Otitis Media (Acute and Chronic Forms)

1. Clinical Overview

Summary

Otitis Media encompasses a spectrum of inflammatory conditions affecting the middle ear cleft, representing one of the most common reasons for paediatric consultation and antibiotic prescription worldwide. [1] The two principal entities are Acute Otitis Media (AOM), an acute purulent bacterial infection presenting with otalgia, fever, and bulging tympanic membrane; and Otitis Media with Effusion (OME), also called "Glue Ear," characterized by non-purulent fluid accumulation causing painless conductive hearing loss.

AOM affects approximately 80% of children by age 3 years, with peak incidence between 6-18 months. [2] The condition accounts for over 30 million healthcare visits annually in developed countries and remains a leading indication for antibiotic prescribing in primary care despite most cases being viral or self-limiting. [3] OME is the commonest cause of acquired hearing impairment in childhood, affecting 90% of children by age 10 years, with 5-10% developing persistent bilateral effusions requiring surgical intervention. [4]

The pathophysiology centres on Eustachian tube dysfunction unique to young children: shorter (17-18mm vs adult 31-38mm), more horizontal orientation (10° vs 45°), and functional immaturity of the tensor veli palatini muscle predispose to negative middle ear pressure, fluid accumulation, and ascending bacterial colonization from the nasopharynx. [5]

Management has evolved significantly with emphasis on antimicrobial stewardship. Current NICE NG91 guidelines recommend a "no antibiotic" or "delayed prescribing" strategy for most AOM cases, reserving immediate antibiotics for systemically unwell children, those under 2 years with bilateral disease, or those with perforation/otorrhoea. [6] For OME, watchful waiting for 3 months is standard, with surgical insertion of ventilation tubes (grommets) reserved for persistent bilateral disease with hearing loss > 25-30 dB HL affecting development. [7]

Key Facts

• AOM vs OME Distinction: AOM = Acute infection with pain, fever, and bulging drum. OME = Chronic effusion with hearing loss, no pain, retracted/dull drum.
• Microbiology Triad: Streptococcus pneumoniae (25-30%), Haemophilus influenzae non-typeable (20-25%), Moraxella catarrhalis (10-15%). [8]
• Anatomical Vulnerability: Paediatric Eustachian tube is 50% shorter and 75% more horizontal than adults, with incomplete cartilaginous support.
• Spontaneous Resolution: 60% of AOM cases resolve within 24 hours without antibiotics; 80% within 2-3 days. [9]
• Grommet Surgery: Most common elective surgical procedure in childhood (> 30,000 insertions annually in UK). [10]
• Vaccine Impact: Introduction of PCV7/PCV13 pneumococcal conjugate vaccines has reduced AOM incidence by 20-30% but increased non-vaccine serotype and H. influenzae cases. [11]

Clinical Pearls

"The Bulging Drum vs The Red Drum": Diagnostic accuracy for AOM requires evidence of middle ear effusion (bulging, immobile drum on pneumatic otoscopy) PLUS acute inflammation (erythema). A simply "red" drum in a crying, febrile child with viral URTI is NOT diagnostic of AOM - the hyperaemia may be from crying, fever, or mucosal inflammation. True AOM shows a bulging, opaque drum with loss of bony landmarks (handle of malleus, cone of light). Specificity increases from 50% (erythema alone) to 95% (bulging + erythema). [12]

"Nature's Myringotomy": Spontaneous tympanic membrane perforation with purulent otorrhoea, though alarming to parents, is actually therapeutic - "Nature's myringotomy." The perforation releases accumulated pus under pressure, providing immediate pain relief (often dramatic overnight improvement). Small perforations (1-2mm) heal spontaneously in 95% of cases within 7-10 days without intervention. Advise water precautions (no swimming, cotton wool with Vaseline for bathing) and ensure follow-up to confirm healing. [13]

"Unilateral OME in an Adult = NPC Until Proven Otherwise": Bilateral OME in children is physiological due to adenoidal hypertrophy and Eustachian tube immaturity. However, unilateral OME in an adult is highly suspicious for Nasopharyngeal Carcinoma (NPC) causing extrinsic Eustachian tube obstruction. This is an absolute indication for nasendoscopy (flexible nasal endoscopy) to visualize the post-nasal space and fossa of Rosenmüller. Endemic areas (Southeast Asia, Southern China) have particularly high NPC incidence. Never dismiss unilateral adult OME as "Glue Ear." [14]

"The Pinna Push - Acute Mastoiditis": If a child presents with postauricular swelling, erythema, tenderness, and the pinna is pushed forward and downward (proptosis of the auricle), this is acute mastoiditis until proven otherwise. The pathognomonic sign is loss of the postauricular sulcus (crease behind ear obliterated by boggy swelling). Urgent CT temporal bones, IV antibiotics (ceftriaxone + metronidazole), and ENT referral for possible cortical mastoidectomy are required. This represents coalescent mastoiditis with destruction of the bony septa. [15]

"Tympanometry Over Otoscopy": In medico-legal terms, tympanometry provides objective, reproducible documentation of middle ear status, whereas otoscopy is subjective and operator-dependent. Type B (flat) tympanogram has 90% sensitivity/specificity for middle ear effusion. Type C (negative pressure peak < -200 daPa) indicates Eustachian tube dysfunction but not necessarily fluid. Always document tympanometry when considering grommet surgery - it forms the medico-legal evidence base for intervention. [16]

"When NOT to Prescribe Antibiotics": The majority of AOM does NOT require antibiotics. Do NOT prescribe if: (1) Child > 2 years with unilateral AOM, (2) Mild symptoms, (3) No systemic features, (4) No perforation. Offer "delayed prescription"

• advise parents to wait 2-3 days and only collect prescription if deterioration or no improvement. This strategy reduces antibiotic use by 80% without increasing complications. [6]

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2. Epidemiology

Incidence and Prevalence

Acute Otitis Media:

• By age 1 year: 60% of children have had at least one episode
• By age 3 years: 80-90% have had at least one episode
• By age 7 years: 95% have had at least one episode [2]
• Recurrent AOM (≥3 episodes in 6 months or ≥4 in 12 months): 10-20% of affected children
• Annual incidence: Peaks at 6-18 months (60-70 episodes per 100 child-years), declining to 10-20 per 100 child-years by age 5-7 years

Otitis Media with Effusion:

• Point prevalence: 15-20% of preschool children at any given time [4]
• Cumulative incidence: 90% of children have at least one episode by age 10 years
• Persistent OME (> 3 months): 5-10% of children
• Bilateral OME with hearing loss > 25 dB HL: 2-3% (surgical candidates)

Demographic Patterns

Age Distribution:

• Peak AOM incidence: 6-18 months (coincides with waning maternal antibodies, daycare exposure, Eustachian tube immaturity)
• Peak OME prevalence: 2-5 years (adenoidal hypertrophy maximal)
• Adult OME: Rare (less than 1%), investigate for NPC or other pathology

Seasonal Variation:

• AOM incidence peaks in winter months (November-March in Northern Hemisphere)
• Follows 2-3 weeks after peak viral URTI season (RSV, influenza, rhinovirus)
• Summer months show 50-60% reduction in incidence

Geographic Variation:

• Indigenous populations (Native American, Australian Aboriginal, Inuit): 2-3× higher incidence, earlier onset, more severe disease
• Possible factors: genetic predisposition (altered Eustachian tube anatomy), overcrowding, malnutrition, limited healthcare access

Risk Factors

Host Factors:

1. Age 6-24 months: Peak anatomical and immunological vulnerability
2. Male sex: 1.3-1.5× increased risk (unclear mechanism) [17]
3. Craniofacial anomalies:
   • Cleft palate (with/without lip): 95% develop OME due to tensor veli palatini dysfunction - muscle fails to open Eustachian tube
   • Down syndrome: 60-80% have OME (mid-face hypoplasia, small Eustachian tube, immune dysfunction)
   • Pierre Robin sequence: Micrognathia impairs Eustachian tube function
4. Immunodeficiency: Selective IgA deficiency, IgG subclass deficiency, HIV
5. Ciliary dyskinesia: Primary ciliary dyskinesia (Kartagener syndrome) - impaired mucociliary clearance

Environmental Factors:

