Eustachian Tube (ET) Dysfunction Eustachian Tube (ET) Dysfunction

 Diagnosis of ET dysfunction  Diagnosis of ET dysfunction depends upon: depends upon: – Subjective symptoms of aural – Ruling out presence of middle fullness and/or ear “popping” ear effusion (with or without a history of  Tympanogram usually will reveal environmental ) reduced middle ear pressure – Careful otoscopic examination of the tympanic membrane with pneumatic insufflation to rule out effusion

Eustachian Tube (ET) Dysfunction Middle Ear Effusion

 Treatment  Diagnosis of middle ear effusion: – Otalgia with hearing loss – Nasal steroids/saline lavage – Otoscopic examination reveals – Antihistamines/Decongestants middle ear effusion with absent movement – Insufflation of ET – In an adult, a mass in the – Oral nasopharynx must be considered as a possible etiology – GERD treatment – Middle ear ventilation tube placement (only in rare instances)

Middle Ear Effusion Middle Ear Effusion

 Audiogram will demonstrate a  Treatment conductive hearing loss with a – Oral “flat” tympanogram – Oral corticosteroids – Middle ear pressure equalization tube (PET) placement if persists Hemotympanum Tympanosclerosis (aka Myringosclerosis)

 Bloody middle ear effusion  White plaque-like deposit on usually secondary to trauma tympanic membrane (TM)  Workup should include a surface thorough neurologic examination – Usually secondary to frequent and CT scan of temporal bones otitis media and audiogram   Blood will usually reabsorb No treatment necessary spontaneously over 4-12 weeks (unless impairment of TM  If no resolution, PET is indicated mobility is noted)

Tympanic Membrane Perforation Tympanic Membrane Perforation

 Occurs secondary to pressure  Treatment should include: and/or fluid accumulation in – Oral antibiotics the middle ear (can be post – Ear drops head trauma) – Dry ear precautions

 Conductive hearing loss  If perforation is small and/or  Potential for otorrhea and post-traumatic, may recurrent middle ear infections spontaneously heal in 3-8 weeks without

Otitis Externa Otitis Externa

 Infection of external auditory  Treatment should include: canal (EAC) – Oral antibiotics with anti- – Exquisitely painful Psudomonal coverage – Severe canal edema (conductive hearing loss) – Otowick placement – History of EAC trauma nearly – Otic drops with anti- always elicited Pseudomonal coverage – Multiple bacterial species (including Pseudomonas) are usually present Otitis Externa Exostosis

 Higher incidence in  Hypertrophy of the bony external immunocompromised auditory canal populations  Secondary to chronic exposure to cold water (surfing, ocean swimming)  If any facial nerve weakness or  No treatment needed unless near-total cranial neuropathies are present, EAC occlusion and/or secondary possibility of “malignant otitis conductive hearing loss externa” (skull base  Need for meticulous ear cleaning after osteomyelitis) must be considered water exposure

Nasal Polyps Nasal Polyps

 Inflammatory growths associated  Diagnosis also depends upon with chronic allergies radiographic appearance of  Can cause anatomic obstruction sinuses (limited CT scan) of sinus ostia with secondary acute sinusitis  Associated with asthma and aspirin (Sampter’s triad)

Nasal Polyps Nasal Septal Hematoma

 Treatment  Usually secondary to trauma – Antibiotics  Not always an associated nasal – Oral corticosteroids bone fracture – Antihistamines/Decongestants  Needle aspiration and/or incision and drainage – Nasal/sinus lavage – Surgery  High incidence of recurrence Nasal Septal Hematoma Mucocele

 If hematoma is left undrained,  Accumulation of mucous in secondary compromise of the submucosal space  Most common on labial and vascular supply to nasal dorsal buccal surfaces cartilage can result is so-called  Usually secondary to dental saddle nose deformity trauma  Occasional superinfection in which case surgical excision may be indicated

Oral Leukoplakia Oral Leukoplakia

 “White plaque”  Workup should include thorough  Presents most commonly on examination of mucosa of upper lateral aspect of tongue and aerodigestive tract (especially in buccal mucosa tobacco-users)  Associated with trauma or  Biopsy of areas of erythroplakia chronic inflammation/irritation more important than representative sampling  Low (less than 5%) premalignant potential

Geographic Tongue Torus Palatini and Torus Mandibularis

 Asymmetric hypertrophy of  Bony overgrowths present in papillae of tongue palate and inner cortex of  Unknown etiology mandible  Rarely symptomatic  Unknown etiology  Treatment with antifungal or  Unless overlying mucosa becomes not indicated inflamed, no treatment indicated for these benign lesions  May be exacerbated by GERD Tonsillitis Tonsillar Lymphoma

 Infection of palatine tonsillar tissue with  Lymphoma (usually B-cell type) exudates and trismus comon in the acute that develops within the setting lymphoid tissue of the palatine  Chronic infections are associated with tonsils (part of Waldeyer’s ring) hypertrophy and possibly tonsoliths (tonsil stones)  Important to keep high index of  Treatment simultaneously with oral suspicion if significant corticosteroids and antibiotics for acute infections asymmetry, cervical adenopathy,  Surgical excision may be indicated for constitutional symptoms frequent infections, airway obstruction, halitosis, or noticeable asymmetry

Peritonsillar Abscess Parotitis

 Acute, suppurative infection with the  Inflammation of the parotid ductal submucosal space around tonsils system with associated swelling, pain,  Will always be uvular deviation, bulging erythema, fevers of soft palate, trismus, and muffled-  Increased incidence in diabetics but can sounding voice occur secondary to episode of  Treatment involves either needle dehydration aspiration and/or incision and drainage  Rarely can occur secondary to parotid with oral antibiotics and corticosteroids stone (sialolith)  Can re-accumulate following needle  Treatment includes antibiotics, aspiration hydration, oral sialogogues, heat and massage directly over the involved gland

Submandibular Sialoadenitis/Sialolithiasis Parotid Neoplasm

 Acute inflammation of submandibular  Firm mass within the substance of salivary gland parotid salivary gland  Can be secondary to dehydration (as in  Approximately 80% benign parotitis) but more commonly due to  Presence of ipsilateral facial nerve sialolith (stone) weakness, pain, or adenopathy increase  Physical exam can often palpate stone likelihood of malignancy along course of submandibular duct  Diagnostic workup should include MRI (within the floor of mouth) of parotid gland followed by fine needle  Treatment is same as for parotitis aspiration biopsy except that frequent infections with an  Treatment involves surgical excision of associated sialolith mandate surgical gland excision of gland Second Branchial Cleft Cyst Thyroglossal Duct Cyst

. painless, fluctuant mass in the  most common congenital lateral aspect of the neck that is neck mass (70%) situated deep to the sternomastoid muscle  elevates on protrusion of . most common branchial cleft tongue or swallowing anomaly (95%)  may develop draining sinus . often becomes apparent after on skin surface recent URI  presentation varies depending upon age

Thyroglossal Duct Cyst Bell’s Palsy

 Usually present at or just inferior  Paralysis of all branches (upper to the hyoid bone and lower) of facial nerve – may be associated with ectopic  Sudden onset thyroid tissue (1-2%) therefore imaging to confirm  Viral prodrome (usually) the presence of normal  Diagnosis of exclusion thyroid tissue is recommended  Must rule out presence of co-  Treatment is surgical excision existing mastoiditis, otitis (Sistrunk Procedure) externa, parotid tumor

Bell’s Palsy

 Likely secondary to infection of facial nerve with herpes simplex virus  Treatment includes oral corticosteroids and possibly also with an antiviral medication with reassessment after 7-10 days