---

Acute Suppurative Otitis Media (ASOM)

---

1. Definition

• K. J. Lee's Essential Otolaryngology, p. 441
• Cummings Otolaryngology, p. 3767

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2. Epidemiology

• Most common reason for pediatrician visits in children in the United States.
• Nearly all children experience at least one AOM episode in early life.
• By 6 months of age: 20% have had 2+ AOM episodes.
• By 3 years of age: 50% have had 3+ episodes.
• Global AOM incidence: ~10.8 new episodes per 100 people per year.
  • Ranges from 3.6 in Central Europe to 43.4 in Sub-Saharan West Africa.
  • Highest in children aged 1-4 years (61 new episodes per 100 per year).
• Peak incidence: ages 6-24 months.

• Cummings Otolaryngology, p. 3767

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3. Risk Factors

Environmental

• Day care attendance (4+ children doubles risk)
• Tobacco smoke exposure
• Pacifier use
• Having older siblings
• Supine bottle feeding
• Absence of breastfeeding in first 6 months
• Low socioeconomic status
• Fall and winter season

Anatomic

• Cleft palate
• Eustachian tube dysfunction
• Craniofacial syndromes (Treacher Collins, Down syndrome)

Host Factors

• Age < 12 months at first AOM episode (powerful predictor of recurrence)
• Male sex
• Aboriginal/indigenous ancestry (Native American, Inuit, Native Australian)
• Premature birth, low birthweight
• Obesity
• Immunodeficiency
• Adenoid hypertrophy
• Genetic predisposition (greater concordance in monozygotic twins)

Protective Factors

• Breastfeeding
• Pneumococcal conjugate vaccination (PCV7, PCV13)
• Hib vaccination
• K. J. Lee's Essential Otolaryngology, p. 441
• Cummings Otolaryngology, p. 3768

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4. Etiology and Pathogenesis

Role of the Eustachian Tube (ET)

1. Ventilation - equalization of pressure between middle ear and nasopharynx
2. Drainage - clearance of middle ear secretions
3. Protection - barrier against nasopharyngeal pathogens

Sequence of Events

1. Preceding upper respiratory infection (URI) causes nasopharyngeal mucosal edema
2. Gerlach tonsil (peritubular lymphoid tissue) becomes inflamed, compromising ET function
3. ET dysfunction leads to negative middle ear pressure and transudation of fluid
4. Nasopharyngeal bacteria reflux or are aspirated into the middle ear
5. Adenoid pad acts as a bacterial reservoir, perpetuating infection
6. Middle ear inflammation ensues - ASOM
7. Biofilm formation by bacteria promotes persistence and recurrence

• K. J. Lee's Essential Otolaryngology, p. 441-442
• Cummings Otolaryngology, p. 3768

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5. Microbiology

Bacteria

• Introduction of PCV7 and PCV13 (Prevnar 13) has altered pneumococcal serotype prevalence and decreased invasive complications.
• Nontypeable strains predominate for H. influenzae since the Hib vaccine.
• Day-care attendees and children with older siblings are at risk for resistant strains.

Viruses

• RSV, rhinovirus, coronavirus, parainfluenza, enterovirus, adenovirus
• Viruses are isolated in up to 75% of AOM aspirates
• Viral infection initiates mucosal inflammation, paving way for bacterial superinfection
• K. J. Lee's Essential Otolaryngology, p. 441-442
• Cummings Otolaryngology, p. 3768

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6. Stages / Stages of ASOM

Stage 1: Hyperemia (Tubal Occlusion)

• ET blocked; negative pressure in middle ear
• Retraction of TM, congestion of vessels along handle of malleus
• Mild otalgia, sense of fullness

Stage 2: Pre-suppuration (Exudation)

• Middle ear fills with serous/serosanguineous exudate
• TM appears red and bulging
• Increasing otalgia and fever

Stage 3: Suppuration (Frank Pus)

• Mucopurulent exudate fills middle ear
• TM is bright red, tense, and bulging
• Severe throbbing otalgia, fever, systemic toxicity
• Risk of spontaneous perforation

Stage 4: Perforation

• TM perforates (usually small, anteroinferior)
• Immediate relief of otalgia with mucopurulent discharge (otorrhoea)
• Fever subsides; child looks better

Stage 5: Resolution/Complications

• With treatment: perforation heals, infection resolves
• Without treatment: risk of complications (mastoiditis, meningitis, etc.)

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7. Clinical Features

Symptoms

• Otalgia - rapid onset (< 48 hours), often severe
• Fever (may be > 39°C in severe cases)
• Irritability (especially in young children)
• Ear pulling/tugging (non-specific in infants)
• Hearing loss (conductive)
• Otorrhoea - if TM perforated (relieves pain)
• Preceding URTI symptoms in most cases

Signs

• Tympanic membrane changes (key finding):
  • Erythema (redness)
  • Bulging (pus under pressure)
  • Loss of light reflex
  • Loss of normal landmarks (handle of malleus obscured)
  • Air-fluid level visible (if TM translucent)
  • Perforation with mucopurulent discharge
• Reduced/absent TM mobility on pneumatic otoscopy
• Systemic: fever, toxicity in severe cases

Pneumatic otoscopy is the key diagnostic tool and is required to make the diagnosis of AOM - K. J. Lee's Essential Otolaryngology

• K. J. Lee's Essential Otolaryngology, p. 441
• Cummings Otolaryngology

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8. Diagnosis

Diagnostic Criteria (AAP 2013 Guidelines)

1. Moderate to severe bulging of TM, OR new onset otorrhoea not due to acute otitis externa
2. OR mild bulging of TM AND recent onset otalgia (<48 hours) OR intense erythema of TM

Tools

• Pneumatic otoscopy - gold standard; shows reduced/absent TM mobility
• Tympanometry - type B (flat) or C curve; useful in equivocal cases
• Tympanocentesis/myringotomy - allows culture; indicated in:
  • Treatment failure
  • Immunocompromised patient
  • Neonates and infants < 6 weeks
  • Severe toxicity

Differential Diagnosis

• Otitis media with effusion (OME) - no acute signs, TM not bulging
• Acute otitis externa - canal inflamed, TM normal, pain on tragal pressure
• Myringitis bullosa - bullae on TM surface
• Dental/TMJ pain referred to ear

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9. Treatment

A. Pain Control (Cannot Be Overlooked)

• Oral analgesics/antipyretics:
  • Paracetamol (acetaminophen)
  • Ibuprofen
  • Narcotics - use sparingly (risk of respiratory depression)
• Topical: Benzocaine eardrops (short-lived effect)
• Myringotomy - relieves middle ear pressure immediately

B. Observation (Watchful Waiting)

• Children ≥ 2 years with non-severe, unilateral AOM
• Children 6-23 months with non-severe, unilateral AOM
• Diagnosis uncertain or symptoms mild

• Compliant parents
• Ready access to healthcare
• Clear instructions to return if no improvement in 48-72 hours

• 80% of children with AOM improve within 3 days WITHOUT antibiotics
• 92% improve within 3 days WITH antibiotics (absolute benefit ~12%)

C. Antibiotic Treatment

• Any child < 6 months
• Children 6-23 months with bilateral AOM (even if non-severe)
• Children 6-23 months with severe unilateral or bilateral AOM
• Children ≥ 2 years with severe symptoms (otalgia > 48 hours, OR fever > 39°C)
• Otorrhoea present
• Children with craniofacial anomalies, immunodeficiency, cochlear implants

• High-dose amoxicillin (90 mg/kg/day) achieves middle ear tissue concentrations to overcome intermediate-resistant pneumococcal strains (MIC 0.1-1 µg/mL).
• Highly resistant pneumococcal strains (MIC > 2 µg/mL) will not respond to amoxicillin.
• Amoxicillin should NOT be used if: received amoxicillin in past 30 days, concurrent purulent conjunctivitis, or PCN allergy.

• Switch to amoxicillin-clavulanate if on amoxicillin
• Ceftriaxone IM 50 mg/kg/day for 3 days if unable to tolerate oral
• Consider tympanocentesis for culture and drainage
• K. J. Lee's Essential Otolaryngology, p. 442-443
• Cummings Otolaryngology, p. 3769

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10. Recurrent Acute Otitis Media (rAOM)

Antibiotic Prophylaxis

• Half therapeutic daily dose of amoxicillin for months
• Reduces recurrences by 1-2 episodes per year
• Not routinely recommended due to: GI/allergic side effects, antibiotic resistance

Surgical Options

• Provide surrogate ET function (middle ear ventilation + drainage)
• Reverse and prevent MEE formation
• AOM episodes with tubes present as otorrhoea (generally less severe)
• Can be treated with topical fluoroquinolone eardrops rather than systemic antibiotics
• Effect: ~1 AOM episode prevented by 6 months post-insertion (modest)
• Largest benefit in children with MEE persisting between AOM episodes

• AAP: Tympanostomy tubes are an option for children with rAOM who fail preventive/medical treatment
• AAO-HNS: Recommend against tubes in rAOM WITHOUT MEE; recommend as option in rAOM WITH persistent MEE

• Adenoids are a nasopharyngeal reservoir for respiratory pathogens
• Obstruct nasal airway and impair ET function when enlarged
• Meta-analysis (10 RCTs): Adenoidectomy ± tympanostomy tubes is most beneficial in children < 2 years with rAOM (modest effect size; must balance against surgical risks)
• Cummings Otolaryngology, p. 3770

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11. Complications

Intratemporal (Within the Temporal Bone)

Intracranial

Facial Nerve Palsy in ASOM (Special Note)

• Usually incomplete but may progress in first 2-3 days
• Child is typically not severely unwell
• Mechanism: erosion of bony Fallopian canal OR congenital dehiscence (present in 56% of temporal bones) + nerve inflammation
• Most common site of dehiscence: oval window area (micro-dehiscence in 1/3 of temporal bones)
• Most common pathogen: pneumococcus (80%)
• Treatment: Wide myringotomy + systemic antibiotics; if mastoiditis suspected: CT + cortical mastoidectomy
• Prognosis: Usually full recovery of facial nerve function
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 1223-1259
• Bailey and Love's Surgery, p. 7805
• Textbook of Family Medicine

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12. Biofilm Formation and Persistence

• Early dense nasopharyngeal colonization by S. pneumoniae, NTHi, and M. catarrhalis predisposes to early and recurrent AOM.
• Bacteria form biofilms in the middle ear - a sessile community embedded in extracellular matrix.
• Biofilms resist host immune defenses and antibiotics, contributing to chronic/recurrent disease.
• The final outcome of untreated or poorly treated AOM may be severe chronic ear disease (CSOM, cholesteatoma).
• Cummings Otolaryngology, p. 3768

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13. Prevention

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14. Summary Algorithm

Child with otalgia + fever + ear findings
           ↓
Pneumatic otoscopy
           ↓
Bulging / erythematous TM with reduced mobility?
           ↓ YES → ASOM confirmed
           ↓
Age + severity assessment
    ↓                          ↓
< 6 months                ≥ 6 months, bilateral,
OR severe symptoms        severe, or immunocompromised
    ↓                          ↓
IMMEDIATE antibiotics     6 months - 2 years, unilateral,
(Amoxicillin 90 mg/kg/d)  non-severe → OBSERVE 48-72 hrs
                               ↓
                    No improvement → Antibiotics
                               ↓
                    Amox-clav if failure at 48-72 hrs
                               ↓
                    Watch for complications
                    (mastoiditis, facial palsy, meningitis)

---

Key Mnemonics

• S - Streptococcus pneumoniae (~50%)
• H - H. influenzae non-typeable (~45%)
• M - Moraxella catarrhalis (~10%)

• Deep Eye pain (V1 - ophthalmic division)
• Ear discharge (otorrhoea)
• Face - lateral rectus palsy (VI nerve)

• Mastoiditis
• Brain abscess
• Epidural abscess
• Facial nerve palsy
• Labyrinthitis
• Meningitis
• Sigmoid sinus thrombosis

---

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Chronic Suppurative Otitis Media (CSOM)

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1. Definition

• The word "chronic" implies duration > 3 months from the initial perforation/infection.
• "Suppurative" implies active or intermittent purulent discharge.
• CSOM is broadly divided into:
  • Tubotympanic (Safe/Mucosal) type - involves the pars tensa; generally considered safe
  • Atticoantral (Unsafe/Squamous) type - involves the pars flaccida; associated with cholesteatoma and dangerous complications
• Scott-Brown's Otorhinolaryngology, Vol 2
• Shambaugh Surgery of the Ear, p. 527

