Adenoids and JNA ENT MBBS 4TH YR

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ADENOIDS & JUVENILE NASOPHARYNGEAL ANGIOFIBROMA (JNA)

ENT - MBBS 4th Year


PART 1: ADENOIDS

Embryology

  • Adenoids develop at 16 weeks as subepithelial infiltration of lymphocytes in the nasopharynx
  • They form part of Waldeyer's ring (along with palatine tonsils, lingual tonsil, tubal tonsils)
(K.J. Lee's Essential Otolaryngology, p. 959)

Anatomy

  • Located on the posterior wall of the nasopharynx (roof and posterior wall)
  • Covered by ciliated pseudostratified columnar epithelium (respiratory type); luminal aspect has multiciliated and secretory cells
  • Unlike palatine tonsils, adenoids have no crypts - they have surface folds/rugae
  • They are not encapsulated and have no afferent lymphatics

Physiology / Role

  • Part of the mucosal immune system; produce secretory IgA (sIgA)
  • Act as first-line defense against inhaled antigens
  • Adenoid size peaks at 4-10 years, then undergoes spontaneous involution at puberty
  • In children with CRS (chronic rhinosinusitis):
    • Adenoids serve as a bacterial reservoir - bacteria from middle meatal swabs and adenoidal core cultures are near-identical (S. pneumoniae, Group A strep, H. influenzae, S. aureus, coagulase-negative staphylococci)
    • Positive predictive value of adenoid core culture for predicting middle meatal culture: 91.5%
    • Biofilms cover 88-99% of adenoid surface in CRS children vs 0-6.5% in simple obstructive adenoid hypertrophy
    • Lower IgA expression in CRS adenoids; higher TGF-β1, MMP-2, MMP-9
(Scott-Brown's ORL, Vol 2; Cummings Otolaryngology)

Adenoid Hypertrophy - Clinical Features

Age group: Most common between 4-10 years
Symptoms:
SystemSymptom
NasalMouth breathing, nasal obstruction, hyponasal voice (rhinolalia clausa)
OtologicalRecurrent otitis media, serous otitis media (glue ear), conductive hearing loss
SleepSnoring, obstructive sleep apnoea (OSA), restlessness during sleep, unusual sleep positions
Face"Adenoid facies" - open mouth, high arched palate, elongated face, dull appearance
SystemicFailure to thrive (in severe cases)
Adenoid facies = characteristic look due to chronic mouth breathing: elongated face, open mouth, pinched nostrils, dental malocclusion.
Investigation:
  • Lateral soft tissue X-ray of nasopharynx - shows pad of adenoid tissue in postnasal space (arrow visible on soft tissue radiograph)
Lateral X-ray showing large adenoid pad in postnasal space (arrow)
Plain lateral radiograph showing a large pad of adenoid tissue (arrow) in the postnasal space - Bailey & Love's Surgery
  • Flexible nasendoscopy (gold standard)
  • Note: adenoid size alone does not correlate with severity of CRS on CT

Adenoid and Otitis Media with Effusion (OME / Glue Ear)

  • Adenoid hypertrophy causes Eustachian tube dysfunction → OME
  • Adenoidectomy alone improves OME/recurrent AOM (due to both mechanical obstruction relief and elimination of bacterial reservoir)
  • Added for children ≥4 years when distinct indications exist

Medical Treatment

  • Intranasal corticosteroids may significantly improve nasal obstruction symptoms in moderate-to-severe adenoid hypertrophy and may reduce adenoid size (Cochrane evidence - limited but supportive)

Indications for Adenoidectomy

(Bailey & Love's Surgery, 28th Ed; KJ Lee's Otolaryngology)
  1. OSA associated with postnasal obstruction
  2. Recurrent acute otitis media or prolonged serous otitis media (>3 months duration)
  3. Recurrent rhinosinusitis
  4. Postnasal discharge / chronic adenoiditis
  5. Failure to thrive due to airway obstruction
Tonsillectomy indications (for comparison):
  • 6-7 episodes of acute tonsillitis in 1 year
  • 5 episodes/year for 2 years
  • 3 episodes/year for 3 years (Paradise criteria)
  • Peritonsillar abscess

Adenoidectomy - Operative Technique

  • Patient supine, oropharynx exposed with Boyle-Davis mouth gag + Doughty's tongue plate
  • Nasopharynx palpated; adenoid curette (St. Clair Thompson) used to scrape adenoid pad
  • Haemostasis with post-nasal pack or suction cautery
  • Important: Avoid sedative premedications and postoperative opiates in OSA patients (risk of respiratory depression)


PART 2: JUVENILE NASOPHARYNGEAL ANGIOFIBROMA (JNA)

Definition

A benign but locally invasive vascular tumour of the nasopharynx occurring almost exclusively in adolescent males. Accounts for <1% of all head and neck tumours.
(Cummings Otolaryngology Head & Neck Surgery)

Epidemiology

  • Age: typically 10-25 years, predominantly males
  • Extremely rare in females (some cases in maxillary sinus site)
  • Androgen-dependent: androgen receptors (esp. estrogen receptors) present in tumour tissue - explains male predominance and puberty-related onset

Site of Origin

  • Arises from the sphenopalatine foramen at the root of the pterygoid process on the lateral nasal wall
  • This is the most important fact - the tumour originates here

