STRIDOR

1. Definition

 Stridor is defined as a harsh, crowing, musical sound caused by turbulent airflow through a
partially obstructed upper airway.
 It is usually inspiratory but may be expiratory or biphasic depending on the level of obstruction.

2. Classification of Stridor (Based on site of obstruction)

Type Phase of breathing Level of obstruction

Inspiratory During inspiration Supraglottic or glottic
Expiratory During expiration Intrathoracic trachea
Biphasic During both phases Subglottic or cervical trachea

3. Causes of Stridor

A. Congenital Causes

 Laryngomalacia (most common cause of stridor in infants)

 Vocal cord paralysis
 Subglottic stenosis
 Laryngeal web
 Laryngeal cyst
 Congenital laryngeal atresia

B. Acquired Causes

 Infections:
o Acute laryngotracheobronchitis (Croup)
o Epiglottitis
o Diphtheria
 Trauma:
o Intubation injury
o External trauma to the neck
 Foreign body in larynx/trachea
 Neoplasms:
o Papillomas
o Carcinomas of larynx or trachea
 Inflammatory causes:
o Tuberculosis
o Sarcoidosis
 Allergic reactions:
o Anaphylaxis
o Angioedema
 Neurological causes:
o Bilateral vocal cord paralysis
4. Clinical Presentation

 Noisy breathing (depends on site and severity)

 Respiratory distress, use of accessory muscles
 Voice change (e.g., hoarseness or cry weakness in infants)
 Feeding difficulty in infants
 Cough: Barking or brassy
 Intermittent or persistent cyanosis

5. Investigations

 Indirect laryngoscopy (in adults) or flexible nasolaryngoscopy (in children)

 X-ray soft tissue neck (AP and lateral views):
o Steeple sign in Croup
o Thumb sign in Epiglottitis
 CT scan of neck and chest (if lesion is suspected deeper or to define extent)
 Microlaryngoscopy and bronchoscopy: Definitive examination under general anesthesia
 Pulse oximetry and ABG: For assessing oxygenation and acidosis

6. Management

Depends on cause and severity. General principles include:

 Maintain airway: Intubation or tracheostomy in severe obstruction

 Oxygen therapy
 Nebulized adrenaline and systemic steroids (for acute laryngeal edema or Croup)
 Antibiotics in case of bacterial infections (e.g., epiglottitis)
 Removal of foreign body under general anesthesia
 Surgical intervention:
o For laryngeal webs, papillomas, tumors, subglottic stenosis
 Treatment of underlying disease: Tuberculosis, allergic conditions, etc.

7. Emergency Airway Measures

 Endotracheal intubation (preferably by skilled personnel)

 Cricothyrotomy or emergency tracheostomy if intubation fails
 Close monitoring in ICU setting for respiratory failure or sepsis

8. Important Points (Exam-Oriented)

 Most common cause of congenital stridor: Laryngomalacia

 Most common infectious cause of stridor in children: Croup
 Thumb sign on X-ray: Epiglottitis
 Always classify stridor as inspiratory, expiratory, or biphasic
  Stridor in adults is a medical emergency and requires urgent airway assessment

OTOSCLEROSIS
(As per PL Dhingra ENT, 6th Edition)

1. Introduction & Definition

 Otosclerosis is a primary disease of the bony labyrinth capsule characterized by replacement of

normal bone with spongy, vascular bone (otospongiosis), followed by sclerosis.
 It usually affects the stapes footplate, leading to stapes fixation and conductive hearing loss.
 When it involves the cochlea, it may also cause sensorineural hearing loss.

2. Anatomy & Pathophysiology

 The otic capsule is normally formed by endochondral bone which remains stable throughout life.
 In otosclerosis, active bone remodeling occurs at certain foci, typically:
o Fissula ante fenestram (anterior to oval window) — most common site
 Histologically, two phases are seen:
o Otospongiosis (active phase): Resorption and vascular spongy bone formation
o Sclerosis (inactive phase): Hard dense bone
 Types of fixation:
o Stapedial otosclerosis – Stapes footplate is fixed
o Cochlear otosclerosis – Involvement of cochlea → sensorineural loss

3. Etiology & Risk Factors

 Exact cause is unknown, but possible factors:

o Hereditary (autosomal dominant with incomplete penetrance)
o Hormonal: Worsens during pregnancy or menopause
o Viral: Measles virus has been implicated
o Autoimmune mechanisms

4. Clinical Features

 Onset: Common in 2nd to 4th decade, more in females

 Bilateral in ~70–80% cases

Symptoms:

1. Progressive hearing loss (conductive > mixed)

2. Paracusis Willisii: Hearing better in noisy surroundings
3. Tinnitus (in 75% cases)
4. Vertigo is rare
5. No history of ear discharge (important to differentiate from CSOM)
5. Examination Findings