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2. Epidemiology

• Common globally, especially in areas with limited health resources and low socioeconomic status.
• Most common in children less than 2 years old; frequently follows recurrent AOM.
• Prevalence is disproportionately high in indigenous populations: Native Americans, Inuit, Native Australians, Native New Zealanders.
• A major cause of preventable hearing loss in the developing world.
• By 14 years of age, studies show 7% of AOM-prone children develop collapse of posterior superior TM, central perforation, or CSOM.
• K. J. Lee's Essential Otolaryngology, p. 445
• Scott-Brown's Otorhinolaryngology, Vol 2

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3. Risk Factors

Host Factors

• Multiple episodes of AOM (strongest predictor)
• AOM in first few months of life
• Chronic secretory otitis media (glue ear / OME)
• Genetic predisposition (higher incidence in certain ethnic groups)
• Male sex
• Craniofacial anomalies (cleft palate - impairs ET function)
• Immunodeficiency

Environmental Factors

• Low socioeconomic status
• Overcrowding, poor housing
• Day-care attendance
• Tobacco smoke exposure
• Malnutrition (impairs immunity)

Pathological Risk

• Nasopharyngeal reflux - contamination of middle ear via ET
• Tympanostomy tube or existing perforation allows contamination from the external auditory canal (EAC)
• Adenoid hypertrophy - nasopharyngeal bacterial reservoir
• K. J. Lee's Essential Otolaryngology, p. 445

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4. Etiology and Pathogenesis

Step-by-Step Pathogenesis

Repeated AOM / Untreated AOM
          ↓
Eustachian tube dysfunction → negative middle ear pressure
          ↓
Transudation → persistent middle ear effusion (serous → purulent)
          ↓
Bacterial infection → inflammatory mediators + bacterial toxins
          ↓
Mucosal edema → submucosal glands form (secretory mucosa) → perpetuates effusion
          ↓
Granulation tissue formation (basement membrane rupture)
→ Fibroblasts, neovascularization, polyp formation
          ↓
Enzymes in effusion degrade TM collagen → TM weakened
          ↓
Negative ME pressure + weakened TM → retraction pockets
          ↓
Deep retraction pockets → contact with mucosa → fibrous adhesions → PERFORATION
          ↓
Perforation + retraction pockets → cholesteatoma (squamous epithelium in ME)

Role of Biofilms

• Highly organized networks of sessile bacteria in an extracellular matrix
• Resistant to host immunity (escape phagocytosis; impenetrable matrix blocks humoral immunity)
• Increased antibiotic resistance - efflux pumps, decreased metabolic rate, altered gene expression
• Frequently polymicrobial - harder to target
• Located on respiratory epithelium, within mucous, or intracellularly
• Create multiple reservoirs for persistent infection
• Pseudomonas aeruginosa is most common biofilm organism in CSOM
• K. J. Lee's Essential Otolaryngology, p. 445
• Shambaugh Surgery of the Ear, p. 527

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5. Classification of CSOM

Type 1: Tubotympanic (Safe / Mucosal) CSOM

Type 2: Atticoantral (Unsafe / Squamous) CSOM

Key mnemonic: Central = Safe; Marginal = Dangerous

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6. Microbiology

In CSOM (Mixed and Polymicrobial)

Note: Organisms in CSOM differ significantly from AOM (Pseudomonas and Staph replace Strep pneumoniae as dominant pathogens)

• K. J. Lee's Essential Otolaryngology, p. 445
• Cummings Otolaryngology, p. 3072

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7. Cholesteatoma

Definition

Types

A. Congenital Cholesteatoma

• Expanding cystic mass of keratinizing squamous epithelium medial to an intact TM
• No prior history of otorrhoea, perforation, or ear surgery
• Caused by persistence of epidermoid cell rests in the anterior epitympanum (normally regress in fetal life)
• Most arise from the anterior middle ear
• Also can be found at the petrous apex (congenital rests)

B. Primary Acquired Cholesteatoma

• Most common type (around 98% of all cholesteatomas)
• Arises from invagination of pars flaccida (attic retraction pocket)
• Keratin accumulates in the lateral epitympanic (Prussak) space
• Causes: scutum erosion, medial displacement of ossicular chain, ossicular erosion
• Associated with poor ET function → negative middle ear pressure → pars flaccida retraction

C. Secondary Acquired Cholesteatoma

• Squamous epithelium migrates into the ME via a TM perforation (especially marginal/attic)
• Usually arises from the pars tensa
• Located medial to the ossicular chain
• Causes early erosion of the long process of incus (LPI)
• More erosion of inner ear structures

Growth and Behavior of Cholesteatoma

• Grows as an expanding cyst accumulating keratin debris
• Contains enzymes (collagenases, proteases) that erode bone
• Destroys ossicles (long process of incus most commonly), tegmen, lateral semicircular canal, facial canal
• Can erode into the labyrinth (labyrinthine fistula), dura, or sigmoid sinus
• NOT malignant but behaves aggressively due to bone erosion and risk of dangerous complications
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 768-822
• Cummings Otolaryngology (pediatric CSOM chapter)

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8. Clinical Features

Symptoms

Red flags in CSOM: Otalgia, headache, vertigo, facial weakness - all warrant urgent investigation for complications

Signs on Examination

• Shambaugh Surgery of the Ear, p. 527-528
• K. J. Lee's Essential Otolaryngology, p. 446

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9. Investigations

Audiological

• Pure Tone Audiometry (PTA): Conductive hearing loss (CHL), mixed hearing loss possible
  • CHL > 30 dB suggests ossicular erosion
  • Paradoxically preserved hearing with ossicular erosion can occur if cholesteatoma bridges the oval window
• Tympanometry: Type B or Type C curve (confirms perforation / ET dysfunction)
• Speech audiometry in selected cases

Microbiological

• Aural swab for culture and sensitivity - guide topical/systemic antibiotic therapy
• Essential before starting treatment

Imaging

CT has high NPV for absence of cholesteatoma if normal. MRI-DWI has high positive predictive value for cholesteatoma.

Other

• Biopsy of granulation tissue unresponsive to topical therapy - to rule out malignancy
• Aural toilet + otomicroscopy - essential for proper diagnosis; discharge often obscures landmarks
• K. J. Lee's Essential Otolaryngology, p. 446
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 757-796

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10. Treatment

Goals of Treatment

1. Primary goal: Create a safe, dry ear (no otorrhoea; no dangerous collection of keratin/debris)
2. Eradication of disease
3. Prevention of recurrence
4. Preservation or restoration of hearing

---

A. Medical Treatment (for CSOM without Cholesteatoma)

Step 1: Aural Toilet

• Thorough cleaning of the ear canal under otomicroscopy
• Remove debris, purulent discharge, and granulation tissue
• Essential before applying topical drops (discharge reduces efficacy of drops)
• Methods: dry mopping, syringing, microsuction

Step 2: Topical Antibiotics (First-Line)

• 4-6 week course following aural toilet
• Fluoroquinolone drops (ciprofloxacin, ofloxacin) - first choice; broad spectrum; covers Pseudomonas; ototopically safe
• Acetic acid (2%) drops - antiseptic; acidifies the canal; effective against Pseudomonas; low resistance risk
• Avoid aminoglycoside drops (neomycin, gentamicin) in perforated ears - ototoxic
• Avoid aminoglycoside/polymyxin B combinations in perforated ears

Note: Biofilms are frequently resistant to topical medication; biofilms have multicellular strategies to overcome high antibiotic concentrations, including efflux pumps.

Step 3: Topical Steroids

• Reduce mucosal inflammation and granulation tissue formation
• Often combined with antibiotic drops

Step 4: Systemic Antibiotics (Selected Cases)

• For acute flares with systemic signs (fever, adenitis)
• Based on culture and sensitivity
• Fluoroquinolones (ciprofloxacin) - oral route; good pseudomonal coverage
• Not routinely used for chronic disease

Water Precautions

• Keep ears dry - avoid swimming, bathing with ear submerged
• Cotton wool + petroleum jelly plug during bathing

Indications to Proceed to Surgery (Medical Failure)

• Failure of multiple attempts at medical treatment
• Symptoms suspicious of complications (vertigo, facial weakness, headache)
• Persistent granulation tissue unresponsive to topical therapy
• Cholesteatoma identified on examination
• K. J. Lee's Essential Otolaryngology, p. 446
• Shambaugh Surgery of the Ear, p. 528

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B. Surgical Treatment

Surgical Priorities (in order)

1. Eradication of disease
2. Prevention of recurrence
3. Preservation/restoration of hearing

Key Procedures

1. Myringoplasty / Tympanoplasty

• Myringoplasty: Repair of the TM perforation only (no ossicular work)
• Tympanoplasty: Repair of TM ± ossicular reconstruction

• Temporalis fascia - most commonly used; excellent results
• Tragal cartilage with perichondrium - stiffer; good for retraction-prone ears or revision surgery
• Perichondrium alone
• Fat - for small perforations

• Ear must be dry for at least 3 months before tympanoplasty
• Optimal age for children: around 10 years (when ET function matures and AOM episodes reduce)
• Younger age = higher failure rates (immature ET, AOM recurrence, adenoid hypertrophy)
• A healthy contralateral ear is a more reliable predictor of success than age alone
• Earlier surgery in children with troublesome otorrhoea or significant hearing loss

• Underlay technique (temporalis fascia placed medial to TM remnant) - most common
• Overlay/Lateral graft technique - for anterior perforations
• Endoscopic tympanoplasty - increasingly used; avoids post-auricular incision

2. Ossiculoplasty

• Ossicular chain reconstruction to restore hearing
• Performed at primary surgery or as a staged procedure
• Materials:
  • Autologous bone (incus, cortical bone)
  • Hydroxyapatite prostheses
  • Titanium PORP/TORP (partial/total ossicular replacement prosthesis)
• Often staged because: residual cholesteatoma may prevent primary ossiculoplasty; graft needs to heal first

3. Mastoidectomy

• Cholesteatoma (absolute)
• Disease not eradicable by tympanoplasty alone
• Refractory CSOM with mastoid involvement
• Complications requiring surgical drainage

• CWD has historically shown lower disease recurrence in meta-analyses
• CWU preferred in children to avoid lifelong cavity care
• Anatomical position of cholesteatoma more important than canal wall status for recurrence risk
• Endoscopic approaches are increasingly used

4. Second-Look Surgery

• Planned re-exploration 6-12 months after CWU surgery to check for residual cholesteatoma
• Increasingly being replaced by MRI-DWI surveillance (high positive predictive value for cholesteatoma)
• Avoids unnecessary general anaesthetic in children
• Shambaugh Surgery of the Ear, p. 529-530
• Cummings Otolaryngology (pediatric chapter)
• Scott-Brown's Otorhinolaryngology, Vol 2

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11. Complications of CSOM

Intratemporal Complications

Intracranial Complications

Any patient with CSOM + headache, vertigo, or facial weakness must be urgently investigated with CT/MRI for complications.