1. Passive smoking: Strongest modifiable risk factor. Tobacco smoke paralyzes respiratory cilia, increases upper respiratory infections, promotes adenoidal hypertrophy. Dose-dependent: > 20 cigarettes/day in household increases AOM risk 2-3× [18]
2. Daycare attendance: Children in daycare have 2-3× increased AOM incidence vs home care, due to viral pathogen exposure (especially RSV, influenza)
3. Bottle feeding (especially supine):
   • Breastfeeding > 3 months reduces AOM risk by 30-40%
   • Mechanisms: passive immunity (IgA in breast milk), improved orofacial muscle development, avoidance of supine feeding (prevents milk reflux into Eustachian tube)
   • "Bottle propping" (baby drinks lying flat) is particularly high-risk
4. Lack of breastfeeding: Exclusive breastfeeding for 6 months is protective
5. Pacifier use beyond 6 months: Alters oropharyngeal pressure dynamics, promotes bacterial colonization
6. Season: Winter respiratory virus season

Medical Factors:

1. Previous AOM: Each episode increases recurrence risk (sensitization, bacterial colonization)
2. First episode before 6 months: Predicts recurrent AOM (indicates high susceptibility)
3. Adenoidal hypertrophy: Mechanically obstructs Eustachian tube orifice, serves as bacterial biofilm reservoir
4. Allergic rhinitis: Controversial association - may promote Eustachian tube oedema
5. Gastro-oesophageal reflux: Acidic refluxate may reach Eustachian tube, causing inflammation (weak evidence)

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3. Pathophysiology

Anatomical Basis: The Eustachian Tube

The Eustachian tube (pharyngotympanic tube) is the key to understanding all forms of otitis media. This ~36mm long structure connects the middle ear to the nasopharynx, serving three critical functions:

1. Ventilation: Equalizes middle ear pressure with atmospheric pressure
2. Drainage: Mucociliary clearance of middle ear secretions toward nasopharynx
3. Protection: Prevents nasopharyngeal reflux and ascending infection

Paediatric Vulnerability:

The infant Eustachian tube functions as a "horizontal drainpipe" that readily obstructs and facilitates bacterial reflux, whereas the adult tube is a "sloped drain" with effective clearance. [5]

Pathophysiological Sequence

Stage 1: Viral Upper Respiratory Tract Infection (Day 0-3)

• Rhinovirus, RSV, influenza, adenovirus, coronavirus infect nasopharyngeal mucosa
• Mucosal inflammation and oedema extend to Eustachian tube orifice and lumen
• Ciliary beat frequency reduced by inflammatory cytokines (IL-1, TNF-α)
• Result: Functional Eustachian tube obstruction

Stage 2: Middle Ear Underpressure (Day 1-4)

• Blocked Eustachian tube prevents air entry to middle ear
• Oxygen absorbed from middle ear cavity into blood (mucosal perfusion continues)
• Negative pressure develops (-50 to -200 daPa)
• Tympanic membrane retracts medially
• Vascular engorgement of middle ear mucosa → transudation of sterile fluid
• Result: OME (Otitis Media with Effusion) - if uncomplicated, may resolve spontaneously over weeks

Stage 3: Bacterial Colonization (Day 3-7)

• Negative pressure creates "suction pump" effect, aspirating nasopharyngeal secretions (contaminated with bacteria) into middle ear
• Normal nasopharyngeal flora: S. pneumoniae (20-40% carriage), H. influenzae non-typeable (30-50%), M. catarrhalis (60-70%) colonize middle ear fluid
• Warm, nutrient-rich effusion provides ideal culture medium
• Result: Bacterial superinfection of sterile OME

Stage 4: Acute Purulent Otitis Media (Day 5-10)

• Bacterial proliferation (10^6-10^9 CFU/mL)
• Neutrophil infiltration → purulent exudate
• Increasing volume of pus under pressure → bulging tympanic membrane
• Pain from tympanic membrane stretch and middle ear pressure (otalgia)
• Systemic inflammatory response → fever
• Result: Acute Otitis Media (AOM) - clinical syndrome of infection

Stage 5 a: Spontaneous Resolution (70-80% of cases)

• Host immune response (opsonization, neutrophil killing)
• Antibody formation (if previous exposure to serotype)
• Eustachian tube patency restored (viral infection resolves, oedema subsides)
• Mucociliary clearance resumes → drainage to nasopharynx
• Resorption of effusion over 1-3 weeks
• Result: Complete resolution

Stage 5 b: Tympanic Membrane Perforation (10-15% of cases)

• Increasing pus volume under pressure exceeds tensile strength of tympanic membrane
• Perforation typically occurs at pars tensa, most commonly postero-inferior quadrant (thinnest region)
• Immediate drainage of pus → dramatic pain relief ("Nature's myringotomy")
• Small perforations (less than 2mm) heal spontaneously in 95% of cases within 2 weeks
• Result: Acute perforation with otorrhoea - usually benign, self-healing

Stage 5 c: Progression to Complications (1-2% of cases)

• Infection spreads beyond middle ear cleft:
  • Posteriorly → Mastoid air cells → Acute mastoiditis
  • Medially → Petrous apex → Petrositis (Gradenigo syndrome)
  • Intracranially → Meningitis, epidural/subdural abscess, brain abscess, lateral sinus thrombosis
  • Laterally → Facial nerve canal (dehiscent in 10%) → Facial nerve palsy
  • Inferiorly → Labyrinth → Labyrinthitis (vertigo, sensorineural hearing loss)
• Result: Suppurative complications - medical/surgical emergency

Microbiology

Bacterial Pathogens (in order of frequency): [8]

1. Streptococcus pneumoniae (25-30%)

   • Gram-positive diplococci
   • Vaccine serotypes (4, 6B, 9V, 14, 18C, 19F, 23F in PCV7) now rare
   • Non-vaccine serotypes (3, 19A, 22F, 33F) have increased post-PCV introduction
   • Most likely to cause severe disease, complications, and antibiotic resistance
   • Penicillin resistance: ~10-30% (varies by region)

2. Haemophilus influenzae non-typeable (20-25%)

   • Gram-negative coccobacillus
   • Not the same as H. influenzae type b (Hib vaccine does NOT protect)
   • Lacks polysaccharide capsule (hence "non-typeable")
   • β-lactamase production: ~30-50% (amoxicillin resistance)
   • Incidence has increased in post-PCV era (niche replacement)

3. Moraxella catarrhalis (10-15%)

   • Gram-negative diplococci
   • β-lactamase production: > 95% (almost universally resistant to amoxicillin)
   • Generally causes milder disease than S. pneumoniae
   • Self-limiting in many cases

4. Streptococcus pyogenes (Group A Strep) (5%)

   • More common in older children (> 5 years)
   • Associated with concurrent pharyngitis
   • Can cause severe complications (mastoiditis)

5. Staphylococcus aureus (less than 5%)

   • Rare cause of AOM
   • Associated with chronic ear disease, post-grommet insertion, or immunocompromise
   • MRSA may occur in nosocomial settings

Viral Pathogens (detected in 60-90% of AOM cases, often co-infection with bacteria):

• Respiratory Syncytial Virus (RSV) - most common
• Rhinovirus
• Influenza A and B
• Adenovirus
• Coronavirus
• Parainfluenza

Sterile OME:

• ~30% of OME aspirates are culture-negative ("sterile effusion")
• Likely represents post-viral inflammatory exudate without bacterial superinfection

Molecular Pathophysiology

Inflammatory Cascade:

• Bacterial cell wall components (pneumococcal peptidoglycan, lipoteichoic acid; H. influenzae LPS) activate Toll-like receptors (TLR2, TLR4) on middle ear epithelial cells and macrophages
• Signaling cascade → NF-κB activation → transcription of pro-inflammatory cytokines
• IL-1β, IL-6, IL-8, TNF-α released → neutrophil chemotaxis, vascular permeability
• Prostaglandins (PGE2), leukotrienes mediate pain and inflammation
• Matrix metalloproteinases (MMPs) degrade extracellular matrix → tissue damage

Effusion Characteristics:

• Serous (thin, watery): Early OME, viral-mediated
• Mucoid ("Glue Ear"): Chronic OME, high viscosity due to goblet cell metaplasia and mucin hypersecretion
• Purulent (thick, opaque, yellow-green): Acute bacterial infection (AOM)

Biofilms:

