Etiology:

• Since it occurs in the second decade of life, it is proposed that nasopharyngeal angiofibroma is a testosterone dependent tumour
• A nidus of hamartomatous vascular tissue in the nasopharynx undergoes proliferation in response to hormonal stimulation

Site of occurence:

• The site of occurrence was initially thought to be the posterior wall and roof of nasopharynx
• But recent studies indicate that the site of origin is in fact the posterior part of nasal cavity, near sphenopalatine foramen

Pathology:

• Angiofibroma as the name suggests is composed of both fibrous and vascular elements
• The vascular elements are composed of endothelium lined blood vessels without muscle coat
• Hence there is increased risk of bleeding which is not responsive to application of adrenaline

Pathways of spread:

• Nasal cavity
• Paranasal sinuses
• Pterygomaxillary fossa
• Orbit – through superior or inferior orbital fissure
• Infratemporal fossa
• Cranial cavity
  • Usually the middle cranial fossa is involved. Spread can be through:
    • In front of foramen lacerum – lateral to carotid artery
    • Through wall of sphenoid sinus to region of sella turcica – medial to carotid artery
  • Anterior cranial fossa spread can occur through
    • Roof of ethmoid sinus
    • Cribriform plate

Clinical features:

• The usual presentation is one of recurrent, profuse epistaxis which is not necessarily associated with any provocative factor
• Nasal blockage and denasal speech
• Blockage to the eustachian tube opening results in conductive hearing loss and serous otitis media
• Extension to the orbit results in proptosis and involvement of II, III, IV and VI cranial nerves
• Swelling of cheek and broadened nasal bridge

Investigations:

• X-ray lateral view nasopharynx reveals the presence of a mass
• X-ray paranasal sinuses
• CT scan of head with contrast enhancement shows the extend of involvement and bony destruction – it is the investigation so choice
  • Anterior bowing of posterior wall of maxillary sinus – Holman Miller sign – is pathognomonic of angiofibroma
• MRI helps to better understand the soft tissue involvement
• Carotid angiography helps to ascertain the level of vascularity and has to be done before attempting embolization

Treatment:

• Surgical resection
  • There are different approaches available
    • Transpalatine
    • Transmaxillary
    • Intracranial – Extracranial
    • Extended lateral rhinotomy
    • Extended Denker’s approach
    • Infratemporal fossa
    • Endoscopic
  • Endoscopic resection is the preferred method
  • Blood loss during surgery is a major problem
  • Blood loss can be minimised by decreasing the vascularity of the tumor by any of the following methods
    • Hormonal therapy with diethyl stilbestrol
    • Cryotherapy
    • Embolization
• Hormonal therapy
  • Since nasopharyngeal angiofibroma is a androgen dependent tumour, diethyl stilbestrol or flutamide can be tried
• Radiotherapy
• Chemotherapy
  • For treatment of recurrence or residual lesions after surgery

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3. Vocal nodule – Etiology, Pathogenesis, Clinical features and Management

Etiology:

• Voice abuse is the most important etiological factor
  • Speaking in low tones or high intensity for long periods to time
• It is seen in people who tend to use their voice a lot like singers, singers and children
• Hence it is also known by the following alternate names:
  • Singer’s nodules
  • Speaker’s nodules
  • Minister’s nodules
  • Teacher’s nodules
  • Screamer’s nodules

Pathogenesis:

• Voice abuse initially results in oedema and haemorrhage in the submucosal space
• Later it undergoes hyalinisation and fibrosis
• The overlying epithelium undergoes hyperplasia and forms a nodule

Clinical features:

• Hoarseness of voice is the main complaint
• Voice fatigue
• Pain in neck

Laryngoscopy findings:

• Bilaterally symmetrical nodules on both vocal cords in their free border
• Location – At the junction of anterior one third and posterior two third (this is the area which undergoes maximum vibration during speech)
• Size – Pin head sized to half the size of a small pea
• Appearance – Initially appear red and oedematous, later changing to grey and fibrosed

Management:

• Voice rest is the most important intervention
• The patient should be advised on how to use their voice properly
• Early lesions, especially in children heal well with voice rest alone
• Late lesions, especially in adults may require excision under operating microscope
• Speech therapy is essential to prevent recurrence

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2. Septal perforation – Causes, Clinical features, Management
3. Clinical signs in allergic rhinitis – nasal, ocular, otologic, pharyngeal, laryngeal

• Traumatic perforation
  • Septal surgery
  • Cautery for epistaxis
  • Habitual nose picking
  • Deliberate perforation for putting ornaments
• Pathological perforation
  • Septal abscess
  • Nasal myiasis
  • Rhinolith
  • Chronic granulomatous diseases
    • Leprosy, Lupus, Tuberculosis – perforation of cartilaginous septum
    • Syphilis – perforation of bony septum
  • Wegener’s granuloma
• Drugs and Chemicals
  • Long term use of steroid nasal sprays
  • Exposure to certain chemicals in industry
    • eg: chromium
  • Cocaine addicts
• Idiopathic

Clinical features:

• Small perforations result in a whistling sound
• Large perforations cause crusting which bleed upon removal

Management:

• The identification of the cause is essential
• Small perforations can be closed by using plastic flaps
• In case of large perforations, removal of crusts can be done using alkaline nasal douche and application of bland ointment
• Silastic buttons can be used to close large perforations

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2. Vocal nodule – Etiology, Pathogenesis, Clinical features and Management
3. Juvenile nasopharyngeal angiofibroma – Etiology, Pathology, Clinical Features and Management

• Congenital Laryngeal Stridor

1. Laryngomalacia
2. CNPAS – Acronym
3. RDI – Acronym

• Nasal signs
  • Transverse nasal crease (allergic crease)
    • A black transverse line across the middle of nose
    • Occurs due to constant rubbing of the nose in the upward direction resembling a salute – allergic salute
  • Swollen turbinates
  • Pale, oedematous, bluish nasal mucosa
  • Thin watery discharge
• Ocular signs
  • Lid oedema
  • Cobblestone appearance and congestion of conjunctiva
  • Dark circles under eyes – allergic shiners
• Otologic signs
  • Retraction of tympanic membrane and serous otitis media due to eustachian tube dysfunction
• Pharyngeal signs
  • Granular pharyngitis due to hyperplasia of submucosal lymphoid tissue
• Laryngeal signs
  • Hoarseness of voice
  • Oedema of vocal cords

1. Atrophic rhinitis (Ozaena)
2. Tympanic membrane – central perforation
3. Bullous myringitis

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2. Juvenile nasopharyngeal angiofibroma – Etiology, Pathology, Clinical Features and Management
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Alternate names:

• Transitional cell papilloma
• Schneiderian papilloma

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2. Juvenile nasopharyngeal angiofibroma – Etiology, Pathology, Clinical Features and Management
3. Vocal nodule – Etiology, Pathogenesis, Clinical features and Management

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2. Indications for tonsillectomy
3. Aegophony

• Obstructive Sleep Apnoea

1. Respiratory Disturbance Index (RDI)
2. Indications for tonsillectomy
3. RDI – Acronym

1. Ankle brachial index
2. OSA – Acronym
3. RDI – Acronym