• K. J. Lee's Essential Otolaryngology, p. 446
• Shambaugh Surgery of the Ear
• Scott-Brown's Otorhinolaryngology, Vol 2

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12. Hearing Loss in CSOM

• Type: Predominantly conductive; mixed HL in labyrinthine involvement
• Cause of CHL:
  • TM perforation alone: 10-15 dB loss (larger/anteroinferior perforations = greater loss)
  • Ossicular erosion: CHL > 30 dB
  • Ossicular discontinuity: maximum CHL ~60 dB
• Special situation: CHL may be paradoxically mild if cholesteatoma bridges the ossicular gap and transmits sound directly to the oval window (acoustic coupling)
• SNHL: Can coexist due to: labyrinthitis, labyrinthine fistula, toxins crossing the round window, or cochlear damage from long-standing infection
• Audiometric finding: Negative Rinne at 512 Hz (BC > AC); Weber lateralizes to the diseased ear (if SNHL present, lateralizes to better ear)

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13. CSOM in Special Situations

CSOM + Cochlear Implant Candidacy

• Cochlear implantation was initially contraindicated in CSOM, but selective studies show OM prevalence does not increase post-implantation
• Pre-implantation ear must be dry
• Options:
  • Dry perforation: first-stage myringoplasty → implant after 3 months
  • Cholesteatoma/unstable cavity: radical mastoidectomy + obliteration → implant after months
  • Stable cavity: one-stage obliteration + implantation
• Fungal overgrowth (Candida) is a risk in ears treated with prolonged topical ciprofloxacin
• Cummings Otolaryngology, p. 3072

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14. Prevention

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15. Summary Comparison Table: Tubotympanic vs Atticoantral CSOM

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16. Key Mnemonics

• Pseudomonas aeruginosa (most common)
• Staphylococcus aureus
• Anaerobes (Bacteroides)
• Klebsiella / Proteus
• Fungi (especially post-antibiotics)

• Otorrhoea
• Retro-orbital pain (V1)
• Diplopia (VI nerve palsy)

Mnemonic: "O.R.D." (Order of dysfunction - Ear, Eye pain, Eye movement)

• Mastoiditis
• Brain abscess
• Epidural abscess
• Facial nerve palsy
• Labyrinthitis / Labyrinthine fistula
• Otitic hydrocephalus
• Sigmoid sinus thrombosis
• Subdural abscess

• Crusty attic discharge (foul-smelling)
• Hearing loss > 30 dB
• Ossicular erosion on CT
• Lateral canal fistula sign (vertigo on pneumatic otoscopy)
• Erosion of scutum
• Suction/aural polyp in attic
• TM - attic/marginal perforation
• External auditory canal white pearly mass
• Attic retraction pocket

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17. Summary Algorithm

Chronic Otorrhoea > 3 months + TM perforation
              ↓
Otomicroscopy + Aural Toilet
              ↓
          ┌────────────────────────────┐
          ↓                            ↓
CENTRAL perforation         ATTIC/MARGINAL perforation
(Pars tensa; mucoid)        (Pars flaccida; foul-smelling)
          ↓                            ↓
  TUBOTYMPANIC CSOM         ATTICOANTRAL CSOM
          ↓                            ↓
Medical treatment           HRCT Temporal Bone
(Aural toilet + cipro drops)       ↓
          ↓                Cholesteatoma confirmed
   No improvement in 4-6 wks         ↓
          ↓               SURGERY MANDATORY
   TYMPANOPLASTY      (CWU or CWD mastoidectomy
                       + tympanoplasty ± ossiculoplasty)
                               ↓
                  Post-op surveillance:
                  MRI-DWI for residual/recurrent cholesteatoma

---

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Epistaxis (Nosebleed)

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1. Definition

• ~16% of the US population suffers from epistaxis annually
• Accounts for approximately 500,000 emergency room visits per year in the USA
• 90% are anterior and self-limited; only ~10% are posterior and potentially dangerous
• Most do not require medical attention
• K. J. Lee's Essential Otolaryngology, p. 584

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2. Surgical Anatomy of Nasal Blood Supply

External Carotid Artery (ECA) Supply

• Sphenopalatine Artery (SPA) - the principal supply; enters the nasal cavity via the sphenopalatine foramen
  • Posterior septal artery - supplies the posterior nasal septum
  • Lateral nasal artery - supplies the lateral nasal wall and turbinates
• Greater Palatine Artery - supplies the anterior nasal septum and floor of the nose; runs through the incisive canal

• Angular artery - runs in the nasofacial crease; supplies the nose externally
• Superior labial artery - sends small branches to the nasal vestibule and anterior nasal septum

Internal Carotid Artery (ICA) Supply

• Anterior Ethmoidal Artery (AEA) - exits the orbit via the anterior ethmoidal foramen; supplies the lateral wall and anterior third of the nasal cavity + superior septum
• Posterior Ethmoidal Artery (PEA) - smaller; supplies the superior turbinate and adjacent posterior septum

Key Vascular Plexuses

Kiesselbach's Plexus (= Little's Area)

• Located on the anteroinferior nasal septum (anterior 1-1.5 cm)
• Most common site of anterior epistaxis (>90% of all nosebleeds)
• Formed by anastomosis of 5 arteries:
  1. Anterior ethmoidal artery (ICA system)
  2. Posterior ethmoidal artery (ICA system)
  3. Sphenopalatine artery (ECA system)
  4. Greater palatine artery (ECA system)
  5. Superior labial artery (ECA system)
• Represents an anastomotic highway between internal and external carotid systems
• The overlying mucosa is thin, making these vessels highly susceptible to trauma and drying

Woodruff's Plexus (= Naso-nasopharyngeal Plexus)

• Located at the posterior 1 cm of the nasal floor, inferior meatus, and middle meatus
• Site of posterior epistaxis
• Supplied predominantly by the sphenopalatine artery (SPA) and ascending pharyngeal artery
• K. J. Lee's Essential Otolaryngology, p. 584
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 1846-1856

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3. Classification

By Location

By Severity

• Mild - self-limiting; resolves with simple first aid
• Moderate - requires medical intervention; nasal packing
• Severe - haemodynamically significant; requires hospitalisation, packing, surgery, or embolisation
• Rosen's Emergency Medicine
• K. J. Lee's Essential Otolaryngology

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4. Aetiology / Causes

Local Causes

Systemic Causes

Key point: In adolescent males with severe unilateral epistaxis - suspect Juvenile Nasopharyngeal Angiofibroma (JNA). Do NOT biopsy - risk of catastrophic haemorrhage.

• Scott-Brown's Otorhinolaryngology, Vol 2, p. 1898-1910
• Bailey and Love's Surgery, p. 788

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5. Pathogenesis

• The mucosa over Kiesselbach's plexus is thin and has poor submucosal support.
• Drying and crusting over Little's area is the most common precursor to epistaxis in children.
• Rhinitis sicca: dry air → mucosal desiccation → crust formation → removal of crust tears vessels.
• Staphylococcus aureus colonisation of the nasal cavity may contribute to recurrent epistaxis by causing low-grade inflammation → release of inflammatory mediators → neovascularisation of the septal mucosa → thin-walled arterioles and capillaries with a surrounding inflammatory infiltrate (visible as prominent vessels on Little's area).
• Digital trauma (nose picking) is the triggering event in the majority of cases.
• Posterior epistaxis typically involves arterial bleeding from the SPA territory, hence more profuse and dangerous.
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 1859-1886

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6. Clinical Assessment

History

• Duration and frequency of bleeding
• Which nostril; unilateral vs. bilateral
• Amount of blood loss (cups? soaked tissues?)
• Direction: anterior (from nose) or posterior (blood in throat, spitting blood)
• Precipitating factors (trauma, nose blowing, dry environment)
• Current medications (anticoagulants, antiplatelets, NSAIDs, topical steroids, decongestants)
• Past medical history: hypertension, coagulopathy, renal/liver disease, HHT
• Family history of bleeding disorders
• Red flags: recurrent unilateral epistaxis + nasal obstruction → suspect tumour; adolescent male + massive bleed → JNA

Examination

• General: HR, BP (hypertension), pallor, signs of haemodynamic compromise
• Anterior rhinoscopy: (with head light + nasal speculum)
  • Inspect Little's area for visible bleeding point, prominent vessels, crusting
  • Note any polyps, foreign body, septal deviation, perforation
• Nasal endoscopy (rigid/flexible): For posterior bleeds or when anterior source not found
  • Can identify SPA territory bleeding at posterior septum and lateral wall
  • Even in apparently posterior epistaxis, the point can often be identified and treated endoscopically
• Oropharynx: Blood trickling down posterior pharyngeal wall confirms posterior source

Investigations

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7. First Aid (Pre-hospital / Self-management)

1. Sit the patient upright - lean slightly forward (prevents blood tracking posteriorly into airway/pharynx; avoids aspiration and swallowing of blood)
2. Pinch the soft cartilaginous part of the nose (not the bony bridge) firmly for 10-15 minutes continuously without releasing
3. Breathe through the mouth
4. Apply ice pack to the nose or back of neck for vasoconstriction
5. Topical vasoconstrictors (oxymetazoline/xylometazoline) applied with cotton wool
6. Spit out blood - do not swallow (causes nausea/vomiting)
7. Do NOT tilt head back

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8. Medical Management

Step-Up Approach (Escalation Ladder)

Step 1: First Aid (pinch, lean forward, ice, topical decongestant)
         ↓ (if fails)
Step 2: Chemical / Silver Nitrate Cautery (anterior bleeds)
         ↓ (if fails)
Step 3: Electrocautery (bipolar) under endoscopic guidance
         ↓ (if fails)
Step 4: Anterior Nasal Packing
         ↓ (if posterior bleed or fails)
Step 5: Posterior Nasal Packing
         ↓ (if fails - 38% failure rate with packing)
Step 6: Endoscopic Sphenopalatine Artery Ligation / Cautery (TESPAL)
         ↓ (if fails or not available)
Step 7: Internal Maxillary Artery Ligation / Anterior Ethmoidal Artery Ligation
         ↓ (if fails or haemodynamically unstable)
Step 8: Endovascular Embolisation

---

A. Anterior Epistaxis - Mild

1. Inspect nasal cavity with headlight and speculum; remove obscuring clots
2. Topical decongestant + anaesthesia (cottonoids with xylometazoline + lidocaine or cocaine 5-10%; atomizer, or soaked pledgets held in nose for 10 minutes)
3. Silver nitrate chemical cautery - apply to bleeding point or prominent vessels; generally sufficient for most anterior bleeds
   • Apply only unilaterally to avoid septal perforation from bilateral cautery
4. Absorbable haemostatic agents (Gelfoam / Surgicel) applied over cauterization site to minimize rebleeding
5. Topical antibiotic ointment (Naseptin / Bacitracin) to prevent crust formation and secondary infection
6. Advise: avoid anticoagulants for 7-10 days (if safe); avoid strenuous activity and nose blowing; nasal saline sprays; humidification; avoid nose picking

B. Anterior Epistaxis - Moderate to Severe

1. Office or emergency treatment with formal diagnostic nasal endoscopy to identify and control source
2. Transoral greater palatine foramen block - to reduce bleeding from SPA territory
3. Inject bleeding area with lidocaine + adrenaline (epinephrine) (1:200,000)
4. Bipolar electrocautery for definitive control under endoscopic visualisation
5. If patient unable to tolerate office treatment or medically unstable: proceed to operating room under GA
6. Anterior nasal packing if cautery fails:
   • Vaseline-impregnated ribbon gauze (BIPP - bismuth iodoform paraffin paste) - layered from floor to roof
   • Non-absorbable sponge packs (Merocel / RhinoRocket) - expand on contact with moisture; easy to insert
   • Absorbable packs (Nasopore, Surgicel, Gelfoam) - dissolve; no removal needed; less trauma
   • Pack kept in situ for 24-48 hours (up to 72 hours max)
   • Antibiotic cover (co-amoxiclav or similar) while packed - to prevent TSS and sinusitis

C. Posterior Epistaxis

1. ABC stabilisation (airway, breathing, circulation); establish IV access; bloods; oxygen
2. Formal diagnostic nasal endoscopy - often reveals the bleeding point (SPA territory, posterior septum)
3. Endoscopic cautery first line - can often control posterior bleeds directly
4. Posterior nasal packing if endoscopy not immediately available or unsuccessful:
   • Foley catheter (30 ml balloon) - passed through the nose into the nasopharynx, balloon inflated with water/saline, pulled forward to tamponade the choana; anterior cavity then packed with Vaseline gauze
   • Dual balloon epistaxis device (e.g., Brighton Epistat, Rapid Rhino) - posterior + anterior balloon in one device
   • Anteroposterior (AP) gauze pack under GA - gauze pack in nasopharynx via the mouth
   • Patients require HDU/ICU observation with cardiac monitoring and supplemental oxygen (nasal packing → hypoxia via naso-pulmonary reflex + nasal airway obstruction)
   • Antibiotic therapy to prevent toxic shock syndrome (S. aureus)
   • Failure rate of posterior packing: 38% (high!)
   • Complications: mucosal trauma, alar necrosis, oroantral fistula, otitis media, respiratory obstruction, aspiration, significant pain, cardiopulmonary compromise
5. Endoscopic Sphenopalatine Artery Ligation/Cautery (TESPAL) - preferred method for intractable posterior epistaxis in endoscopic era:
   • Performed under GA
   • Mucosal incision anterior to the crista ethmoidalis of the palatine bone
   • Medially-based mucosal flap raised from the lateral nasal wall
   • SPA identified at the sphenopalatine foramen; clipped or cauterised
   • Definitive control of terminal blood supply; success rate > 90%
   • Essentially has replaced posterior packing as the definitive treatment
6. Internal Maxillary Artery (IMA) Ligation - now rarely needed:
   • Gingivobuccal (Caldwell-Luc) approach to the pterygomaxillary fossa
   • Vascular clips applied to IMA trunk and branches
   • 10-15% failure rate (due to collateral supply)
   • Complications: facial numbness, CN palsies, epiphora, damage to tooth roots, oroantral fistula
7. Anterior Ethmoidal Artery Ligation - for bleeds from the AEA territory (superior/posterior septum):
   • Approached via a small medial canthal (Lynch) incision or endoscopically
   • AEA clipped in the orbit close to where it enters the ethmoid
8. External Carotid Artery Ligation - historic; last resort; ligation above the origin of the lingual artery

