Chapter 7Head and Neck Examination (excluding Lymph Nodes)

Pediatric Ear Pain – [1, 3]

• Otalgia (ear pain): Can be divided into:
  • Primary otalgia (pain originating from ear – commonly acute otitis media, AOM; or otitis externa)
  • Secondary otalgia (pain originating from outside the ear – commonly temporomandibular joint disorders, dental infections, or malignancies of the pharynx/larynx)
• Onset: Acute vs. chronic?
  • Acute otalgia:
    • Head trauma; barotrauma (e.g. diving, airplane, noise) → e.g. Tympanic Membrane (TM) perforation
    • Recent upper respiratory tract infection (URTI) or seasonal allergies? → e.g. Acute otitis media
    • History of tympanostomy tubes, myringoplasty → e.g. Recurrent acute otitis media
    • Recent swimming or prior ear instrumentation → e.g. Otitis externa, Foreign body
    • Pain out of proportion to exam findings → e.g. Herpez zoster oticus (Ramsay Hunt Syndrome – also presents with tinnitus, hearing loss, vertigo, vesicular rash/crusting of ear, and ipsilateral facial paralysis)
  • Chronic otalgia:
    • Primary causes: e.g. Mastoiditis (otitis media complication, may be acute or subacute), necrotizing otitis externa, or cholesteatoma (sense of aural fullness)
    • Secondary causes: e.g. Temporomandibular joint disorders, dental infections, or head/neck tumors
• Provoking/Palliating:
  • Worse with manipulation of tragus/ear → e.g. Otitis externa
  • Worse with eating/chewing:
    • Primary causes: e.g. necrotizing otitis externa or malignancy - extending to temporomandibular joint
    • Secondary causes: e.g. Temporomandibular joint disorders, dental infection (e.g. worse with hot or cold foods), head and neck malignancies (typically with swallowing – odynophagia)
• Quality: Throbbing? Sharp/stabbing?
• Region: Post-auricular pain/swelling → e.g. mastoiditis
• Severity:
  • Otalgia severity suddenly reduced spontaneously → e.g. TM perforation
  • Otitis externa may vary from pruritus (itching) to severe pain.
  • Severe Pain: e.g. Necrotizing otitis externa; Mastoiditis; HZV oticus (pain out of proportion to exam)
• Timing:
  • Intermittent: Consider secondary otalgia e.g. Temporomandibular joint disorders or dental infections.
  • Constant: Consider primary otalgia e.g. AOM, Otitis Externa, Necrotizing Otitis Externa, Mastoiditis
• Associated Symptoms:
  • Hearing Loss:
    • Acute: e.g. Otitis media with effusion; Otitis externa; foreign body; TM perforation; Herpes zoster oticus
    • Chronic: e.g. Head/Neck malignancy; or Cholesteatoma (also presents with aural fullness)
  • Otorrhea (Fluid/discharge from ear) suggests a primary otalgia cause:
    • Acute: Otalgia generally precedes otorrhea in acute otitis media, whereas otalgia occurs concurrently with otorrhea in Otitis externa. Also consider necrotizing otitis externa, mastoiditis.
    • Chronic: e.g. chronic otitis media or cholesteatoma (typically malodorous drainage)
  • Vertigo: Consider inner ear involvement – e.g. labyrinthitis (inner ear infection), Herpes zoster oticus (Ramsay Hunt Syndrome)
  • Bruxism (grinding teeth at night): ↑ likelihood of Temporomandibular joint syndrome or dental causes.
  • Dysphagia (difficulty swallowing), Odynophagia (painful swallowing), Hoarseness of voice:
    • Acute: e.g. Deep Neck Space infection (e.g. retropharyngeal abscess or peritonsillar abscess – Can’t Miss Diagnoses requiring urgent assessment/intervention)
    • Chronic: e.g. head/neck cancer (e.g. pharyngeal, laryngeal tumor) – especially if >50 years old and history of smoking / alcohol abuse
  • High Fever (>40°C): Assess for infectious etiology other than acute otitis media (e.g. meningitis, necrotizing otitis externa, mastoiditis)
  • Headache: e.g. rhinosinusitis; necrotizing otitis externa; mastoiditis – or referred causes such as meningitis; brain abscess; or cavernous sinus thrombosis
• Pediatric Presentation: Otalgia may present with non-verbal behaviors such as ear rubbing/tugging; crying; refusal to eat/drink, particularly if patient is unable to articulate their pain verbally (e.g. infants)

• Hearing Loss Definition: The complete or partial inability to hear – with loss exceeding 25 decibels (dB) at frequencies between 250 and 8000 Hz. Note that conversational speech is at 45-60 dB.
  • Sensorineural hearing loss (SNHL) affects conversion of mechanical sound to neuroelectric signals in inner ear or auditory nerve.
  • Conductive hearing loss (CHL) affects transmission of sound and conversion to mechanical vibrations.
  • Mixed hearing loss includes elements of both Sensorineural and Conductive Hearing Loss.
• Single Screening Question for Hearing Loss for Adults ≥ 50 years old¹: Do you think you have a hearing loss? – LR+ve 3.1 (95% CI 2.0-4.7), LR-ve 0.27 (95% CI 0.18-0.41) for moderate hearing loss (threshold 35-40 dB); LR+ve 2.7 (95% CI 2.2-3.4), LR-ve 0.45 (95% CI 0.38-0.53) for mild hearing loss (20-25 dB).
• Onset: Sudden (< 72 hours) or gradual?
  • Type: Sensorineural Hearing Loss (SNHL)
    • Sudden Onset:
      • Can’t Miss Diagnoses: Sudden sensorineural hearing loss; temporal bone fracture (see Red Flags below)
      • Meniere’s Disease (triad = episodic vertigo, tinnitus, unilateral SNHL)
      • Autoimmune disease
      • Infectious causes (e.g. meningitis, labyrinthitis)
    • Gradual Onset:
      • Most Common Causes: Presbycusis (age-related hearing loss); Chronic noise exposure
      • Drug-induced (Ototoxic medications – see Below)
      • Cerebellopontine angle tumor
      • Pediatrics: TORCH infection in utero (e.g. Toxoplasmosis, Rubella, CMV, HSV); Syphilis; or Genetic conditions
  • Type: Conductive Hearing Loss (CHL)
    • Sudden Onset:
      • Cerumen impaction; Foreign body
      • Otitis externa
      • Tympanic membrane perforation or retraction
      • Otitis media with effusion
    • Gradual Onset:
      • Otosclerosis (bony overgrowth involving stapes footplate, often +ve FMHx)
      • Cholesteatoma
      • Tumor (e.g. vascular glomus tumor) or Head/Neck Malignancy
• Provoking/Palliating Factors: Is the hearing loss fluctuating or progressive?
  • Provoking – Recent barotrauma or head/ear trauma: Consider Tympanic membrane perforation; or temporal bone fracture (see Red Flags below – emergency).
  • Palliating – Hearing Amplification: e.g. Hearing Aids; Bone Conduction Hearing Devices; Cochlear Implants (see Past Surgical History – below).
• Quality: Affecting high-frequency sounds? Low frequency sounds? Both? How is your hearing in a noisy environment (can be sign of early SNHL)
• Region: Unilateral or bilateral hearing loss?
• Severity: How is your hearing loss affected your functioning and quality of life?
• Timing: Fluctuating – suggestive of Meniere’s disease
• Associated Symptoms:
  • Otalgia (Ear pain): e.g. Otitis media with effusion; Tympanic membrane perforation; Head/Neck malignancy; or Cholesteatoma (sense of aural fullness)
  • Otorrhea (Fluid/discharge from ear): e.g. Otitis externa; Otitis Media with effusion; Cholesteatoma (risk factors – history of tympanic membrane perforation, recurrent otitis media)
  • Vertigo: e.g. Meniere’s Disease; labyrinthitis
  • Tinnitus: typically associated with most hearing loss, not specific to any diagnosis
• Red Flag Symptoms:
  • Unilateral sudden sensorineural hearing loss (SNHL): Sudden ↓ hearing of at least 30 dB (on an audiogram / hearing test) across three consecutive frequencies occurring acutely over 72 hour. may be accompanied by unilateral tinnitus –most commonly Idiopathic (80-90% of cases)
  • Bilateral sudden SNHL (rare), typically from other causes such as:
    • Ototoxic drugs: see Medications for list of ototoxic drugs (below)
    • Autoimmune: e.g. autoimmune inner ear disorder, lupus, Cogan’s disease
    • Neoplasms: e.g. neurofibromatosis type 2, bilateral vestibular schwannoma
    • Infectious: e.g. Lyme disease, Herpes Simplex Virus, Varicella, HIV, Tuberculosis, syphilis
    • Stroke
    • Barotrauma (e.g. diving, airplane, noise)
  • Head trauma, temporal bone fracture: Presents with lacerations or bruising around ear (Battle’s sign – bruising over mastoid process); blood in ear canal; hemotympanum - pooling of blood behind tympanic membrane on middle ear otoscopy; facial nerve paralysis (facial nerve runs through the temporal bone)
  • Stroke: Presenting with focal neurologic symptoms and signs.