• Bacteria in OME and recurrent AOM often exist as biofilms (organized bacterial communities encased in extracellular matrix attached to mucosal surface)
• Biofilms confer antibiotic resistance (1000× higher MIC), immune evasion
• Difficult to eradicate → recurrent/chronic disease
• Adenoidal biofilms serve as bacterial reservoir

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4. Clinical Presentation

A. Acute Otitis Media (AOM)

Diagnostic Criteria (All 3 required for definitive diagnosis): [6,12]

1. Acute onset of symptoms (less than 48 hours)
2. Presence of middle ear effusion:
   • Bulging of tympanic membrane, OR
   • Otorrhoea (if perforated), OR
   • Decreased/absent tympanic membrane mobility on pneumatic otoscopy
3. Signs/symptoms of middle ear inflammation:
   • Otalgia (ear pain), OR
   • Marked erythema of tympanic membrane

Symptoms (by age):

Infants (less than 1 year):

• Irritability, crying (often high-pitched, inconsolable)
• Fever (38-40°C in 60-70% of cases)
• Poor feeding, reduced oral intake
• Sleep disturbance, frequent waking
• Ear tugging/pulling (unreliable sign - often absent)
• Vomiting, diarrhoea (systemic features)
• Preceding viral URTI symptoms (runny nose, cough)

Toddlers/Children (1-5 years):

• Otalgia (explicitly verbalized if old enough: "My ear hurts")
• Fever (may be absent in 30-40%)
• Hearing loss (child may turn up TV, not respond to voice)
• Balance problems (middle ear pressure affects vestibular system)
• Preceding viral URTI

Older Children (> 5 years):

• Severe otalgia (often describes as "stabbing" or "throbbing")
• Hearing loss (unilateral or bilateral)
• Feeling of "fullness" or "pressure" in ear
• Autophony (hearing own voice loudly)
• Fever less common

If Perforated (10-15% of AOM):

• Sudden-onset purulent otorrhoea (yellow, green, or blood-stained discharge from ear canal)
• Immediate pain relief after perforation (dramatic improvement - "pain gone overnight")
• Discharge may be pulsatile (synchronous with heartbeat) if drum is freshly perforated

Signs on Otoscopy (Pneumatic Otoscopy is Gold Standard):

1. Hyperaemia (Redness):

   • Erythema of tympanic membrane
   • May be diffuse or concentrated along handle of malleus or around periphery
   • CAUTION: Erythema alone is NOT diagnostic (occurs with crying, fever, viral URTI)

2. Bulging:

   • Tympanic membrane convex (bulges outward into ear canal)
   • Loss of normal concavity
   • Loss of bony landmarks: Handle of malleus obscured, no cone of light reflex
   • "Doughnut sign"

• circumferential bulge
  • Most specific sign for AOM

3. Opacity:

   • Loss of translucency (normally can see through to middle ear)
   • Opaque, milky appearance
   • May see yellow/white purulent fluid behind drum

4. Immobility (on pneumatic otoscopy):

   • Gentle positive/negative pressure applied via pneumatic bulb
   • Normal drum moves briskly in/out
   • Effusion-filled middle ear → no movement (drum "fixed")
   • Sensitivity/specificity: 90%/80% for effusion [12]

5. Perforation (if occurred):

   • Visible defect in pars tensa (most common: postero-inferior quadrant)
   • Purulent discharge visible in ear canal or draining through perforation
   • Margins may be ragged (acute) vs smooth (chronic)

Systemic Features:

• Fever: 60-70% (usually 38-40°C, occasionally > 40°C)
• Lethargy, malaise
• Gastrointestinal symptoms: vomiting, diarrhoea (10-20%)

B. Otitis Media with Effusion (OME / Glue Ear)

Diagnostic Criteria:

• Presence of middle ear effusion without signs of acute infection
• Absence of acute symptoms (no pain, no fever)

Symptoms:

1. Hearing Loss (cardinal symptom):
   • Conductive hearing loss, typically 20-40 dB HL
   • Bilateral in 80% of cases (unilateral in 20%)
   • Parent reports: "Turning TV volume up"

• "Ignoring me when I call"
• "Saying 'What?' repeatedly"
  • Teacher reports: "Not paying attention in class"
• "Sitting at front of classroom"
  • May be fluctuating (varies day-to-day as effusion consistency changes)

2. Speech and Language Delay:

   • Hearing loss during critical language acquisition period (1-3 years) may impair phonological development
   • Delayed speech milestones
   • Articulation errors (especially high-frequency sounds: s, f, th)
   • Controversial: Some studies show association with language delay, others show minimal long-term impact [4]

3. Behavioural Changes:

   • Inattention, "daydreaming"
   • Social withdrawal (difficulty hearing peers)
   • Frustration, behavioural problems
   • Poor academic performance

4. Balance Problems:

   • Clumsiness
   • Delayed gross motor milestones (less common)
   • Vestibular dysfunction in some cases

5. Otalgia (uncommon):

   • Usually painless
   • Occasional mild discomfort or "fullness"
   • If pain develops: Consider superimposed AOM

6. Tinnitus (older children):

   • Low-pitched ringing or buzzing

Signs on Otoscopy:

1. Retracted Tympanic Membrane:

   • Drum pulled medially (concave, "sucked in" appearance)
   • Handle of malleus appears shortened and more horizontal
   • Short process of malleus prominent
   • Loss of light reflex

2. Dull, Opaque Appearance:

   • Loss of normal pearly-grey translucency
   • Amber/Yellow colour (serous effusion)
   • Grey/Blue colour (mucoid "glue" effusion)
   • "Ground glass" appearance

3. Visible Fluid Level or Bubbles:

   • Air-fluid interface visible as horizontal line behind drum (pathognomonic)
   • Air bubbles in effusion (appear as circular shadows)
   • Best seen with good light and magnification (otomicroscope)

4. Immobility on Pneumatic Otoscopy:

   • No movement with positive/negative pressure (fluid prevents drum excursion)
   • Most reliable sign

5. Atelectasis (severe cases):

   • Extreme retraction, drum draped over ossicles
   • May contact medial wall of middle ear (promontory)
   • Risk of adhesive otitis media (fibrous adhesions)

Associated Features:

• Adenoidal facies: Mouth breathing, open-mouth posture, long face (from chronic nasal obstruction due to adenoidal hypertrophy)
• Nasal speech (hyponasal quality - "talking through nose blocked")
• Snoring, obstructive sleep apnoea (if large adenoids)

C. Recurrent Acute Otitis Media

Definition:

• ≥3 episodes of AOM in 6 months, OR
• ≥4 episodes of AOM in 12 months

Clinical Features:

• Repeated cycles of otalgia, fever, bulging drum
• Episodes separated by periods of complete symptom resolution (unlike chronic suppurative otitis media)
• Often has underlying persistent OME between acute episodes
• Risk factors: Early first episode (less than 6 months), daycare, passive smoking, craniofacial anomaly

D. Chronic Suppurative Otitis Media (CSOM)

Definition:

• Chronic otorrhoea (> 6-12 weeks) through persistent tympanic membrane perforation

Clinical Features:

• Continuous or intermittent purulent discharge
• Painless (unlike AOM)
• Conductive hearing loss
• Dry perforation may be asymptomatic between discharge episodes
• Danger: Risk of cholesteatoma, intracranial complications

(Detailed coverage in separate CSOM topic)

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5. Investigations

1. Otoscopy

The PRIMARY Diagnostic Tool

Standard Otoscopy:

• Direct visualization of tympanic membrane using handheld otoscope
• Operator-dependent: Requires experience, good technique
• Proper technique:
  1. Child position: Infant cradled, older child seated (parent can hold if uncooperative)
  2. Gently pull pinna upward and backward (adult) or downward and backward (infant less than 3 years) to straighten ear canal
  3. Largest speculum that fits comfortably in external canal
  4. Insert gently, avoid pushing against canal walls (painful)
  5. Systematic examination: colour, contour, translucency, landmarks, mobility

Pneumatic Otoscopy:

• Gold standard for diagnosing middle ear effusion [12]
• Insufflator (pneumatic bulb) attached to otoscope
• Requires airtight seal between speculum and ear canal
• Gentle squeeze/release of bulb → positive/negative pressure
• Normal: Drum moves briskly in/out (excursion 1-2mm)
• Effusion: No movement or minimal sluggish movement
• Sensitivity: 94%, Specificity: 80% for detecting middle ear effusion (superior to visual inspection alone) [12]