D. Endovascular Embolisation (Interventional Radiology)

• Indicated for: life-threatening epistaxis failing packing; unsuitable for surgery (elderly, comorbid); massive JNA bleeding pre-operatively
• Technique:
  • Bilateral selective ICA and ECA angiography to visualise feeders
  • Superselective catheterisation of IMA, facial, and ascending pharyngeal arteries
  • Embolisation of SPA, facial artery branches with small particles (150-400 µm); distal occlusion reduces collateral recurrence
  • Success rate: 91-97%; complication rate: 0-3%
• Complications: stroke (if ICA/ophthalmic artery embolised), facial nerve palsy, skin necrosis, blindness (if particles enter ophthalmic artery)
• K. J. Lee's Essential Otolaryngology, p. 584-585
• Bailey and Love's Surgery, p. 789
• Cummings Otolaryngology, p. 2063-2067

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9. Special Conditions

Hereditary Haemorrhagic Telangiectasia (HHT) / Osler-Weber-Rendu Disease

• Autosomal dominant; mutations in ENG (endoglin) or ACVRL1 (ALK1) genes
• Recurrent, multifocal epistaxis from thin-walled vessels deficient in muscle and elastic tissue
• Telangiectasias on lips, tongue, nasal mucosa, fingers, GI tract, lung (AVMs), liver, brain
• Diagnostic criteria (Curaçao criteria): epistaxis + telangiectasias + visceral AVMs + family history (3/4 = definitive; 2/4 = suspected)
• Treatment: laser photocoagulation, topical oestrogens, bevacizumab (anti-VEGF), embolisation, septal dermoplasty (Young's procedure)

Juvenile Nasopharyngeal Angiofibroma (JNA)

• Exclusively in adolescent males
• Benign but locally aggressive vascular tumour arising from the lateral nasopharyngeal wall / sphenopalatine foramen area
• Presents with massive, recurrent, unilateral epistaxis + progressive nasal obstruction
• Diagnosis: contrast CT (highly vascular mass with anterior bowing of posterior antral wall - Holman-Miller/antral sign) + MRI for soft tissue extent
• DO NOT BIOPSY - risk of uncontrollable haemorrhage
• Treatment: pre-operative embolisation of feeding vessels → endoscopic or open excision by experienced surgeon; image guidance often used

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10. Epistaxis in Children

• Age peak: 2-10 years; rare in infants
• Most common cause: digital trauma (nose picking)
• Rhinitis sicca (dry air, winter, low humidity) is a significant contributor
• Almost all childhood epistaxis arises from Kiesselbach's plexus (venous/arteriolar)
• Posterior bleeds rare in children but high risk if present (airway compromise, aspiration)
• Most resolve with conservative measures (pinching + ice + topical vasoconstrictors)
• Indication for haematologist referral: recurrent/severe epistaxis + family history of bleeding disorder OR abnormal PT/APTT → ~1/3 will have a diagnosable coagulopathy, most often von Willebrand disease type 1
• Adolescent male + massive unilateral epistaxis requiring packing: evaluate with CT for JNA
• Tintinalli's Emergency Medicine, p. 945-959
• Scott-Brown's Otorhinolaryngology, Vol 2, p. 1861-1916

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11. Epistaxis in the Elderly

• Predominantly posterior epistaxis (arterial)
• Most common causes: hypertension and anticoagulant/antiplatelet therapy
• Bleeding from SPA territory - profuse, difficult to control
• Often requires packing ± TESPAL
• Nasal packing in the elderly is associated with significant risk: hypoxia (naso-pulmonary reflex), cardiac arrhythmias, pulmonary complications
• TESPAL is the preferred definitive procedure to avoid prolonged packing

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12. Complications of Epistaxis and its Treatment

Epistaxis itself

• Hypovolaemia / haemorrhagic shock (rare)
• Aspiration of blood
• Anaemia
• Anxiety / syncope

Complications of Treatment

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13. Summary Algorithm

EPISTAXIS
     ↓
First Aid: Sit upright, lean forward, pinch soft nose x 10-15 mins
Topical vasoconstrictor (oxymetazoline / cocaine pledgets)
     ↓
Anterior rhinoscopy / nasal endoscopy
     ↓
        ┌────────────────────────────────────┐
        ↓                                    ↓
  ANTERIOR SOURCE                    POSTERIOR / NOT VISIBLE
  (Little's area visible)             or profuse / uncontrolled
        ↓                                    ↓
Silver nitrate cautery            ABC resuscitation
  ± Bipolar electrocautery         IV access, bloods, oxygen
        ↓ (fails)                           ↓
Anterior packing                  Endoscopic cautery (GA or awake)
(Merocel / BIPP gauze)                      ↓ (fails)
  + Antibiotics                    Posterior packing
        ↓ (fails)                  (Foley catheter / dual balloon)
TESPAL (SPA ligation)              + Antibiotics, HDU monitoring
        ↓ (fails)                           ↓ (38% fail)
AEA ligation / IMA ligation        TESPAL (preferred)
        ↓ (fails)                           ↓ (fails)
   Embolisation                     Embolisation

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14. Key Facts / Mnemonics

• Labial (superior labial artery)
• Ethmoidal - Anterior
• Greater palatine
• Sphenopalatine
• Anterior ethmoidal (same; sometimes listed as "ethmoidal A+P")

• Hypertension / HHT
• Infection (rhinitis, sinusitis)
• Trauma (nose picking, fractures)
• Systemic (coagulopathy, liver, renal, leukaemia)
• Vascular (JNA, haemangioma, AVM)
• Anticoagulants / Antiplatelet drugs
• Drug abuse (cocaine)

• Adolescent male + massive bleed = JNA
• Recurrent + family history = von Willebrand / HHT
• Unilateral + nasal obstruction = tumour
• Elderly + hypertensive + posterior = SPA territory bleed (needs TESPAL)
• Skin telangiectasias + recurrent = HHT (Osler-Weber-Rendu)

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Epistaxis - All Relevant ENT Headings

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1. Definition

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2. Surgical Anatomy of Nasal Blood Supply

External Carotid Artery (ECA) Contributions

• Internal Maxillary Artery (IMA) →
  • Sphenopalatine Artery (SPA) - terminal branch; enters via sphenopalatine foramen
    • Posterior septal artery (posterior septum)
    • Lateral nasal artery (lateral wall + turbinates)
  • Greater Palatine Artery - supplies anterior septum and nasal floor via incisive canal
• Facial Artery →
  • Angular artery (external nose)
  • Superior labial artery (vestibule + anterior septum)

Internal Carotid Artery (ICA) Contributions

• Anterior Ethmoidal Artery (AEA) - anterior and lateral 1/3 of nasal cavity; superior septum
• Posterior Ethmoidal Artery (PEA) - small; superior turbinate and adjacent posterior septum

Kiesselbach's Plexus (= Little's Area)

• Located on the anteroinferior nasal septum (anterior 1-1.5 cm)
• Most common site of epistaxis (>90% of all nosebleeds)
• Anastomosis of 5 arteries:
  1. Anterior ethmoidal artery (ICA)
  2. Posterior ethmoidal artery (ICA)
  3. Sphenopalatine artery (ECA)
  4. Greater palatine artery (ECA)
  5. Superior labial artery (ECA)
• Anastomotic highway between ICA and ECA systems
• Thin overlying mucosa → highly susceptible to trauma and drying

Mnemonic for Kiesselbach's plexus supply: "SPAG-E" - Sphenopalatine + Palatine (greater) + Anterior ethmoidal + Greater labial (superior labial) + Ethmoidal (posterior)

Woodruff's Plexus (= Naso-nasopharyngeal Plexus)

• Posterior 1 cm of nasal floor, inferior and middle meatus
• Site of posterior epistaxis
• Supplied by SPA and ascending pharyngeal artery (both ECA)

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3. Classification

By Location

By Severity

• Mild - self-limiting; first-aid measures
• Moderate - requires clinical intervention; packing
• Severe - haemodynamically significant; hospitalisation, surgery, or embolisation

---

4. Aetiology / Causes

Local Causes

Systemic Causes

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5. Pathogenesis

• Thin mucosa overlying Kiesselbach's plexus → easily traumatised
• Rhinitis sicca / dry air: mucosal desiccation → crust formation → crust removal tears vessels
• Staphylococcus aureus colonisation → low-grade inflammation → neovascularisation → thin-walled arterioles on Little's area (histologically: capillaries with inflammatory infiltrate)
• Posterior bleeds: arterial bleed from SPA branches → profuse, difficult to control
• HHT: thin-walled vessels deficient in smooth muscle and elastic tissue → rupture with minimal trauma

---

6. Clinical Assessment

History

• Which side; unilateral vs. bilateral
• Anterior (blood from nose) vs. posterior (blood in throat/mouth)
• Volume and duration; frequency and recurrence
• Preceding events (trauma, URTI, nose blowing, nose picking)
• Medications (anticoagulants, antiplatelets, steroids, cocaine)
• PMH: hypertension, liver disease, renal failure, HHT, coagulopathy
• Family history of bleeding disorders
• Red flags:
  • Adolescent male + massive unilateral bleed → JNA
  • Unilateral + nasal obstruction + mass → tumour
  • Recurrent + family history → von Willebrand / HHT
  • Skin telangiectasias → HHT

Examination

• Vital signs: HR, BP (hypertension), signs of haemodynamic compromise
• Anterior rhinoscopy (headlight + Thudichum speculum):
  • Little's area for bleeding point, prominent vessels, crusting, telangiectasias
  • Septal deviation, perforation, polyps, foreign body
• Rigid/flexible nasal endoscopy: identifies posterior source; essential in refractory/posterior epistaxis
• Oropharynx: blood trickling down posterior pharyngeal wall = posterior source
• Skin / lips / tongue: telangiectasias (HHT)

Investigations

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7. First Aid / Pre-hospital Management

1. Sit upright, lean forward (prevents posterior aspiration of blood)
2. Pinch the soft cartilaginous part of nose firmly for 10-15 minutes continuously - do NOT release early
3. Breathe through the mouth
4. Apply ice pack to nose / forehead / back of neck
5. Topical vasoconstrictor soaked cotton - oxymetazoline / xylometazoline
6. Spit out blood - do NOT swallow (causes nausea, vomiting, masks blood loss)
7. Do NOT tilt head back

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8. Management - Step-Up Escalation Ladder

Step 1: Chemical Cautery (Anterior - Mild)

• Inspect with headlight + speculum; remove clots
• Apply topical decongestant + anaesthesia: cottonoids soaked in cocaine 5-10% OR xylometazoline + lidocaine (atomiser or pledgets × 10 mins)
• Silver nitrate cautery to bleeding point or prominent vessels
  • Apply to one side only at a time - bilateral cautery risks septal perforation
  • Wait 4-6 weeks before cauterising opposite side if needed
• Absorbable haemostatic agents (Gelfoam / Surgicel) over cauterised site
• Topical antibiotic ointment (Naseptin / Mupirocin) - prevents crust and Staph colonisation
• Advise: saline spray, humidification; avoid nose blowing/picking; avoid anticoagulants 7-10 days if safe

Step 2: Electrocautery (Anterior - Moderate to Severe)

• Rigid nasal endoscopy under topical anaesthesia to identify source
• Transoral greater palatine foramen block (reduces SPA territory bleeding)
• Submucosal injection of lidocaine 1% + adrenaline 1:200,000
• Bipolar electrocautery under direct endoscopic vision
• If patient unable to tolerate or medically unstable → operating room under GA

Step 3: Anterior Nasal Packing

• Pack in situ 24-48 hours (max 72 hours)
• Antibiotic cover while packed (co-amoxiclav) - prevent TSS (S. aureus), sinusitis, otitis media
• Analgesia

Step 4: Posterior Packing (if anterior fails or posterior source)

• Failure rate of posterior packing: 38% (high - proceed to TESPAL)
• Requires HDU / monitored bed with:
  • Cardiac monitoring (naso-cardiac reflex → bradycardia, arrhythmias)
  • Supplemental oxygen (naso-pulmonary reflex → hypoxia, bronchospasm)
  • Regular obs
• Antibiotic therapy - TSS prophylaxis

• Mucosal trauma, alar necrosis, oroantral fistula
• Otitis media (ET occlusion)
• Respiratory obstruction, aspiration
• Significant pain
• Cardiopulmonary compromise (especially in elderly)
• TSS (S. aureus)

