20.1 Dizziness, Vertigo & Epistaxis
Key Takeaways
- Disorders of the nose and paranasal sinuses, diseases of the ear, diseases of the oral cavity and pharynx, and diseases of the larynx and airway are the four enumerated subsections.
- Benign paroxysmal positional vertigo is diagnosed by the Dix-Hallpike maneuver and treated with the Epley repositioning maneuver.
- A normal head impulse test, direction-changing nystagmus or skew deviation indicates a central cause of acute vestibular syndrome.
- Early magnetic resonance imaging can miss small posterior circulation infarcts, so a reassuring scan does not override concerning examination findings.
- Most epistaxis is anterior and controlled with direct pressure and topical vasoconstriction, while posterior bleeding requires packing and specialist care.
Last updated: August 2026
Disorders of the ear, nose, throat, and vestibular apparatus represent a large volume of ambulatory encounters and urgent hospital admissions. A structured clinical approach to dizziness, cranial neuropathies, deep neck space infections, epistaxis, and acute hearing loss is a high-yield competency for the ABIM exam.
1. Clinical Approach to Dizziness & Vertigo
The initial diagnostic step in any patient presenting with "dizziness" is categorizing the symptom into one of four distinct clinical subtypes:
- Vertigo (Vestibular): The false illusion of rotational motion, spinning, tilting, or swaying of the self or the environment. Reflects asymmetric neural input within the vestibular pathways (peripheral labyrinth/vestibular nerve vs central brainstem/cerebellum).
- Presyncope (Cardiovascular / Hemodynamic): Sensation of impending loss of consciousness, lightheadedness, diaphoresis, and graying-out of vision. Reflects global transient cerebral hypoperfusion (orthostatic hypotension, cardiac dysrhythmias, vasovagal syncope, aortic stenosis).
- Disequilibrium (Neuromuscular / Proprioceptive): Sensation of unsteadiness, imbalance, and wobbliness experienced exclusively while standing or ambulating, without a spinning sensation. Reflects peripheral sensory polyneuropathy, bilateral vestibulopathy, Parkinsonian gait disorders, cerebellar ataxia, or visual impairment.
- Non-Specific Lightheadedness / Psychogenic: Vague, floating, disconnected feeling often accompanied by chronic anxiety, panic disorder, hyperventilation, or Persistent Postural-Perceptual Dizziness (PPPD).
Peripheral vs. Central Vertigo: Key Clinical Distinctions
| Clinical Parameter | Peripheral Vertigo (Labyrinth / CN VIII) | Central Vertigo (Brainstem / Cerebellum) |
|---|---|---|
| Onset & Severity | Sudden, explosive onset; intense spinning; severe nausea and vomiting | Gradual or sudden; moderate or mild spinning sensation; variable nausea |
| Episode Duration | Seconds (BPPV), minutes to hours (Ménière), days with rapid improvement (Vestibular Neuritis) | Constant, persistent, lasting days to weeks without spontaneous compensation |
| Nystagmus Characteristics | Unidirectional horizontal-torsional; fast phase beats away from affected ear; suppresses with visual fixation; does NOT change direction with eccentric gaze | Direction-changing horizontal, pure vertical (downbeat/upbeat), or pure torsional; does NOT suppress with visual fixation |
| Auditory Symptoms | Common (tinnitus, fluctuating low-frequency sensorineural hearing loss, aural fullness in Ménière/Labyrinthitis) | Rare (unless AICA territory infarction involving the internal auditory artery) |
| Postural Instability & Gait | Mild to moderate; patient can ambulate independently with caution; leans toward lesion side | Severe ataxia / postural imbalance; patient unable to stand or walk unassisted, even with eyes open |
| Neurological Signs | Absent (strictly isolated vestibular/auditory signs) | Present (dysmetria, dysdiadochokinesia, Horner syndrome, facial numbness, diplopia, dysarthria, limb weakness) |
| Common Etiologies | BPPV, Vestibular Neuritis, Labyrinthitis, Ménière Disease | Posterior circulation ischemic stroke (PICA/AICA/Vertebrobasilar), Cerebellar hemorrhage, Multiple Sclerosis plaque |
| Visual Fixation Effect | Nystagmus inhibited/suppressed by visual fixation | Nystagmus unaffected or accentuated by visual fixation |
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2. Specific Vertigo Syndromes & the HINTS Examination
Benign Paroxysmal Positional Vertigo (BPPV)
- Pathophysiology: Mechanical disorder caused by displaced calcium carbonate crystals (otoconia) from the utricular macula that migrate into the semicircular canals (canalithiasis, involving the posterior semicircular canal in 85–90% of cases).
