DISEASES OF THE EXTERNAL EAR Flashcards
What are the components of the external ear?
Auricle and External Auditory Canal (EAC).
What lines the auricle and EAC?
Skin.
What is the approximate length of the external ear?
2.5 cm.
Where does the external ear end?
At the tympanic membrane.
What percentage of the EAC is cartilage and what percentage is bony?
~40% cartilage and ~60% bony.
What is the narrowest portion of the EAC called?
Isthmus (at the bony-cartilage junction).
What are the contiguous structures related to the EAC?
Tympanic membrane, mastoid, glenoid fossa, cranial fossa, and infratemporal fossa.
What cranial nerves innervate the external ear?
CN V, VII, IX, X, and the greater auricular nerve.
What causes nystagmus?
A rapid lateral oscillation of the eyes with fast and slow phases.
What symptom is associated with nystagmus?
Vertigo, a spinning sensation.
What are the arterial supplies of the external ear?
Superficial temporal, posterior auricular, and deep auricular branches.
What is the most common problem related to the EAC?
Impacted cerumen.
What glands produce cerumen?
Sebaceous and apocrine glands.
What is the difference between impacted and retained cerumen?
Impacted cerumen obstructs the entire EAC; retained cerumen partially obstructs it.
What is the leading cause of impacted cerumen?
Excessive use of Q-tips or cotton buds.
How can impacted cerumen be removed?
Using a curette, suction tip, or water irrigation (if tympanic membrane is intact).
What is the preferred empiric antibiotic for auricular lacerations?
Amoxicillin.
What should not be sutured in auricular lacerations?
Cartilage.
What is a common complication of untreated auricular hematoma?
Cauliflower ear.
What are the three degrees of burns of the auricle, and how are they treated?
First-degree: Conservative; Second-degree: Antibiotics/creams; Third-degree: Debridement and reconstructive surgery.
What is perichondritis/chondritis?
Infection of the perichondrium or cartilage, often caused by trauma.
What are common symptoms of perichondritis?
Pain, pruritus, induration, and edema.
What is the most common foreign body in the EAC?
Insects (e.g., cockroaches, crickets, ants).
What is otitis externa?
Inflammation of the external ear, often caused by infection or trauma.
What are the types of otitis externa?
Furunculosis, diffuse otitis externa (swimmer’s ear), otomycosis, herpes zoster oticus, contact dermatitis, seborrheic dermatitis, and psoriasis.
What is furunculosis, and how is it treated?
Infection of the outer third of the EAC caused by Staphylococcus species; treated with incision, drainage, systemic antibiotics, and analgesics.
What is diffuse otitis externa, and what causes it?
Swimmer’s ear; caused by Pseudomonas species or viruses.
What is otomycosis, and what causes it?
Fungal infection of the EAC, commonly caused by Aspergillus niger or Candida albicans.
What is the treatment for otomycosis?
Aural toilette, local debridement, and otic antifungal preparations.
What is herpes zoster oticus?
Infection of the geniculate ganglion by the chickenpox virus, causing vesicles in the EAC and auricle.
What is the treatment for herpes zoster oticus?
Acyclovir, systemic steroids, and analgesics for neuropathic pain.
What is contact dermatitis, and what causes it?
Localized reaction in the ear due to inciting agents like hearing aids, ear plugs, or neomycin.
What is seborrheic dermatitis, and what causes it?
Erythematous, greasy scaling caused by Malassezia furfur.
What is the treatment for seborrheic dermatitis?
Topical steroids and keratolytics.
What is psoriasis of the external ear, and how is it treated?
Erythematous patches with hyperkeratosis; treated with topical steroids, UV phototherapy, and immunosuppressants like cyclosporin.
What can cause temporary hearing loss in psoriasis?
Accumulation of debris in the EAC.
What is the main complication of untreated diffuse otitis externa?
Severe swelling, preventing medication from reaching the EAC.
What is otowick, and when is it used?
A cotton/gauze soaked in medication inserted into a swollen EAC to allow medication absorption.
Why is cerumen protective for the EAC?
It acts as an antifungal, antiviral, antibiotic, and insect repellent.
Which cranial nerve innervates the posteroinferior walls of the EAC?
CN X (Vagus nerve).
What happens if water enters the EAC and changes its pH?
It predisposes the EAC to fungal, viral, or bacterial infections.
What is the most common fungal species causing otomycosis?
Aspergillus niger.
What is the difference between paralysis and palsy?
Paralysis: Complete loss of motion; Palsy: Partial loss of motion.
What can hematoma of the auricle lead to if untreated?
Cartilage necrosis and cauliflower ear.
Why is the cartilage in the auricle prone to necrosis?
It is alymphatic and avascular, relying on diffusion from the skin for nutrition.
What should you avoid in the case of perforated tympanic membrane during cerumen removal?
Water irrigation.
What is necrotizing external otitis (NEO)?
A potentially lethal infection of the EAC and surrounding structures, commonly seen in diabetics and immunocompromised patients.
What is the usual causative agent of necrotizing external otitis?
Pseudomonas aeruginosa, followed by Staphylococcus aureus.