• Tinnitus Definition: Perception of sound in the absence of external stimulation (e.g. ringing, hissing, whistling, humming, buzzing, chirping, clicking sounds). Typically occurs in the presence of hearing loss.
• Onset:
  • Acute (<6 months): e.g. noise exposure, trauma, otitis media, or ototoxic medication exposure
  • Chronic (≥6 months): Less likely to resolve spontaneously
• Provoking/Palliating:
  • Exertional (e.g. worse on exertion, improves with rest): Concern for vascular cause
  • Positional (e.g. worse on standing up, improves with lying down): Concern for vascular cause
  • Sound Amplification: Some patients with tinnitus find hearing amplification (e.g. hearing aids) helps to mask tinnitus by introducing ambient noise.
• Quality: Is it low-pitched (e.g. buzzing, humming, rumbling) or high-pitched (e.g. ringing, hissing – most common, suggesting Sensorineural hearing loss)?
  • Red Flag Symptom – Pulsatile:
    • Pulse synchronous (synchronous with heartbeat at radial pulse with rushing, flowing or humming quality) – concern for vascular cause e.g. idiopathic intracranial hypertension, arterial bruits, venous hums, aneurysms, systemic hypertension, arteriovenous malformation, or vascular tumor
    • Pulse asynchronous (not synchronous with heartbeat, e.g. rhythmic clicking) – usually mechanical cause e.g. palatal myoclonus (e.g. due to stroke, trauma, encephalitis, multiple sclerosis), eustachian tube contraction.
• Region:
  • Unilateral, non-pulsatile (Note: Unilateral tinnitus may represent more serious pathology vs. bilateral):
    • With focal neurological deficits on exam: Suggests central causes (e.g. multiple sclerosis, cerebellopontine angle tumor, brainstem infarction) – explored in Chapter 31 – Neuro Exam – MF4
    • Without focal neurological deficits on exam: Suggests peripheral causes (e.g. chronic noise exposure, acoustic trauma, semicircular canal dehiscence, Meniere’s disease)
    • Abnormal otoscopy findings on exam: e.g. cerumen impaction, chronic otitis media, tympanic membrane perforation, cholesteatoma
  • Bilateral and non-pulsatile with normal otoscopy findings: e.g. Presbycusis (age-related hearing loss), chronic noise exposure, acoustic trauma, head trauma, otosclerosis, ototoxic medication exposure
• Severity: Is it bothersome (e.g. causing distress, impacting quality of life or function), or non-bothersome (e.g. aware of tinnitus but not affecting quality of life or function)?
• Associated Symptoms:
  • Otorrhea (Fluid/discharge from ear) or Otalgia (ear pain): e.g. infectious, inflammatory, allergic causes
  • Vertigo (see below): e.g. vestibular schwannoma; migraine; Meniere’s Disease (triad = episodic vertigo, tinnitus, unilateral sensorineural hearing loss); Herpes zoster oticus (Ramsay Hunt Syndrome – also occurs with otalgia, vesicular rash, facial paralysis)
  • Hearing loss: Tinnitus will typically accompany hearing loss for a broad range of causes
  • Headache: e.g. Migraine – explored in Chapter 31 – Screening Neuro Exam – MF4

• Rhinosinusitis Definition: Symptomatic inflammation of nasal cavity and paranasal sinuses, divided into Acute (<4 weeks), Subacute (4-12 weeks), and Chronic (>12 weeks).
• Chronic Rhinosinusitis (CRS): Suggestive diagnosis with ≥ 2 of 4 Cardinal Symptoms for 12 consecutive weeks. Confirmation requires objective evidence through a nasal endoscopy to evaluate for pus/polyps coming from the sinonasal passage
  • Nasal obstruction/blockage/congestion – clarify whether unilateral or bilateral – if truly unilateral symptoms, consider septal deviation, benign polyp, or tumor.
  • Anterior and/or posterior nasal mucopurulent discharge – commonly opaque white or light yellow
  • Facial pain/pressure/fullness – cheek (maxillary sinus), above eye (frontal sinus), between eyes (ethmoid sinus)
  • Reduction (hyposmia) or loss (anosmia) of smell – more common in patients with nasal polyposis.
• Acute Rhinosinusitis: Diagnosis with ≥ 2 of 3 Symptoms for < 4 weeks:
  • Pain/pressure – as above for chronic rhinosinusitis, cheeks/periorbital
  • Obstruction
  • Nasal drainage/discharge ; and either of severe nasal obstruction or facial pain/pressure/fullness
  • Reduction (hyposmia) or loss (anosmia) of smell
  • Other symptoms: ear fullness, cough, headache, dental pain
  • Presumed Acute Bacterial Rhinosinusitis – Symptom Progression and Duration: In acute bacterial rhinosinusitis, may see pattern of initial improvement followed by worsening symptoms in Day 5-10, with symptoms persisting >10 days without evidence of improvement.
  • Presumed Acute Viral Rhinosinusitis - Symptom Progression and Duration: In acute viral rhinosinusitis, symptoms generally last < 10 days (may gradually resolve after 10 days), and do not worsen in biphasic pattern seen in acute bacterial rhinosinusitis.
• Red Flags of Complicated Rhinosinusitis:
  • Preorbital / preseptal cellulitis: Eye pain; eyelid swelling and erythema without proptosis (bulging of eye
  • Orbital cellulitis: Eye pain; eyelid swelling and erythema along with proptosis (bulging of eye), pain with eye movements, double vision (diplopia)
  • Orbital abscess: Eye pain, eyelid swelling, proptosis (bulging of eye), pain with eye movements – may be limitation of ROM, double vision (diplopia), decrease in visual acuity / vision
  • Others: Fever/rigors; Severe headache (e.g. meningitis, intracranial abscess); focal neurologic deficits (e.g. cranial nerve palsies, abnormal extraocular movements); papilledema; nuchal rigidity/altered mental status (e.g. meningitis); recurrent/severe epistaxis
• Allergic Rhinitis: Disease caused by IgE-mediated inflammatory response of nasal mucous membranes after exposure to inhaled allergens. Part of Atopic Triad with Atopic Dermatitis (eczema) and Asthma.
  • Diagnosis with allergic cause and 1 or more of the following symptoms: Nasal congestion; rhinorrhea (often clear discharge – coloured may indicate comorbid process e.g. chronic rhinosinusitis); itchy nose/eyes/palate; or sneezing.
  • Environmental allergen triggers – common: Pollens, pets, flooring/upholstery, mold, tobacco smoke, humidity levels at home, occupational triggers at work
  • Ask about seasonality: e.g. for allergic rhinitis triggered by specific pollens which peak seasonally in a predictable way, such as trees (spring), grasses (summer) and ragweed (fall)
  • Other symptoms: postnasal drip; pale discoloration of nasal mucosa, red/watery eyes; cough; malaise/fatigue (especially in pediatrics)
  • Severity:
    • Intermittent: Symptoms present < 4 days/week or < 4 consecutive weeks
    • Persistent: Symptoms present > 4 days/week or > 4 consecutive weeks
    • Signs of Moderate-Severe Disease: Abnormal sleep; impaired daily activities/sport/leisure; problems at work/school; or bothersome symptoms (otherwise considered mild disease)

• Snoring: Do you snore loudly (loud enough to be heard through closed doors or your bed-partner elbows you for snoring at night)?
• Tired: Do you often feel tired, fatigued or sleepy during the daytime (such as falling asleep during driving or talking to someone)?
• Observed: Has anyone observed you stop breathing or choking/gasping during sleep?
• Pressure: Do you have or are being treated for high blood pressure?
• BMI: >35kg/m²?
• Age: >50 years old?
• Neck Size Large (Measured around Adams Apple): For males, is your shirt color 17”/43cm or larger? For females, is your shirt collar 16”/41cm or larger?
• Gender: Male?

Key Task in Acute Pharyngitis: Differentiate viral pharyngitis (typically self-limiting with minimal sequelae) from bacterial and fungal infections which can be more severe and lead to serious sequelae. This is challenging given significant overlap in clinical presentations.