Pathology

Macroscopy:
  • Sessile, lobulated, rubbery, dark red to tan-gray
  • Unencapsulated, sessile, wide-based attachment to nasopharynx
  • No mucosal ulceration
Microscopy:
  • Admixture of vascular tissue + fibrous stroma
  • Vessel walls lack elastic fibres and have incomplete or absent smooth muscle → accounts for profuse bleeding
  • Vascular cavities with endothelial layer but no muscle layer (unlike normal arteries)
  • Similarities between nasal mucosal cells, genital erectile tissue, and vascular spaces

Growth Pattern

  • Locally infiltrative, slow-growing
  • Expands laterally via pterygopalatine fossa → infratemporal fossa
  • Extends into nasopharynx and choanal space → anterior nasal cavity and sinuses
  • Can expand to: maxillary/ethmoid sinuses, orbit, cheek, cavernous sinus
  • Intracranial extension (middle/anterior cranial fossa) - uncommon but serious

Clinical Features

FeatureDetails
Age/sexAdolescent males, 10-25 years
EpistaxisMost common presentation - recurrent, severe, may lead to anaemia
Nasal obstructionUsually unilateral
OtherBlood-stained sputum, serous otitis media, nasal discharge, facial swelling, proptosis, anosmia
DurationUsually long history, often mild and innocuous initially

Diagnosis

Endoscopy: Rubbery vascular mass protruding into anterior nasal space; bleeds excessively on contact - biopsy avoided due to risk of haemorrhage
CT with contrast:
  • Enhancing soft tissue mass from nasopharynx/lateral nasal wall
  • Widening of pterygopalatine fossa
  • No bone erosion generally
  • Holman-Miller sign (classical): anterior bowing of posterior wall of maxillary sinus
CT showing widening of left sphenopalatine foramen by JNA
CT scan showing widening of the left sphenopalatine foramen from a juvenile angiofibroma - Cummings Otolaryngology
MRI:
  • Vascular tumour with flow voids within the mass
  • Enhancement on gadolinium imaging
  • Best for delineating intracranial extension and follow-up
MR Angiography / DSA (Digital Subtraction Angiography):
  • Shows feeding vessels arising from branches of the external carotid artery (mainly internal maxillary artery)
  • If intracranial spread: internal carotid artery also feeds the tumour
  • DSA shows enlarged intratumoral vessels + intense inhomogeneous blush in venous phase
Histology: Final confirmation - required before definitive treatment

Chandler Staging (1984)

StageExtent
Stage IConfined to nasopharynx
Stage IIExtension into nasal cavity or sphenoid sinus
Stage IIIInvolvement of maxillary sinus, ethmoid sinus, infratemporal fossa, orbit, cheek, cavernous sinus
Stage IVIntracranial extension

Management

Primary treatment: Surgical excision
Pre-operative embolization:
  • Well-established adjunct to induce tumour shrinkage, improve surgical access, reduce intra-operative blood loss
  • Done transarterially with particles (PVA) or liquids (NBCA/Onyx)
  • For tumours supplied by branches of external carotid - relatively straightforward
  • Intracranial supply (internal carotid) increases risk of neurological deficit
  • Direct tumour puncture technique with Onyx injection - improves devascularization
Surgical approaches:
  • Traditional: Open approaches (transpalatal, lateral rhinotomy, midfacial degloving)
  • Modern: Endoscopic surgical resection - now preferred for smaller tumours (Stage I-II) without spread; some consider preoperative embolization unnecessary for smaller endoscopic cases
  • Large/intracranial tumours: Combined skull base approach (head and neck surgeon + neurosurgeon)
Radiotherapy:
  • Used when surgery is contraindicated or for recurrence
  • Primary radiation therapy has been reported
  • Gamma knife used in some cases
Hormonal therapy (adjunct):
  • Flutamide (androgen antagonist) - shown to reduce tumour size, may have role as pre-operative adjunct
Natural history:
  • Spontaneous regression reported after cessation of androgen stimulation (post-puberty)
  • Rare malignant transformation reported

Key Exam Points - JNA

FeatureValue
Tumour typeBenign, locally invasive, vascular
WhoAdolescent males (10-25 years)
Origin siteSphenopalatine foramen / lateral nasal wall
Classic sign on CTHolman-Miller sign (anterior bowing of posterior maxillary wall)
Classic imaging findingFlow voids on MRI
Feeding arteryBranches of external carotid (internal maxillary artery)
Biopsy in clinicAVOID - risk of catastrophic haemorrhage
Pre-op adjunctEmbolization
Primary treatmentSurgical excision
HistologyVascular spaces with absent smooth muscle + fibrous stroma
StagingChandler staging (I-IV)

Comparison Table: Adenoids vs JNA

FeatureAdenoids (Hypertrophy)JNA
TypeLymphoid hyperplasiaBenign vascular tumour
AgeChildren, 4-10 yearsAdolescent males, 10-25 years
SexBothAlmost exclusively male
LocationRoof/posterior nasopharynxSphenopalatine foramen
Main symptomNasal obstruction, OMEEpistaxis, nasal obstruction
InvestigationLateral X-ray, nasendoscopyCT, MRI, DSA
Classic signAdenoid faciesHolman-Miller sign
TreatmentAdenoidectomySurgery (±embolization)
BiopsySafeDANGEROUS

Sources: Cummings Otolaryngology Head and Neck Surgery; Bailey & Love's Short Practice of Surgery 28th Ed; Scott-Brown's Otorhinolaryngology Head & Neck Surgery; K.J. Lee's Essential Otolaryngology
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