In the endoscopic era, posterior packing is largely a temporary/bridge measure before TESPAL

Step 5: Transnasal Endoscopic Sphenopalatine Artery Ligation / Cautery (TESPAL)

• Performed under GA
• Technique:
  • Topical decongestion of lateral nasal wall
  • Mucosal incision anterior to the crista ethmoidalis of the palatine bone (posterior end of middle meatus)
  • Medially-based mucosal flap raised from the lateral nasal wall
  • SPA identified at the sphenopalatine foramen as it exits the pterygopalatine fossa
  • Vascular clips or bipolar cautery applied to the SPA and its branches
  • Can perform endoscopically without any external incision
• Success rate > 90%
• Advantages over packing: avoids prolonged hospital stay, avoids packing complications, definitive control
• Failure: consider contralateral SPA branch, AEA contribution, or collateral supply

Step 6: Anterior Ethmoidal Artery (AEA) Ligation

• For bleeds from the AEA territory (superior, posterior nasal septum / superior turbinate area) failing TESPAL
• Approached via:
  • Lynch incision (medial canthal skin incision, Lynch-Howarth)
  • Endoscopically (emerging technique)
• AEA clipped in the orbit just medial to where it enters the ethmoid
• Landmarks: AEA lies ~24 mm posterior to the anterior lacrimal crest

Step 7: Internal Maxillary Artery (IMA) Ligation

• Rarely needed in endoscopic era (largely superseded by TESPAL)
• Gingivobuccal (Caldwell-Luc) approach to pterygopalatine/pterygomaxillary fossa
• Vascular clips applied to IMA trunk and branches
• 10-15% failure rate (collateral supply)
• Complications: facial hypoesthesia, CN palsies, epiphora, damage to tooth roots, oroantral fistula, sinusitis, blindness

Step 8: Endovascular Embolisation (Interventional Radiology)

• Life-threatening epistaxis failing all conservative measures
• Patients unsuitable for GA / surgery (elderly, high surgical risk)
• Massive JNA bleeding (pre-operative embolisation to reduce intraoperative blood loss)
• Vascular malformations (HHT)

• Bilateral selective ICA and ECA angiography to visualise feeders
• Superselective catheterisation (microcatheter) of IMA, facial, and ascending pharyngeal arteries
• Distal embolisation of SPA, facial artery branches with particles 150-400 µm
• Distal rather than proximal occlusion reduces collateral recurrence
• If no clear bleeding point: empirical bilateral embolisation of distal IMA + facial arteries

• Success rate: 91-97%
• Complication rate: 0-3%

• Stroke (inadvertent ICA/ophthalmic artery embolisation)
• Facial nerve palsy
• Skin necrosis
• Blindness (ophthalmic artery occlusion - most feared)
• Facial pain

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9. Epistaxis in Special Situations

Hereditary Haemorrhagic Telangiectasia (HHT) / Osler-Weber-Rendu Disease

• Autosomal dominant; mutations in ENG (endoglin) gene or ACVRL1 (ALK-1)
• Recurrent, multifocal bleeds from thin-walled vessels (no smooth muscle / elastic tissue)
• Telangiectasias: lips, tongue, nasal mucosa, fingers, GI mucosa; AVMs in lung, liver, brain

1. Recurrent spontaneous epistaxis
2. Mucocutaneous telangiectasias (lips, oral cavity, fingers, nose)
3. Visceral AVMs (lung, liver, brain, GI)
4. First-degree family member with HHT

• Laser photocoagulation (Nd:YAG or KTP) - repeated sessions
• Topical oestrogen cream (anti-angiogenic)
• Bevacizumab (anti-VEGF) - IV or topical intranasal
• Embolisation (for pulmonary AVMs)
• Septal dermoplasty (Young's procedure) - replacement of nasal mucosa with split-thickness skin graft to reduce telangiectatic vessel exposure

Juvenile Nasopharyngeal Angiofibroma (JNA)

• Exclusively in adolescent males
• Benign but locally aggressive, highly vascular, hormonally sensitive tumour
• Arises from the lateral nasopharyngeal wall / sphenopalatine foramen region
• Presentation: massive recurrent unilateral epistaxis + progressive unilateral nasal obstruction ± cheek swelling

• Contrast CT: highly vascular mass + Holman-Miller sign (anterior bowing of posterior antral wall)
• MRI: soft tissue extent; intracranial extension; "salt and pepper" appearance on T1 (flow voids)
• Angiography: highly vascular; primarily fed by IMA/SPA
• Do NOT biopsy - catastrophic haemorrhage risk

1. Pre-operative embolisation of feeding vessels (48-72 hrs before surgery)
2. Endoscopic resection by experienced surgeon, often with image guidance
3. Open approaches (mid-facial degloving, infratemporal fossa) for extensive disease
4. Radiotherapy in selected cases (intracranial extension)

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10. Paediatric Epistaxis

• Peak age: 2-10 years; rare in infants
• Almost always anterior (Kiesselbach's plexus)
• Most common cause: digital trauma (nose picking)
• Other causes: allergic rhinitis, viral URTI, rhinitis sicca, foreign body
• Manage with conservative measures (90% resolve)

• Recurrent/severe epistaxis + family history of bleeding disorder
• Abnormal PT or APTT on screening
• ~1/3 will have coagulopathy - most commonly von Willebrand disease type 1

• Recurrent unilateral epistaxis + nasal obstruction → CT scan
• Adolescent male + profuse unilateral epistaxis requiring packing → JNA

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11. Complications of Epistaxis and its Management

---

12. Prevention / Recurrence Reduction

---

13. Summary Table: Anterior vs. Posterior Epistaxis

---

14. Key Mnemonics

• Sphenopalatine artery
• Posterior ethmoidal artery
• Anterior ethmoidal artery
• Greater palatine artery
• Labial (superior labial artery)

• Local trauma (nose picking, fractures)
• Osler-Weber-Rendu (HHT)
• Coagulopathy (VWD, Haemophilia, ITP)
• Anticoagulants / Antiplatelets
• Leukaemia / liver / renal disease
• Hypertension (elderly, posterior)
• Inflammation (rhinitis, sinusitis, granulomatous)
• Tumours (JNA, SCC, rhabdomyosarcoma)
• Structural (septal deviation, perforation, rhinitis sicca)

• Male adolescent + massive bleed = JNA
• Unilateral + obstruction = tumour
• Abnormal PT/APTT + family history = VWD
• Telangiectasias + recurrent = HHT

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Rhinitis - All Relevant ENT Headings

---

1. Definition

• Nasal obstruction / blockage
• Rhinorrhoea (anterior or posterior nasal drip)
• Sneezing
• Nasal pruritus (itching)

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2. Classification

Master Classification

RHINITIS
├── ALLERGIC RHINITIS (AR)
│   ├── Seasonal (SAR) - "Hay fever"
│   ├── Perennial (PAR)
│   └── Occupational (allergic type)
│
└── NON-ALLERGIC RHINITIS (NAR)
    ├── Infectious Rhinitis
    │   ├── Viral (most common)
    │   ├── Bacterial
    │   └── Fungal
    ├── Idiopathic (Vasomotor) Rhinitis
    ├── Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES)
    ├── Hormonal Rhinitis
    │   ├── Pregnancy rhinitis
    │   ├── Puberty / menopause
    │   └── Hypothyroidism / acromegaly
    ├── Medication-Induced Rhinitis (Rhinitis Medicamentosa)
    ├── Atrophic Rhinitis
    │   ├── Primary (ozaena)
    │   └── Secondary
    ├── Occupational Rhinitis (non-allergic type)
    ├── Irritant-Induced Rhinitis
    ├── Gustatory Rhinitis
    ├── Senile Rhinitis
    ├── Granulomatous Rhinitis
    ├── Rhinitis from Mechanical Obstruction
    └── Neoplastic Rhinitis

ARIA (Allergic Rhinitis and its Impact on Asthma) Classification of Allergic Rhinitis

• Cummings Otolaryngology
• Scott-Brown's Otorhinolaryngology, Vol 1

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3. Allergic Rhinitis (AR)

Epidemiology

• 5th most common chronic disease in the United States by economic impact
• Annual direct costs: up to $5 billion in the USA; ~355 Euros per patient per month in Europe
• 3.5 million lost workdays per year in the USA attributable to AR
• Significantly decreases quality of life and impairs sleep
• Strong association with asthma (united airway disease concept)
• Prevalence increasing in Westernised populations

Pathophysiology - Two Phases

Phase 1: Sensitisation (Initial Exposure)

1. Allergen deposited on nasal mucosa
2. Mucosal epithelial cells secrete TSLP (thymic stromal lymphopoietin) → matures dendritic cells into TH2-promoting subtypes
3. Antigen Presenting Cells (APCs/dendritic cells) engulf antigen and process it
4. Presentation to TH2 lymphocytes → TH2 dominance established
5. TH2 cells release IL-4, IL-5, IL-13 → stimulate B cells to produce allergen-specific IgE
6. IgE binds to Fc epsilon RI receptors on mast cells and basophils in nasal mucosa
7. → Patient is now sensitised (no symptoms yet)

Phase 2: Re-exposure (Clinical Disease)

1. Re-exposure to same allergen → cross-links IgE on mast cells
2. Mast cell degranulation → release of preformed mediators:
   • Histamine (H1 receptors) → vasodilation, increased permeability, pruritus, sneezing
   • Tryptase, chymase (proteases)
   • Leukotrienes (LTC4, LTD4) → bronchoconstriction, mucus secretion
   • Prostaglandin D2 → vasodilation
   • Bradykinin → vascular permeability
3. → Sneezing, rhinorrhoea, pruritus within minutes

1. Recruitment of eosinophils, basophils, T lymphocytes, neutrophils to nasal mucosa
2. IL-5 (from TH2 cells) → eosinophil survival and activation
3. Eosinophil products (MBP, ECP) → chronic mucosal damage
4. Nasal hyperreactivity develops → heightened response to specific AND non-specific stimuli
5. → Nasal congestion, hyposmia (dominates in late phase)

Allergens

Seasonal Allergens (trigger SAR / hay fever)

• Tree pollens (spring): Birch, oak, alder, hazel
• Grass pollens (summer): Timothy, rye, Bermuda grass
• Weed pollens (late summer/autumn): Ragweed, mugwort, plantain

Perennial Allergens (trigger PAR)

• House dust mite (HDM) - Dermatophagoides pteronyssinus / farinae - most important perennial allergen
• Animal danders - cat (Fel d 1), dog, horse
• Cockroach allergens
• Mould spores - Aspergillus, Alternaria, Cladosporium

Clinical Features of Allergic Rhinitis

Symptoms

• Sneezing - often paroxysmal (bouts of multiple sneezes)
• Rhinorrhoea - thin, watery, clear discharge (anterior + posterior)
• Nasal pruritus - itching inside the nose
• Nasal obstruction / blockage - bilateral; worse at night
• Post-nasal drip - causes throat clearing, cough
• Conjunctival symptoms (allergic conjunctivitis) - itching, tearing, redness - especially in SAR
• Reduced smell (hyposmia)
• Fatigue, headache, sleep disturbance (especially with nasal obstruction)
• Ear fullness (ET dysfunction from nasal oedema)
• Eustachian tube dysfunction → OME

Signs on Examination

Note: No single appearance of nasal mucosa is pathognomonic for AR - pale/swollen turbinates can occur in any cause of rhinitis

• Cummings Otolaryngology, p. 2782-3108

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4. Diagnosis of Allergic Rhinitis

Step-wise Diagnostic Approach

• Timing of symptoms (seasonal vs. perennial)
• Specific triggers (pollens, pets, dust)
• Work-related exacerbations
• Associated conditions: asthma, atopic dermatitis, conjunctivitis, food allergy
• Family history of atopy
• Drug history (NSAIDs, beta-blockers, ACE inhibitors, OCP, topical decongestants)

• Anterior rhinoscopy / nasal endoscopy
• Look for turbinate hypertrophy, polyps, septal deviation, discharge quality
• Examine eyes, skin, chest (united airway)

• CT sinuses: chronic rhinosinusitis, polyps, anatomical anomalies
• Nasal endoscopy: polyps, tumours, structural causes
• Ciliary function tests: if primary ciliary dyskinesia suspected (Kartagener's syndrome)
• Sweat chloride / CF screen: if CF suspected
• Serum ACE: sarcoidosis
• ANCA: Granulomatosis with polyangiitis (GPA/Wegener's)

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5. Treatment of Allergic Rhinitis