• Modified Centor Score (estimating probability that pharyngitis is streptococcal): 1 point for: (1) History of Fever (>38°C); (2) Anterior Cervical Adenopathy; (3) Tonsillar Exudate; (4) Absence of Cough. In addition, assign 1 additional point if Age < 15; as well as subtract 1 point if the patient’s Age is over 45.
  • Other symptoms of bacterial pharyngitis: Nausea/vomiting; headache; abdominal pain. Pharyngitis caused by Group A streptococcus may also present with scarlatiniform rash (classically erythematous rash blanching on pressure, with sandpaper texture, worse in flexor creases, starting on the trunk and spreading outwards usually sparing palms and soles), arthralgia (Joint pain) or myalgia (muscle pain)
• Common Symptoms of Viral Pharyngitis: Cough; rhinorrhea; diarrhea; fatigue; conjunctivitis; tonsillar hypertrophy; oropharyngeal erythema/edema; pharyngeal “cobble stoning”
• Common Symptoms of Fungal Pharyngitis: Altered or decreased sense of taste; mouth numbness; oropharyngeal white curd-like (pseudomembranous) plaques that can be scraped off and smooth red patches; angular cheilitis (painful fissures at corners of mouth)

Red Flags of pharyngitis complications:

• Upper Airway Obstruction (ENT emergency): May present with muffled or “hot potato” voice (late finding); drooling/pooling of saliva; stridor (late finding); respiratory distress (tachypnea, shortness of breath, accessory muscle use); sniffing/tripod positioning (to maintain airway patency – e.g. in epiglottitis).
• Peritonsillar abscess: Presents with progressive trismus (decreased mouth opening), and bulging of tonsillar area and soft palate
• Deep Neck Space Infection (e.g. retropharyngeal or parapharyngeal abscess – requires ENT surgical consult): May present with severe unilateral pharyngitis; bulging of pharyngeal wall; neck pain/swelling; crepitus; trismus (inability to open jaw); stiff neck and impaired neck movement; toxic appearance with fever/rigors; may be associated with history of penetrating trauma to oropharynx

• Onset: Was it sudden, gradual or insidious onset?
• Palliating/Provoking:
  • Provoking – Triggers:
    • Key Question: What were you doing when the dizziness started?
    • Head Movements: laying down or turning over in bed, bending over, leaning or turning (Benign Paroxysmal Positional Vertigo)
    • Postural changes affecting cerebral blood-flow: e.g. Movement to upright position (e.g. from lying down to sitting up – Orthostatic hypotension)
    • Barotrauma (sudden change in pressure in middle ear): Diving, sneeze, cough, airplane descending
    • Medications/Toxins: e.g. Alcohol, Skeletal muscle relaxants, Benzodiazepines
    • Exertion: exertional dizziness may suggest cardiac (e.g. aortic stenosis, bradycardia) or general medical problem (e.g. anemia)
• Quality: Do you feel like you, or the room, is moving or spinning even when you are still (vertigo)?
  • Important note: Quality of dizziness is not a reliable means of differentiating different causes of dizziness. Patient subjective report of dizziness quality (e.g. spinning/not spinning, lightheaded, off balance etc) cannot be used to rule in or rule out any cause of dizziness.
• Severity: How does your dizziness affect your functional abilities?
• Timing: Is the dizziness constant, or does it come and go? How long do episodes of dizziness last (seconds, minutes, hours, days)?
• Associated Symptoms:
  • Hearing: Do you notice any hearing loss? Do you hear ringing in your ears? Which side (e.g. tinnitus and hearing loss on Left side only vs. Right side only vs. both)
  • Neurological Symptoms: Do you have any numbness or tingling? Any localized weakness? Any headaches? Double vision? Trouble swallowing? Trouble moving? Trouble speaking?
    • IMPORTANT RED FLAGS for a serious central cause of acute dizziness (eg stroke, bleed):
    • New significant headache or neck pain (generally not seen in benign causes of dizziness, but may be present in intracranial hemorrhage or vertebral artery dissection)
    • New inability to walk unaided
    • Any new focal neurologic deficit (eg weakness/numbness/sensory change, visual field defect)
    • Vertical nystagmus that is present at rest (ie when patient is not moving)
    • 5 Dangerous D’s (mnemonic for posterior circulation stroke symptoms): dysarthria, diplopia, dysmetria, dysphonia, dysphagia
  • Migraine-like symptoms (may suggest vestibular migraine): photophobia, phonophobia, visual disturbances (eg scintillating scotoma), nausea/vomiting, activity avoidance, headache/head pressure
  • General Medical Symptoms: fevers, GI symptoms, Respiratory Tract Infection symptoms, weakness, myalgias, rash
  • Cardiac/Respiratory Symptoms: chest pain, dyspnea, palpitations, exertional intolerance

Note: Key examination tests to differentiate peripheral and central causes of vertigo include the HINTS Exam (see below), the Dix-Hallpike Exam (see below), and a Screening Neurologic Exam. These are more fully explored in Chapter 31 – “Complete” Screening Neurological Examination – MF4.

• Arrhythmias (e.g. sinus bradycardia, long QT interval, heart block): ↑ risk of cardiac cause of syncope; Atrial fibrillation also associated with obstructive sleep apnea (OSA)
• Coronary Artery Disease (CAD): ↑ risk of cardiac cause of syncope; CAD also associated with OSA
• Heart Failure (HF): ↑ risk of cardiac cause of syncope
• Valvular heart disease (e.g. Aortic stenosis, Mitral regurgitation): ↑ risk of cardiac cause of syncope
• Bleeding Disorders: ↑ risk epistaxis, including risk of posterior epistaxis – ENT emergency
• Cerebrovascular disease: Untreated obstructive sleep apnea ↑ risk of stroke
• Body Mass Index ≥ 30 kg/m² (Class ≥1 Obesity): ↑ risk of tinnitus
• Hypertension: Associated with Obstructive Sleep Apnea (OSA); ↑ risk of tinnitus, and ↑ risk hypertensive retinopathy and other eye conditions, ↑ risk posterior epistaxis – ENT emergency
• Diabetes: Associated with Obstructive Sleep Apnea (OSA), ↑ risk of tinnitus and necrotizing otitis externa; ↑ risk of diabetic retinopathy – Explored in Ch 14 – Diabetes Exam – MF3
• Thyroid diseases: Graves disease (Autoimmune hyperthyroidism) causes Exophthalmos (bulging of eye) and restricted extraocular movements which cause diplopia – Explored in Ch 15 – Thyroid Exam – MF3
• Scleroderma (Progressive Systemic Sclerosis): Contributes to Dry eyes
• Autoimmune Diseases (e.g. Ankylosing Spondylitis, Psoriatic Arthritis, Inflammatory Bowel Disease): Can cause Iritis.
• Mood disorders: May be an atypical symptom of OSA – Explored in Ch 33 – Assessment of Mood and Anxiety – MF4
• Viral Infections with increased risk of Head and Neck Cancers: Epstein-Barr Virus (EBV), Human Papilloma Virus (HPV), Human Immunodeficiency Virus (HIV)
• Hearing Loss: Most recent audiology testing? Most recent fitting with hearing aids? Recurrent ear infections as child?
• Pediatrics – TORCH Infections (Toxoplasmosis, Rubella, Cytomegalovirus, Herpes Simplex) or Syphilis during pregnancy: May cause progressive sensorineural hearing loss (SNHL) for pediatric patients.
• Craniofacial abnormalities (e.g. Down Syndrome, Cleft Palate): ↑ risk of sinusitis or acute otitis media

Relevant Clinical Scores:

• STOP-BANG Score – Screening for Obstructive Sleep Apnea
• CENTOR Score – Estimating probability of Strep Pharyngitis

• Tympanostomy tubes (e.g. patients with conductive hearing loss from middle ear effusion or recurrent acute otitis media)
• Tonsillectomy (e.g. patients with airway obstruction, or recurrent/chronic infection)
• Myringoplasty / Tympanoplasty (surgical closure of perforated tympanic membrane e.g. to remove tympanostomy tubes)
• Hearing Amplification:
  • Hearing Aids (air conduction hearing devices for mild-to-moderate hearing loss): goal to significantly improve communicative ability and quality of life, not to restore previous hearing.
  • Bone Conduction Hearing Devices (transmit sound directly through skull to functioning cochlea): e.g. for patients with congenital atresia of external auditory canal canal, chronic middle/outer ear infection exacerbated by standard hearing aid, or single-sided deafness
  • Cochlear Implants (surgically implanted device using electrical stimulation to provide hearing): e.g. for severe-to-profound sensorineural hearing loss (deafness)

• Atopic Triad: Allergic rhinitis, Asthma, Eczema
• Family history of sudden cardiac death (↑ risk of cardiac cause of syncope)
• Family history of hearing loss (many congenital syndromes can present with hearing loss)
• Otosclerosis (bony overgrowth involving stapes footplate) – cause of progressive conductive or mixed hearing loss

• Pack years = packs/day x years smoking: Use of cigarettes? E-cigarettes? Vapes?
  • Have you thought about quitting within the next 6 months? How long ago did you quit smoking?
  • The benefits of smoking cessation begin with the last cigarette; quit before Age 35, life expectancy same as non-smokers; quit age 35-65, add 5 years to life expectancy; quit age 65-74, add 1 year.
  • 5As approach taking a smoking Hx (Explored in Chapter 38 – Motivational Interviewing – IF)
  • Note: Smoking, Chewing Tobacco use ↑ risk of Head/Neck Cancer, tinnitus, chronic rhinosinusitis (CRS)
  • Pediatric second-hand smoke exposure: ↑ risk of sinusitis, acute otitis media
• Pro-Comp Connection: Regarding patient’s position, do not jump to thinking in terms of “compliance” with recommendations for smoking cessation.