 Otoscopy: Normal tympanic membrane

o Schwartze’s sign: Pinkish hue over promontory (active phase)
 Tuning fork tests:
o Rinne negative (BC > AC)
o Weber lateralizes to affected ear
o Absolute bone conduction (ABC) normal

6. Investigations

Audiometry:

 Conductive hearing loss

 Carhart’s notch: Dip at 2000 Hz in bone conduction (due to stapes fixation)
 Air-Bone Gap: Often 20–40 dB
 Sensorineural loss if cochlear otosclerosis

Impedance Audiometry:

 Type As tympanogram (shallow compliance)

 Absent stapedial reflex

CT Temporal Bone:

 Rarely needed but may show radiolucent foci in otic capsule

 Useful in cochlear otosclerosis or revision surgery

7. Treatment & Management

Conservative:

 Hearing aids – Effective in stapedial otosclerosis when surgery contraindicated

 Sodium fluoride (controversial) – May slow progression in active phase

Surgical:

 Stapedectomy (removal of stapes and insertion of prosthesis) – Treatment of choice

 Stapedotomy (preferred) – Small fenestra in footplate, piston prosthesis inserted
 Contraindications to surgery:
o Only hearing ear
o Active infection
o Poor general health
o Cochlear otosclerosis

8. Complications of Surgery
  Sensorineural hearing loss
 Perilymph fistula
 Floating footplate
 Vertigo
 Tinnitus worsening
 Chorda tympani injury – Taste disturbance

9. Differential Diagnosis

 Otitis media with effusion

 Adhesive otitis media
 Ossicular chain discontinuity
 Tympanosclerosis

LARYNX

1. Introduction & Definition

 The larynx is a cartilaginous structure located in the midline of the neck, extending from the level
of C3 to C6 vertebrae.
 It forms the upper part of the respiratory tract and houses the vocal cords, making it the organ of
voice.
 It serves as a valve mechanism, important in phonation, respiration, and protection of the airway
during swallowing.

2. Anatomy of the Larynx

A. Cartilages

 Unpaired:
o Thyroid – largest, forms Adam’s apple
o Cricoid – signet-ring shaped, complete ring
o Epiglottis – leaf-shaped, prevents aspiration
 Paired:
o Arytenoid – pyramidal, mobile (controls vocal cords)
o Corniculate – atop arytenoids
o Cuneiform – embedded in aryepiglottic folds

B. Joints

 Cricothyroid joint – tenses vocal cords

 Cricoarytenoid joint – adducts/abducts cords

C. Muscles

 Intrinsic muscles (control vocal cords):

 o Adductors: Lateral cricoarytenoid, transverse arytenoid
o Abductor: Posterior cricoarytenoid (safety muscle)
o Tensors: Cricothyroid
o Relaxers: Thyroarytenoid, vocalis
 Extrinsic muscles: Move larynx as a whole (e.g., infrahyoid, suprahyoid)

D. Cavities

 Supraglottic: Above vocal cords

 Glottic: Vocal cords and rima glottidis
 Subglottic: Below cords to lower border of cricoid

E. Membranes

 Thyrohyoid membrane – connects thyroid cartilage and hyoid bone

 Cricothyroid membrane – site of emergency airway (cricothyrotomy)

3. Nerve Supply

 Motor:
o All intrinsic muscles by Recurrent laryngeal nerve
o Cricothyroid by External branch of superior laryngeal nerve
 Sensory:
o Above cords – Internal branch of superior laryngeal nerve
o Below cords – Recurrent laryngeal nerve

4. Blood Supply

 Superior laryngeal artery – from superior thyroid artery (external carotid)

 Inferior laryngeal artery – from inferior thyroid artery (thyrocervical trunk)

5. Physiology of the Larynx

 Phonation – Vibration of vocal cords as air passes

 Respiration – Maintains open airway
 Protection – Epiglottis and closure reflex prevent aspiration
 Cough reflex – Larynx highly sensitive to foreign material

6. Disorders of the Larynx (Brief Overview)

Condition Key Points

Acute Laryngitis Viral, hoarseness, resolves in days
Chronic Laryngitis Due to smoking, vocal abuse, GERD; long-term hoarseness
Vocal Cord Nodules Singer’s nodule – bilateral, at junction of anterior 1/3 and posterior 2/3
Reinke’s Edema Polypoidal degeneration in smokers
 Condition Key Points
Laryngeal Papilloma HPV related, multiple in children (juvenile form)
Laryngeal Cancer Hoarseness, dysphagia, stridor; more common in glottic region
Laryngomalacia Most common cause of congenital stridor in infants
Laryngotracheobronchitis (Croup) Barking cough, inspiratory stridor in children
Epiglottitis Acute, life-threatening airway obstruction in children

7. Clinical Features of Laryngeal Disease

 Hoarseness of voice
 Stridor (inspiratory, expiratory, biphasic)
 Dysphagia or odynophagia
 Aphonia
 Throat pain or foreign body sensation
 Cough (dry or brassy)
 Neck swelling (in malignancy or abscess)