Otomicroscopy:

• Binocular microscope (operating microscope or examination microscope)
• Superior visualization: magnification (6-40×), depth perception, both hands free
• Used in ENT specialist clinics
• Allows microsuction of wax/debris, myringotomy, grommet insertion

2. Tympanometry (Impedance Audiometry)

Objective, reproducible assessment of middle ear function

Principle:

• Probe in ear canal delivers pure tone (226 Hz in children, 1000 Hz in infants less than 6 months)
• Varies ear canal pressure from +200 to -400 daPa (decaPascals)
• Measures acoustic admittance (compliance) - how much sound energy is reflected vs transmitted through drum
• Plots graph of compliance vs pressure

Tympanogram Types (Jerger Classification): [16]

Clinical Use:

• Diagnosis of OME: Type B tympanogram (flat trace) is 90% sensitive/specific for middle ear effusion [16]
• Monitoring OME: Serial tympanometry tracks effusion resolution
• Pre-operative assessment: Documents effusion before grommet surgery (medico-legal)
• Post-operative: Type A suggests grommet patent, Type B suggests blocked/extruded grommet
• Screening: Some countries use tympanometry in school screening programs

Limitations:

• Wax occlusion of canal → flat trace (mimics Type B)
• Uncooperative child movement → artifact
• Probe seal issues → inaccurate results
• Does NOT diagnose AOM (cannot differentiate sterile OME from infected OME)

3. Pure Tone Audiometry (Hearing Assessment)

Purpose: Quantify degree and type of hearing loss

Technique:

• Age-appropriate method:
  • less than 6 months: Otoacoustic emissions (OAE), Auditory Brainstem Response (ABR)
  • 6 months - 2.5 years: Visual Reinforcement Audiometry (VRA) - child turns toward sound, rewarded with visual stimulus (toy lights up)
  • 2.5 - 5 years: Play Audiometry - child performs action (put block in bucket) in response to sound
  • > 5 years: Conventional Pure Tone Audiometry - raise hand when hear beep

Findings in OME:

• Conductive hearing loss:
  • Air conduction thresholds elevated (20-40 dB HL typical)
  • Bone conduction thresholds normal (0-20 dB HL)
  • Air-Bone Gap > 10 dB = conductive component
  • Flat audiogram (all frequencies equally affected, unlike sensorineural loss which affects high frequencies first)
• Mild-Moderate severity: Most OME causes 20-35 dB loss (equivalent to earplugs or listening underwater)
• Bilateral in 80% of OME cases

Thresholds for Intervention:

• > 25-30 dB HL bilaterally: Consider intervention (grommets) if persistent > 3 months [7]
• > 40 dB HL: Definite hearing impairment, intervention warranted
• Unilateral: Controversial - may consider observation unless severe or affecting schooling

4. Imaging (NOT routine)

Indications for CT Temporal Bones:

1. Suspected Mastoiditis:

   • Postauricular swelling/erythema, pinna proptosis
   • CT shows: Mastoid air cell opacification, bony septae destruction (coalescence), subperiosteal abscess
   • Protocol: High-resolution CT temporal bones, axial + coronal, bone windows

2. Suspected Intracranial Complication:

   • Severe headache, altered consciousness, neck stiffness, focal neurology
   • CT brain + CT temporal bones → may need MRI brain for better soft tissue detail (abscess)
   • Findings: Intracranial abscess, venous sinus thrombosis, meningeal enhancement

3. Recurrent AOM with Suspected Anatomical Anomaly:

   • Persistent recurrent AOM despite appropriate treatment
   • CT may reveal: Facial nerve canal dehiscence, ossicular anomaly, tegmen tympani defect

4. Pre-operative Planning for Cholesteatoma:

   • If cholesteatoma suspected (attic perforation, foul discharge, granulation tissue)
   • CT delineates extent, erosion of ossicles/bone

MRI Temporal Bones:

• Rarely indicated in otitis media
• Use: Suspected cholesteatoma (DWI-MRI detects keratin), labyrinthitis ossificans, petrous apex lesion

Do NOT routinely image simple AOM or OME - diagnosis is clinical + tympanometry/audiometry

5. Microbiological Sampling

NOT routine for uncomplicated AOM or OME

Indications for Ear Swab/Culture:

1. Perforated AOM with otorrhoea: Swab of discharge if severe/not responding to empiric antibiotics
2. CSOM: Culture of discharge to guide targeted antibiotic (often polymicrobial, Pseudomonas)
3. Post-grommet otorrhoea: Persistent discharge through grommet
4. Immunocompromised patient: Higher risk of unusual organisms (fungi, Pseudomonas)
5. Neonatal AOM: Rare, concerning for unusual pathogens (E. coli, S. aureus)

Technique:

• Microsuction of canal debris/wax first (to avoid contamination)
• Swab discharge at tympanic membrane perforation or from middle ear (via grommet)
• Specify "Ear swab (middle ear)" to lab

Myringotomy/Tympanocentesis with Aspiration:

• Needle aspiration of middle ear fluid through intact drum
• Rarely performed outside research settings
• Indications: Severe sepsis, immunocompromised, failed multiple antibiotic courses, neonatal AOM
• Provides most accurate microbiology (uncontaminated by ear canal flora)

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6. Management

A. Acute Otitis Media (AOM)

Management Principles:

1. Analgesia is the mainstay - AOM is painful; pain relief is priority [6]
2. Most AOM is self-limiting - 60% resolve in 24 hours, 80% in 2-3 days without antibiotics [9]
3. Antibiotics provide modest benefit - reduce pain at 2-7 days by ~10% (NNT ~15), reduce perforation by ~5% (NNT ~20) [6]
4. Antimicrobial stewardship - reserve antibiotics for high-risk groups to reduce resistance

NICE NG91 Guideline: "No Antibiotic" or "Delayed Antibiotic" Strategy [6]

Step 1: Analgesia (ALL patients)

First-line:

• Paracetamol:
  • Dose: 15 mg/kg every 4-6 hours (max 4 doses/24h)
  • Infants > 3 months: 60-120 mg per dose
  • Children 1-5 years: 120-250 mg per dose
  • Children 6-12 years: 250-500 mg per dose
• Ibuprofen (if > 3 months, > 5 kg):
  • Dose: 10 mg/kg every 6-8 hours (max 3 doses/24h)
  • Max single dose: 400 mg
  • Can alternate with paracetamol for severe pain
• Do NOT use codeine in children (risk of respiratory depression, poor metabolism)

Adjuncts:

• Topical analgesics (limited evidence): Lidocaine drops (if no perforation)
• Warm compress to ear (comfort measure)
• Reassurance to parents: Pain typically improves dramatically within 24-48 hours

Step 2: Antibiotic Decision Algorithm

ACUTE OTITIS MEDIA CONFIRMED
         ↓
   ASSESS RISK FACTORS
         ↓
    ┌────┴────┐
  HIGH RISK   LOW RISK
    ↓           ↓
IMMEDIATE    "NO ANTIBIOTIC" or
ANTIBIOTIC   "DELAYED PRESCRIPTION"
             (reassess in 2-3 days)

HIGH RISK (Immediate Antibiotic):

1. Systemically very unwell:
   • Signs of sepsis
   • Severe vomiting (unable to tolerate oral)
2. High-risk comorbidities:
   • Immunocompromised (primary immunodeficiency, chemotherapy, HIV, post-transplant)
   • Cystic fibrosis
   • Congenital heart disease with risk of endocarditis
   • Cochlear implant (high risk of meningitis)
3. Age less than 2 years with BILATERAL AOM
4. AOM with perforation and otorrhoea
5. Symptoms > 4 days with no improvement

LOW RISK (No Antibiotic or Delayed Prescription):

• Age > 2 years
• Unilateral AOM
• Mild-moderate symptoms
• No systemic features
• Otherwise healthy

"Delayed Prescribing" Strategy:

• Provide prescription but advise parents to wait 2-3 days before collecting/using
• Use antibiotics only if: (1) No improvement after 2-3 days, OR (2) Deterioration at any time
• Reduces antibiotic use by 80% without increasing complications [6]
• Improves parental satisfaction (empowered to make decision)

Step 3: Antibiotic Choice (if indicated)

First-line: AMOXICILLIN [6]