• How often do you drink alcohol (Drinks/Week)? What is the size of 1 drink? What kinds of drinks?
• Note: Alcohol use ↑ risk of Head and Neck Cancer
• Can be cause of Dizziness, and worsen Tinnitus

• Intranasal drug use (e.g. Cocaine, methamphetamine, opioids) – ↑ risk epistaxis, esp. anterior epistaxis.
• Note: Excessive use of caffeine can worsen Tinnitus

• Occupations with exposure to toxins with ↑ risk for head and neck cancer: Dry cleaning (exposure to perchloroethylene dry cleaning agent); Farming (exposure to pesticides); Textile workers; Wood workers; Manufacturing; Automobile mechanics; construction workers (cement)
• Occupational exposure to allergens: E.g. Food allergies (e.g. food preparation); Insect stings (e.g. farming); Latex (e.g. cleaning, healthcare, etc.)
• Untreated Obstructive Sleep Apnea: Associated with ↓ work productivity, and ↑ risk occupational injury
• Occupational noise exposure¹³: ↑ risk of tinnitus and hearing loss – Ontario Occupational Health and Safety Act (OSHA) noise regulation requires employers ensure no worker is exposed to sound level > 85 dBA (weighted decibels) averaged over an 8 hour work shift – 85 dB e.g. heavy traffic, noisy restaurant; normal conversation is about 60 dB

• Known allergies, past allergic reactions (if known)
• Allergies (e.g. Allergic rhinitis) ↑ risk of sinusitis, acute otitis media (AOM)
• Anaphylaxis (true allergy): Typically onset <1 hour of exposure, involving 2 or more of:
  • Integumentary – Skin or mucosal (Pruritus, generalized hives/urticaria, flushing, swelling of face, lips, tongue or uvula)
  • Respiratory – Dyspnea, Wheeze-Bronchospasm, Hypoxemia, stridor, persistent cough/ throat clearing
  • Cardiac – Hypotension (Systolic BP <90mmHg or decrease >30% from baseline)
  • Gastrointestinal – Persistent crampy abdominal pain, persistent vomiting

• Allergic Rhinitis:
  • Saline rinses (using distilled/sterilized/boiled water re. ↑ infection risk if contaminated)
  • Glucocorticoid nasal sprays (e.g. fluticasone, mometasone, ciclesonide)
  • Oral antihistamines: 1st generation is more sedating (e.g. Diphenhydramine); 2nd generation is less sedating (e.g. Cetirizine, Loratadine, Fexofenadine)
  • Leukotriene Receptor Antagonist (e.g. patients with comorbid asthma): Montelukast
• Emergency Medication for Anaphylaxis: Epinephrine IM Autoinjector

(Note: Explored further in MF2)

• Relevance: ↑ risk of Epistaxis (particularly posterior epistaxis – an ENT emergency)
• Anti-platelets (primary hemostasis) – e.g. Acetylsalicylic Acid (ASA), Clopidogrel, Ticagrelor
• Anti-coagulants (secondary hemostasis) –
  • Heparins: e.g. Unfractionated Heparin, Low Molecular Weight Heparin (LMWH)
  • Vitamin K Antagonist: Warfarin
• Direct Oral Anticoagulants (DOACs): e.g. Dabigatran, Apixaban, Rivaroxaban, Edoxaban

• Continuous Positive Airway Pressure (CPAP): Current settings (e.g. 6-14cm H₂O pressure); comfortable fit; adherence to wearing CPAP.
• Oral Appliance (OA) – e.g. Mandibular advancement or tongue-retaining devices
• Bilevel Positive Airway Pressure (BiPAP): Current settings (e.g. Inspiration Positive Airway Pressure of 10cm H₂O and Expiratory Positive Airway Pressure of 5cm H₂O); comfortable fit; adherence to wearing BiPAP

• Cardiac Effects (Hypotension, postural hypotension, torsade’s, other arrhythmias)
  • Cardiac medications: Class 1a antiarrhythmics (e.g. Quinidine); Digoxin; Nitroglycerin
  • Neurology medications: Cholinesterase inhibitors (e.g. Rivastigmine, donepezil, galantamine for dementia); Antiepileptics (e.g. phenytoin, phenobarbital for epilepsy); Antiparkinsonian agents (e.g. Levodopa/Carbidopa)
  • Oral anti-hyperglycemics: SGLT2 inhibitor (e.g. empagliflozin, dapagliflozin)
  • Antihypertensives: e.g. ACE-i/ARB, Beta blocker, calcium channel blocker, thiazides, etc.
  • Urinary anticholinergics (e.g. overactive bladder): e.g. Oxybutynin, Solifenacin
  • Phosphodiesterase 5 Inhibitors: e.g. Sildenafil
• Central Anticholinergic Effects: Skeletal muscle relaxants (e.g. Cyclobenzaprine, baclofen); Antihistamines (e.g. Dimenhydrinate)
• Cerebellar Toxicity: Benzodiazepines (e.g. Lorazepam, Clonazepam, Diazepam); Lithium
• Hypoglycemia: Oral antihyperglycemic medications; insulin; beta-blockers (particularly non-selective betablockers e.g. propranolol, labetalol, carvedilol)
• Ototoxicity: e.g. Aminoglycoside antibiotics (e.g. gentamicin); chemotherapy (e.g. cisplatin, fluorouracil); high dose Loop diuretics (e.g. furosemide)

• Rehabilitation: e.g. Particle Repositioning maneuvers for Benign Paroxysmal Positional Vertigo (BPPV); Vestibular rehabilitation for vestibular neuritis.
• Symptom management:
  • Betahistine (Specifically for Meniere’s disease)
  • Antihistamines (e.g. diphenhydramine, dimenhydrinate)
• Antiemetics for severe nausea/vomiting (e.g. ondansetron, metoclopramide)

• Aminoglycoside Antibiotics (e.g. gentamicin, tobramycin, amikacin, neomycin)
• Macrolide Antibiotics (e.g. azithromycin, erythromycin)
• Glycopeptide Antibiotics (e.g. vancomycin)
• Tuberactinomycin Antibiotics (e.g. viomycin)
• Anti-neoplastic drugs (e.g. cisplatin, carboplatin, oxaliplatin)
• Salicylates (e.g. High dose Acetylsalicylic Acid 6-8g/day – usually reversible)
• Antimalarial Drugs (e.g. quinine, chloroquine – usually reversible)
• Loop Diuretics (e.g. furosemide – usually temporary)

• Fever could be indicative of an infection or a constitutional symptom

Say: I will inspect the head for signs of trauma, masses, lesions or scars.

Do: Check scalp for signs of trauma (Battle sign or mastoid ecchymosis; Racoon eyes or periorbital ecchymosis).

Report: I note no visible signs of trauma or lesions.

Why Check: External signs of a traumatic brain injury and basilar skull fracture (Assessment of Traumatic brain injury and concussion explored in Ch 31 – Screening Neuro Exam – MF4)

Say: Can you open one eye and pull the lower eyelid down? Now the other side?

Do: Check for scleral icterus (jaundice), conjunctivitis (increased vascular markings), discharge (differentiate watery from mucopurulent), or conjunctival pallor (anemia). Look for infraorbital edema/ darkening (“allergic shiners”)

Report: No scleral icterus, conjunctivitis, discharge or conjunctival pallor noted.