A. Allergen Avoidance (First Principle)

B. Pharmacotherapy

1. Intranasal Corticosteroids (INCS) - First-line for moderate-severe / perennial AR

• Most effective single agent for allergic rhinitis
• Reduce all 4 cardinal symptoms (obstruction, rhinorrhoea, sneezing, pruritus)
• Particularly effective for nasal congestion (unlike antihistamines)
• Reduce nasal mucosal oedema, eosinophilic infiltration, goblet cell hyperplasia
• Onset: 12-24 hours but full effect may take 1-2 weeks of regular use
• Must be used regularly (not PRN)
• Examples:
  • Fluticasone propionate (Flixonase) 2 sprays/nostril OD
  • Fluticasone furoate (Avamys) 2 sprays/nostril OD
  • Mometasone furoate (Nasonex) 2 sprays/nostril OD
  • Budesonide (Rhinocort) 2 sprays/nostril OD
  • Beclometasone dipropionate
  • Triamcinolone acetonide
• Side effects: nasal irritation, epistaxis, nasal dryness, septal perforation (rare); systemic bioavailability very low (especially fluticasone / mometasone)
• Technique: direct spray laterally towards the outer wall of the nostril (avoid septal direction)

2. Antihistamines (H1 Receptor Antagonists)

• First-line for mild/seasonal AR; particularly for sneezing, pruritus, rhinorrhoea
• Less effective for nasal congestion than INCS

• Chlorphenamine (chlorpheniramine), promethazine, diphenhydramine
• Significant sedation (~20% of patients); anticholinergic side effects
• Warn patients about driving / machinery
• May be useful for night-time relief of symptoms

• Azelastine (2 sprays/nostril BD) - rapid onset within minutes; some somnolence; bitter taste
• Olopatadine 0.6% (2 sprays/nostril BD) - safe, effective for SAR; bitter taste
• When adding antihistamine to INCS - intranasal antihistamine preferred over oral (superior efficacy as add-on)
• Dymista = azelastine + fluticasone combined intranasal spray - highly effective

3. Decongestants

• Xylometazoline, oxymetazoline, naphazoline
• Alpha-adrenergic agonists → vasoconstriction → rapid nasal decongestion
• Onset: minutes; very effective
• Use limited to 5-7 days maximum - prolonged use → rhinitis medicamentosa (rebound congestion)
• Indications: facilitate INCS penetration in severe congestion; acute flare; pre-examination; sleep during acute exacerbations

• Pseudoephedrine (most effective; now sold behind pharmacy counter - risk of methamphetamine conversion)
• Phenylephrine - meta-analysis shows lack of efficacy vs. placebo
• Cause systemic vasoconstriction → side effects: insomnia, irritability, hypertension, arrhythmias, urinary retention (men)
• Contraindicated: hypertension, ischaemic heart disease, hyperthyroidism, glaucoma, MAOI use, pregnancy

4. Intranasal Cromones (Sodium Cromoglicate)

• Mast cell stabiliser; prevents degranulation
• Weak effect; requires 4-6 times daily dosing (compliance poor)
• Useful in children (very safe, no systemic side effects)
• Best used prophylactically before allergen exposure
• Also useful in pregnancy (safe profile)

5. Leukotriene Receptor Antagonists (LTRA)

• Montelukast 10 mg OD (adults); 5 mg OD (children 6-14 yrs)
• Blocks CysLT1 receptors → reduces nasal congestion, rhinorrhoea
• Less effective than INCS or antihistamines as monotherapy
• Most useful as add-on therapy especially when concomitant asthma present (licensed for both)
• FDA black box warning (2020): neuropsychiatric events (suicidal ideation, aggression, depression) - use with caution

6. Anticholinergic Agents

• Ipratropium bromide nasal spray (0.03%)
• Reduces watery rhinorrhoea by blocking muscarinic receptors on nasal glands
• Does NOT help sneezing, pruritus, or nasal blockage
• Most useful for vasomotor / gustatory rhinitis and URTI-associated rhinorrhoea

7. Anti-IgE Therapy (Omalizumab)

• Monoclonal antibody against free IgE → reduces IgE levels → mast cell desensitisation
• Licensed for severe allergic asthma + moderate-severe AR refractory to standard therapy
• Expensive; requires subcutaneous injection every 2-4 weeks

Summary - Treatment Choice by AR Type

C. Allergen Immunotherapy (AIT)

Subcutaneous Immunotherapy (SCIT)

• Injections of gradually increasing doses of allergen extract subcutaneously
• Build-up phase: weekly injections for 3-6 months (increasing dose)
• Maintenance phase: monthly injections for 3-5 years
• Must be given in clinical setting with 30-minute observation post-injection (risk of anaphylaxis)
• Adrenaline (epinephrine) must be immediately available
• Efficacy: reduces symptoms, reduces medication use, induces long-term tolerance (persists years after stopping)
• Can prevent new sensitisations developing
• Can prevent progression of AR to asthma

Sublingual Immunotherapy (SLIT)

• Allergen drops or tablets placed under the tongue
• Self-administered at home - no injection required
• FDA-approved tablets available for: grass pollen (Grazax, Oralair), house dust mite (Acarizax/Odactra), ragweed (Ragwitek)
• Slightly less effective than SCIT but better compliance and safety profile
• Also given for 3-5 years
• Contraindications (both SCIT and SLIT): severe/uncontrolled asthma (FEV1 < 70%), ischaemic heart disease, beta-blocker use, malignancy, autoimmune disease, pregnancy (not new course)

Mechanism of Immunotherapy

• Shifts immune response from TH2 → TH1/Treg dominance
• Induces regulatory T cells (Tregs) secreting IL-10 and TGF-β
• Reduces allergen-specific IgE; increases blocking IgG4
• Reduces mast cell and eosinophil recruitment to nasal mucosa
• Cummings Otolaryngology, p. 3100-3108
• Goldman-Cecil Medicine, p. 2553-2558

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6. Non-Allergic Rhinitis (NAR)

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6A. Idiopathic (Vasomotor) Rhinitis

• Most common type of NAR
• Cause: unknown; likely autonomic dysregulation of nasal vasomotor tone (hence "vasomotor")
• Triggered by non-specific irritants and environmental changes (not allergens)
• Triggers:
  • Cold, dry air; changes in temperature/humidity
  • Barometric pressure change
  • Strong smells (perfumes, cologne, incense, cleaning products, paint)
  • Tobacco smoke
  • Strong emotions / stress
  • Exercise
  • Alcohol
• Subtypes:
  • "Runners" - predominantly watery rhinorrhoea
  • "Blockers" - predominantly nasal congestion; many patients have both
• Features: perennial, constant symptoms; no pruritus or conjunctival symptoms; negative allergy tests
• Treatment:
  • INCS - moderately effective for congestion
  • Ipratropium bromide nasal spray - for rhinorrhoea
  • Oral decongestants - for congestion
  • Avoid identified triggers
  • Capsaicin nasal spray (desensitises TRPV1 channels) - emerging evidence
  • Surgery (turbinate reduction) for refractory nasal obstruction

6B. Non-Allergic Rhinitis with Eosinophilia Syndrome (NARES)

• Characterised by eosinophilia on nasal smear despite negative allergy tests
• Most often seen in adults
• Symptoms: profuse rhinorrhoea, sneezing, nasal pruritus, hyposmia (similar to AR but no atopy)
• Pathophysiology: "entopy" theory - localised allergic TH2 pathway confined to the nasal mucosa (local IgE production) without systemic atopic markers
• Eosinophilic infiltrate → chronic nasal mucosal dysfunction, prolonged ciliary clearance → may progress to nasal polyposis
• Strong association with Aspirin-Exacerbated Respiratory Disease (AERD / Samter's triad)
• Treatment: INCS (highly effective), oral/topical antihistamines; treat underlying aspirin sensitivity

6C. Infectious Rhinitis

• Most common cause: Rhinovirus (>50%), coronavirus, RSV, parainfluenza, adenovirus
• Presentation: profuse watery then mucopurulent rhinorrhoea, nasal obstruction, mild fever, malaise, sneezing, sore throat
• Duration: 7-10 days; self-limiting
• Treatment: symptomatic - saline irrigation, decongestants (short-term), paracetamol; antibiotic NOT indicated

• Secondary infection of viral rhinitis most common
• Pathogens: S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus
• Produces mucopurulent/purulent discharge; may progress to acute rhinosinusitis
• Treatment: antibiotics if bacterial sinusitis develops (amoxicillin/co-amoxiclav)

• Rhinoscleroma (Klebsiella rhinoscleromatis) - hard nodular lesions in nose, pharynx
• Syphilis (Treponema pallidum) - tertiary: gumma, saddle nose deformity
• Tuberculosis (MTB) - rare; granulomatous disease of nasal mucosa
• Leprosy - affects nasal mucosa early; causes saddle nose

6D. Granulomatous Rhinitis

6E. Hormonal Rhinitis

• Affects ~20-22% of pregnant women; onset typically 3rd trimester; resolves within 2 weeks post-delivery
• Mechanism: oestrogens → vascular engorgement, increased glandular activity, increased mucopolysaccharide production, decreased mucociliary clearance; increased blood volume → vasodilation
• Only known risk factor: smoking (increases risk by 69% relative risk)
• Neither pre-existing asthma nor rhinitis is a risk factor
• Treatment: saline irrigation (safe); INCS (topical, low systemic bioavailability - relatively safe); short-term topical decongestants; ipratropium for rhinorrhoea; avoid oral decongestants (vasoconstriction risk to fetus)

• Hypothyroidism - nasal congestion; treat the underlying condition
• Acromegaly (excess GH) - nasal mucosal hypertrophy
• Puberty / menstrual cycle - hormonal fluctuations can trigger symptoms
• Menopause - oestrogen withdrawal → mucosal atrophy → rhinitis sicca

6F. Drug-Induced Rhinitis / Rhinitis Medicamentosa

• Rebound nasal congestion from chronic use of topical alpha-adrenergic decongestants (oxymetazoline, xylometazoline, naphazoline)
• Mechanism: prolonged vasoconstriction → ischaemic mucosal damage → paradoxical vasodilation + rebound congestion → increased medication use → vicious cycle
• Onset after >5-7 days of continuous use
• On examination: red, raw, congested nasal mucosa (unlike allergic rhinitis with pale/oedematous mucosa)
• Treatment:
  • Abrupt withdrawal of topical decongestant (cold turkey)
  • INCS - reduces rebound inflammation (use for 4-6 weeks during withdrawal)
  • Short course oral prednisolone if severe
  • Reassurance; often very difficult for patients to stop

6G. Atrophic Rhinitis (Ozaena)

• Chronic condition predominantly in women in developing countries (subtropical/temperate climates)
• Progressive atrophy of nasal mucosa and underlying bone of turbinates
• Paradox: wide nasal cavities but patient feels blocked (no turbinate resistance to airflow)
• Thick, foul-smelling green/brown crusts (ozaena) filling the nasal cavities
• Anosmia (mucosal atrophy destroys olfactory epithelium)
• Associated bacteria: Klebsiella ozaenae, Staphylococcus spp., Proteus mirabilis, E. coli
• Possible mechanism: iron deficiency, nutritional deficiency, infection → mucosal atrophy → secondary bacterial colonisation

• Post-surgical (excessive turbinate resection → Empty Nose Syndrome)
• Granulomatous disease (GPA, sarcoidosis)
• Radiation therapy
• Trauma
• Rhinitis medicamentosa (late)

• Nasal irrigation with saline / alkaline nasal douche (dissolves crusts, moistens mucosa)
• Glucose 25% in glycerine nasal spray (antimicrobial + moisturising)
• Topical antibiotics (based on culture: rifampicin drops, ciprofloxacin) - eradicate Klebsiella
• Oestrogen nasal spray (increases vascularity)
• Vitamin A/D supplements (mucosal regeneration)
• Young's operation (surgical): nasal closure (nostril occlusion) to reduce airflow and allow mucosal regeneration → nasal passages re-opened after 6 months
• Submucosal implants to narrow nasal cavity and create turbulence

6H. Occupational Rhinitis

• Rhinitis caused by airborne agents in the workplace
• Two types:
  • Allergic (IgE-mediated): sensitisation to high molecular weight agents (flour, latex, animal proteins, enzymes) or low molecular weight chemicals (isocyanates, anhydrides, wood dust)
  • Non-allergic (irritant/toxic): aldehydes, isocyanates, solvents, cold air, diesel exhaust (see irritant table above)
• Predisposes to occupational asthma (united airway disease)
• Often under-diagnosed
• Management: reduce exposure (engineering controls, PPE), change work role, pharmacotherapy as for AR/NAR

