BMS 200 HEENT 2 Fall 2023 PDF

HEENT 2 Ear and vestibular apparatus pathologies General anatomy of the mouth and sinuses Neurology of the olfactory and gustatory pathways BMS 200 Outcomes – to come later Pathologies of the ear Conductive vs. sensorineural hearing loss Otitis externa & otomycosis Otit...

HEENT 2 Ear and vestibular apparatus pathologies General anatomy of the mouth and sinuses Neurology of the olfactory and gustatory pathways BMS 200 Outcomes – to come later Pathologies of the ear Conductive vs. sensorineural hearing loss Otitis externa & otomycosis Otitis media  Acute otitis media (AOM)  Otitis media with effusion (OME)  Chronic otitis media Cholesteatoma Tympanic membrane perforations Hearing loss - generalities One of the most common sensory defects  15% between 20 and 69 years have some degree of high-frequency hearing loss due to noise Outer and inner hair cells are damaged by noise, but the outer are more vulnerable  Presbycusis (age-induced) hearing loss is likely due to a combination of neuronal loss and hair cell loss  Many substances are ototoxic Antibiotics, chemotherapeutic agents, diuretics are often implicated Many of these substances damage either the outer hair cells or the stria vascularis Hearing loss - generalities Conductive hearing loss – impaired sound transmission in the external or middle ear, impacts all frequencies  Trauma to the tympanic membrane, infection, plugging of the external auditory meatus/canal, otosclerosis, cholesteatoma Sensorineural hearing loss – often loss of higher frequencies more than lower  Presbycusis, ototoxic agents, noise (most common)  Problems with endolymph (Meniere’s), infections of the labyrinth or 8th CN, tumours (acoustic neuroma, brainstem tumours)  Tuning fork investigation of hearing Rinne Weber Method Base of vibrating tuning fork placed Base of vibrating tuning on vertex of skull fork placed on mastoid process until subject no longer hears it, then held in air next to ear Normal Hears equally on both sides Hears vibration in air after bone conduction is over Conduction Sound louder in diseased ear Vibrations in air not deafness (one because masking effect of heard after bone ear) environmental noise is absent on conduction is over diseased side Sensorineural Sound louder in normal ear Vibration heard in air deafness (one after bone conduction is ear) over, as long as nerve deafness is partial  Audiometry Human ear can hear from 20 – 20000 Hz  We’re best at hearing 1000 – 4000, human speech ranges from 500 – 2000 Hz Audiometry assesses hearing at particular tones (see FYI graphic below) and is much better at characterizing hearing loss than tuning fork tests Different forms of audiometry  i.e. speech audiometry Otitis externa 90% of otitis externa is bacterial  Usually staphylococcal, pseudomonas aeruginosa, or E. coli Risk factors include:  Humidity, loss of cerumen (trauma, excessive Q-tip use), heat, increased pH, obstruction of the ear canal, exposure The secretions of the ear are somewhat acidic, and this acts as a form of barrier immunity Infection can lead to an increase in pH (occlusion of secretions) Water (especially water colonized by bugs) in the ear canal is a prominent risk factor Otitis externa Clinical Features  Otalgia – movement of the pinna/tragus can elicit this Movement of the outer ear doesn’t exacerbate otitis media  Otorrhea (ear discharge) which can be purulent  Itching of the external canal  Edema  occlusion of the ear canal  conductive hearing loss  Severe infection can lead to cellulitis (deeper layers, skin involvement) Treatment – topical antibiotics  Make sure not to use ototoxic antibiotics with a perforated TM  Otitis externa - variations Furunculosis – otitis externa of the outer 1/3 of the ear canal, usually staphylococcal Chronic otitis externa – less painful, more itchy  Usually caused by repetitive trauma, chronic drainage from a middle ear infection Malignant/necrotizing otitis externa – bad news  Progressive, slowly developing infection, severe otalgia, lots of otorrhea, granulation/necrotic tissue in the auditory canal Can be life-threatening if the infection colonizes temporal bone, intracranial structures Cranial nerve palsies and systemic infection also possible  More common in the elderly, diabetics, immunocompromised – usually P. aeruginosa  Medical emergency Otitis externa - variations Otomycosis – fungal infection of the external auditory canal, up to 10% of otitis externa  Usual agent is Aspergillus (80%), next most common is Candida species  More likely in: Diabetes, elderly, past history of HEENT surger in the mastoid  Often seen in those with poor response to antibacterial antibiotics Fungal debris is often present on otoscopy Otitis Media This has been discussed to some degree in CMS Acute otitis media (AOM): rapid onset of signs and symptoms, including fever and otalgia Recurrent AOM = 3 or more episodes within a 6-month period or four or more episodes within a 12-month period - complete resolution of symptoms between episodes Usually due to auditory tube dysfunction Up to age 7, eustachian tube is shorter, wider, and more horizontal than in adults – predisposes to upper airway/oral bacteria colonization Blockage of the tube – swelling of adenoid lymphatic tissue, swelling due to URTI or allergic rhinitis, inadequate tensor palatini function Lack of breastfeeding (breast milk has antimicrobial sustances in it) Otitis Media AOM – General pathogenesis  Obstruction of the auditory tube  air absorbed in middle ear  negative pressure  edema of mucosa with exudate and