Scleral Icterus¹⁴, Conjunctival Pallor¹⁵, Viral Conjunctivitis¹⁶

Bacterial Conjunctivitis¹⁷, Allergic Conjunctivitis¹⁸, Infraorbital edema/darkening¹⁹

Why Check: Scleral icterus is a possible sign of liver disease. Conjunctival pallor is a sign of anemia. Acute conjunctivitis can represent:

• Viral conjunctivitis: Classically appears as a pink or red colour, with minimal-to-no itching and watery discharge, which usually begins unilateral but may progress to bilateral. Ask about sick contacts, where contact with another person with red-eye mildly increases the likelihood of viral conjunctivitis (LR+ 2.5, LR- 0.89). Ask if eyelids are stuck together on awakening which mildly decreases the likelihood of viral conjunctivitis (LR+ 0.72, LR- 3.5). On exam, look for mucopurulent ocular discharge (LR+ 0.47, LR- 2.7) which moderately decreases the likelihood of viral conjunctivitis. Also look for pharyngitis (LR+ 5.4-9.9, LR- 0.48-0.48) and preauricular lymphadenopathy (LR+ 2.5-5.6, LR- 0.73-0.89) which moderately increase the likelihood of viral conjunctivitis.
• Bacterial conjunctivitis: Classically appears as a pink or red colour, with minimal-to-no itching and mucopurulent discharge which is usually unilateral. Ask about sick contacts, where contact with another person with red-eye moderately reduces the likelihood of bacterial conjunctivitis (LR+ 0.40). Ask if eyelids are stuck together on awakening (LR+ 1.4, LR- 0.29) which mildly increases the likelihood of bacterial conjunctivitis. On exam, assess for ocular discharge, where watery discharge greatly reduces the likelihood of bacterial conjunctivitis (LR+ 0.03), as well as mucopurulent discharge (LR+ 2.1, LR- 0.37) and otitis media (LR+ 2.5, LR -0.84) which mildly increase the likelihood of bacterial conjunctivitis. look for pharyngitis (LR+ 0.10-0.19, LR- 2.1-2.14) and preauricular lymphadenopathy (LR+ 0.18-0.40, LR- 1.1-1.4) which moderately decrease the likelihood of bacterial conjunctivitis.
• Allergic conjunctivitis: Pink; Prominent itching; Watery discharge; bilateral. In allergic rhinitis, can also see infraorbital edema/darkening due to subcutaneous venodilation re. “allergic shiners”.

Say: I will inspect the nose.

Do: Look for epistaxis (nose bleeds), rhinorrhea (runny nose), and a transverse nasal crease (“allergic salute”). Using anterior rhinoscopy (with otoscope, or nasal speculum with headlight), look at the septum and nares for symmetry or deviations. Look at the nasal mucosa – is it hyperemic (inflamed), bluish/pale, congested or dry? Look for discharge – is it clear or mucopurulent? Look for any nasal polyps and/or masses (rare) – but do NOT confuse with the turbinates which are normal anatomy**.**

Report: I note no swelling, trauma, or deviation of the nares, which show good symmetry.

Why Check: Assessing for conditions listed above. Specific diseases include:

• Chronic rhinosinusitis (CRS) requires evidence of mucosal inflammation (e.g. hyperemic nasal mucosa, mucopurulent discharge, polyposis) in addition to the 4 cardinal symptoms of CRS – Nasal obstruction/blockage/congestion; Anterior and/or posterior nasal mucopurulent discharge; Facial pain/pressure/fullness; and Reduction or loss of smell (hyposmia or anosmia).
• In allergic rhinitis, look for a transverse nasal crease (“allergic salute”) which occurs due to patient’s repeated rubbing of the tip of the nose with their hand, in addition to clear rhinorrhea and bluish/pale swelling of nasal mucosa.
• Note that clear rhinorrhea (nasal discharge) and clear otorrhea (ear discharge) in the setting of a traumatic brain injury raise concern for a basilar skull fracture (Assessment of Traumatic brain injury and concussion explored in Ch 31 – Screening Neuro Exam – MF4)

Say: I will now palpate the nasal bones. Please tell me if you are in discomfort.

Do: As you palpate, assess for step deformities and pain. Stop the exam if the patient is in distress.

Report: I note no signs of nasal fracture or pain evident on palpation of nasal bones.

Why Check: Assessing for step deformities and pain in nasal fracture / trauma to face

Say: I will now inspect the mouth; can you open the mouth wide?

Setup: Have both a light source and a tongue depressor available

Do: Inspect outer lips for symmetry, colour, moisture, ulcers, cracking, scaling and masses. Have the patient open mouth and shine a light to inspect for colour, ulcers, white patches and nodules. Look for signs of inflammation on gums, and abnormalities of teeth (e.g. dental infections such as carries). Look at the surface of tongue – should be symmetrical, rough with papillae, and possibly covered with white coating, or clear. Look for white plaques that can scrape off on the tongue (thrush). Look at the hard palate, under-surface of tongue and floor of mouth for nodules, ulcers, or white, erythematous or cyanotic areas.

Report: I note no abnormalities to the outer lips, gums, or teeth. I note no oral ulcers, nodules, or erythematous areas.

Oral Candidiasis²⁰, Oral Cancer²¹

Aphthous Ulcer²², Dental Carries²³

Why Check: Important to detect thrush (common in patients who are immunosuppressed, including e.g. on glucocorticoid medications); cysts, calculi in sub-mandibular ducts; and oral cancers (e.g. of tongue). Note that dental infections are a common cause of secondary otalgia (ear pain originating outside the ear). Trismus (inability to open the jaw), drooling and pooling of saliva in the mouth raises concern for deep neck space infection and upper airway obstruction (Emergency).

Say: I will now inspect the at the back of the throat for the palate, tonsils and uvula. Can you say “Aaaah”?

Setup: Have both a light source and a tongue depressor available

Normal Inspection²⁴, Strep Pharyngitis²⁵, Peritonsillar Abscess²⁶

Do: Look at soft palate and uvula for redness and swelling. When patient says “Aaaah”, the soft palate should rise symmetrically, and the uvula should remain in midline. You may need to use your tongue depressor to visualize the soft palate adequately. This is easier to see with the patient keeping their tongue in their mouth while saying ahh. Assess tonsils for evidence of hyperplasia, inflammation, or exudates.

Report: Uvula is midline on palate elevation. Tonsils are a Grade 0 with no focal inflammation or exudates.

• You can report your tonsil findings based on the Tonsillar Hypertrophy Grading Scale (Grade 0: Tonsils absent/atrophied***;*** Grade 1: Tonsils 0-25% of oropharyngeal diameter; Grade 2: 25-50% of oropharyngeal diameter; Grade 3: 50-75% of oropharyngeal diameter; Grade 4: 75-100% of oropharyngeal diameter)

Why Check: Important in assessment of Acute Infectious Pharyngitis (e.g. Strep Pharyngitis vs. Viral Pharyngitis – in photo of Strep Pharyngitis above, note tonsillar exudate seen bilaterally – part of CENTOR score). With respect to tonsillar enlargement or snoring as chief complaint, this may require referral to ENT or Sleep Study for further study if clinically significant. Inspection for Acute Infectious Pharyngitis should be followed by a Lymph Node Exam (explored in Ch 11 – Lymph Node Exam – MF2). Oropharyngeal tumours and masses can cause deviations in the symmetry of the palate. Asymmetry of the oropharynx and bulging of pharyngeal wall/soft palate/floor of oropharynx raises concern for deep neck space infection and upper airway obstruction (Emergency). Specifically, deviation of the uvula towards the unaffected side raises concern for peritonsillar abscess.

Modification for Patients with Obesity: Use a tongue depressor to visualize the posterior oropharynx. This may make it easier to see the oropharynx if the view is obstructed.

Conditional test

(Also seen in Ch 39 – Anesthesia Pre-Op Assessment – Integration Foundation)

Say: I will inspect the mouth to look at airway structures. Can you briefly open the moth and stick the tongue out?

Do: Inspect the patient’s oropharynx structures for the soft palate, uvula, fauces, and pillars.

Scoring: see image. Mallampati 1 = soft palate, uvula, pillars completely visible. Mallampati 2 = soft palate and part of uvula visible. Mallampati 3 = only soft palate and base of uvula visible. Mallampati 4 = soft palate not visible.

Report: I can visualize all of the soft palate, uvula and pillars. The Mallampati Score is 1.

Why Check: Part of the airway assessment in the pre-op anesthesia exam. Useful in collaboration with other tests to assess the difficulty of intubation by direct laryngoscopy. Can help classify a patient’s airway as easy (Mallampati Class I or II) or a difficult (Mallampati Class III or IV) intubation and helps direct the anesthesia pre-op planning process. Risk factors of a difficult airway can be assessed by as LEMON: Look (e.g. C-spine immobilization, trauma, facial swelling, teeth); Evaluate (3-3-2 rule: 3 fingerbreadths of mouth opening, 3 fingerbreadths of hyomental distance, 2 fingerbreadths of thyromental distance); Mallampati score; Obstruction/obesity; Neck mobility (C-spine ROM).

A Mallampati Score of 3 or 4 is also significant in assessing patients for Obstructive Sleep Apnea.

Typically followed by lymph node (Ch 11 – MF2) and Thyroid (Ch 15 – MF3) exams

Say: I will now inspect the neck.

Do: Look for swelling or scars, masses or lesions; goiter; or muscular hypertrophy. Palpate the Temporomandibular Joint (TMJ) and ask the patient to open and close their mouth repeatedly, checking for tenderness and instability. Also, ask the patient to swallow in good lighting.

Report: I note no neck swelling scars, masses, or lesions.