What are the symptoms of necrotizing external otitis?
Deep-seated aural pain, chronic purulent otorrhea, aural fullness, otorrhagia, and otalgia.
What is the treatment for necrotizing external otitis?
IV antibiotics for at least 4 weeks, serial gallium scans, and local canal debridement.
What is relapsing polychondritis?
A progressive destruction of cartilage affecting the nose, ears, and larynx.
What is the treatment for relapsing polychondritis?
Steroids to control acute attacks and suppress recurrences.
What deformity is associated with relapsing polychondritis?
Saddle nose deformity and enlarged fossa due to cartilage resorption.
What is erysipelas?
Acute superficial cellulitis caused by Group A beta-hemolytic streptococci.
What is the characteristic appearance of erysipelas?
Bright red skin with well-demarcated, advancing margins.
What is the treatment for erysipelas?
Oral or IV antibiotics, such as 3rd generation cephalosporins like ceftriaxone.
What is keratosis obturans?
Accumulation of squamous epithelium in the EAC, leading to pain, hyperemia, and conductive hearing loss.
What is the treatment for keratosis obturans?
Regular debridement and topical steroids.
What is canal cholesteatoma?
A cystic collection of squamous epithelium that causes pain, purulent otorrhea, and bony erosion.
What is the treatment for canal cholesteatoma?
Frequent debridement, topical antibiotics, and surgery for complicated cases.
What are exostoses?
Benign bony outgrowths in the periosteum of the EAC.
What is the treatment for symptomatic exostoses?
Excision using a diamond burr for large or obstructive cases.
What percentage of EAC tumors are squamous cell carcinoma (SCC)?
0.2
What is the treatment for squamous cell carcinoma of the EAC?
Wide local excision for small tumors; radical en bloc resection for large or invasive tumors.
What is basal cell carcinoma (BCC)?
A proliferation of basal cells in the epithelium that is locally aggressive but does not metastasize.
What is the treatment for basal cell carcinoma of the EAC?
Wide surgical excision and frozen section examination to ensure clear margins.
What is malignant melanoma of the EAC?
An extremely rare tumor developed from a darkly pigmented nevus that ulcerates and bleeds.
What is adenoid cystic carcinoma of the EAC?
A malignant tumor arising from ceruminous glands, also known as cylindroma.
What is the treatment for adenoid cystic carcinoma of the EAC?
Surgical excision.
What is aural atresia and stenosis?
Congenital malformations of the EAC due to defects in the 1st and 2nd branchial arches or 1st branchial cleft.
What are the three groups of aural atresia and stenosis?
Group I: Mild malformations; Group II: Moderate malformations (microtia); Group III: Severe malformations.
What are first branchial cleft anomalies?
Congenital anomalies due to failure of normal obliteration of the 1st branchial cleft, presenting as cysts, sinuses, or fistulas.
What is the difference between Type I and Type II first branchial cleft anomalies?
Type I: Ectodermal origin, duplication of membranous EAC; Type II: Ectodermal and mesodermal origin, involving parotid and surrounding structures.
What is the treatment for first branchial cleft anomalies?
Complete surgical excision with facial nerve preservation.
What are the common symptoms of necrotizing external otitis?
Deep-seated aural pain, chronic purulent otorrhea, and ear fullness.
What is the common treatment for cartilage-related ear injuries?
Antibiotics, debridement, and pressure dressing to prevent hematoma formation.
What are the signs of canal cholesteatoma?
Unilateral pain, foul-smelling purulent otorrhea, and bony erosion.
What are the common causes of erysipelas of the ear?
Group A beta-hemolytic streptococci.
What complications can arise from untreated aural hematoma?
Cartilage necrosis and cauliflower ear.
What structures are commonly affected in relapsing polychondritis?
Cartilage of the nose, ears, and larynx.
What is the significance of Moh’s Micrographic Surgery?
Ensures clear surgical margins for excision of malignant lesions like SCC and BCC.
What distinguishes BCC from SCC in the EAC?
BCC is less common, locally aggressive, and destroys soft tissue but does not metastasize, while SCC can metastasize.
What is the primary cause of necrotizing external otitis?
Pseudomonas aeruginosa.
What are exostoses composed of?
Concentric lamellar bony structures formed by continuous bone deposition.
What type of cells proliferate in basal cell carcinoma?
Basal cells in the epithelium, which can differentiate into various epithelial components.
What is the treatment for keratosis obturans?
Regular debridement and topical steroids.
What is the main cause of canal cholesteatoma?
Squamous epithelium in abnormal areas, secreting enzymes that cause bony erosion.
What is the most common fungal cause of otomycosis?
Aspergillus niger.
What congenital anomaly involves an additional ear canal or duplication of the EAC?
Type I first branchial cleft anomaly.
What congenital anomaly involves both ectoderm and mesoderm, often involving the parotid gland?
Type II first branchial cleft anomaly.
What is the most common location for adenoid cystic carcinoma in the EAC?
Ceruminous glands.
Which congenital malformation of the EAC is commonly associated with craniofacial syndromes?
Aural atresia and stenosis.