• Dose: 40 mg/kg/day divided TDS (in UK) or 80-90 mg/kg/day divided BDS-TDS (high-dose, in US/Canada)
  • UK standard: 125-250 mg TDS (less than 5 years), 250-500 mg TDS (> 5 years)
  • High-dose (for areas with high pneumococcal resistance): Double the dose
• Duration: 5 days (some evidence 5 days non-inferior to 10 days for uncomplicated AOM in > 2 years) [6]
• Coverage: Excellent for Strep pneumoniae (including most resistant strains if high-dose), covers H. influenzae (if not β-lactamase producing)
• Cheap, safe, well-tolerated

Second-line (if Penicillin Allergy - NOT anaphylaxis):

• Co-amoxiclav (amoxicillin + clavulanate):
  • If treatment failure after 2-3 days of amoxicillin (suggests β-lactamase-producing H. influenzae or M. catarrhalis)
  • Dose: 0.25 mL/kg of 125/31 suspension TDS (less than 12 years)
  • Duration: 5 days
  • Clavulanate inhibits β-lactamase → effective against resistant H. flu, M. catarrhalis
  • Side effect: Diarrhoea (20-30% - clavulanate disrupts gut flora)

Penicillin Allergy (non-anaphylactic):

• Clarithromycin:

  • Dose: 7.5 mg/kg BD (max 500 mg BD)
  • Duration: 5 days
  • Macrolide - covers Strep pneumoniae, H. influenzae (variable)
  • Resistance: Increasing macrolide resistance in pneumococcus (10-30% in some regions)

• Erythromycin:

  • Alternative macrolide if clarithromycin unavailable
  • Dose: 10 mg/kg QDS
  • More GI side effects than clarithromycin

Penicillin Anaphylaxis:

• Ceftriaxone (3rd-generation cephalosporin):
  • Single IM dose: 50 mg/kg (max 1g)
  • Highly effective, used for severe AOM or vomiting (unable to tolerate oral)
  • less than 1% cross-reactivity with penicillin in true IgE-mediated allergy
  • Hospital/acute setting

Treatment Failure (Persistent Symptoms > 3 Days After Starting Antibiotics):

• Reassess: Is it AOM or viral URTI with red drum? Re-examine drum
• If definite AOM persists:
  • Switch to Co-amoxiclav (covers resistant organisms)
  • Consider referral to ENT if second-line failure
  • Consider myringotomy/tympanocentesis for culture in severe cases

Step 4: Follow-up

Routine follow-up NOT required for uncomplicated AOM

Follow-up indicated for:

1. AOM with perforation: Review at 4-6 weeks to confirm healing
2. Recurrent AOM: Audiology assessment + ENT referral for consideration of grommets
3. Treatment failure: Reassess at 3 days if symptoms not improving
4. Concern for complications: Immediate review if develops red flag features

B. Otitis Media with Effusion (OME / Glue Ear)

Management Principles:

1. Most OME resolves spontaneously within 3 months [7]
2. Watchful waiting is first-line for asymptomatic or mild cases
3. Intervention indicated if persistent bilateral OME with hearing loss affecting development
4. Surgery (grommets) is definitive but temporary - effusion may recur

NICE CG60 Guideline: Management of OME in Under 12s [7]

Stage 1: Active Monitoring (First 3 Months)

Indications for Active Monitoring:

• Asymptomatic OME (incidental finding)
• Mild hearing loss (less than 20-25 dB HL)
• Unilateral OME
• No developmental concerns

Management:

1. Reassure parents: OME is common, usually self-resolves
2. Advice:
   • Optimize environment: Face child when speaking, reduce background noise, preferential seating at school (front of classroom)
   • Treat nasal obstruction if present (adenoidal hypertrophy, allergic rhinitis)
   • Avoid passive smoking
3. Review in 3 months:
   • Repeat otoscopy + tympanometry
   • Hearing assessment (audiometry)
   • If resolved → discharge
   • If persists → proceed to Stage 2

Stage 2: Autoinflation (3-6 Months)

Autoinflation (Otovent/Eargym):

• Child blows up balloon using nose (nostrils pinched around nozzle)
• Valsalva-like manoeuvre forces air up Eustachian tube → "pops" open tube
• Evidence: Modest benefit - Cochrane review shows small improvement in effusion resolution at 1 month (NNT ~6), but not sustained long-term [7]
• Suitable for: Children > 3 years who can cooperate
• Technique: Inflate balloon 3 times daily for 1-3 months

Do NOT use:

• Decongestants (oral or nasal) - no evidence of benefit
• Antihistamines - no benefit unless concurrent allergic rhinitis
• Antibiotics - not effective for OME (no infection)
• Steroids (oral/intranasal) - limited short-term benefit, not sustained, significant side effects

Stage 3: Surgical Intervention (Persistent OME > 3 Months)

Indications for Surgery (Grommets ± Adenoidectomy): [7]

1. Persistent bilateral OME > 3 months (confirmed on 2 occasions 3 months apart), AND
2. Bilateral hearing loss > 25-30 dB HL (based on audiometry), AND
3. Impact on development:
   • Speech/language delay
   • Educational difficulties (poor attention, academic underperformance)
   • Social/behavioural problems attributed to hearing loss

Grommet Insertion (Myringotomy + Ventilation Tube Insertion):

Procedure:

• Day-case surgery, general anaesthetic (inhalational, short procedure 10-15 min)
• Examination Under Anaesthetic (EUA): Both ears examined with otomicroscope
• Microsuction: Wax/debris removed
• Myringotomy: Small incision in tympanic membrane, typically antero-inferior quadrant (to avoid ossicles, round window, facial nerve)
  • Incision site chosen to avoid: Superior (incus, malleus), Posterior (stapes, round window, facial nerve)
• Aspiration: Middle ear effusion suctioned (viscous "glue" requires wide-bore suction)
• Grommet insertion: Ventilation tube inserted half-in, half-out of myringotomy
  • Types: Shah (short-term, 6-9 months), T-tube (long-term, 12-18 months)
  • Function: Allows air entry into middle ear → restores atmospheric pressure → effusion drains via Eustachian tube

Mechanism of Action (Important Concept):

• Grommets do NOT "drain fluid out"
• Grommets ventilate the middle ear (allow air in)
• Ventilation breaks the negative pressure vacuum → effusion drains naturally down Eustachian tube (mucociliary clearance)
• Restores normal middle ear aeration

Grommet Extrusion:

• Tympanic membrane heals and pushes grommet out as epithelium migrates
• Typical extrusion time: 6-12 months (Shah grommet), 12-18 months (T-tube)
• Extrusion is expected, not a complication
• Leaves small perforation which heals spontaneously in 95% of cases

Adenoidectomy:

• Often performed with grommets (especially age > 3 years, recurrent OME)
• Evidence: Reduces OME recurrence and need for repeat grommets by ~25% [10]
• Mechanism:
  • Removes mechanical obstruction of Eustachian tube orifice
  • Eliminates biofilm reservoir of bacteria (source of recurrent infection)
• Indications:
  • Recurrent OME (previous grommets extruded with recurrence)
  • Nasal obstruction symptoms (mouth breathing, snoring, OSA)
  • Recurrent adenoiditis
• Technique: Curettage or suction diathermy of adenoid pad via transoral approach

Post-operative Management:

Water precautions:

• No swimming until grommets extruded (or use silicone earplugs + swimming cap - controversial)
• Bath/shower: Cotton wool soaked in Vaseline in ear (to prevent water entry)
• No diving (pressure changes may displace grommet)
• Rationale: Water entry through grommet → infection (otorrhoea)

Grommet otorrhoea (discharge through grommet):

• Occurs in 10-25% of cases
• Triggers: Water contamination, URTI, biofilm
• Management:
  1. Topical antibiotic-steroid drops: Ciprofloxacin 0.3% + dexamethasone (or gentamicin + hydrocortisone) - quinolones are non-ototoxic
  2. Microsuction (ENT clinic) if profuse/persistent
  3. Avoid systemic antibiotics (topical is superior - direct delivery to infection)
  4. Rarely: Grommet removal if persistent infection

Outcome:

• Immediate hearing improvement: ~12 dB improvement (from 35 dB to 23 dB HL average) [10]
• Symptom resolution: 80-90% parents report improved hearing, attention, behaviour
• Recurrence: 20-30% require repeat grommets after extrusion