6I. Gustatory Rhinitis

• Copious watery rhinorrhoea triggered by eating (especially spicy foods, hot food, alcohol)
• Mechanism: hyperactive neurogenic reflex with increased parasympathetic activity in response to salivary reflexes; capsaicin activates TRPV1 channels
• Isolated symptom - no sneezing, pruritus, congestion
• Can cause social embarrassment
• Treatment: ipratropium bromide nasal spray (anticholinergic → blocks glandular secretion); take 30-60 mins before meals

6J. Senile Rhinitis

• Rhinitis of elderly patients without identifiable allergic or inflammatory cause
• Mechanism: age-related changes - decreased ciliary function, decreased mucosal glandular secretions, reduced nasal valve support → anterior rhinorrhoea (clear, watery drip)
• Exacerbated by: cold air, position change
• Treatment: ipratropium bromide nasal spray; saline irrigation; humidification

6K. Rhinitis from Mechanical Obstruction

6L. Neoplastic Rhinitis

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7. Differential Diagnosis of Rhinitis

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8. Investigation Summary

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9. United Airway Disease (AR and Asthma)

• The nasal passages and lower airways share contiguous mucosa and unified immunology
• Epidemiology: 40-80% of asthma patients have rhinitis; 30-40% of AR patients have asthma
• AR worsens asthma and increases ER visits for asthma
• Untreated AR → nasal obstruction → mouth breathing → bypass of nasal air conditioning → exacerbates asthma
• Treating AR effectively improves asthma control
• Montelukast (LTRA) is licensed for both conditions
• Same patient needs integrated management of both upper and lower airway disease

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10. Complications of Rhinitis

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11. Surgical Treatment of Rhinitis

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12. Key Mnemonics

• Sneezing
• Nasal discharge (watery)
• Obstruction (nasal)
• Block (nasal pruritus/itch)

• Allergic shiners
• Dennie-Morgan lines
• Dysnasal salute (allergic salute)
• Transverse nasal crease
• Adenoid facies
• Swollen pale turbinates

• Avoidance
• Intranasal corticosteroids (first-line moderate-severe)
• Decongestants (short-term)
• Eliminators of IgE (antihistamines - first-line mild)
• Immunotherapy (disease-modifying)

Topical decongestant use → initial relief → rebound congestion on wearing off → more frequent use → ischaemic mucosal damage → worsening congestion → cannot stop

• Idiopathic (vasomotor)
• Vasomotor (same - most common NAR)
• Hormonal (pregnancy, thyroid, puberty)
• Atrophic (primary/secondary - ozaena)
• Granulomatous (GPA, sarcoidosis)
• Occupational (irritant/allergic)
• Gustatory (spicy food → rhinorrhoea)
• Senile (elderly)

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Rhinosinusitis (Sinusitis) - All Relevant ENT Headings

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1. Definition

• The nasal mucosa is virtually always involved alongside sinus inflammation
• Isolated sinusitis without nasal involvement is rare

• Nasal obstruction/congestion OR nasal discharge (anterior or posterior) PLUS
• Facial pain/pressure OR loss/reduction of smell

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2. Classification

By Duration

By Aetiology

By Sinus Involved

• Maxillary sinusitis - most common (drained via OMC)
• Ethmoidal sinusitis - most common in children; most serious anatomically (proximity to orbit)
• Frontal sinusitis - risk of intracranial / osteomyelitis complications
• Sphenoidal sinusitis - rare; dangerous (proximity to optic nerve, ICA, pituitary)
• Pansinusitis - all sinuses affected

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3. Applied Anatomy of the Paranasal Sinuses

The Paranasal Sinuses

The Ostiomeatal Complex (OMC) / Osteomeatal Unit (OMU)

• Key anatomical unit for sinus drainage - the bottleneck of sinus pathophysiology
• Comprises:
  • Uncinate process - hook-shaped process of the ethmoid
  • Hiatus semilunaris - crescent-shaped gap between uncinate process and ethmoid bulla
  • Infundibulum - passage connecting maxillary sinus ostium to middle meatus
  • Ethmoid bulla - largest anterior ethmoidal air cell
  • Middle meatus - space under the middle turbinate receiving drainage
• The anterior ethmoid cells, maxillary sinus, and frontal sinus all drain via the OMC
• Obstruction of the OMC → impaired mucociliary clearance → stasis → infection of all three sinuses
• The OMC is the primary target of FESS

Mucociliary Clearance

• Nasal and sinus mucosa lined by pseudostratified ciliated columnar epithelium with goblet cells
• Cilia beat at 10-15 Hz in coordinated waves, propelling mucus toward sinus ostia then to nasopharynx
• Mucus has two layers:
  • Sol layer (periciliary, watery) - cilia beat freely
  • Gel layer (thick, sticky) - traps particles; propelled by cilia tips
• Rate of mucociliary clearance: ~6 mm/min in sinuses
• Disruption (viral infection, drying, ciliotoxic agents) → stasis → infection

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4. Pathophysiology of Rhinosinusitis

Initiating Events

1. Viral URTI (rhinovirus most common) → mucosal inflammation + oedema
2. Mucosal oedema → obstruction of sinus ostia and OMC
3. Loss of mucociliary function (virus-induced epithelial damage)
4. Stagnation of secretions → reduced oxygen tension (hypoxia) in sinus
5. Anaerobic environment → bacterial overgrowth and superinfection
6. Sinus mucosa → goblet cell hyperplasia → thick mucus → further ostial occlusion

Predisposing Factors (why OMC gets obstructed)

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5. Acute Rhinosinusitis (ARS)

Aetiology

• Rhinovirus > Coronavirus > RSV > Parainfluenza > Adenovirus > Influenza
• Duration: 7-10 days; self-limiting

• Streptococcus pneumoniae (~30-35%)
• Non-typeable Haemophilus influenzae (~25-30%)
• Moraxella catarrhalis (~15-20%, especially children)
• Streptococcus pyogenes (occasional)
• Staphylococcus aureus (sphenoid/hospital-acquired)
• Anaerobes (odontogenic maxillary sinusitis)

Despite bacteria causing <2% of ARS, antibiotics are prescribed at >70% of office visits for sinusitis - major driver of antibiotic resistance

Clinical Features

• Purulent nasal discharge (mucopurulent/yellow-green) - anterior or posterior
• Facial pain/pressure/fullness - worse on bending forward
  • Maxillary: cheek pain; may radiate to upper teeth
  • Frontal: forehead pain
  • Ethmoid: medial canthal / retro-orbital pain
  • Sphenoid: vertex / occipital / retro-orbital pain
• Nasal obstruction/congestion (bilateral or unilateral)
• Hyposmia or anosmia
• Post-nasal drip → throat clearing, cough, halitosis
• Fever (more common in bacterial ARS)
• Ear pressure/fullness (ET dysfunction)
• Fatigue and malaise
• Maxillary toothache (upper molar roots project into maxillary sinus)

• Anterior rhinoscopy / nasal endoscopy: excess mucus, purulence in middle meatus
• Facial tenderness on palpation over sinuses (especially maxillary / frontal)
• Erythema and swelling over cheek (severe maxillary sinusitis)
• Sinus transillumination - NOT accurate for diagnosing sinusitis (unreliable)

Criteria: Viral vs. Bacterial ARS

"Double sickening": Initial improvement followed by acute worsening = hallmark of secondary bacterial ARS

Investigations for ARS

• Clinical diagnosis - imaging NOT routinely recommended for uncomplicated ARS
• CT sinuses (non-contrast): only if:
  • Suspected complication (orbital / intracranial)
  • Diagnosis uncertain
  • Immunocompromised patient
  • Failure to respond to treatment
• Nasal swab / middle meatal culture (guided by endoscopy) - for treatment failure
• Blood tests (FBC, CRP): if systemic sepsis suspected

Radiological Features of ARS

• Air-fluid level in sinus - hallmark of acute bacterial ARS
• Mucosal thickening (smooth, peripheral) - can be acute or chronic
• Complete sinus opacification
• CT scan: intermediate attenuation (10-25 HU) for acute watery secretions
• MRI: watery secretions = hypointense T1, hyperintense T2

Treatment of Acute Rhinosinusitis

Symptomatic / Supportive (ALL patients)

1. Saline nasal irrigation (isotonic or hypertonic saline)
   • High-volume Nasal saline rinses (e.g., Neti pot, NeilMed) - clears secretions, improves ciliary function
   • More effective than sprays
2. Topical decongestants (oxymetazoline/xylometazoline) - relieves pain, pressure, rhinorrhoea; max 5 days
3. Oral decongestants (pseudoephedrine 120 mg BD) - reduce oedema
4. Analgesics/antipyretics (paracetamol, ibuprofen) - pain and fever
5. Intranasal corticosteroids (INCS) - modest benefit; recommended particularly when allergic component; reduces mucosal oedema
6. Steam inhalation - symptom relief; no proven benefit on outcome
7. Adequate hydration

Antibiotic Therapy (Bacterial ARS only)

• Symptoms ≥ 10 days without improvement
• "Double sickening" (initial improvement then deterioration)
• Severe symptoms (fever >39°C, severe facial pain) from outset
• Complications developing

• Puncture of maxillary sinus through inferior meatus (or canine fossa)
• Obtain material for culture; irrigate with saline
• Indications: diagnostic (treatment failure), therapeutic (severe pain, hospitalized patient)
• Largely replaced by endoscopic culture

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6. Recurrent Acute Rhinosinusitis (RARS)

• Definition: ≥ 4 episodes per year with complete symptom resolution between episodes
• Investigate for:
  • Allergy (SPT, specific IgE)
  • Anatomical variants on CT (OMC obstruction)
  • Immune deficiency (IgG, IgG subclass, IgA levels, vaccine antibody titres)
  • Primary ciliary dyskinesia (saccharin test, ciliary biopsy)
  • Cystic fibrosis (sweat chloride, CF gene)
• Management:
  • Treat underlying cause
  • FESS if anatomical obstruction
  • Prophylactic INCS

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7. Chronic Rhinosinusitis (CRS)

Definition

Important: Symptom-based diagnosis alone is unreliable - >40% of patients with CRS symptoms have normal CT and endoscopy. Objective confirmation required.

Types of CRS

Pathophysiology of CRS

• Loss of normal mucosal homeostasis due to persistent inflammatory stimulus
• Chronically inflamed sinuses: loss of bacterial diversity → overgrowth of pathological species
• S. aureus superantigens - stimulate massive T-cell activation and IL-5 → eosinophilia → polypogenesis
• Biofilm formation on sinus mucosa (especially Pseudomonas, S. aureus) → antibiotic resistance
• In CRSwNP: TH2 cytokines (IL-4, IL-5, IL-13) → eosinophilic inflammation → mucosal oedema → polyp formation
• Impaired mucociliary clearance → perpetuating cycle

Symptoms of CRS (must have ≥ 2 for ≥ 12 weeks, one of which must be nasal obstruction OR discharge):

Headache alone is NOT a criterion for CRS - virtually all patients labelled as having "sinus headaches" actually have atypical migraine

Nasal Polyps

• Pale/grey/yellow, translucent, soft, grape-like masses
• Arise from the middle meatus (lateral wall / ethmoid region)
• Mobile; non-tender; insensitive (unlike turbinates - valuable diagnostic distinction)
• Bilateral in most inflammatory causes; unilateral polyp → suspect inverted papilloma or malignancy
• Associated with: CRSwNP, AFRS, AERD/Samter's triad, cystic fibrosis, Kartagener's syndrome (PCD)
• Antrochoanal polyp (Killian's polyp): single, unilateral; arises from maxillary sinus mucosa; extends through enlarged natural ostium through choana to nasopharynx; usually in young adults

Diagnosis of CRS

• Polyps (white, grey, translucent)
• Mucopurulent discharge in middle meatus
• Mucosal oedema / hypertrophy of turbinates
• Septal deviation

• Indicated for all CRS patients being considered for surgery
• Shows: mucosal thickening, sinus opacification, polyps, osteitis, OMC obstruction, anatomical variants, bone erosion
• Dense secretions (30-60 HU) - more chronic/concentrated
• Lund-Mackay CT score - quantifies extent of disease (0-24 scale; used for surgical planning and research)
• OMU opacification - key finding indicating OMC obstruction

• Correlation of CT + endoscopy findings: 70-80%
• CT alone may miss mucosal disease seen on endoscopy
• Modest CT changes in asymptomatic individuals in ~1/3 of population

