9.2 Otitis Media, Epistaxis & Vertigo

Management of Middle and External Ear Infections

Ear pain (otalgia) and discharge (otorrhea) are frequent reasons for consultation. Accurately localizing the pathology to either the external canal or the middle ear space is the key to appropriate therapy.

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Differentiating Otitis Media and Otitis Externa

1. Acute Otitis Media (AOM)

AOM is a bacterial infection of the middle ear fluid, most common in young children due to their shorter, more horizontal eustachian tubes.

• Diagnosis: Requires acute onset of symptoms, middle ear effusion (documented by bulging TM or decreased mobility on pneumatic otoscopy), and signs of middle ear inflammation (erythema or otalgia).
• Management:
  • First-line: High-dose oral amoxicillin (80–90 mg/kg/day) divided into two doses.
  • Alternative (Penicillin Allergy): Cefdinir, cefuroxime, or azithromycin (in severe anaphylactic allergies).
  • Second-line / Treatment Failure (no improvement in 48-72 hours): Amoxicillin-clavulanate (90 mg/kg/day of amoxicillin component) to cover beta-lactamase producing organisms.
  • Complications: Mastoiditis, meningitis, tympanic membrane perforation.

2. Acute Otitis Externa (AOE)

Commonly known as "swimmer's ear," AOE is an infection of the external auditory canal skin.

• Diagnosis: Characterized by intense pain on manipulation of the auricle or tragus, canal swelling, and white/yellow discharge.
• Management: Topical therapy is highly effective because it delivers high concentrations of medication directly to the site of infection.
  • First-line: Topical fluoroquinolone-corticosteroid drops (e.g., ciprofloxacin 0.3% / dexamethasone 0.1%).
  • Alternative: Neomycin/polymyxin B/hydrocortisone drops. Note: Avoid neomycin-containing drops if the tympanic membrane is perforated or cannot be fully visualized, as aminoglycosides are ototoxic.
  • Severe Cases: If the canal is completely occluded, insert an ear wick to facilitate drug delivery.

Epistaxis Management: Stepwise Clinical Protocols

Epistaxis is classified by the anatomical source of bleeding. Proper localization guides the clinical response.

1. Anterior Epistaxis

• Source: Over 90% of bleeds arise from Kiesselbach's plexus (an anastomosis of five arteries: sphenopalatine, anterior ethmoidal, greater palatine, septal branch of superior labial, and ophthalmic) on the anterior nasal septum.
• Stepwise Management:
  1. Direct Compression: Instruct the patient to blow out clots, then apply firm, continuous pressure to the cartilaginous nasal flares (pinching the nostrils) for 10–15 minutes. The patient must lean forward to prevent swallowing blood.
  2. Topical Vasoconstrictors: If pressure fails, apply topical vasoconstrictors, such as oxymetazoline 0.05% spray or a cotton pledget soaked in epinephrine or cocaine solution.
  3. Chemical Cautery: If a single bleeding vessel is clearly visible on the anterior septum, perform chemical cauterization using silver nitrate sticks. Apply the tip to the surrounding mucosa first, then directly to the bleeding point for 3–5 seconds. Caution: Never cauterize both sides of the nasal septum during the same visit, as this can cause ischemic necrosis leading to septal perforation.
  4. Anterior Packing: If cauterization fails, insert an anterior nasal pack (e.g., Merocel nasal tampon or pneumatic balloon tamponade). Packs are typically left in place for 24–72 hours. Prophylactic oral antibiotics (e.g., cephalexin or amoxicillin-clavulanate) are often prescribed to reduce the risk of toxic shock syndrome, although evidence is mixed.

2. Posterior Epistaxis

• Source: Arises from the sphenopalatine artery (Woodruff's plexus) in the posterior nasal cavity. More common in patients with pre-existing hypertension, atherosclerosis, coagulopathies, or those on anticoagulant therapy.
• Clinical Presentation: Profuse bleeding from both nares, blood dripping rapidly down the posterior oropharynx even when anterior pressure is applied, and failure to control bleeding with anterior packing.
• Management: Requires posterior nasal packing using a double-balloon catheter (e.g., Epistat) or a Foley catheter.
• Critical Safety Directive: Posterior packing is highly painful and stimulates the nasopulmonary reflex, which can cause significant vagal stimulation, hypoventilation, hypoxemia, and bradycardia. All patients requiring posterior packing must be admitted to the hospital with continuous cardiac monitoring and pulse oximetry. Surgical ligation of the sphenopalatine artery or endovascular embolization is indicated if packing fails.

Differential Diagnosis of Peripheral Vertigo

Vertigo is the illusion of motion, typically spinning. Differentiating peripheral (inner ear) from central (brainstem/cerebellum) causes is a core clinical skill. Peripheral vertigo is characterized by horizontal-torsional, unidirectional nystagmus that is fatigable and suppressed by visual fixation.

1. Benign Paroxysmal Positional Vertigo (BPPV)

• Pathophysiology: Calcium carbonate crystals (otoconia) dislodge from the utricle and migrate into the semicircular canals (usually the posterior canal).
• Clinical Features: Recurrent, brief episodes of vertigo (lasting less than 60 seconds) triggered by specific head movements (e.g., rolling over in bed, tilting the head back). No hearing loss or tinnitus.
• Diagnosis: Dix-Hallpike maneuver, which elicits geotropic, torsional, upbeating nystagmus after a brief latency of a few seconds. The nystagmus is fatigable (decreases with repeated testing).
• Management: Epley maneuver (canalith repositioning). Vestibular suppressants (e.g., meclizine) are ineffective and contraindicated, as they do not resolve the mechanical issue and can delay recovery.

2. Meniere's Disease (Endolymphatic Hydrops)

• Pathophysiology: Increased volume and pressure of endolymph within the membranous labyrinth.
• Clinical Features: Episodic vertigo lasting 20 minutes to several hours, accompanied by fluctuating low-frequency sensorineural hearing loss, low-pitched tinnitus, and a sensation of aural fullness in the affected ear.
• Management:
  • Acute Attacks: Vestibular suppressants (meclizine, benzodiazepines) and antiemetics.
  • Maintenance: Lifestyle modifications including a strict low-sodium diet (<2,000 mg/day), avoiding caffeine, alcohol, and nicotine. Oral diuretics (e.g., hydrochlorothiazide) or betahistine can be used to prevent attacks.

3. Vestibular Neuritis and Labyrinthitis

• Pathophysiology: Post-viral inflammatory condition of the vestibular portion of cranial nerve VIII (vestibular neuritis) or both the vestibular and cochlear branches (labyrinthitis).
• Clinical Features: Sudden, severe, continuous vertigo lasting days, accompanied by nausea, vomiting, and gait instability.
  • Vestibular Neuritis: Hearing is preserved.
  • Labyrinthitis: Associated with unilateral sensorineural hearing loss and/or tinnitus.
• Exam Findings: Unidirectional, horizontal nystagmus beating away from the affected side, and an abnormal head impulse test (catch-up saccades when turning head toward the lesion).
• Management:
  • Symptomatic: Short-term vestibular suppressants (e.g., meclizine 25mg or diazepam 2-5mg every 6 hours) for the first 48–72 hours only (prolonged use delays central vestibular compensation).
  • Anti-inflammatory: A 10-14 day course of oral prednisone initiated early improves functional recovery. Vestibular rehabilitation exercises are recommended for persistent imbalance.