Hearing Aids (Alternative to Surgery):

• Bone conduction headband (Baha Softband) or conventional behind-the-ear (BTE) hearing aids
• Indications:
  • Child unfit for anaesthesia
  • Parents decline surgery
  • Recurrent OME despite multiple grommet insertions
• Limitations: Compliance issues (young children remove aids), stigma, cost

C. Recurrent Acute Otitis Media

Definition: ≥3 episodes in 6 months or ≥4 in 12 months

Management:

Conservative:

1. Address modifiable risk factors:
   • Cease passive smoking exposure
   • Avoid supine bottle feeding
   • Consider reducing daycare hours (if feasible)
   • Ensure pneumococcal + influenza vaccinations up-to-date
2. Prophylactic antibiotics: NOT recommended (NICE) - no evidence of benefit, promotes resistance
3. Xylitol chewing gum/syrup: Some evidence for prevention (reduces bacterial adhesion) - not widely used

Surgical:

• Grommet insertion: Consider if underlying persistent OME between acute episodes
• Adenoidectomy: If > 3 years, evidence of adenoidal hypertrophy, or recurrent adenoiditis
• Both (grommets + adenoidectomy): Often performed together for recurrent AOM with OME

---

7. Complications

Overall Rate: Rare (1-2% of AOM) in antibiotic era, but potentially life-threatening

A. Intratemporal Complications

1. Acute Mastoiditis

Pathophysiology:

• Infection spreads from middle ear to mastoid air cells (via aditus ad antrum)
• Initially: Coalescent mastoiditis - pus under pressure erodes bony septa between air cells → large abscess cavity
• Later: Pus breaches cortical bone → subperiosteal abscess (between bone and periosteum)

Clinical Features: [15]

• Postauricular swelling: Boggy, tender, erythematous swelling behind ear
• Pinna proptosis: Ear pushed forward and downward
• Loss of postauricular crease (sulcus obliterated)
• Sagging of posterosuperior ear canal wall (on otoscopy)
• Fever, otalgia, hearing loss
• May have preceding AOM (50%) or no history of AOM (silent mastoiditis)

Investigations:

• CT temporal bones (contrast-enhanced): Mastoid opacification, bony erosion, subperiosteal collection
• Blood: FBC (leukocytosis), CRP/ESR (elevated), blood cultures

Management:

• Admission for IV antibiotics
• Antibiotics: Ceftriaxone 50 mg/kg/day IV (covers resistant S. pneumoniae, H. influenzae) + Metronidazole (anaerobic cover)
• ENT referral (urgent)
• Surgical drainage (Cortical Mastoidectomy) if:
  • Subperiosteal abscess > 1 cm
  • No improvement after 24-48h IV antibiotics
  • Intracranial extension
• Myringotomy + grommet: To drain middle ear pus, ventilate

Prognosis:

• Excellent with prompt treatment
• Risk of intracranial spread if untreated

2. Facial Nerve Palsy

Pathophysiology:

• Facial nerve (CN VII) traverses middle ear in facial canal (bony tunnel)
• In 10% of population, canal is dehiscent (bony covering incomplete) → nerve exposed to middle ear
• AOM inflammation/infection causes neuropraxia (pressure ischaemia) or neuritis
• Usually Lower Motor Neuron (LMN) palsy: inability to close eye, forehead weakness, mouth droop

Clinical Features:

• Acute onset facial weakness during AOM episode
• Complete LMN palsy (cannot close eye, raise eyebrow, smile)
• House-Brackmann Grade III-VI
• Risk of exposure keratitis (cornea dries, ulcerates due to incomplete eyelid closure)

Management:

• Urgent ENT referral
• Antibiotics: High-dose IV (ceftriaxone)
• Myringotomy: Drain pus, relieve pressure on nerve
• Eye care: Lubricating drops (daytime), lacrilube ointment (night), tape eyelid closed at night (prevent exposure keratopathy)
• Steroids: Controversial - some use prednisolone 1 mg/kg/day for 5-7 days (reduce inflammation)

Prognosis:

• 90-95% full recovery if treated promptly (within 24-48 hours)
• Delayed treatment → permanent palsy (5-10%)

3. Labyrinthitis

Pathophysiology:

• Inflammation spreads to labyrinth (inner ear: cochlea + vestibular apparatus)
• Routes: (1) Round/oval window, (2) Erosion of lateral semicircular canal (cholesteatoma), (3) Haematogenous
• Causes sensorineural hearing loss + vertigo

Clinical Features:

• Severe vertigo (room spinning), nausea, vomiting
• Sensorineural hearing loss (may be permanent)
• Nystagmus (horizontal, toward affected ear in acute phase)
• Tinnitus
• Background AOM or CSOM

Management:

• Urgent ENT referral + audiometry
• IV antibiotics (ceftriaxone + metronidazole)
• Steroids: High-dose prednisolone (to preserve hearing)
• Myringotomy: Drain infection
• Vestibular suppressants: Prochlorperazine, cyclizine (short-term for severe vertigo)
• Consider cochlear implant if progresses to profound deafness

Prognosis:

• Vertigo resolves in days-weeks (central compensation)
• Hearing loss may be permanent (30-50% have residual SNHL)

4. Chronic Suppurative Otitis Media (CSOM)

Definition: Chronic otorrhoea (> 6-12 weeks) through persistent TM perforation

Pathophysiology:

• Perforation from AOM fails to heal → chronic pathway for bacterial entry
• Recurrent/persistent infection
• Risk of cholesteatoma (if attic/marginal perforation)

Types:

• Mucosal CSOM ("Safe ear"): Central perforation, mucoid discharge
• Squamous CSOM ("Unsafe ear"): Attic/marginal perforation, foul discharge, cholesteatoma

(Detailed management in separate CSOM topic)

B. Intracranial Complications (Rare but Life-Threatening)

Routes of Spread:

1. Direct erosion: Through tegmen tympani (roof of middle ear) or tegmen mastoideum (roof of mastoid)
2. Thrombophlebitis: Via valveless emissary veins (infection travels retrograde)
3. Pre-formed pathways: Petrosquamous suture, labyrinthine windows

1. Meningitis

Pathophysiology:

• Infection spreads to subarachnoid space
• Causative organisms: S. pneumoniae (most common), H. influenzae

Clinical Features:

• Headache, photophobia, neck stiffness (Kernig's sign, Brudzinski's sign)
• Fever, altered consciousness
• Seizures (20%)
• Background AOM/mastoiditis (50% have no ear symptoms)

Management:

• Medical emergency: Admit ICU
• Lumbar puncture (if no raised ICP): CSF shows neutrophils, low glucose, high protein, organisms on Gram stain
• Antibiotics: IV ceftriaxone 2g BD + vancomycin (empiric for meningitis - broad cover)
• Imaging: CT/MRI brain + temporal bones (identify source)
• ENT/neurosurgery: Surgical drainage of mastoid/middle ear if source

Prognosis:

• Mortality: 5-10% (even with treatment)
• Morbidity: Deafness (30%), neurological sequelae (20%)

2. Brain Abscess

Pathophysiology:

• Localized pus collection in brain parenchyma
• Locations: Temporal lobe (nearest to petrous bone), Cerebellum (via posterior fossa)
• Stages: Cerebritis → Early capsule → Late capsule (mature abscess)

Clinical Features:

• Headache (severe, progressive)
• Focal neurology: Hemiparesis, dysphasia, visual field defect (depends on location)
• Seizures (30-50%)
• Reduced GCS (late sign, raised ICP)
• Fever (may be absent - "cold" abscess)

Investigations:

• MRI brain (contrast): Ring-enhancing lesion (capsule), central low signal (pus), surrounding oedema
• CT brain: Less sensitive, but faster (use if unstable)

Management:

• Neurosurgical emergency
• Aspiration/Excision: Stereotactic aspiration (if less than 3 cm) or craniotomy + excision
• Antibiotics: IV ceftriaxone + metronidazole (anaerobes common) for 6-8 weeks
• Dexamethasone: Reduce cerebral oedema
• Anticonvulsants: If seizures

Prognosis:

• Mortality: 10-20%
• Morbidity: Epilepsy (50%), neurological deficit (30%)

3. Lateral (Sigmoid) Sinus Thrombosis

Pathophysiology:

• Infection spreads to lateral venous sinus (sigmoid sinus)
• Thrombophlebitis → septic thrombosis → venous infarction
• Embolization → septic emboli to lungs

Clinical Features:

• "Picket fence" fever: Spiking fevers with rigors (intermittent bacteraemia)
• Headache (raised ICP from venous obstruction)
• Griesinger's sign: Tender swelling over mastoid emissary vein (pathognomonic but rare)
• Papilloedema (raised ICP)
• Septic pulmonary emboli: Cough, pleuritic chest pain, haemoptysis

Investigations:

• MRI venography (MRV) or CT venography (CTV): Filling defect in sigmoid sinus
• D-dimer: Elevated
• Blood cultures: Positive (intermittent bacteraemia)

Management:

• IV antibiotics: Ceftriaxone + metronidazole
• Anticoagulation: Controversial - some advocate heparin/LMWH (prevent thrombus propagation), others avoid (risk of haemorrhagic transformation)
• Mastoidectomy: Surgical drainage of mastoid, may need sinus decompression

Prognosis:

• Mortality: 5-15%
• Morbidity: Chronic headaches (venous hypertension), seizures

---

8. Prognosis

Natural History of AOM

Without Antibiotics:

• 60% resolve within 24 hours (pain-free) [9]
• 80% resolve within 2-3 days
• Spontaneous perforation: 10-15% (usually heals without sequelae)
• Complications: less than 1% in otherwise healthy children

With Antibiotics:

• Modest reduction in symptom duration (~1 day earlier resolution)
• Slightly reduced perforation rate (absolute risk reduction ~5%, NNT ~20)
• No difference in long-term hearing outcomes

Recurrence:

• After first episode: 20-30% have recurrent AOM
• Risk factors for recurrence: First episode less than 6 months old, daycare, passive smoking, craniofacial anomaly

Natural History of OME

Spontaneous Resolution:

• 50% resolve within 3 months (without intervention) [4]
• 80% resolve within 6-12 months
• Resolution more likely if: Unilateral, serous (thin) effusion, older age, summer season

Persistence:

• 20% have persistent OME > 12 months
• Persistent bilateral OME with hearing loss: Surgical candidates (grommets)

Long-term Outcomes:

Hearing:

• With grommets: Immediate improvement (~12 dB gain), maintained while grommets in situ [10]
• After grommet extrusion: 60-70% remain dry (cured), 30-40% recur (may need repeat grommets)
• Long-term (age 9-11): No significant difference in hearing between operated and non-operated groups (OME eventually resolves in most)

Speech and Language:

• Controversial: Some studies show transient delay during active OME, others show no long-term impact
• UK TARGET trial: No difference in language scores at age 9 between grommet vs watchful waiting groups [10]
• Consensus: Short-term hearing loss may affect development in vulnerable children (pre-existing language delay, learning difficulties) - these benefit most from intervention

Academic Performance:

• Mild association between persistent OME in early childhood and lower reading scores at age 7 (correlation, not causation)
• Likely confounded by socioeconomic factors

Behavioural:

• Parental reports of improved behaviour/attention after grommets (not consistently shown in formal studies)

Special Populations

Down Syndrome

• 60-80% have OME (vs 15-20% general population)
• Multifactorial: Mid-face hypoplasia, narrow Eustachian tube, immune dysfunction, adenoidal hypertrophy
• Persistent OME common → early grommet insertion often required
• Higher recurrence rate after grommet extrusion → may need long-term (T-tube) grommets or hearing aids

Cleft Palate

• 95% develop OME (due to tensor veli palatini muscle dysfunction - muscle inserts abnormally, cannot open Eustachian tube)
• Universal grommets: Many centres insert grommets prophylactically at time of cleft repair (age 3-6 months)
• Persistent OME until palate repair (restores muscle function) - often requires multiple grommet insertions
• Long-term: 50% require grommets into teenage years

Immunocompromised

• Higher risk of recurrent AOM, complications, unusual organisms (Pseudomonas, fungi, atypical mycobacteria)
• Lower threshold for antibiotics, ENT referral
• Grommets may help reduce recurrent AOM but higher risk of persistent otorrhoea

---

9. Prevention

Vaccination

1. Pneumococcal Conjugate Vaccine (PCV13)

• Protects against 13 Streptococcus pneumoniae serotypes (including most common AOM serotypes)
• Impact: 20-30% reduction in AOM incidence [11]
• Serotype replacement: Increase in non-vaccine serotypes (3, 19A) and non-pneumococcal AOM (H. influenzae)
• Schedule: 2, 4, 12-13 months (UK), or 2, 4, 6, 12-15 months (US)

2. Influenza Vaccine

• Annual influenza vaccination reduces AOM incidence by ~30% during influenza season
• Influenza is common trigger for AOM (viral infection → Eustachian tube dysfunction → bacterial superinfection)
• Recommended for all children > 6 months (UK: nasal live attenuated; US: injectable inactivated)

3. Hib Vaccine (Haemophilus influenzae type b)

• Protects against H. influenzae type b (invasive disease)
• Does NOT protect against non-typeable H. influenzae (cause of AOM)
• Schedule: 2, 3, 4, 12 months (UK)

Modifiable Risk Factors

1. Breastfeeding

• Exclusive breastfeeding for ≥3-6 months reduces AOM incidence by 30-40%
• Mechanisms: Passive immunity (IgA), reduced supine feeding, improved orofacial development

2. Avoid Passive Smoking

• Single most important modifiable risk factor
• Eliminate household smoking exposure
• Dose-dependent effect (more cigarettes = higher AOM risk)

3. Avoid Supine Bottle Feeding

• Do not prop bottles (feeds infant lying flat)
• Milk reflux into Eustachian tube → inflammation, bacterial colonization
• Hold infant semi-upright during feeds

4. Limit Pacifier Use

• Discontinue pacifier after 6 months if possible
• Associated with 30% increased AOM risk (mechanism unclear - altered oropharyngeal pressures, bacterial colonization)

5. Reduce Daycare Exposure (if feasible)

• Small daycare groups (less than 6 children) have lower AOM risk than large centres
• Home care has lowest risk
• (Acknowledge: Not feasible for most families due to work commitments)

Prophylactic Interventions (NOT Recommended)

1. Prophylactic Antibiotics

• Not recommended (NICE, AAP guidelines)
• Minimal benefit (~0.5 episodes prevented per year)
• Significant harms: Antibiotic resistance, side effects (diarrhoea, rash), cost

2. Xylitol

• Sugar alcohol (birch sugar) in chewing gum or syrup
• Reduces bacterial adhesion to nasopharyngeal mucosa
• Some evidence for ~25% AOM reduction (Finnish studies)
• Not widely adopted (compliance issues, cost)

3. Probiotics

• Insufficient evidence for AOM prevention

---

10. Key Guidelines and Evidence

NICE NG91: Otitis Media (Acute) - Antimicrobial Prescribing (2018) [6]

Key Recommendations:

1. No antibiotic or delayed antibiotic for most children with AOM
2. Immediate antibiotic if: Systemically unwell, high-risk comorbidities, age less than 2 with bilateral AOM, perforation with otorrhoea
3. First choice: Amoxicillin 5 days
4. Alternative (penicillin allergy): Clarithromycin or erythromycin
5. Analgesia: Paracetamol or ibuprofen for all

NICE CG60: Otitis Media with Effusion in Under 12s (2008) [7]

Key Recommendations:

1. Active observation for 3 months (most resolve spontaneously)
2. Surgical referral if persistent bilateral OME > 3 months with hearing loss > 25-30 dB HL affecting development
3. Autoinflation may be tried (modest evidence)
4. Do NOT routinely offer: Decongestants, antihistamines, antibiotics, steroids
5. Hearing aids as alternative to surgery in selected cases

Cochrane Reviews

1. Antibiotics for AOM (Venekamp et al., 2015) [9]

• 13 RCTs, 3,401 children
• Findings: Antibiotics reduce pain at 2-7 days by ~10% (NNT 15), reduce perforation by ~5% (NNT 20)
• Harms: Increased vomiting, diarrhoea, rash (NNH 14)
• Conclusion: Modest benefit; reserve for high-risk groups

2. Grommets for OME (Browning et al., 2010) [10]

• 10 RCTs, 1,609 children
• Findings: Grommets improve hearing by ~12 dB at 6-12 months (statistically significant)
• Long-term: No difference at 3-5 years (OME resolves naturally in controls)
• Conclusion: Short-term benefit; long-term benefit unclear

