Otitis externa

Question 1

Definition

Answer 1

Infection of the external auditory canal (EAC)

Question 2

Aetiology

Answer 2

MC caused by:
- Pseudomonas aeruginosa
- Staphylococcus aureus
10-15% are fungal predominantly:
- Aspergillus
- Candida spp

Question 3

Epidemiology and Risk Factors

Answer 3

Otitis externa is a common GP presentation, with an incidence >1% per year:
- Diabetes
- Dermatitis : any disruption of the normal skin barrier
- Trauma
- Moisture: swimming, humid environment

Question 4

Risk factors for necrotising otitis externa

Answer 4

• Head & neck radiotherapy
• Diabetes
• Advancing age
• Immunosuppression

Question 5

What is the cerumen?

Answer 5

Produced by glands in the EAC is acidic, providing a protective barrier for the thin dermis of the canal

Question 6

Pathophysiology

Answer 6

Disruption of the cerumen barrier can occur with instrumentation (cotton buds, hearing aids, earplugs) leading to accumulation of moisture and a rise in pH.
This environment is conducive to the proliferation of organisms, invasion and inflammation.

Question 7

Necrotising otitis externa (NOE)

Answer 7

AKA: malignant otitis externa
Invasive form of otitis externa that can lead to osteomyelitis of the temporal bone, multiple cranial nerve palsies and death.
The tight binding of the skin layer to the periosteum in the deep portions of the EAC accounts for the severe otalgia experienced by these patients.

Question 8

Signs

Answer 8

Ottohoea
Erythema: EAC, may extend to pinna
Fever
Cranial nerve palsies: NOE
Granulation tissue in EAC: NOE

Question 9

Symptoms

Answer 9

• Pain: ear, jaw, headache. Severe in NOE (patients may wake at night)
• Discharge
• Pruritus
• Hearing loss: conductive resolve with treatment
• Facial weakness (NOE)

Question 10

Diagnosis

Answer 10

Not required in uncomplicated cases in primary care.
- Swab: for microbiological analysis when there are persistent or recurrent symptoms, or suspicion of necrotising otitis externa
Blood glucose: poor blood glucose control in a diabetic may exacerbate infection

Question 11

Investigations for potential NOE

Answer 11

• FBC (leukocytosis), CRP, ESR,
• Biopsy: granulation tissue in the EAC or any polyp = sent for MC+S and histology to exclude malignancy
• Contact CT temporal bones: thickened + enhanced tissue (EAC) + bone erosion in NOE
• Technetium-99m bone scan : increased uptake with bony involvement, highly sensitive for NOE
  Gallium-67 citrate scan : detects granulocyte: Assess treatment success, as changes to bone turnover detected by technetium scanning will persist through infection clearance

Question 12

Treatment AOE

Answer 12

• Analgesia: Para, Ibuprofen, Codiene
• Topical therapy:
  = ACETIC ACID (mild)
  = Abx +/- topical steroids:
• Ciprofloxacin 3%
• Dexamethasone 0.1%
  or Clotrimazole 1%
  ENT referral
• Microsuction - to allow topical Abx to reach affected tissue
• Wick insertion = aids delivery of topical therapy

Question 13

Treatment NOE

Answer 13

• Admission under ENT : potentially with joint input from medical/infectious diseases team
• Vascular access : for long term therapy (minimum 6 weeks)
• IV antibiotics: ceftazidime/as per local formulary

Question 14

Complications

Answer 14

• Pinna cellulitis
• Chronic otitis externa: prolonged topical antibiotics are a risk factor for fungal overgrowth
• Myringitis

Necrotising otitis externa:
- Meningitis
-Cranial nerve palsies
- Subdural empyema
- Dural sinus thrombophlebitis (dural sinus occlusive disease)