• Microbiological swab - endoscopically guided middle meatal or maxillary sinus culture
• Allergy testing (SPT, serum IgE) - for allergic component
• Olfactory testing - Sniffin' Sticks, UPSIT - baseline + follow-up
• MRI - if malignancy, intracranial extension, or AFRS suspected
• Immunological workup - IgG/IgA/IgM, IgG subclasses, vaccine titres, HIV
• CF screen (sweat chloride, CFTR gene) - if young patient + bilateral polyps + bronchiectasis
• ANCA, ACE - GPA, sarcoidosis
• Histology of polyps / granulation tissue - rule out malignancy, GPA, sarcoidosis

Medical Treatment of CRS

1. Saline Nasal Irrigation (First-Line for All)

• High-volume isotonic or hypertonic saline rinses (250-500 ml twice daily)
• Budesonide added to saline rinse (budesonide rinse) - higher volume + higher potency than spray; highly effective in CRSwNP
• Removes allergens, bacteria, crusts; improves mucociliary function

2. Intranasal Corticosteroids (INCS) - Cornerstone of Medical Treatment

• First-line pharmacotherapy for all CRS types
• Reduce mucosal oedema, eosinophilic inflammation; shrink polyps
• High-potency sprays: mometasone furoate, fluticasone propionate/furoate
• Drops or rinses (budesonide, beclometasone) better penetrate polyp-filled sinuses
• Must be used regularly for sustained effect; titrate to lowest effective dose

3. Systemic Corticosteroids

• Oral prednisolone short course (20-40 mg/day for 2-3 weeks) for CRSwNP
• Dramatically shrinks polyps; improves smell
• Useful pre-operatively to reduce polyp size and bleeding
• Not for long-term use (HPA suppression, osteoporosis, diabetes, infection)
• IV dexamethasone in severe/complicated cases

4. Antibiotics for CRS

• Long-term low-dose macrolide therapy (e.g., roxithromycin 150 mg OD / azithromycin 250 mg MWF for 3 months):
  • Mechanism: anti-inflammatory + immunomodulatory (not purely antibacterial)
  • Reduces cytokine production, inhibits biofilm formation
  • Most effective in CRSsNP with low serum IgE and low eosinophils
  • Less effective in eosinophilic CRS/CRSwNP
• Culture-directed antibiotics for acute exacerbations (2-4 weeks)

5. Antileukotriene Agents

• Montelukast - useful in CRS with concomitant asthma and AERD

6. Biological/Targeted Therapy (for severe refractory CRSwNP)

• Dupilumab (Dupixent) - anti-IL-4Rα (blocks IL-4 and IL-13 signalling)
  • First biologic licensed for CRSwNP
  • Dramatically reduces polyp size, improves smell and QoL
  • Given as subcutaneous injection every 2 weeks
• Mepolizumab - anti-IL-5 (reduces eosinophils)
• Omalizumab - anti-IgE (if atopic component)
• Biologics are used when CRS has failed surgery + medical treatment

7. Aspirin Desensitisation (AERD / Samter's Triad)

• In patients with CRSwNP + asthma + aspirin sensitivity
• High-dose aspirin desensitisation (300-600 mg/day maintenance) reduces polyp recurrence
• Requires specialist management

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8. Fungal Rhinosinusitis

Non-Invasive Forms

A. Fungal Ball (Mycetoma)

• Single sinus (maxillary most common) packed with dense fungal hyphae
• Patient is immunocompetent
• Organism: usually Aspergillus fumigatus
• CT: speckled / chunky calcifications within opacified sinus; unilateral; no bone erosion
• MRI: hypointense on T1 and T2 (absence of free water in dense fungal mass)
• Treatment: surgical removal (FESS); no antifungals needed

B. Allergic Fungal Rhinosinusitis (AFRS)

• Immunocompetent patient with atopic history (allergic rhinitis, asthma)
• Usually young (20s-30s); warm/humid climates
• Organisms: dematiaceous fungi (Bipolaris, Curvularia, Alternaria) > Aspergillus
• Mechanism: IgE-mediated hypersensitivity to fungal antigens → eosinophilic mucin ("allergic mucin") - thick, greenish-brown, peanut-butter consistency with hyphae
• Features: bilateral or unilateral; multiple sinuses; nasal polyps; bone erosion (pressure necrosis)
• CT: bilateral sinus opacification + high-attenuation areas (paramagnetic metals - iron, manganese in fungal debris) + sinus expansion + bone erosion (may mimic malignancy)
• MRI: very low signal (signal void) on T2 - characteristic; due to paramagnetic metals
• BENT criteria for AFRS diagnosis:
  • Bilateral disease
  • Eosinophilia (peripheral)
  • Non-invasive histology
  • Type I hypersensitivity (positive skin test to fungi)
• Treatment: FESS (debridement of allergic mucin) + systemic steroids + INCS; antifungals controversial; immunotherapy to fungi may reduce recurrence

Invasive Forms

C. Acute Invasive Fungal Sinusitis (AIFS) - EMERGENCY

• Occurs in severely immunocompromised patients:
  • Uncontrolled diabetes mellitus (DKA - classic)
  • Haematological malignancy (leukaemia, lymphoma)
  • Bone marrow / solid organ transplant recipients
  • HIV/AIDS
  • Long-term steroids / immunosuppressants
• Organisms: Mucorales (Rhizopus, Mucor, Absidia) (most common in DKA), Aspergillus
• Mechanism: fungi invade blood vessels → tissue infarction and necrosis → black eschar
• Clinically: rapidly progressive; fever + nasal pain/fullness → facial pain → cranial nerve involvement (diplopia, facial numbness) → orbital swelling, proptosis, chemosis → vision loss → intracranial spread
• Black turbinate sign on MRI (non-enhancing devitalized tissue) - characteristic; suggests mucormycosis
• Early CT may show only unilateral mucosal thickening/opacification with perisinus soft tissue infiltration; bone erosion is later finding
• Management - requires urgent multidisciplinary approach:
  1. Urgent ENT review + nasal endoscopy + biopsy (black/necrotic mucosa diagnostic)
  2. Aggressive surgical debridement (endoscopic or open; orbital exenteration if orbital invasion)
  3. Systemic antifungal therapy:
     • Liposomal amphotericin B (AmBisome) 5-10 mg/kg/day IV - first-line for Mucorales
     • Voriconazole - first-line for Aspergillus
     • Isavuconazole - alternative for both
  4. Control/reverse underlying immunosuppression (optimise diabetes, reduce steroids)
  5. Hyperbaric oxygen (adjunctive)
• Prognosis: mortality 50-80% in haematological malignancy; better if DKA-related and treated early

D. Chronic Invasive Fungal Sinusitis (CIFS)

• Mildly immunocompromised (e.g., diabetics) or immunocompetent
• Slowly progressive; months-years
• Aspergillus most common
• CT: homogeneous soft tissue opacification; unilateral; limited bone erosion; extra-sinus extension
• Treatment: surgical debridement + antifungal therapy (voriconazole)

E. Chronic Granulomatous Invasive Fungal Sinusitis (CGIFS)

• Usually in Africa (Sudan) and South Asia
• Immunocompetent individuals
• Aspergillus species
• Granulomatous histology; slow progression; orbital involvement common
• No focal high-density CT areas (unlike AFRS)

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9. Complications of Rhinosinusitis

Orbital Complications - Chandler Classification

Key rules:

• ANY decrease in visual acuity or afferent pupillary defect → EMERGENCY orbital decompression
• Class I and II may be managed medically with very close monitoring
• Class III and above: CT scan mandatory; surgical drainage usually required
• Paediatric SPA: some advocate trial of IV antibiotics before surgery (higher rate of resolution vs. adults)

Intracranial Complications

Bony Complications

Pott's puffy tumour: forehead swelling from frontal sinus osteomyelitis - looks like a soft lump on the forehead - requires prolonged antibiotics (8-12 weeks) as abrupt cessation leads to chronic osteomyelitis or delayed intracranial sepsis

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10. Odontogenic Sinusitis

• Dental root infection → periapical abscess → maxillary sinus floor
• Account for ~10% of maxillary sinusitis cases
• Upper molar teeth (particularly 1st and 2nd molars) roots project into or close to maxillary sinus floor
• Features:
  • Unilateral maxillary sinusitis (key distinguishing feature)
  • Foul-smelling discharge (anaerobes - Fusobacterium, Bacteroides, Prevotella)
  • Dental pain / recent dental procedure
  • Fails to respond to standard antibiotics (need anaerobic coverage)
• Investigations: OPG / dental X-ray; CT (shows dental root periapical infection)
• Treatment: dental extraction / treatment (root canal therapy) + metronidazole ± amoxicillin; FESS if sinus fails to clear

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11. Surgical Treatment - FESS

Functional Endoscopic Sinus Surgery (FESS)

• Restore normal mucociliary function by re-establishing adequate sinus drainage
• Target the OMC - the key bottleneck
• Conservative approach: preserve normal mucosa; only remove diseased tissue
• Endoscopic approach via the nostrils - no external incisions

• Recent CT scan (mandatory) - must be available throughout surgery
• Nasal endoscopy + medical therapy optimised first
• Eyes left exposed or limited taping during surgery (allows intraoperative orbital monitoring)
• Intraoperative image navigation (IGN/IGS) - computer-linked stereotactic guidance system; reduces complications in revision cases

• CRS with or without polyps failing ≥ 3 months of optimal medical therapy
• Recurrent ARS with OMC obstruction
• Complications of sinusitis
• Mucocele
• Fungal ball
• AFRS
• Antrochoanal polyp
• Orbital decompression (Graves' disease, orbital abscess)
• CSF leak repair (anterior skull base)
• Optic nerve decompression
• Pituitary surgery (transsphenoidal approach)
• Tumour removal (selected cases)

• Uncinate process is the first structure removed in FESS
• Free edge identified with Freer's elevator
• Sickle knife on inferior portion is discouraged (risk of orbital penetration)
• Back-biting forceps used for safer excision
• Superior uncinate: protected by hard bone of frontal process of maxilla

• Saline nasal irrigation (high volume) - critical for healing
• INCS (sprays + rinses)
• Regular endoscopic debridement (synechia lysis, crusting removal) in first 4-6 weeks
• Review at 1, 3, and 6 months
• Continue treating underlying condition (allergy, asthma)

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12. Special Situations

Sinusitis in Children

• Ethmoid sinuses most important in children (present from birth; maxillary and frontal develop later)
• Commonest organisms: S. pneumoniae, H. influenzae, M. catarrhalis (same as ASOM)
• Periorbital / orbital cellulitis is the most common serious complication
• Adenoid hypertrophy → nasopharyngeal bacterial reservoir → sinusitis
• Treat with amoxicillin; co-amoxiclav if resistant
• Adenoidectomy may benefit children with recurrent sinusitis (reduces nasopharyngeal bacterial load)

Nosocomial / Hospital-Acquired Sinusitis

• Occurs in critically ill ICU patients, especially with nasotracheal intubation or NG tube
• Suspect in hospitalised patients with fever without another identified cause
• Organisms: S. aureus, Pseudomonas, Gram-negative enteropathogens, fungi
• Maxillary sinus most affected
• Treatment: remove nasal tube; antral puncture + culture + irrigation; IV antibiotics

Sinusitis in Cystic Fibrosis

• Almost universal CRS with polyps
• Due to thick mucus (CFTR dysfunction → abnormal chloride transport) → impaired mucociliary clearance
• Organisms: Pseudomonas aeruginosa, S. aureus, Burkholderia cepacia
• FESS provides temporary relief; high recurrence
• Ivacaftor/Lumacaftor (CFTR modulators) - disease-modifying

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13. Summary Table: ARS vs. CRS

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14. Key Mnemonics

• Facial pain / pressure
• Nasal discharge (purulent)
• Hyposmia / anosmia
• And
• Post-nasal drip

• Streptococcus pneumoniae
• Haemophilus influenzae (NTHi)
• Moraxella catarrhalis

• Pre-septal Cellulitis → Orbital Cellulitis → Subperiosteal Abscess → Orbital Abscess → Cavernous Sinus Thrombosis

• "MAF" = Maxillary + Anterior ethmoid + Frontal

• Non-invasive: Fungal ball, AFRS
• Invasive: Fulminant (acute - immunocompromised) / Tardive (chronic - mild immunocompromise) / granulomatous
• Yes to urgent surgery + amphotericin in AIFS

• Bilateral disease
• Eosinophilia
• Non-invasive histology
• Type I hypersensitivity

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What's Covered

Long Essays (10 Marks) - 5 topics

Short Notes (5 Marks) - 25 topics