External Ear Flashcards
√Describe the 6 nerves innervating to the EAC and Auricle (and sources of referred otalgia)
- Auriculotemporal nerve (V3)
- Innervates: Anterior auricle, tragus, anterior EAC, tensor tympani (medial ptergoid nerve)
- Etiologies in referred otalgia: TMJ disease, dental pathology, parotid tumor/inflammation - Posterior Auricular Nerve (VII)
- Innervates: Posterior surface of auricle/posterior auricular skin, posterior EAC, stapedius (nerve to stapedius)
- Etiologies in referred otalgia: CPA tumors, Herpes zoster, Geniculate neuralgia - Jacobsen’s nerve (IX)
- Innervates: Medial surface of TM, promontory, eustachian tube
- Etiologies in referred otalgia: Tonsillitis/pharyngitis, Eagle’s syndrome, sinusitis, pharyngeal tumor, sinusitis - Arnold’s nerve (X)
- Innervates: Lateral surface of TM, floor of EAC, Concha
- Etiologies in referred otalgia: Laryngeal tumor, GERD, Thyroid inflammation/tumor pathology - Great auricular nerve (C2-3)
- Innervates: Inferior preauricular overlying parotid, medial postauricular overlying mastoid, and posterior auricle
- Etiologies in Referred otalgia: Cervical spine degenerative diseases, Whiplash/trauma, Cervical meningiomas - Lesser occipital (C2-3)
- Innervates: Mastoid region
- Etiologies in referred otalgia: Cervical spine degenerative diseases, Whiplash/trauma, Cervical meningiomas
Vancouver Page 274
√What is the difference between osteoma and exostoses? What is their management?
Exostoses:
- Epidemiology: Common
- Type of tumor: Periostitis secondary to cold temperature (cold water)
- Location: Usually bilateral, medial in EAC (medial to the sutures on the tympanic bone)
- Clinical presentation: Multiple, broad based (sessile)
- Histology: Parallel layers of subperiosteal bone, no or poorly developed trabeculated fibrovascular channels
- Radiographic: Intact cortex
Osteoma:
- Epidemiology: Rare
- Type of tumor: True benign neoplasm
- Location: Unilateral, lateral in EAC (rise from tympanosquamous or tympanomastoid suture)
- Clinical presentation: Single, pedunculated
- Histology: Lamellar bone around trabecular cancellous bone with marrow and fibrovascular tissue
Management:
- Conservative
- Canaloplasty
Describe and differentiate Keratosis Obturans and EAC cholesteatoma
Keratosis Obturans:
- Pathophysiology: Keratin debris obliterates the EAC due to abnormal epithelial migration and/or hyperplastic epithelium with increased desquamation
- Age: Young adults
- Associations: Sinusitis, Bronchiectasis
- Pain: Acute, severe
- Hearing loss: Moderate, conductive
- Otorrhea: Rare
- Lateralization: Usually bilateral
- Bony Erosion: Circumferential widens canal but does not destroy bone (just pushes it)
- Organization of squamous debris: Layered
- Meatal Skin (most reliable differentiation): In tact
- Osteonecrosis (most reliable differentiation): Absent
- Treatment: Regular, lifelong, suctioning of debris
EAC cholesteotoma
- Pathophysiology: Invasion of squamous tissue into a localized area of periosteitis in the canal wall; may be acquired (due to surgery, trauma, chronic inflammation) or spontaneous
- Age: Elderly
- Associations: None
- Pain: Chronic, dull
- Hearing loss: Little to none
- Otorrhea: Frequent
- Lateralization: Usually unilateral
- Bony Erosion: Localized
- Organization of squamous debris: Random
- Meatal Skin (most reliable differentiation): Focal ulceration
- Osteonecrosis (most reliable differentiation): Usually present
- Treatment: Small limited lesion = conservative approach; Bony destruction extends into middle ear/mastoid and unresponsive to medical therapy = surgery removal of cholesteatoma and affected bone, grafting of skin
√What are 2 diseases associated with keratitis obturans?
- Sinusitis
- Bronchiectasis
Compared to cholesteatoma, patients with keratitis obturans have 4 main differences, which are what?
- Younger patients
- Less or no draining ear
- More generalized position, compared to cholesteatoma which are just localized to lateral to annulus
- Widens EAC (but does not destroy bone)
√What is the differential diagnosis of a painful nodule on the ear? Describe 6.
- Chondrodermatitis Helicis Nodularis
- Necrotic, extruding auricular cartilage (thought to be a pressure ulcer-type phenomenon); can simulate BCC or SCC - Skin malignancies
- BCC, SCC, melanoma, adenoid cystic carcinoma, cerumoma - Furuncle
- Staph aureus infection of hair follicle/pilosebaceous unit in outer EAC.
- Treated with antibiotics ointment, warm compresses, +/- I+D
- IV cloxacillin if cellulitis - Gout
- Purine metabolic disorder, uric acid deposited in tissues
- Acute pain treated with colchicine
- Allopurinol (overproducers) or Probenecid (underexcretors) for long term maintenance - Ochronosis
- Disorder characterized by a clinical appearance of blue-black or gray-blue pigmentation
- Alkaptonuria (black urine disease), homogentisic acid metabolic disorder; turns black when oxidized, deposited in cartilage - Darwin’s Tubercle
- Autosomal dominant, incomplete penetrance
- Painless normal anatomic variation on the postero-superior helix (little nub)
See Vancouver page 276
What is the infection caused by Pseudomonas Pyocyaneus and its sequelae?