Why Check:

• Goiter – thyroid condition (non-specific re hypo/eu/hyperthyroid); good for swallow assessment.
• Muscular Hypertrophy – chronic problems with breathing re. work of breathing.
• Jaw Claudication – pain on chewing is a diagnostic clue to Temporal Arteritis (Giant Cell Arteritis), classically presenting with new onset headache in patient of age >50 years old.
• TMJ Tenderness – important to detect mechanical disease of the jaw or TMJ pathology, which can be an important cause of secondary otalgia (ear pain)

Say: I will now inspect the ears.

Setup: Stand lateral to patient.

Do: Examine external auditory canal and auricle. Look for vesicles (small <1cm fluid filled lesions)

Report: I note normal external auditory canal (some hair, ± yellow/brown cerumen i.e. earwax = cerumen); the auricle shows no signs of scars, inflammation, or deformity.

Otitis Externa²⁷

Why Check: Looking for gross damage to external ear. Inflammation of the canal (edema, erythema) may point to otitis externa, along with otorrhea (drainage – in otitis externa, otorrhea often occurs with otalgia; whereas in otitis media, otalgia often precedes otorrhea which can occur in perforated otitis media). In a patient with history of recent trauma, a temporal bone fracture (emergency) may present with lacerations or bruising around the ear. Vesicles in the ear canal or external ear may indicate Herpes zoster oticus (Ramsay Hunt syndrome – otalgia can be present before lesions develop).

Say: I will palpate the pinna and peri-auricular area of each ear. Please tell me if you are in discomfort.

Do: Assess for tenderness, nodules, or inflammation on palpation; push tragus (small eminence of external ear anterior to the concha); palpate mastoid bone (immediately behind ear re structures draining ear). Look for erythema, edema & pain vs. mastoid tip tenderness. Stop the exam if the patient is in distress.

Report: I note no pain induced on pushing of tragus or palpation of mastoid bone.

Why Check: Looking for signs of mastoiditis (e.g. a middle ear infection that spread – pain, edema & erythema on palpation of mastoid bone. Tenderness while pushing down on the tragus is suggestive of otitis externa.

Gen - [3, 4] Peds Acute Otitis Media – [1, 3]

Say: I will use an otoscope to look at the eardrums in each ear (tympanic membranes).

Do: Standing laterally, pull the auricle (superior cartilaginous prominence) up and back in an adult, or down/ down and back in kids. Slowly guide the otoscope into the ear canal, until you can see the tympanic membrane.

• Pneumatic Insufflation: With a pneumatic otoscope (if available), a gentle application of positive then negative pressure will cause the normal tympanic membrane to move inwards and then outwards. When the middle ear is filled with fluid (as in acute otitis media or otitis media with effusion), the tympanic membrane will be poorly mobile.

Report: I have identified the drum’s colour (red, white, yellow); translucency (transparent, opaque); position (retracted, neutral or bulging); and cerumen (wax). I note no signs of inflammation or effusion (with air-fluid level along the tympanic membrane) or perforation. The tympanic membrane is mobile with pneumatic insufflation.

Why Check: Can assess for signs of otitis media (middle ear inflammation), tympanic membrane (TM) perforation, middle ear effusion (MEE), or ↑ inner ear pressure. Note that in otitis externa, the tympanic membrane may be only partially visible due to ear canal edema.

• Acute Otitis Media (AOM): Acute onset of symptoms (e.g. otalgia) with a purulent middle ear effusion (MEE) and significant middle ear inflammation. In children, TM findings increasing likelihood of AOM include bulging (LR+ 51), cloudy (LR+ 34) or distinctly red (LR+ 8.4), and distinctly impaired mobility (LR+ 31).
• Otitis Media with Effusion (OME): Presence of MEE without signs acute middle ear inflammation.
• A cholesteatoma may present and appears as epithelial debris behind the tympanic membrane.
• A glomus tumor may present with a bulging erythematous mass behind the tympanic membrane, accompanied by unilateral pulsatile tinnitus.
• In a patient with history of traumatic brain injury, a basilar skull fracture may present with pooling of blood behind the tympanic membrane called hemotympanum (Assessment of Traumatic brain injury and concussion explored in Ch 31 – Screening Neuro Exam – MF4)

(See Ch 31 – Screening Neuro Exam – MF4)

Say: I will now assess hearing. I will stand behind you, cover one of the ears with one finger, then whisper a combination of 3 numbers and letters. Please repeat back the 3 numbers or letters you hear.

Setup:

• With patient seated, stand arm’s length (2 feet) behind the patient (to prevent lip reading).
• Mask the hearing in one ear using your finger to gently occlude and rub the external auditory canal.
• A trial run using a loud voice to ensure the patient understands the instructions may be helpful.

Do:

• Examiner takes in a full breath, exhales, then whispers 3 random numbers and letters (e.g. “5, B, 6”).
• Ask the patient to repeat the 3 numbers and letters. If the patient repeats all 3 numbers and letters correctly, this is a normal result.
• If the patient responds incorrectly, repeat the test using a new combination of numbers and letters (e.g. “D, 1, C”). The screening test is normal if the patient repeats 3 out of 6 total letters/numbers correctly.
• Repeat with the other ear, using new combination of numbers and letters.

Report: You repeated 3 out of 6 letters correctly with each ear. This is a normal whispered voice screening test for hearing loss.

Why Check: The whispered voice test is a helpful initial screening test for hearing loss, with an alternative screening test being the Finger Rub Test (below). The likelihood of hearing loss is moderately increased by an abnormal whispered voice test (LR+ 6.0) and greatly decreased by a normal whispered voice test (LR- 0.03). This test cannot differentiate sensorineural from conductive hearing loss, where Weber and Rinne testing (see below) can help delineate conductive, sensorineural and mixed hearing loss. An abnormal screening test should be referred for formal audiology assessment.

Say: I will now assess hearing. I will stand behind you and rub my fingers together close to one of your ears with your eyes closed and arms at the sides. Please raise your hand on the side you hear the fingers rubbing.

Do: Standing in front of the patient, once their eyes are closed, bring your arms close to each side of the patient’s ears, ensuring there is no contact with the patient’s outer ear or hair. On each side in a random order, rub your thumb against your index finger while progressing to the middle finger and then back to the index finger three times. Test this with a strong rub (as loud as you can muster); as well as a faint rub (the softest you can hear as the clinician). Monitor for the patient raising their hand to the side they hear the finger rub. Randomize the order of these 4 maneuvers (e.g. left ear, right ear, right ear, left ear).

Report: The patient heard both a strong and faint rub in bilateral ears. This is a normal finger rub screening test for hearing loss.

Why Check: The finger rub test is a helpful initial screening test for hearing loss, with an alternative screening test being the Whispered Voice Test (above). The test can also be performed by standing in front of the patient. The likelihood of hearing loss is greatly increased by being unable to hear a strong finger rub (LR+ 355.4)²⁸. Being able to hear a faint finger rub greatly decreases the likelihood of hearing loss (LR- 0.02)²⁸. Note that ambient noise can impact the performance of this test, where a study demonstrated that being unable to hear a strong finger rub in a quiet environment greatly increases the likelihood of hearing loss (LR+ 16.73), while the same result in a noisy environment moderately increases the likelihood of hearing loss (LR+ 6.76)²⁹. This test cannot differentiate sensorineural from conductive hearing loss, where Weber and Rinne testing (see below) can help delineate conductive, sensorineural and mixed hearing loss. An abnormal screening test should be referred for formal audiology assessment.

Part 1: Weber’s:

Say: I will now use tuning forks to assess hearing.

Setup: Place vibrating 512 Hz tuning fork on the midline of the patient’s head.

Do: Ask where the sound is heard – left ear, right ear, or in the middle. For example, if the sound is heard louder in the right ear, then it is described as “Weber lateralizes to right ear”.

Part 2: Rinne’s Test:

Setup: Place vibrating 512 Hz tuning fork against patient’s mastoid bone. Then move it to just in front of the tragus.

Do: Ask the patient if the sound is louder at the back or front.

• Sound is heard louder at the front = air conduction better than bone conduction (AC > BC). This can be normal but can also be present in sensorineural hearing loss.
• Sound is heard louder at the back = bone conduction better than air conduction (BC > AC). This is abnormal and suggests conductive hearing loss.

Repeat for opposite ear.

Report: Based on table below – can determine nature of the hearing loss as Conductive or Sensorineural:

Why Check: The Weber and Rinne tests help assess for conductive hearing loss (CHL), sensorineural hearing loss (SNHL) or mixed hearing loss.

