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Otitis Externa

Definition & Overview

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Classification

1. Acute Localized OE (Furunculosis)

• One or more pustules/furuncles in the EAC
• Causative organism: S. aureus
• Symptoms: itching, pain, swelling, redness, occasionally decreased hearing

2. Acute Diffuse OE ("Swimmer's Ear" / "Tropical Ear")

• Rapid onset (<48 hours) of canal inflammation
• Most common causative organism: P. aeruginosa (>90% of AOE is bacterial; P. aeruginosa and S. epidermidis are the dominant pathogens)
• Associated with water exposure or local trauma

3. Erysipelas of the Ear

• Caused by group A Streptococcus (S. pyogenes)
• Diffusely red, painful ear; hemorrhagic bullae may appear on canal walls

4. Chronic Otitis Externa (COE)

• Prolonged EAC inflammation; bilateral in >50% of patients; affects 3–5% of the population
• Mild discomfort, pruritus, aural fullness; skin shows atrophy ± stenosis
• Causes include: allergic/contact reactions (commonly neomycin), systemic diseases (psoriasis, seborrhoea, sarcoidosis, Sjögren), and chronic infection

5. Eczematous (Dermatitic) OE

• Severe pruritus, scaling, crusting, oozing, erythema
• Underlying skin conditions: contact dermatitis, seborrhoeic or atopic dermatitis

6. Malignant (Necrotizing) OE

• Aggressive, life-threatening form
• Predominantly in diabetics and immunocompromised patients
• Organism: P. aeruginosa
• Progression: apparent OE → canal maceration, granulation tissue → temporal bone osteomyelitis → intracranial extension → cranial nerve palsies (VII, IX, X, XII) or meningitis
• Bacteria are thought to access the temporal bone via the fissures of Santorini between ear cartilages

7. Fungal OE (Otomycosis)

• ~10% of AOE cases
• Severe pruritus, clear drainage, "cotton-like" debris filling the canal
• Candida: typical white discharge
• Aspergillus flavus: "wet newspaper" appearance — moist white plug with black dots

8. Viral OE (Rare)

• Organisms: varicella, measles, herpesvirus
• Herpes Zoster Oticus (HZO): canal involvement without facial palsy
• Ramsay Hunt syndrome: HZO + facial paralysis ± sensorineural hearing loss or vertigo

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Predisposing Factors

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Clinical Features

• Moderate-to-severe otalgia worsened by pinna manipulation (key distinguishing feature vs. mastoiditis, where tenderness is over the mastoid tip)
• Pruritus → progresses to seropurulent discharge, oedema, aural fullness, conductive hearing loss
• Signs: circumferential EAC erythema and oedema, otorrhoea, preauricular/cervical lymphadenopathy
• Weber test lateralises to the affected side (conductive loss from canal obstruction)

• Predominantly pruritus with mild discomfort
• Secretory (wet) or dry/squamous type
• Periodic waxing and waning course; may progress to medial canal fibrosis

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Investigations

• Clinical diagnosis in most cases; examination under binocular microscopy preferred
• Canal culture (bacteria + fungi) for persistent or recurrent infection
• Biopsy if treatment-resistant — to exclude malignancy
• Imaging (CT/MRI): reserved for suspected spread beyond EAC
  • CT: demonstrates bony erosion in necrotizing OE
  • MRI with gadolinium: preferred for soft tissue and intracranial extension in malignant OE

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Treatment

Acute OE (Uncomplicated)

• Canal debridement/cleaning — removes obstructive debris, allows drop penetration
• Topical antibiotic drops — effective for most cases; systemic antibiotics are not indicated in immunocompetent patients with infection confined to the canal
  • Fluoroquinolone drops (e.g., ciprofloxacin/ofloxacin): first choice; safe with tympanic membrane perforation
  • Aminoglycoside drops (e.g., neomycin, gentamicin): effective but contraindicated with TM perforation (ototoxic)
  • Topical corticosteroids often combined to reduce inflammation
• Acidifying drops (acetic acid) useful for mild cases and prophylaxis

