12.2 ENT Presentations: Infections, Epistaxis, Vertigo, Hearing Loss & Head and Neck Lumps

ENT Presentations: Infections, Epistaxis, Vertigo, Hearing Loss & Head and Neck Lumps

Acute ear, nose, and throat (ENT) presentations account for a substantial volume of emergency department attendances and acute primary care consultations. Clinical mastery requires distinguishing self-limiting viral illnesses from deep neck space infections, skull base osteomyelitis, refractory arterial epistaxis, and posterior fossa stroke mimicking peripheral vertigo.

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Acute Ear Infections & Complications

Acute Otitis Media (AOM)

Acute otitis media represents acute inflammation and effusion within the mucoperiosteal-lined middle ear cleft, most prevalent in children between 6 and 24 months due to short, horizontal, anatomically immature Eustachian tubes.

• Microbiology: Viral respiratory precursors (RSV, rhinovirus) commonly precede secondary bacterial infection driven by Streptococcus pneumoniae, non-typeable Haemophilus influenzae, and Moraxella catarrhalis.
• Clinical Presentation & Otoscopy: Severe acute otalgia, irritability, fever, and pulling at the ears. Otoscopic examination demonstrates an intensely erythematous, bulging tympanic membrane (TM) with cloudiness, loss of normal light reflex, and loss of landmarks (obscuration of the handle and lateral process of the malleus). Perforation of the TM causes a sudden relief of acute otalgia followed immediately by purulent, non-foul-smelling otorrhoea.
• Management Guidelines (NICE): Approximately 80% of uncomplicated cases resolve spontaneously within 3–7 days without antimicrobial therapy. Initial management focuses on regular analgesia with paracetamol and ibuprofen.
  • Indications for Immediate Oral Antibiotics: First-line oral amoxicillin (for 5–7 days; clarithromycin or erythromycin in penicillin allergy) is specifically indicated if:
    1. The patient is systemically unwell, toxic, or clinically compromised.
    2. The child is younger than 2 years of age with bilateral AOM.
    3. AOM is complicated by tympanic membrane perforation and purulent discharge.
    4. Symptoms fail to improve or deteriorate following 3 days of conservative observation (delayed prescription strategy).
• Critical Complication — Acute Mastoiditis: Spread of middle ear infection into the mastoid air cells produces acute osteitis. Manifests as persistent otalgia, high fever, post-auricular boggy swelling, erythema, tenderness over the mastoid tip, and anterior and inferior displacement (proptosis) of the pinna. Mastoiditis is an emergency requiring immediate admission, IV ceftriaxone, urgent high-resolution CT of the temporal bones, and possible cortical mastoidectomy.

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Acute Otitis Externa

Otitis externa ("swimmer's ear") is generalised inflammation of the skin lining the external auditory canal (EAC), commonly precipitated by swimming, water entry, mechanical trauma (cotton buds), or eczema.

• Microbiology: Pseudomonas aeruginosa (~60%) and Staphylococcus aureus (~30%) are the predominant pathogens; fungal superinfections (Aspergillus niger, Candida albicans) occur after prolonged antibiotic therapy.
• Clinical Features: Intense otalgia, pruritus, hearing fullness, and non-mucoid seropurulent ear discharge. Physical examination elicits exquisite tragal tenderness on direct palpation and severe pain upon traction of the pinna. Otoscopy reveals an erythematous, edematous EAC narrowed by inflammatory exudate and debris, whilst the TM remains intact and normal.
• Management: First-line therapy requires gentle aural toilet (microsuction or dry swabbing under direct vision), followed by topical antibiotic-corticosteroid combination ear drops (e.g. neomycin + dexamethasone or ciprofloxacin + dexamethasone) for 7–14 days. If canal edema prevents drop penetration, insert an expandable Pope sponge ear pack/wick to stent the canal and facilitate delivery. Aminoglycoside drops are contraindicated if tympanic membrane perforation cannot be excluded, due to ototoxicity risk.

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Malignant (Necrotising) Otitis Externa

Malignant otitis externa is an aggressive, life-threatening osteomyelitis of the temporal bone and skull base, caused almost exclusively by Pseudomonas aeruginosa tracking through the fissures of Santorini from the external auditory canal.