• Sensorineural hearing loss (SNHL) affect conversion of mechanical sound to neuroelectric signals in inner ear or auditory nerve. The most common causes are presbycusis (age-related hearing loss – slowly progressive and symmetrical) and noise-induced – both with gradual onset***. The exam of the tympanic membrane is often normal.*** Other causes include:
  • Gradual Onset: Drug-induced (Ototoxic medications); Cerebellopontine angle tumors
  • Fluctuating Symptoms: Meniere’s Disease (caused by endolymphatic hydrops of labyrinthine system of inner ear – triad = episodic vertigo, tinnitus, unilateral SNHL)
  • Other causes: Genetic conditions; or Infections in-utero (e.g. TORCH infections – Toxoplasmosis, Rubella, Cytomegalovirus, Herpes Simplex; or Syphilis)
• Conductive hearing loss (CHL) interferes with the transmission of sound and conversion to mechanical vibrations. Otoscopy is critical in assessing for conductive causes of hearing loss, for example:
  • Abnormal ear canal exam: Consider Cerumen impaction; foreign body; otitis externa; or neoplasm
  • Abnormal middle ear otoscopy: Consider Tympanic membrane perforation or retraction; otitis media; middle ear effusion; glomus tumor; or cholesteatoma
  • Normal otoscopic exam: Consider otosclerosis (bony overgrowth involving stapes footplate)
• Mixed hearing loss includes elements of both Sensorineural and Conductive Hearing Loss. Example causes include severe otosclerosis, cholesteatoma, or neoplasms.

The likelihood of conductive hearing loss is greatly increased by abnormal Rinne’s test (LR+ 16.8, LR- 0.2). The likelihood of sensorineural hearing loss is mildly increased by Weber Test lateralizing to the good-hearing ear (LR+ 2.7). An abnormal Weber and Rinne test should be referred for formal audiology assessment.

Say: I will now inspect the eyes more closely. Can you look straight ahead?

Setup: Have a flashlight and direct ophthalmoscope present, facing patient. Have lights dimmed. If available, a Snellen Pocket Card is helpful.

Do:

• Look at eyelids for a drooping eyelid → Ptosis.
• Look at the margins of the iris: If you see white sclera under the bottom iris margin (± top margin too) → Exophthalmos.
• Using a flashlight and standing in front of patient, have patient look straight ahead. Inspect pupil size (Snellen Pocket Card tends to have a guide). ≤1 mm difference between two eyes is normal.
• Using a flashlight, shine light in one eye. Look for pupillary constriction both direct and consensual (part of the Pupillary Light Reflex). Repeat in the other eye. Then, swing the flashlight back and forth between both eyes. Each pupil should constrict (i.e. no relative afferent pupillary defect).

Report: Pupils are equal and reactive to light, and there is no relative afferent pupillary defect.

Ptosis³⁰, Exophthalmos³¹

Why Check:

• Ptosis: Cranial Nerve injury or sympathetic nerve injury (Horner Syndrome –Ophtho Exam – Ch 40 – Integration Foundation)
• Exophthalmos: Sign of Thyroid disease (Ch 15 – Thyroid Exam – MF3)
• Pupillary Light Reflex Lost: Optic nerve or Oculomotor nerve lesion (Ch 31 – Screening Neuro Exam – MF4)
• Positive relative afferent pupillary defect (RAPD): Dilation of one pupil during swinging flashlight test suggests a Retina or Optic nerve injury.

(Also explored in Ch 14 – Diabetes Exam – MF3; Ch 31 – Neuro Exam – MF4; and Ch 40 – Ophtho Exam – IF)

Say: I will now inspect each eye using a direct ophthalmoscope. You will feel my hand touch the shoulder to keep the ophthalmoscope steady. Please look at an object on the wall in the distance at your eye level (preventing constriction due to pupillary accommodation reflex)

Setup: Room should still be dim. Stand facing the patient; if you’re examining the patient’s right eye first, use your right eye to look (vice versa). Adjust the scope’s focus (if you’re not wearing your nearsighted prescription glasses, may take more adjusting) by focusing on an object in room. Use low-moderate light intensity typically with medium aperture.

Do: Steady your hand on their shoulder. Shine the light from ophthalmoscope in patient’s eye; should see the red reflex. Follow reflex and slowly move toward patient. Find an artery and follow that towards the centre. You should come upon the optic disc (head of optic nerve, a confluence of retinal nerve fibers exiting the globe) and the optic cup (white centre of optic disc). Look for signs of optic disc swelling, and loss of venous pulsations. Follow the Superonasal Arcade, Inferonasal Arcade, Superotemporal Arcade, and Inferotemporal Arcade. Focus on Macula (temporal to optic disc), which contains Fovea where you can see a Yellow Reflex in healthy people. Look for signs of hemorrhages, neovascularization (small branching vessels) and cotton wool spots (fluffy white patches).

Report: The optic disc was visualized in each eye, with no signs of optic disc swelling, neovascularization or loss of venous pulsations.

Why Check: Direct fundoscopy allows for a focused exam of intraocular structures, alongside external examination and the slit lamp examination (explored in Ch 40 – Ophtho Exam – IF). Fundoscopy also forms a part of the screening neurological examination (See Chapter 31 –Neuro Exam – MF4). Major pathologies to look for include:

• Absent Red Reflex: Can be due to cataracts, retinoblastoma, retinal detachment, vitreous hemorrhage, etc.
• Glaucoma (Chronic): Enlarged cup/disc ratio >0.5 (normal cup-to-disc ratio ≤0.5)
• Papilledema: Swollen optic disc with no clear demarcated disc border due to ↑ Intracranial Pressure, coupled with loss of venous pulsations. Important to assess for in patients with new onset headaches.
• Retinal Detachment/Tear/Break: Can occur inside field of view on direct ophthalmoscopy.
• Cotton Wool Spots: Sign of vascular insufficiency or ischemia to an area of retina – most common causes being hypertensive and diabetic retinopathy (Ch 14 – Diabetes Exam – MF3)
• Hypertensive Changes: Arteriolar spasm, exudates, flame-shaped hemorrhages, loss of venous pulsations, ghost vessels, cotton wool spots.
• Diabetic Retinopathy: Cotton wool spots, dot and blot hemorrhages, neo-vascularisations

(Conditional Test for Sinusitis)

Say: I will examine the sinuses using a light source. Please remove any dentures. Please keep the neck slightly extended back and mouth open during the assessment.

Setup: Examination must be conducted in completely darkened room with patient’s dentures removed. Ideal test requires use of a transilluminator (a focused light source); otoscope may also be used.

Do: Begin with the maxillary sinus: angle light toward mouth – a normal transillumination is dim glow on hard palate. Progress to the frontal sinus: light source below eyebrow, angling light superomedially – a normal transillumination is dim glow over frontal area.

Report: I note normal bilateral transillumination of frontal and maxillary sinuses.

Transillumination of maxillary sinus, Transillumination of frontal sinus

Why Check: Abnormal transillumination mildly increases the likelihood of sinusitis (LR+ 1.6) while normal sinus transillumination moderately decreases the likelihood of sinusitis (LR- 0.5). Note frontal sinuses may have non-pathologic unequal transillumination – may develop asymmetrically. This is not recommended as part of routine physical exam by otolaryngologists.

Pediatrics – Sinus Development: Ethmoid Sinuses present & pneumatized at birth; Maxillary Sinuses present at birth, pneumatized age 4; Sphenoid Sinuses present by Age 5; Frontal Sinuses begin development age 7, fully developed in adolescence (age 14-18). Sinus drainage occurs through narrow ostia (1-3mm) into middle meatus in ostiomeatal complex (OMC). The sphenoid sinus drains into the roof of the nose.

Say: I will assess your hearing. Please hum an “eee” or “hmm” sound at a consistent pitch for a few seconds. It can be helpful to repeat the test with both high- and low-pitch hums. Please tell us which ear is loudest.

Do: Ask patient to hum an “eee” or “hmm” sound at a consistent pitch for a few seconds as noted above, with potential variation of the pitch over multiple trials. Ask the patient which ear hears the hum the loudest.

Report: The patient reports hearing loss in their left ear, and the Hum test lateralizes to the left ear, consistent with conductive hearing loss.

Why Check: For patients with hearing loss, the Hum test is a simple alternative to the Weber’s test which doesn’t require a tuning fork. Interpretation is the same as the Weber’s test: if the sound lateralizes to the affected ear, this suggests conductive loss. If it lateralizes to the unaffected ear, this suggests sensorineural hearing loss. The Hum test can be helpful in Telemedicine and triaging patients needing urgent assessment for Sudden Sensorineural Hearing Loss (SSNHL)³⁰ where tuning forks are unavailable at initial intake.

Pearl: You can test the hum test on yourself: use your finger to plug and unplug your ear (conductive hearing loss) while making a hum, and see which side the sound lateralizes to.