Fungal OE

• Topical antifungal agents after thorough canal cleaning

Chronic OE

• Address underlying cause (allergic: remove offending agent; systemic disease: treat primary condition)
• Periodic aggressive debridement

Malignant (Necrotizing) OE

• Systemic antipseudomonal antibiotics — ciprofloxacin is standard initial therapy
• Aggressive debridement by an otolaryngologist
• MRI with gadolinium for extent assessment
• Surgical intervention for refractory cases
• Coordination with ENT is mandatory

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Clinical Images

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Peripheral Neuropathy

Overview

• Large myelinated — conduct at ~50 m/s; motor axons; also carry vibration/proprioception
• Small myelinated — transmit pain and temperature
• Small unmyelinated — autonomic fibers; also pain/temperature

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Classification

By Distribution

By Pathology

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The Seven Key Diagnostic Questions (Harrison's)

1. What systems are involved? Motor / sensory / autonomic / combined
2. Distribution of weakness? Distal only vs. proximal+distal; focal/asymmetric vs. symmetric
3. Nature of sensory involvement? Small-fiber (pain/temp loss, burning) vs. large-fiber (vibration/proprioception loss)
4. UMN involvement? Suggests central + peripheral pathology (e.g., B₁₂ deficiency, adrenoleukodystrophy)
5. Temporal evolution? Acute (≤4 weeks) / subacute (4–8 weeks) / chronic (>8 weeks)
6. Hereditary neuropathy? Family history; sensory signs without symptoms (asymptomatic at first)
7. Associated medical conditions? Cancer, diabetes, connective tissue disease, infection (HIV, Lyme, leprosy), alcohol, drugs, toxins

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Diagnostic Approach

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Major Causes

1. Diabetic Neuropathy (most common cause in clinical practice)

2. Uremic Neuropathy (CKD)

• Length-dependent axonal degeneration of lower limbs
• Mechanism: accumulated "middle molecules" (300–12,000 Da uremic toxins) inhibit Na⁺/K⁺-ATPase → altered nerve excitability; lower limb motor axons depolarized pre-dialysis, normalise post-dialysis
• Mononeuropathy multiplex in CKD → consider vasculitic neuropathy (ANCA+ vasculitis, polyarteritis nodosa)
• Very slow NCV (<½ normal) suggests coexisting demyelination — Comprehensive Clinical Nephrology 7E

3. Inflammatory / Immune-Mediated

4. Hereditary Neuropathies

5. Toxic / Drug-Induced

• Chemotherapy: vincristine, cisplatin, oxaliplatin, paclitaxel, bortezomib (CIPN — chemotherapy-induced peripheral neuropathy; mechanisms include microtubule disruption, mitochondrial damage, DNA injury → Wallerian degeneration or apoptosis)
• Antibiotics: isoniazid (pyridoxine deficiency), nitrofurantoin, metronidazole
• Others: amiodarone, colchicine, thalidomide, statins, heavy metals (lead, arsenic, thallium), alcohol

6. Infectious

• Leprosy — most common infectious cause of neuropathy worldwide; M. leprae directly invades Schwann cells
• HIV — distal sensory polyneuropathy; also antiretroviral toxic neuropathy
• Lyme disease (B. burgdorferi) — cranial neuropathy, radiculopathy, mononeuropathy multiplex
• Herpes zoster — postherpetic neuralgia; also rare motor neuropathy

7. Other Systemic Causes

• Vitamin B₁₂ deficiency — large-fiber + posterior column involvement (subacute combined degeneration)
• Amyloidosis — small-fiber + autonomic; autonomic dysfunction without diabetes → think amyloid
• Hypothyroidism, paraproteinaemia (MGUS, myeloma), sarcoidosis, paraneoplastic (anti-Hu, anti-CV2)

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Small-Fiber Neuropathy

• Diagnosis confirmed by skin punch biopsy (reduced intraepidermal nerve fiber density) or quantitative sensory testing
• Most common causes: diabetes / impaired glucose tolerance (GTT warranted even when fasting glucose is normal), amyloid, idiopathic

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Investigations

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Treatment Principles

Disease-Modifying

Neuropathic Pain Management

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