• Demographics & Risk Factors: Predominantly occurs in elderly patients with poorly controlled diabetes mellitus or severely immunocompromised individuals (e.g. haematological malignancy, advanced HIV, chemotherapy).
• Clinical Hallmarks: Severe, relentless, boring otalgia that is characteristically unremitting and worse at night, preventing sleep and failing to respond to standard analgesia or topical drops. Otoscopy reveals a classic pathognomonic finding: granulation tissue at the floor of the external auditory canal at the junction between the cartilaginous and bony meatus.
• Neurological Complications: Progressive osteomyelitis invades the stylomastoid foramen, resulting in facial nerve palsy (cranial nerve VII) with unilateral facial droop. Further advancement to the jugular foramen compromises cranial nerves IX, X, and XI (Vernet's syndrome), and hypoglossal nerve XII.
• Emergency Investigation & Care:
  • Markedly elevated inflammatory markers (ESR characteristically >80–100 mm/h and CRP).
  • Urgent CT of the temporal bones and skull base: Demonstrates cortical bone erosion, osteolysis, and soft tissue invasion.
  • Management: Immediate hospital admission under ENT; long-term high-dose intravenous anti-pseudomonal therapy (e.g. IV ciprofloxacin or IV ceftazidime) continued for a minimum of 6–12 weeks until resolution is confirmed by serial Gallium-67 radioisotope scans or MRI; strict optimization of glycaemic control.

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Acute Throat Infections: Tonsillitis & Quinsy

Acute Tonsillitis

Acute tonsillitis represents acute bacterial or viral infection of the palatine tonsils. Approximately 70% of cases are viral (rhinovirus, adenovirus, EBV), while 30% are caused by Group A Beta-Haemolytic Streptococcus (GABHS / Streptococcus pyogenes).

• Clinical Stratification Scores: Clinical decision tools identify patients who derive true benefit from antibiotic therapy:

• First-Line Antibiotic Therapy: When indicated by Centor ≥3 or FeverPAIN ≥4, the antibiotic of choice (NICE NG84) is phenoxymethylpenicillin (penicillin V) 500 mg four times daily (or 1 g twice daily) for 5–10 days; a 5-day course is usually enough for symptom resolution, with longer courses used where eradication matters. For penicillin allergy, use clarithromycin (or erythromycin in pregnancy) for 5 days.

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Peritonsillar Abscess (Quinsy)

A peritonsillar abscess (quinsy) is a collection of purulent material between the fibrous capsule of the palatine tonsil and the superior pharyngeal constrictor muscle, almost always arising as an acute complication of bacterial tonsillitis.

• Clinical Presentation: The patient presents with severe, progressive, almost invariably unilateral sore throat, high-grade fever, systemic lethargy, and severe ipsilateral referred otalgia. Characteristic examination findings include:
  • Severe Trismus: Marked inability to open the mouth secondary to inflammatory irritation and reflex spasm of the adjacent internal pterygoid muscle.
  • "Hot Potato" Voice: Thickened, muffled speech resulting from pharyngeal distortion.
  • Oropharyngeal Distortion: Drooling and pooling of saliva; marked unilateral enlargement of the affected tonsil bulging forward and medially, pushing the edematous uvula across to the contralateral normal side.
• Emergency Management Protocol:
  1. Immediate ENT Referral: Quinsy is an airway-threatening infection.
  2. Definitive Pus Drainage: Urgent needle aspiration (using a 16G/18G needle with a guarded sheath to prevent carotid puncture) or formal incision and drainage (I&D) of the superior peritonsillar space under local anaesthetic spray.
  3. Intravenous Antimicrobial Therapy: IV broad-spectrum antibiotics covering streptococci and oral anaerobes (e.g. IV co-amoxiclav or ceftriaxone + metronidazole).
  4. Systemic Corticosteroids: A single dose of IV dexamethasone (8 mg) dramatically reduces pharyngeal edema, relieves trismus, and accelerates recovery.

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Epistaxis: Stepped Management Protocol

Epistaxis occurs in up to 60% of the population, exhibiting a bimodal age distribution (<10 years and >50 years).

• Vascular Anatomy:
  • Anterior Epistaxis (~90%): Arises from Little's area on the anterior inferior nasal septum, home to Kiesselbach's plexus—an anastomosis of 5 arterial supplies: anterior ethmoidal artery, posterior ethmoidal artery, sphenopalatine artery, greater palatine artery, and the superior labial artery.
  • Posterior Epistaxis (~10%): Arises posteriorly from the sphenopalatine artery or Woodruff's venous plexus on the lateral nasal wall; predominantly affects elderly, hypertensive, and atherosclerotic patients, manifesting with profuse arterial bleeding streaming down the posterior pharynx.

