Otitis externa usually results from bacteria, such as Pseudomonas, Proteus vulgaris, Staphylococcus aureus, and streptococci and, sometimes, from fungi, such as Aspergillus niger and Candida albicans (fungal otitis externa is most common in tropical regions). Occasionally, chronic otitis externa results from dermatologic conditions, such as seborrhea or psoriasis. Allergic reactions stemming from nickel or chromium earrings, chemicals in hair spray, cosmetics, hearing aids, and medications (such as sulfonamide and neomycin, which is commonly used to treat otitis externa) can also cause otitis externa.

Predisposing factors include:

Acute otitis externa characteristically produces moderate to severe pain that’s exacerbated by manipulating the auricle or tragus, clenching the teeth, opening the mouth, or chewing. Its other clinical effects may include fever, foulsmelling discharge, crusting in the external ear, regional cellulitis, partial hearing loss, and itching. It’s usually difficult to view the tympanic
membrane because of pain in the external canal. Hearing acuity is normal unless complete occlusion has occurred.

Fungal otitis externa may be asymptomatic, although A. niger produces a black or gray, blotting, paperlike growth in the ear canal. In chronic otitis externa, pruritus replaces pain, and scratching may lead to scaling and skin thickening. Aural discharge may also occur.

A benign ear tumor is usually asymptomatic, unless it becomes infected, in which case pain, fever, or inflammation may result. (Pain is usually a sign of a malignant tumor.) If the tumor grows large enough to obstruct the ear canal by itself or through accumulated cerumen and debris, it may cause hearing loss and the sensation of pressure.

Otitis media results from disruption of eustachian tube patency. In the suppurative form, respiratory tract infection, allergic reaction, nasotracheal intubation, or positional changes allow nasopharyngeal flora to reflux through the eustachian tube and colonize the middle ear. Suppurative otitis media usually results from bacterial infection with pneumococcus, Haemophilus influenzae (the most common cause in children younger than age 6), Moraxella catarrhalis, beta-hemolytic streptococci, staphylococci (most common cause in children age 6 or older), or gram-negative bacteria. Predisposing factors include the normally wider, shorter, more horizontal eustachian tubes and increased lymphoid tissue in children, as well as anatomic anomalies. Chronic suppurative otitis media results from inadequate treatment for acute otitis episodes or from infection by resistant strains of bacteria or, rarely, tuberculosis.

Secretory otitis media results from obstruction of the eustachian tube. This causes a buildup of negative pressure in the middle ear that promotes transudation of sterile serous fluid from blood vessels in the membrane of the middle ear. Such effusion may be secondary to eustachian tube dysfunction from viral infection or allergy. It may also follow barotrauma (pressure injury caused by the inability to equalize pressures between the environment and the middle ear), as occurs during rapid aircraft descent in a person with an upper respiratory tract infection or during rapid underwater ascent in scuba diving (barotitis media).

Chronic secretory otitis media follows persistent eustachian tube dysfunction from mechanical obstruction (adenoidal tissue overgrowth or tumors), edema (allergic rhinitis or chronic sinus infection), or inadequate treatment for acute suppurative otitis media.

Acute otitis media is common in children; its incidence rises during the winter months,
paralleling the seasonal rise in nonbacterial respiratory tract infections. Chronic secretory otitis media most commonly occurs in children with tympanostomy tubes or those with a perforated tympanic membrane.

Clinical features of acute suppurative otitis media include severe, deep, throbbing pain (from pressure behind the tympanic membrane); signs of upper respiratory tract infection (sneezing or coughing); mild to very high fever; hearing loss (usually mild and conductive); tinnitus; dizziness; nausea; and vomiting. Other possible effects include bulging of the tympanic membrane, with concomitant erythema, and purulent drainage in the ear canal from tympanic membrane rupture. However, many patients are asymptomatic.

Acute secretory otitis media produces a severe conductive hearing loss—which varies from 15 to 35 dB, depending on the thickness and amount of fluid in the middle ear cavity— and, possibly, a sensation of fullness in the ear and popping, crackling, or clicking sounds on swallowing or with jaw movement. Accumulation of fluid may also cause the patient to hear an echo when he speaks and to experience a vague feeling of top-heaviness.

The cumulative effects of chronic otitis media include thickening and scarring of the tympanic membrane, decreased or absent tympanic membrane mobility, cholesteatoma (a cystlike mass in the middle ear) and, in chronic suppurative otitis media, a painless, purulent discharge. The extent of associated conductive
hearing loss varies with the size and type of tympanic membrane perforation and ossicular destruction.

If the tympanic membrane has ruptured, the patient may state that the pain has suddenly stopped. Complications may include abscesses (brain, subperiosteal, and epidural), sigmoid sinus or jugular vein thrombosis, septicemia, meningitis, suppurative labyrinthitis, facial paralysis, and otitis externa.

Acute otitis media may not produce any symptoms in the first few months of life; irritability may be the only indication of earache.

Bacteria that cause mastoiditis include pneumococci, Haemophilus influenzae, Moraxella catarrhalis, beta-hemolytic streptococci, staphylococci, and gram-negative organisms. Mastoiditis is usually a complication of chronic otitis media; less frequently, it develops after acute otitis media. An accumulation of pus under pressure in the middle ear cavity results in necrosis of adjacent tissue and extension of the infection into the mastoid cells. Chronic systemic diseases or immunosuppression may also lead to mastoiditis. Anaerobic organisms play a role in chronic mastoiditis.

Primary clinical features include a dull ache and tenderness in the area of the mastoid process, low-grade fever, headache, and a thick, purulent discharge that gradually becomes more profuse, possibly leading to otitis externa.

Postauricular erythema and edema may push the auricle out from the head; pressure within the edematous mastoid antrum may produce swelling and obstruction of the external ear canal, causing conductive hearing loss.

Otosclerosis appears to result from a genetic factor transmitted as an autosomal dominant trait; many patients report family histories of hearing loss (excluding presbycusis). Pregnancy may trigger onset of this condition.

Otosclerosis occurs in at least 10% of the U.S. population. It’s three times more prevalent in females than in males, usually affecting people between ages 15 and 30. Whites are most susceptible.

Spongy bone in the otic capsule immobilizes the footplate of the normally mobile stapes, disrupting the conduction of vibrations from the tympanic membrane to the cochlea. This causes progressive unilateral hearing loss, which may advance to bilateral deafness. Other symptoms include tinnitus and paracusis of Willis (hearing
conversation better in a noisy environment than in a quiet one).

Acute infectious myringitis usually follows viral infection but may also result from infection with bacteria (pneumococcus, Haemophilus influenzae, beta-hemolytic streptococci, staphylococci) or any other organism that can cause acute otitis media. Myringitis is a rare sequela of atypical pneumonia caused by Mycoplasma pneumoniae. The cause of chronic granular myringitis is unknown.

Acute infectious myringitis frequently occurs epidemically in children.

Acute infectious myringitis begins with severe ear pain, commonly accompanied by tenderness over the mastoid process. Small, reddened, inflamed blebs form in the canal, on the tympanic membrane and, with bacterial invasion, in the middle ear. Fever and hearing loss are rare unless fluid accumulates in the middle ear or a large bleb totally obstructs the external auditory meatus. Spontaneous rupture of these blebs may cause bloody discharge. Chronic granular myringitis produces pruritus, purulent discharge, and gradual hearing loss.