8. Examination of Larynx

A. Indirect Laryngoscopy

 Done with laryngeal mirror; visualizes vocal cords

B. Fibreoptic Laryngoscopy

 Flexible scope to see movement, lesions, foreign body

C. Microlaryngoscopy

 Under GA for biopsy, excision of lesions

D. Stroboscopy

 Assesses vibratory function of vocal cords (useful in vocal cord paralysis, early carcinoma)

ACUTE OTITIS MEDIA (AOM)

Source: PL Dhingra 6th Edition – Chapter on Middle Ear Infections

1. Introduction & Definition

 Acute Otitis Media (AOM) is an acute inflammation of the middle ear cleft, commonly seen in
children, characterized by rapid onset of symptoms like ear pain, fever, and hearing loss.
 It involves the Eustachian tube, middle ear, and mastoid air cells.
2. Anatomy & Physiology (Relevant Points)

 Middle ear communicates with:

o Nasopharynx via the Eustachian tube
o Mastoid air cells via the aditus and antrum
 Eustachian tube is shorter and more horizontal in children → increased susceptibility to infections.
 Function: Equalize pressure, drainage, and protection.

3. Etiology & Pathophysiology

Etiology:

 Age: Common in children (peak 6 months – 3 years)

 Precipitating factors:
o Upper respiratory tract infections (URTI)
o Allergies, Adenoid hypertrophy
o Bottle feeding in supine position
o Passive smoking
o Cleft palate

Pathogens:

 Bacterial:
o Streptococcus pneumoniae
o Haemophilus influenzae
o Moraxella catarrhalis
 Viral: RSV, Influenza virus, Rhinovirus

Pathophysiology:

1. Eustachian tube dysfunction due to URTI/adenoids

2. Negative pressure in middle ear → fluid exudation
3. Invasion by pathogens → suppuration
4. Accumulation of pus → bulging of tympanic membrane
5. If untreated → rupture of tympanic membrane or spread to mastoid

4. Stages of Acute Otitis Media

(Important for exams)

Stage Description Key Signs

1. Tubal Occlusion Eustachian tube blocked Retraction of TM, mild hearing loss
2. Pre-suppuration Inflammation, exudation Red, congested TM, earache, fever
3. Suppuration Pus in middle ear Bulging TM, severe pain, conductive hearing loss
4. Resolution Pus drains, relief Either TM rupture or treatment
5. Complication If not resolved Mastoiditis, CSOM, intracranial spread

5. Clinical Features
Symptoms:

 Earache (otalgia) – severe, throbbing

 Fever
 Hearing loss – conductive
 Irritability, crying, tugging at ear (in children)
 Ear discharge – if TM ruptures (mucoid or purulent)

Signs:

 Otoscopic findings (depending on stage):

o Congested or bulging tympanic membrane
o Loss of light reflex
o Perforation with discharge
 Tenderness over mastoid if mastoiditis develops

6. Investigations & Diagnosis

 Clinical diagnosis – based on history and otoscopy

 Pneumatic otoscopy – reduced mobility of TM
 Tympanometry – may show negative pressure or flat curve
 Pure tone audiometry – shows conductive hearing loss (if cooperative child)
 Ear swab culture – only if discharge is present and persistent

7. Treatment & Management

Medical:

1. Analgesics & Antipyretics – Paracetamol, Ibuprofen

2. Antibiotics (if bacterial suspected):
o First-line: Amoxicillin
o Others: Amoxicillin + clavulanic acid, Cefuroxime
o Duration: 5–10 days
3. Nasal decongestants – Xylometazoline for Eustachian tube function
4. Antihistamines – if allergic component suspected

Surgical (if needed):

 Myringotomy:
o Incision in TM to drain pus
o Indications: Severe bulging TM, intractable pain, complications, no response to antibiotics
 Grommet insertion: If recurrent AOM or OME

8. Complications

Local Intratemporal Intracranial

Tympanic membrane perforation Acute mastoiditis Meningitis
CSOM Facial nerve palsy Brain abscess
 Local Intratemporal Intracranial
Ossicular necrosis Labyrinthitis Lateral sinus thrombosis
Tympanosclerosis

9. Prevention

 Breastfeeding
 Avoid bottle feeding in lying position
 Treat URTIs early
 Adenoidectomy if hypertrophy present
 Pneumococcal and influenza vaccination

10. Important Exam Points & Mnemonics

Mnemonic – “FHEED” for AOM symptoms

 Fever
 Hearing loss
 Earache
 Ear discharge (after rupture)
 Discomfort/Irritability in children

Stages Mnemonic – “T-P-S-R-C”

 Tubal occlusion
 Pre-suppuration
 Suppuration
 Resolution
 Complication

Gold Standard Treatment

 Amoxicillin is first-line antibiotic

 Myringotomy if severe pain or complications