fluid accumulation  infection from nasopharyngeal secretions  Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis  Major viruses implicated: RSV, influenza, parainfluenza, adenovirus (more next semester) AOM – Clinical Features  Triad of otalgia, fever, and conductive hearing loss Rare to have tinnitus, vertigo, or facial nerve paralysis  Otorrhea can occur if the TM is perforated  Otitis Media AOM – Clinical Features cont…  Bulging, red TM (middle ear inflammation)  Often the TM is opaque, bony landmarks are lost  effusion can often be seen behind it, and mobility is limited (pneumatoscopy) Otitis Media OME (AKA serous otitis media)  Often due to untreated or unresolved AOM Persistent effusion in up to 40% of children 30 days after initial AOM, continued for 3 months in 10% Main concern in pediatric population is impact on hearing at early ages (prior to a year)  Delay in language development  Risk factors are similar to those for AOM OME – Clinical Features  Conductive hearing loss with or without tinnitus  Feeling of fullness in the ear, low-grade fever  May or may not involve otalgia  Otitis Media OME on otoscopy:  TM is translucent/gray (limited inflammation) Fluid behind the ear, can often see air-fluid levels or bubbles  Loss of light reflex, reduced mobility on pneumatoscopy Most cases resolve on their own  Tympanostomy tubes can improve hearing  Case-by-case treatment depending on presentation Tympanic membrane perforations Most common causes:  Middle ear infections  Trauma – can be barotrauma or physical injury to the ear TM perforation – Clinical Features  Sudden onset of pain, hearing loss  Can include bloody otorrhea  Vertigo or tinnitus Usually transient Perforations usually heal spontaneously – advisable to wear earplugs while swimming, bathing  Postero-superior damage to the TM is more likely to damage the function of ossicles – more urgent referral to the HEENT Chronic otitis media TM perforation in the setting of recurrent or chronic ear infections  chronic inflammation affecting both the middle ear and the mastoid cavity  Dysfunction of the Eustachian tube is a significant factor in this disease, observed in approximately 70% of patients undergoing middle ear surgery Types include:  Suppurative or serous chronic otitis media – describes character of the drainage through the perforated TM  Benign chronic otitis media – “dry” – no active infection Chronic otitis media Viruses usual cause, though bacteria are more likely to contribute in children  Pathogens invade via the external canal  edema, fibrosis, perforation and persistent infection  Can also be a complication of tympanostomy tubes Clinical features:  Otorrhea  May or may not involve conductive hearing loss, tinnitus, or aural fullness  Can have occasional severe intracranial complications in children Cholesteatomas Very little cholesterol, and not a neoplasm, so may be one of the worst-named entities in medicine – Definition - non-neoplastic, cystic lesions lined by keratinizing squamous epithelium or metaplastic mucus-secreting epithelium, and filled with debris Occur in the middle ear, mostly in the posterior- superior region (sometimes called the attic) Debris contains mostly keratin, other cellular debris Cyst is usually between 1 and 4 cm Three main types: – Primary congenital – keratined epithelium is “misplaced” into area that should only have bone or simple cuboidal mucosa (not very common, will not discuss pathogenesis) – Secondary acquired, Primary acquired – see next few slides Cholesteatoma - complications Why do we care about cholesteatomas? – Lead to conductive hearing loss (most minor complication) Even after surgical intervention, some degree of hearing loss usually ensues – Can cause serious bony destruction of the temporal bone  infected cyst gains access to the dura and intracranial structures  meningitis and death Cholesteatoma should almost always be removed to avoid this Can also migrate and rupture into deep neck structures  another source of potentially life- threatening infection  Cholesteatoma - pathogenesis Secondary acquired: – Traumatic “implantation” of keratined epithelial cells from the “external-ear” side of the tympanic membrane or auditory canal Traumatic causes include blast damage, iatrogenic (surgical, insertion of ear tubes) – not as common as primary acquired Primary acquired: – Most common type – Recent investigations implicate a combination of chronic secondary acquired… inflammation and abnormal TM cell migration Primary Acquired Cholesteatoma - Pathogenesis Most recent and likely best hypothesis: – Inner surface of the TM consists of respiratory epithelium (simple cuboidal ciliated epithelium with goblet cells) that migrates over its surface in postero- superior direction – As it migrates more This migration tends to rapidly in response to chronic inflammation, it occur as a response to becomes “stuck” to the inflammation in teenage – incus adult years Young children do not tend to get primary acquired Primary acquired cholesteatoma - pathogenesis Next stage – mucous accumulates in the pouch  chronic inflammation (often pseudomonas implicated) if it gets infected This is followed by implantation/conversion of some of the cells in this cyst to keratinized epithelial cells – Note that the “outer” surface of the TM is pulled into the cystic structure Outer surface formed from keratinized epithelium, not respiratory epithelium  Primary acquired cholesteatoma - pathogenesis The “stuck” keratinized cells keep dividing, and continued inflammation is likely linked to: – Growth of the