophy of inferior turbinate
5. Tracheostomy
This is an emergency procedure performed in order to secure the airway when the obstruction
is above the level of vocal folds and subglottic area. An opening is created in the anterior wall
of trachea ideally between the second and third tracheal rings. A tracheostomy tube is introduced
into the trachea through the opening.
10. Tympanoplasty:
This is a surgical procedure that is preformed to remove disease from the middle ear cavity
and reconstruct the sound conducting mechanism. There are 5 types of tympanoplasty
procedures devised to reconstruct middle ear conduction system.
Type I tympanoplasty – Is myringoplasty which is performed if all the three ossicles are intact
Type II tympanoplasty – Is indicated when malleus is absent and the neotympanum is grafted
to the intact incus and stapes.
Type III tympanoplasty – Is indicated when the suprastructure of stapes alone is present and the
neotympanum is draped over the suprastructure
Type IV tympanoplasty – is indicated when the suprastructure also is eroded and the neotympanum
is draped over the foot plate (columella effect)
Type V tympanoplasty – is fenestration of lateral canal