                         [ Epistaxis Presentation ]
                                     │
                [ STEP 1: Trotter's First-Aid Manoeuvre ]
                • Sit upright, head tilted forward
                • Pinch soft lower cartilaginous nose firmly for 10-15 min
                • Ice pack on bridge of nose, mouth breathing
                                     │
                       ┌─────────────┴─────────────┐
                       ▼                           ▼
              [ Bleeding Arrested ]       [ Persistent Bleeding ]
                       │                           │
             Apply topical antiseptic      [ STEP 2: Anterior Rhinoscopy ]
             (Naseptin cream for 10d)      • Evacuate clots, apply topical
                                             anaesthetic/vasoconstrictor
                                                   │
                                     ┌─────────────┴─────────────┐
                                     ▼                           ▼
                          [ Vessel Visualised ]        [ Vessel NOT Visualised ]
                                     │                           │
                            [ Silver Nitrate ]         [ STEP 3: Anterior Pack ]
                            • 3-5 sec around/on vessel • Rapid Rhino or Merocel
                            • One side of septum only  • Admit / ENT review
                            • Discharge with Naseptin  • Prophylactic antibiotics
                                                                 │
                                                       [ Ongoing Bleeding ]
                                                                 │
                                                       [ STEP 4: Posterior Pack ]
                                                       • Double-balloon catheter / Foley
                                                       • Emergency surgical ligation
                                                         (ESPAL) or embolisation

• Step 1 (First Aid / Trotter's Manoeuvre): Seat patient upright with head tilted forward (preventing swallowing of blood, nausea, and airway aspiration). Instruct the patient to compress the soft, cartilaginous lower third of the nose firmly and continuously for 10–15 uninterrupted minutes while breathing through the mouth. Apply ice packs to the forehead or bridge of the nose to induce reflex vasoconstriction.
• Step 2 (Direct Visualisation & Silver Nitrate Cautery): If bleeding persists beyond 15 minutes, perform anterior rhinoscopy using a Thudichum speculum and headlight after having the patient blow out clots. Insert cotton pledgets soaked with a topical local anaesthetic and vasoconstrictor (e.g. 5% lidocaine with 0.5% phenylephrine or cophenylcaine spray) for 5 minutes. If an active bleeding vessel is identified on Little's area, apply a silver nitrate stick for 3–5 seconds directly to the vessel periphery and then its centre. Crucial rule: Cauterise only one side of the nasal septum during a single session to avoid bilateral mucosal ischaemia, cartilage necrosis, and permanent septal perforation. Prescribe topical Naseptin cream (chlorhexidine + neomycin; check peanut/soya allergy) twice daily for 10 days.
• Step 3 (Anterior Nasal Packing): If chemical cautery fails or the bleeding source is diffuse, insert an anterior nasal pack (inflatable carboxymethylcellulose Rapid Rhino soaked in sterile water, or PVA Merocel lubricated with saline). Packing usually requires admission or formal observation; prophylactic antibiotics are not routinely needed for anterior packs and are given only according to local ENT policy.
• Step 4 (Posterior Nasal Packing & Surgical Intervention): Refractory epistaxis draining persistently down the oropharynx despite anterior packing necessitates a posterior balloon pack (dedicated double-cuff catheter or a 12F–14F Foley catheter inflated with 10 mL saline in the nasopharynx) and urgent transfer to theater for endoscopic sphenopalatine artery ligation (ESPAL) or interventional radiologic arterial embolisation.

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Vertigo: Peripheral vs Central Differentiation

Vertigo is the illusion of motion (typically rotational spinning) of the patient or their visual surroundings, reflecting vestibular pathway pathology. The primary clinical imperative is differentiating benign peripheral vestibular dysfunction from life-threatening central brainstem or cerebellar stroke.

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Peripheral Vertigo Syndromes

1. Benign Paroxysmal Positional Vertigo (BPPV):

   • Pathophysiology: Canalithiasis; dislodged calcium carbonate crystals (otoconia) from the utricle float into the semicircular canals (posterior semicircular canal in >85% of cases).
   • Clinical Presentation: Recurrent, sudden, brief attacks of violent rotational vertigo lasting strictly <60 seconds, provoked exclusively by changes in head position relative to gravity (turning over in bed, looking up, bending down). Completely normal hearing; no tinnitus.
   • Diagnostic Gold Standard: Dix-Hallpike Manoeuvre: Turn patient's head 45° to one side, rapidly lay them supine with head extended 20° over the edge of the bed. Positive test: after a latency period of 5–20 seconds, paroxysmal torsional, geotropic upbeating nystagmus appears, lasting <60 seconds, accompanied by vertigo. Nystagmus fatigues upon repeated testing.
   • Definitive Treatment: Epley particle repositioning manoeuvre (rotates the head through 4 sequential positions to guide canaliths back into the utricle; curative in >80% on first attempt). Note: Vestibular sedatives (e.g. prochlorperazine) are not indicated for BPPV as they delay central compensation and fail to treat canalithiasis.