cystic structure – Activation of osteoclasts and invasion of the temporal bone – Conductive hearing loss Tend to see them develop in the as the mobility of the pars flaccida (postero-superior ossicles is impaired to handle of malleus) because: This is the direction the inner (remember, the inner surface of the TM got surface of the TM “likes” to stuck to the incus) migrate This part of the TM has a lot of resident inflammatory cells This area is close to the incus Primary acquired cholesteatoma – appearance on otoscopy Normal ear A small cholesteatoma A huge one  Cholesteatomas Not terribly common, but not terribly rare – about 10/100,000/year (about 300 or so in Lower Mainland/year) – By far most common type is primary acquired, but a history of head trauma or HEENT surgeries may imply presence of a secondary acquired Clinical Features: – Painless otorrhea (hallmark finding) Otorrhea increases as infection worsens, almost impossible to treat non-surgically – Conductive hearing loss (sometimes sensorineural as well) Prognosis: very few die from cholesteatomas, as they are usually discovered and surgically treated – Usually results in some hearing loss post-op – With new theories of pathophysiology many existing and new drugs, as well as less invasive procedures, have potential to treat and perhaps better preserve hearing  Cholesteatoma Other clinical features Rarely vertigo or dysequilibrium may arise due to the inflammatory process within the middle ear or due to invasion of the labyrinth Facial nerve palsy, can also result from the inflammatory process or mechanical compression of the nerve Dizziness How is “dizziness” classified? – Vertiginous (vertigo) The environment seems to be moving Caused by inner ear or brainstem-cerebellar disorders – Inner ear = peripheral – Brainstem-cerebellar = central – Non-vertiginous Organic –a pathology that usually involves visual compromise or low blood pressure Functional – common in a wide range of mood disorders Benign paroxysmal positional vertigo Acute attacks of transient rotatory vertigo lasting seconds to minutes initiated by certain head positions – Accompanied by rotatory nystagmus Most common form of positional vertigo (50% of patients with peripheral vestibular dysfunction) – Symptoms are usually brief, caused by changing head position – Typical history = worsening when getting out of bed, extending the neck Usually caused by migration of a free-floating otolith (should not be free-floating, should be attached) BPPV Diagnosis? – Dix-Hallpike Positional Testing Patient rapidly moved from a sitting position to a supine position with the head hanging over the end of the table, turned to one side at 45° and neck extended 20° holding the position for 20 s – Onset of vertigo and rotatory nystagmus indicate a positive test for the dependent side Meniere’s disease Episodic attacks of tinnitus, hearing loss, and vertigo lasting minutes to hours – Inadequate absorption of endolymph leads to endolymphatic over-accumulation that distorts the membranous labyrinth – Usually begins in middle age – Triggered by high salt intake, caffeine, stress, nicotine, and alcohol Diagnostic Criteria for Menière’s Disease (must have all three) – Two spontaneous episodes of Rotational vertigo ≥20 min Audiometric confirmation of Sensorineural Hearing Loss Tinnitus and/or aural fullness Vestibular Neuronitis Acute onset of disabling vertigo often accompanied by nausea, vomiting, and imbalance without hearing loss that resolves over days leaving a residual imbalance that lasts days to weeks – Could be viral, often associated with URTI Acute phase – Severe vertigo with nausea, vomiting, and imbalance lasting 1-5 days – Nystagmus – Patient tends to veer towards affected side Convalescent phase – Imbalance and motion sickness lasting days to weeks – Spontaneous nystagmus away from affected side – Gradual vestibular adaptation requires weeks to months Labyrinthitis Acute infection of the inner ear resulting in vertigo and hearing loss May be serous (viral) or purulent (bacterial) – Occurs as a complication of acute and chronic otitis media, bacterial meningitis Bacterial: S. pneumoniae, H, influenzae, M. catarrhalis, P. aeruginosa, P. mirabilis Viral: rubella, CMV, measles, mumps, varicella zoster Sudden onset of vertigo, N/V, tinnitus, and unilateral hearing loss with no associated fever or pain – Meningitis is a serious complication Acoustic neuroma Intracranial tumours that develop from Schwann cells that myelinate the vestibular and/or cochlear nerve – Can take up much of the space of the cerebellopontine angle (80% of tumours in this area are acoustic neuromas) – Most are from the vestibular component of the nerve Clinically relevant (i.e. big, or impair hearing) acoustic neuromas occur in ~ 1/100,000 – There’s quite a bit of room in that area of the brain, so often do not elevate intracranial pressure until they are quite large – Can also impinge on the nearby facial nerve and trigeminal nerve Most have no risk factors, but some are at a higher Acoustic neuromas Acoustic neuroma Clinical Features: Hearing loss by far the most common – Can be sudden or gradual, constant or fluctuating – Assume that all unilateral neurosensory hearing loss is due to an acoustic neuroma until proven otherwise Vertigo is fairly uncommon, but balance difficulties are common Facial weakness or Treatment/Prognosis: numbness due to CN Microsurgery or radiation VII or V impingement Headache due to used to treat, generally elevated intracranial survival is quite good pressure 30 – 80% maintain hearing