Perichondritis
- Characterized by diffuse inflammation of the pinna and severe pain
- If not treated aggressively with antibiotics +/- drainage, loss of cartilage and permanent deformity can result
√List a complete differential diagnosis for acute otitis externa
- Acute otitis externa
- Chronic otitis externa
- Malignant/Necrotizing otitis externa
- EAC cholesteatoma (± infected)
- Granuloma
- Squamous cell carcinoma
- Otomycosis
- Otitis externa bullosa sive hemorrhagica
- Perichondritis
- Eczema
- Herpes zoster oticus
Phases of chronic otitis externa (> 3 months)
- Pre-inflammatory: Stratum Cornea edema, loss of lipid layer
- Inflammatory: Pain, papules
- Chronic - ulceration, lichenification (thickened, hardened area of skin)
- ± Furuncle: Staph aureus infection of pilosebaceous unit
List 5 bacterial etiologies of acute otitis externa
- Pseudomonas Aeruginosa (most common for malignant OE)
- Proteus mirabilis
- Staphylococci
- Streptococci
- Peptostreptococcus - klebsiella
What is the main bacterial etiology of chronic otitis externa?
Proteus vulgaris
What are the etiologies of fungal chronic otitis externa?
- Aspergillus niger
- Candida albicans
*commonly get granulation at handle of malleus
What are the fissures of santorini?
Fissures present in the lateral cartilaginous EAC which allow passage of infection or neoplasm into the preauricular parotid tissues and glenoid fossa
What is the foramen of Huschke?
An embryologic remnant that forms a defect within the bony EAC which allows passage of infection or neoplasm from the medial EAC into the preauricular parotid tissues and glenoid fossa
Describe 4 basic principles of otitis externa management
- Thorough cleaning and debridement
- Antibiotic treatment - topical ± oral depending on severity
- Counselling patient - avoid instrumentation, keep dry ear
- Analgesia - depending on severity
What are 4 cardinal features of necrotizing otitis externa (malignant OE)?
Skull base osteomyelitis, commonly caused by pseudomonas infections
Features:
1. Otalgia > 1 month
2. Otorrhea/granulation tissue
3. Advanced age, diabetes or immune suppression
4. Cranial neuropathy
Infected granulation tissue on the floor of the
cartilaginous ear canal near the osteo-cartilaginous
junction is a hallmark of malignant OAE
Vancouver notes page 277
What are 3 cranial nerves most often involved in necrotizing otitis externa?
Facial (75%)
Vagus (70%)
Accessory (56%)
What are Investigations that can be done for malignant otitis externa?
Bloodwork:
- HbA1c (diabetes)
- WBC
- CRP
Imaging:
- CT (Anterior TMJ bone erosion)
- MRI (to follow disease and evaluate for dural and intracranial involvement)
Nuclear Medicine Tests:
1. Technetium-99 scan: Used to identify presence of acute or chronic osteomyelitis, identifies increase in osteoblastic activity; stays positive for prolonged period & lags behind gallium for months
- Abnormal = >10% increase in activity
- High sensitivity, low specificity
- Use to follow disease resolution
- PMN Gallium-67 scan: Incorporated into proteins & leukocytes during acute inflammatory process, used to follow resolution of the disease, will fade as disease process settles
- WBC Indium 111: Best for following treatment progress, has largely replaced G-67. Earliest changes seen on MRI (within 1-2 days)
What is the most useful imaging for tracking progress of necrotizing otitis externa?
Single photon emission tomographs (SPECT) with two radionuclide tracers - Indium-111-labeled leukocytes, and technetium-99m
What is the management of malignant otitis externa? List 7 components
- Prolonged IV antibiotics with ID consult (anti-pseudomonas)
- Acidic, antibiotic, or antibiotic/corticosteroid combination otic drops
- Aggressive diabetic control (Endo consult)
- Meticulous cleaning and debridement
- Follow course with periodic indium bone scans or MRI
- ± HBO
- Surgery only if failed medical management or focal abscess present
What are 12 classes of topical agents for otomycosis?
- Nystatin
- Clotrimazole cream or drops (safe for perforations)
- Chloraphenicol
- Ampho B or Tonalfate (antifungals)
- Locacorten Vioform (NOT safe for perforations)
- 1.5% Acetic acid
- 95% isopropyl alcohol
- Merthiolate (Thiomersol)
- Metacresyl-acetate (Cresylate)
- Gentian violet (carcinogenic)
- Aluminum Sulfate-calcium acetate (domboro)
- Drying agents - boric acid, hydrogen peroxide
Four classes of agents used for otitis externa
- Acetic acid solutions
- 2% solution (generic name acetic acid otic)
- Acetic acid 2%, hydrocortisone 1% (generic name acetasol HC) - Ciprofloxacin solutions
- Ciprofloxacin 0.2%, Hydrocortisone 1% (Trade Cipro HC)
- Ciprofloxacin 0.3%, Dexamethasone 0.1% (Trade Ciprodex) - Neomycin, polymyxin B, hydrocortisone
- Trade name Cortisporin Otic - Ofloxacin 0.3%
- Trade name Floxin Otic
What is a complication of chronic otitis externa that may be difficult to manage?
Median canal fibrosis (results in a blind fundus)