2. Vestibular Neuritis vs Acute Labyrinthitis:

   • Pathophysiology: Viral or post-viral inflammatory neuropathy affecting the 8th cranial nerve.
   • Clinical Comparison: Both present with the abrupt onset of severe, continuous, disabling rotational vertigo lasting 2–3 days, accompanied by intense nausea, vomiting, horizontal nystagmus beating away from the affected ear, and severe gait unsteadiness.
   • Crucial Distinguishing Feature: In Vestibular Neuritis, cochlear function is entirely preserved (hearing is completely normal; no tinnitus). In Acute Labyrinthitis, the inflammatory process involves both the vestibular and cochlear labyrinths, producing vertigo PLUS sudden unilateral sensorineural hearing loss and tinnitus.
   • Management: Short-course vestibular sedatives (e.g. buccal or oral prochlorperazine 5–10 mg TDS, or cyclizine) strictly limited to the first 48–72 hours (maximum 3 days). Prolonged administration must be avoided because it blocks central brainstem vestibular compensation. Encourage early mobilisation and Cawthorne-Cooksey vestibular rehabilitation exercises.

3. Meniere's Disease (Endolymphatic Hydrops):

   • Pathophysiology: Excessive accumulation of endolymphatic fluid within the inner ear due to inadequate resorption by the endolymphatic sac.
   • The Diagnostic Tetrad: Recurrent spontaneous vertigo attacks lasting 20 minutes to several hours (typically 2–4 hours); fluctuating, low-frequency sensorineural hearing loss; roaring unilateral tinnitus; and a sensation of aural fullness in the affected ear.
   • Management: Acute attacks: oral or IM prochlorperazine. Prophylactic maintenance: dietary restriction of salt (<2 g/day), caffeine, and alcohol, combined with oral betahistine (H1 agonist / H3 antagonist to enhance inner ear microvascular perfusion).

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Hearing Loss, Chronic Ear Disease & Sinusitis

Tuning Fork Tests

• Sudden sensorineural hearing loss (developing over 3 days or less, with no obvious external or middle ear cause) is an emergency: NICE NG98 advises immediate referral (to be seen within 24 hours) to ENT or audiovestibular medicine if it started within the past 30 days. Early oral corticosteroids are given by the specialist, and MRI of the internal auditory meati looks for a vestibular schwannoma in unilateral or asymmetrical loss.
• Otitis media with effusion (glue ear): the commonest cause of hearing loss in children; active observation for 3 months, then hearing aids or grommets if hearing loss persists.
• Cholesteatoma: a growth of keratinising squamous epithelium in the middle ear, causing chronic painless, foul-smelling discharge and conductive hearing loss, with a retraction pocket or crust in the attic (pars flaccida). It erodes bone and can cause facial palsy, vertigo, meningitis or brain abscess, so it needs ENT referral for surgical removal.

Acute Rhinosinusitis (NICE NG79)

Nasal blockage or discharge with facial pain or pressure and reduced smell, usually after a cold.

• Symptoms for 10 days or less: no antibiotic; self-care with analgesia (most are viral and settle within 2–3 weeks).
• Symptoms for more than 10 days without improvement: no antibiotic, a back-up antibiotic, or a high-dose nasal corticosteroid for 14 days (age 12 and over).
• Antibiotic if systemically very unwell or at high risk of complications: phenoxymethylpenicillin for 5 days (co-amoxiclav if very unwell or worsening).
• Red flags needing same-day referral: periorbital swelling or redness, displaced eye, double vision or reduced acuity, severe frontal headache, meningism or neurological signs (orbital or intracranial spread).

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Head & Neck Lumps and Cancer

Risk factors: smoking, alcohol, betel quid and HPV (oropharyngeal cancer, increasingly common in younger adults).

Thyroid Nodules

Check thyroid function. Most nodules are benign; a suppressed TSH suggests a hyperfunctioning ("hot") nodule, which is rarely malignant. Assess with ultrasound (graded by appearance, such as the British Thyroid Association U1–U5 system) and fine-needle aspiration of suspicious nodules. Red flags needing urgent referral include stridor (same-day), rapid growth, voice change, a hard fixed nodule, cervical lymphadenopathy, a nodule in a child, or previous neck irradiation. Thyroid cancers are mostly papillary (good prognosis, lymphatic spread), follicular (haematogenous spread), medullary (calcitonin, MEN2) and anaplastic (older people, rapid growth, poor prognosis).

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Nasal Polyps

Benign inflammatory swellings in adults with chronic rhinosinusitis, causing nasal blockage, discharge and loss of smell; they are usually bilateral, pale and insensitive to touch. Associations include asthma and aspirin-exacerbated respiratory disease (asthma, polyps and aspirin or NSAID sensitivity) and cystic fibrosis (polyps in a child). Treatment is intranasal corticosteroid (drops or spray), short oral steroid courses for severe disease, and endoscopic sinus surgery if needed. Unilateral polyps, bleeding, pain or a polyp in a child need ENT referral to exclude malignancy or other causes.