- Clinical Presentation: Recurrent, sudden episodes of brief, severe spinning vertigo lasting <60 seconds, provoked specifically by head position changes relative to gravity (rolling over in bed, tilting head back ["top-shelf vertigo"], bending over).
- Diagnostic Maneuver — Dix-Hallpike Test: Patient is seated, head turned 45 degrees toward the tested ear, then rapidly lowered into a supine position with the neck extended 20–30 degrees over the table edge. A positive test elicits:
- Latency: 2 to 10 second delay before onset of vertigo and nystagmus.
- Nystagmus: Mixed torsional and upbeating geotropic nystagmus (beating toward the lower, dependent ear).
- Duration & Fatigability: Vertigo and nystagmus resolve in <60 seconds and fatigue (diminish in intensity) with repeated testing.
- Definitive Management: Epley Canalith Repositioning Maneuver (moves canaliths out of the posterior semicircular canal back into the utricle; achieves >85–90% resolution in 1–2 sessions). Board Pearl: Vestibular suppressant drugs (e.g., Meclizine, Benzodiazepines) are NOT recommended for routine BPPV because they do not clear canaliths, cause sedation, and delay central vestibular compensation.
Vestibular Neuritis vs. Labyrinthitis
- Pathophysiology: Presumed viral infection or reactivation (HSV-1) affecting the vestibular branch of cranial nerve VIII.
- Clinical Presentation: Acute Vestibular Syndrome (AVS) — sudden onset of severe, continuous, unremitting vertigo, postural instability, nausea, and vomiting lasting several days (2–7 days), gradually improving over weeks.
- Key Distinction:
- Vestibular Neuritis: Isolated vestibular nerve involvement -> Normal auditory function (no hearing loss, no tinnitus).
- Labyrinthitis: Involvement of both vestibular and cochlear branches / labyrinth -> Acute unilateral sensorineural hearing loss and tinnitus accompanied by vertigo.
- Treatment: Short-term vestibular suppressants (Meclizine 25–50 mg q8h or Diazepam 2–5 mg q8h) strictly limited to the first 24 to 72 hours to avoid hindering central neuroplastic vestibular compensation; oral corticosteroids (Prednisone 60 mg/day tapered over 10–14 days); early vestibular rehabilitation therapy.
Ménière Disease (Endolymphatic Hydrops)
- Pathophysiology: Excess accumulation and increased hydraulic pressure of endolymph within the membranous labyrinth leading to episodic distension and micro-ruptures.
- Diagnostic Clinical Tetrad:
- Spontaneous episodic vertigo lasting 20 minutes to 12 hours
- Fluctuating low-frequency sensorineural hearing loss (documented on audiometry)
- Low-pitched roaring tinnitus
- Sensation of aural fullness / pressure in the affected ear
- Management Strategy:
- Acute Attacks: Antiemetics (Ondansetron), short-term vestibular suppressants (Meclizine, Diazepam).
- Chronic Maintenance & Prevention: Dietary sodium restriction (<2000 mg/day), avoidance of caffeine, alcohol, and nicotine; maintenance oral diuretics (Hydrochlorothiazide 25 mg / Triamterene 37.5 mg daily or Acetazolamide).
- Refractory Cases: Intratympanic dexamethasone injections; Intratympanic Gentamicin (chemical vestibular ablation; carries risk of hearing loss); endolymphatic sac decompression.
Acute Vestibular Syndrome & the HINTS Exam
The HINTS examination (Head Impulse, Nystagmus, Test of Skew) is a validated 3-step bedside oculomotor evaluation used to differentiate a central posterior circulation cerebellar/brainstem stroke from a benign peripheral vestibular neuritis in patients presenting with Acute Vestibular Syndrome (acute continuous vertigo, spontaneous nystagmus, and nausea). In the first 24–48 hours of stroke onset, HINTS has a sensitivity of 99% and specificity of 96%, outperforming early diffusion-weighted MRI (DWI-MRI can yield false negatives in up to 12–20% of acute small posterior fossa infarctions).