3. Adenoidectomy for OME (van den Aardweg et al., 2010)

• Combined with grommets: Reduces recurrence by ~25%, fewer repeat operations
• Adenoidectomy alone: Less effective than grommets alone

---

11. Controversies and Evolving Evidence

1. High-Dose vs Standard-Dose Amoxicillin

• US/Canada: Recommend 80-90 mg/kg/day (high-dose) to overcome pneumococcal resistance
• UK/Europe: Use 40-50 mg/kg/day (standard-dose)
• Debate: High-dose increases side effects (diarrhoea); unclear if clinically superior in low-resistance settings

2. Duration of Antibiotics (5 vs 10 Days)

• Evidence supports 5-day courses are non-inferior to 10 days for uncomplicated AOM in children > 2 years
• Shorter courses reduce antibiotic exposure, improve compliance
• Some guidelines still recommend 7-10 days (conservative)

3. Tympanostomy Tubes for Recurrent AOM (Without OME)

• Weak evidence: Some studies show reduction in AOM episodes (by ~1-2 episodes/year)
• Not routinely recommended (NICE) - benefits marginal, risks of surgery
• Consider if > 4-6 episodes/year despite addressing risk factors

4. Long-Term Effects of OME on Development

• Ongoing debate: Does persistent OME in early childhood cause lasting language/academic impairment?
• TARGET trial (UK): No long-term benefit of grommets on language at age 9
• Consensus: Short-term intervention warranted if hearing loss affecting current development; long-term effects unclear

5. Water Precautions with Grommets

• Traditional advice: No swimming, strict water precautions
• Recent evidence: Surface swimming (no diving) is low-risk; routine earplugs may not be necessary
• Guidelines vary: Conservative (UK) vs liberal (some US centres)

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12. Patient and Caregiver Information

For Parents: Acute Otitis Media (Ear Infection)

What is it? An ear infection is when bacteria or a virus causes inflammation behind the eardrum. Pus builds up, causing pain and fever.

Will it get better without antibiotics? Yes, in most cases. 60-80% of ear infections clear up on their own within 2-3 days. Your child's immune system fights the infection.

What should I do?

1. Pain relief: Give paracetamol or ibuprofen regularly (every 4-6 hours) for the first 1-2 days. This is the most important treatment.
2. Comfort: Warm compress on the ear, plenty of fluids, rest.
3. Watch and wait: Most children improve within 24-48 hours.

When do I need antibiotics? The doctor may prescribe antibiotics if your child is:

• Very unwell (high fever, vomiting, lethargic)
• Under 2 years old with infection in both ears
• Has discharge coming from the ear
• Has other health problems (heart condition, weak immune system)

"Delayed prescription": Your doctor may give you a prescription to collect in 2-3 days if your child doesn't improve. This avoids unnecessary antibiotics.

When should I worry? See a doctor urgently if:

• Swelling behind the ear
• Severe headache or drowsiness
• Weakness of the face
• No improvement after 3 days

For Parents: Glue Ear (OME)

What is Glue Ear? Glue Ear is when sticky fluid builds up behind the eardrum (in the middle ear). It's like having earplugs in - sounds are muffled. It doesn't hurt and there's no infection.

Why does it happen? After a cold, the tube that drains the ear (Eustachian tube) can get blocked. Air gets absorbed from the middle ear and is replaced by fluid.

Will it get better? Yes, in most children (80%) Glue Ear clears up by itself within 3-6 months. The tube unblocks and the fluid drains away.

What can I do to help?

• Face your child when speaking
• Reduce background noise (turn TV down)
• Ask the teacher to seat your child at the front of the classroom
• Avoid smoking around your child

When is treatment needed? If Glue Ear lasts more than 3 months and your child has:

• Hearing loss (tested by audiology)
• Speech delay
• Difficulty at school
• Behavioural problems from not hearing

What is a grommet? A grommet (ventilation tube) is a tiny plastic tube inserted into the eardrum. It lets air into the middle ear, which dries up the fluid. Hearing is restored immediately.

How long do grommets stay in? Grommets fall out by themselves after 6-12 months. The eardrum heals. Some children need grommets more than once.

Can my child swim with grommets? Ask your doctor - advice varies. Some say avoid swimming; others say surface swimming is fine. Use earplugs and a swimming cap if swimming.

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13. References

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2. Casselbrant ML, Mandel EM. Epidemiology. In: Rosenfeld RM, Bluestone CD, eds. Evidence-Based Otitis Media. 2nd ed. BC Decker; 2003:147-162.

3. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The diagnosis and management of acute otitis media. Pediatrics. 2013;131(3):e964-999. doi:10.1542/peds.2012-3488

4. Rosenfeld RM, Shin JJ, Schwartz SR, et al. Clinical Practice Guideline: Otitis Media with Effusion (Update). Otolaryngol Head Neck Surg. 2016;154(1 Suppl):S1-S41. doi:10.1177/0194599815623467

5. Bluestone CD. Eustachian Tube: Structure, Function, and Role in Middle Ear Disease. 2nd ed. PMPH-USA; 2018.

6. National Institute for Health and Care Excellence. Otitis media (acute): antimicrobial prescribing. NICE guideline [NG91]. Published March 2018. https://www.nice.org.uk/guidance/ng91

7. National Institute for Health and Care Excellence. Otitis media with effusion in under 12 s: surgery. NICE clinical guideline [CG60]. Published February 2008. Updated 2024. https://www.nice.org.uk/guidance/cg60

8. Ngo CC, Massa HM, Thornton RB, Cripps AW. Predominant bacteria detected from the middle ear fluid of children experiencing otitis media: A systematic review. PLoS One. 2016;11(3):e0150949. doi:10.1371/journal.pone.0150949

9. Venekamp RP, Sanders SL, Glasziou PP, Del Mar CB, Rovers MM. Antibiotics for acute otitis media in children. Cochrane Database Syst Rev. 2015;2015(6):CD000219. doi:10.1002/14651858.CD000219.pub4

10. Browning GG, Rovers MM, Williamson I, Lous J, Burton MJ. Grommets (ventilation tubes) for hearing loss associated with otitis media with effusion in children. Cochrane Database Syst Rev. 2010;(10):CD001801. doi:10.1002/14651858.CD001801.pub3

11. Taylor S, Marchisio P, Vergison A, Harriague J, Hausdorff WP, Haggard M. Impact of pneumococcal conjugate vaccination on otitis media: a systematic review. Clin Infect Dis. 2012;54(12):1765-1773. doi:10.1093/cid/cis292

12. Karma PH, Penttila MA, Sipila MM, Kataja MJ. Otoscopic diagnosis of middle ear effusion in acute and non-acute otitis media. I. The value of different otoscopic findings. Int J Pediatr Otorhinolaryngol. 1989;17(1):37-49. doi:10.1016/0165-5876(89)90172-5

13. van Dongen TMA, van der Heijden GJMG, Venekamp RP, Rovers MM, Schilder AGM. A trial of treatment for acute otorrhea in children with tympanostomy tubes. N Engl J Med. 2014;370(8):723-733. doi:10.1056/NEJMoa1301630

14. Wei WI, Sham JST. Nasopharyngeal carcinoma. Lancet. 2005;365(9476):2041-2054. doi:10.1016/S0140-6736(05)66698-6

15. Psarommatis IM, Voudouris C, Douros K, Giannakopoulos P, Bairamis T, Carabinos C. Algorithmic management of pediatric acute mastoiditis. Int J Pediatr Otorhinolaryngol. 2012;76(6):791-796. doi:10.1016/j.ijporl.2012.02.042

16. Onusko E. Tympanometry. Am Fam Physician. 2004;70(9):1713-1720.

17. Vergison A, Dagan R, Arguedas A, et al. Otitis media and its consequences: beyond the earache. Lancet Infect Dis. 2010;10(3):195-203. doi:10.1016/S1473-3099(10)70012-8

18. Jones LL, Hashim A, McKeever T, Cook DG, Britton J, Leonardi-Bee J. Parental and household smoking and the increased risk of bronchitis, bronchiolitis and other lower respiratory infections in infancy: systematic review and meta-analysis. Respir Res. 2011;12:5. doi:10.1186/1465-9921-12-5

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