(Conditional Test – Explored in Ch 31 – Screening Neuro Exam – MF4)

• When to do the HINTS+ Exam? The HINTS+ exam is only indicated with acute onset, continuous dizziness, imbalance, and nystagmus lasting hours to days (Acute Vestibular Syndrome = AVS). Patients must have ongoing nystagmus at rest (involuntary repetitive jerking eye movements) to be eligible for the HINTS exam. Patients presenting with the acute vestibular syndrome could be having a peripheral (nerve) problem (acute vestibular neuritis) or a central (brain) problem (stroke or other acute brain lesion). The HINTS exam is a battery of 3 bedside tests which accurately differentiate peripheral versus central causes of the acute vestibular syndrome – but it is only validated in patients with ongoing, continuous acute dizziness and nystagmus. If the patient does not have continuous nystagmus, the HINTS exam is NOT indicated. Make sure you do a history and physical to exclude any RED FLAGS for stroke (explored in Chapter 7 – Head and Neck Exam) prior to doing the HINTS+ exam.
• Head Impulse (this tests the patient’s vestibular-ocular reflex, a reflex arc which enables the eyes to automatically adjust to head movements to keep vision stable): Patient’s head centred; eyes fixed on your nose. Examiner turns patient’s head slowly 20 degrees to one side, and then briskly and suddenly towards centre. Normally, the patient’s eyes will stay fixed on your nose if their vestibular nerve is intact. If they have impairment of the vestibular-ocular reflex – you will see the eyes momentarily lose focus with the head turn, and then snap back (catch-up saccade) to focus on you. A positive catch-up saccade suggests vestibular nerve dysfunction, which will always occur if the patient has vestibular neuritis (peripheral cause of AVS), but is not typically seen in a stroke or other central cause of AVS.
• Nystagmus: Patient’s head centred; observe their eyes for nystagmus. Ask patient to look to left and observe for nystagmus – is it left-beating or right-beating? Then ask patient to look to right and observe for directional nystagmus – did direction of the nystagmus change (bidirectional) or stay the same (unidirectional)? Unidirectional nystagmus suggests peripheral vertigo, where the fast phase beats away from the side with the lesion. Bidirectional, or vertical nystagmus suggests central vertigo.
• Test of Skew: Patient head centred; eyes fixed on your nose. Examiner covers one eye with their hand. After a second, move to cover the opposite eye. Watch the now uncovered eye – do you see any vertical skew? (post-uncovering correction to refocus on your nose). Repeat with the other eye. Vertical or Diagonal Skew deviation suggests a central lesion.
• + a bedside test of hearing: the plus in HINTS+ is a bedside test of hearing. Use a finger rub 2cm from the patient’s ears to screen for a new significant hearing loss. New hearing loss could indicate Anterior Inferior Cerebellar Artery Stroke infarcting the entire labyrinth, so a new hearing loss raises the concern for a central cause. New hearing loss could also be present in peripheral problems like labyrinthitis and sudden sensorineural hearing loss. Regardless, it is important not to miss a new hearing loss in patients with the acute vestibular syndrome.

Why Check: In a patient with ONGOING dizziness/vertigo lasting hours to days and spontaneous nystagmus (acute vestibular syndrome), it is important to separate central causes (e.g. brainstem/cerebellar ischemia) from peripheral causes (e.g. vestibular neuritis).

• Head Impulse Test: Tests the Vestibulo-ocular reflex – which should be preserved in a central cause and affected in a peripheral cause on the ipsilateral side.
• Nystagmus: In a peripheral cause, there is a unilateral imbalance of vestibular signal from the affected side. This means the unaffected side is unopposed, and eyes are pushed towards the lesioned side. The fast phase of nystagmus gives rise to observed left-beating vs. right-beating. This activity represents the brain correcting for the deficiency of unilateral peripheral vestibular input. By contrast, nystagmus that is vertical or direction changing would not be seen in vestibular neuritis (peripheral cause) and points towards a central cause.
• Test of Skew: Tests vestibular input to the oculomotor system. A positive vertical test of skew is concerning for central vertigo.

(Conditional Test for BPPV – See Ch 31 – Neuro Exam – MF4)

Provocative Testing for Diagnosing BPPV

Benign Positional Paroxysmal Vertigo (BPPV) is caused by loose debris (otoconia) within one of the semi-circular canals of the vestibular apparatus. Each ear has 1 vestibular apparatus and each vestibular apparatus has 3 semi-circular canals. The most common location for otoconia in BPPV is the posterior canal (~65%), followed by the horizontal canal (~30%), while the anterior canal is relatively rare. Movement of loose otoconia within a semicircular canal will reliably produce vertigo with a different type of nystagmus depending on which canal is affected. Therefore, we use provocative testing in BPPV to watch for which type of nystagmus and LOCALIZE which ear and canal the otoconia are in. Once we have localized the otoconia, we can then use the appropriate particle repositioning maneuver to correct the problem and cure our patients.

Provocative tests for BPPV are indicated only if you suspect a diagnosis of BPPV based on a history of brief, (less than one minute), intense attacks of dizziness that are always triggered by head movements (most commonly lying down or turning over in bed). A patient who has continuous dizziness present at rest lasting hours to days should never get provocative tests for BPPV. You should also ensure that the patient does not have any red flags for a serious central cause of dizziness, and that there is not another cause (such as postural hypotension or vestibular migraine or Meniere’s disease) that better explains their symptoms, prior to provocative tests.

Since the most common type of BPPV is posterior canal (~65%), this is the first canal which we test in a patient with suspected BPPV. Posterior canal BPPV is identified using the Dix-Hallpike Test.

Say: I will move you from a sitting to lying down position on the exam table and move the neck to the side and back. Please tell me if these movements reproduce your symptoms of vertigo.

Do: Have patient sit upright on exam table with legs extended. Rotate head by 45° to one side. Maintaining the 45° rotation, lie the patient back, hang their head over edge of the exam table, and extend their neck an additional 20°. Look for reproduction of symptoms AND observe for nystagmus in patient’s eyes. Posterior canal BPPV produces an upwards, torsional nystagmus. There is often a latent reaction for about 5 seconds before the nystagmus is generated. Repeat with rotating head to other side to test the other ear.

Report: I cannot reproduce upwards torsional nystagmus or vertigo with a Dix-Hallpike test on either side, therefore it is unlikely the patient has posterior canal BPPV

Why Check: Used to diagnose and localize the affected ear in patients with Posterior Canal Benign Paroxysmal Positional Vertigo (BPPV). Eliciting ~10-30 seconds of upwards, torsional nystagmus is diagnostic for posterior canal BPPV on the side you are testing. Once you have localized which ear has posterior canal BPPV, you can proceed to particle repositioning maneuver (Epley or Semont) for posterior canal BPPV on the affected side.

(Conditional Test for horizontal canal BPPV – See Ch 31 – Neuro Exam – MF4)

Since the second most common type of BPPV is horizontal canal (~30%), this is the second canal which we test in a patient with suspected BPPV. Horizontal canal BPPV is identified using the Supine Roll test.

Say: I will reposition you to look to one side and then the other side while lying flat on your back.

Do: Have patient lie supine on an exam bed. Turn their head to one side and examine their eyes for nystagmus. Then turn their head to the other side and examine for nystagmus. If they have horizontal canal BPPV, you will see horizontal nystagmus on both head turns which is either towards the ground (geotropic) or away from the ground (apogeotropic).

Report: There is no horizontal nystagmus on supine roll test, therefore it is unlikely the patient has horizontal canal BPPV.

Why Check: Used to localize the affected ear in patients with Horizontal Canal Benign Paroxysmal Positional Vertigo (BPPV). On the side that has the more intense nystagmus, the nystagmus will beat towards the affected ear. When you have identified which ear is affected and whether it is geotropic or apogeotropic, you can proceed with an appropriate particle repositioning maneuver (Gufoni or Barbecue roll) for the affected side.

• Video 1 - Posterior Canal BPPV Diagnosis Using Dix Hallpike Test: https://www.youtube.com/watch?v=kvVnEsGVLUY
• Video 2 - Quick Review of HINTS exam: https://www.youtube.com/watch?v=-VXwD2nskhQ
• Video 3 - Horizontal Canal BPPV Diagnosis Using Supine Roll Test: https://www.youtube.com/watch?v=VRjRTnIw9YE

Note: The widely used Clinical Prediction Rule for Strep Throat is the Centor Score. It is based on assigning 1 point to each of the following: (1) History of Fever; (2) Anterior Cervical Adenopathy; (3) Tonsillar Exudate; (4) Absence of Cough. It can also be modified for pediatric populations → Assign 1 additional point if Age < 15; as well as subtract 1 point if the patient’s Age is over 45. The following table details the evidence behind the Centor Score towards clinical decision making, with or without using a Rapid Strep Point-of-Care test result:

Table 1: Signs, Symptoms and Overall Clinical Impression Findings for Obstructive Sleep Apnea³⁶

Table 2: Diagnostic Odds Ratios of STOP-BANG Scores 3, 4 and 5 (out of 8) for predicting Obstructive Sleep Apnea in Patients with Class I Obesity (BMI 30-35) and Class II-III Obesity (BMI >35)³⁷