The "INFARCT" Central Rule (Any ONE Central Finding Indicates Stroke):
- Impulse Normal: Head Impulse Test (HIT) is NORMAL / Negative (the patient can maintain steady visual fixation on the examiner's nose during a rapid passive horizontal head thrust without needing a corrective catch-up saccade). This proves the peripheral reflex arc (CN VIII) is fully intact, localizing the lesion to the central vestibular pathways.
- Fast-phase Alternating: Direction-changing gaze-evoked nystagmus (nystagmus beats right on rightward gaze, and beats left on leftward gaze) OR pure vertical/torsional nystagmus. Central nystagmus does not suppress with visual fixation.
- Refixation on Cover Test: Skew Deviation present (on alternate eye cover testing, covering and uncovering an eye reveals a vertical refixation movement, indicating central vertical ocular dysconjugacy).
3. Epistaxis Management
Epistaxis is categorized anatomically into anterior and posterior bleeding, which dictate vastly different clinical risks and intervention ladders.
| Parameter | Anterior Epistaxis (90% of cases) | Posterior Epistaxis (10% of cases) |
|---|---|---|
| Vascular Source | Kiesselbach Plexus (Little's Area) on anterior inferior nasal septum (anastomosis of anterior ethmoidal, sphenopalatine, superior labial, and greater palatine arteries) | Woodruff Plexus / Sphenopalatine Artery branches located on the posterior lateral nasal wall / posterior septum |
| Patient Demographics & Triggers | Children, young adults; digital trauma (nose picking), dry air, allergic rhinitis, upper respiratory infections | Older adults; systemic hypertension, severe atherosclerosis, anticoagulation, coagulopathies |
| Clinical Presentation | Unilateral bleeding from anterior nares; brisk but easily visualized bleeding site | Profuse, torrential bilateral bleeding draining down the posterior pharynx; blood swallowed, risk of airway compromise |
| Stepwise Management | Step 1: Direct continuous compression of nasal alae (pinching soft lower third of nose) for 10–15 minutes with head tilted forward.<br/>Step 2: Topical vasoconstrictor (Oxymetazoline 0.05% or Phenylephrine spray) + local anesthetic (Lidocaine 4%) + repeat compression for 10 min.<br/>Step 3: Chemical cautery with Silver Nitrate applicator directly to visible bleeding vessel (apply for 4–5 sec; never cauterize both sides of septum simultaneously due to perforation risk).<br/>Step 4: Anterior Nasal Packing (Rapid Rhino, Merocel sponge) left for 48–72 hours; oral antistaphylococcal antibiotics (Cephalexin or Augmentin) to prevent Toxic Shock Syndrome. | EMERGENCY Management:<br/>1. Posterior Nasal Balloon Packing (Epistat double-balloon catheter or 10–14 Fr Foley catheter inflated with 10–15 mL sterile saline and pulled snug against posterior choana).<br/>2. Mandatory Inpatient Admission to a monitored telemetry/ICU bed (high risk of hypoxemia, hypercapnia, vagally mediated bradycardia/arrhythmias, and airway obstruction).<br/>3. Urgent ENT Consultation for endoscopic sphenopalatine artery ligation (ESPAL) or interventional radiology embolization. |
Test Your Knowledge
A 64-year-old man with a history of hypertension and hyperlipidemia presents to the emergency department with sudden, severe, continuous spinning vertigo, nausea, and vomiting that began 6 hours ago. He is severely unsteady and unable to sit or stand without assistance. On physical examination, spontaneous horizontal nystagmus is noted that beats to the right on rightward gaze and beats to the left on leftward gaze. During the Head Impulse Test (HIT), the patient successfully maintains visual fixation on the examiner's nose without requiring a corrective catch-up saccade. On alternate cover testing, an upward corrective refixation movement of the left eye is observed when uncovered (skew deviation). A non-contrast head CT is completely normal. What is the most appropriate next step in management?
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