Version July 2025
INTRODUCTION —
The term otitis externa (also known as external otitis or swimmer's ear) refers to inflammation of the external auditory canal. Infectious, allergic, and dermatologic disease may all lead to otitis externa. Acute bacterial infection is the most common cause of acute otitis externa (AOE) [1].
This topic will focus on the pathogenesis, clinical features, and diagnosis of AOE. The treatment of AOE is discussed in detail elsewhere. (See "Acute otitis externa in adults: Treatment".)
EPIDEMIOLOGY —
AOE can occur in all age groups [2]. An estimated 10 percent of people develop AOE during their lifetime. Annual rates of ambulatory care visits in the United States for AOE are highest during childhood and decrease with age [3].
AOE is more likely to occur in the summer, compared with winter months [2]. This may be related to increased ambient humidity and participation in outdoor water activities.
ANATOMY —
The external auditory canal is a cylinder measuring approximately 2.5 cm in length and 7.0 to 9.0 mm in width, extending from the conchal cartilage of the auricle to the tympanic membrane (figure 1). It is divided into a lateral (outer) cartilaginous portion that occupies approximately one-third of the canal and a medial (inner) bony portion that occupies the remaining two-thirds. Their junction is termed the isthmus and is the narrowest region of the ear canal. The outer cartilaginous portion is lined by thicker skin with numerous adnexal structures including cerumen glands, sebaceous glands, and hair follicles. The inner bony portion of the canal contains thin skin without subcutaneous tissue. The dermis in this area is in direct contact with the underlying periosteum. Thus, minimal inflammation or instrumentation of the bony canal causes significant pain and/or injury.
The inferior tympanic recess is a small depression in the inferior medial aspect of the ear canal, adjacent to the tympanic membrane. Debris can collect in this area and cause or perpetuate infection.
The lining of the ear canal is a keratinizing squamous epithelium that undergoes continual sloughing. Epithelial migration is a naturally occurring cleaning process for the ear canal that allows egress of keratin debris and cerumen. Epithelial migration begins in the center of the tympanic membrane and continues out to the medial, then lateral aspects of the ear canal.
The ear canal is bound superiorly by the middle cranial fossa, anteriorly by the temporomandibular joint and parotid region, medially by the tympanic membrane, posteriorly by the mastoid cavity, and inferiorly by the skull base and soft tissues of the neck. These boundaries have particular importance when considering the potential complications of otitis externa.
The fissures of Santorini are a series of embryologic fissures in the anterior aspect of the cartilaginous portion of the canal through which neurovascular tissues pass. These fissures also allow potential spread of ear canal disease to the parotid region, temporomandibular joint, and soft tissue of the upper neck.
PATHOGENESIS AND RISK FACTORS —
Several factors may contribute to the development of otitis externa, despite the defense mechanisms of the auditory canal.
The inherent defense mechanisms of the ear canal include:
●The tragus and conchal cartilage partially cover the opening of the ear canal and help to prevent foreign body entrance.
●Hair follicles and the isthmus narrowing inhibit entry of contaminants into the ear canal.
●Cerumen helps create an acidic ear canal environment, which inhibits bacterial and fungal growth. It is also hydrophobic, repelling water that might otherwise create an ideal culture medium. In addition, the sticky quality of cerumen helps to trap fine debris.
Breakdown of the skin-cerumen barrier is the first step in the pathogenesis of otitis externa. Inflammation and edema of the skin then leads to pruritus and obstruction. The pruritus prompts scratching that may create further injury. This sequence of events alters the quality and amount of cerumen produced, impairs epithelial migration, and increases the pH of the ear canal. The resulting dark, warm, alkaline, moist ear canal becomes an ideal breeding ground for numerous organisms.
Specific factors increase the risk of otitis externa [4-7]:
●Swimming or other water exposure is a well-documented risk factor for otitis externa. Excess moisture leads to skin maceration and breakdown of the skin-cerumen barrier, changing the microflora of the ear canal to predominantly gram-negative bacteria. (See 'Microbiology' below.)
●Any trauma such as from excessive cleaning or aggressive scratching of the ear canal not only removes cerumen but can also create abrasions along the thin layer of skin in the ear canal, allowing organisms to gain access to deeper tissue. In addition, part of a cotton swab may become detached or a small piece of tissue paper may be left behind in the ear canal; these remnants can partially disintegrate and fester, causing a severe skin reaction and infection.
●Devices that occlude the ear canal such as hearing aids, earphones, or diving caps can predispose to otitis externa.
●Allergic contact dermatitis can lead to otitis externa (eg, from earrings or chemicals in cosmetics or shampoos).
●Dermatologic conditions can also predispose to otitis externa (eg, psoriasis, atopic dermatitis).
●Prior radiation therapy can cause ischemic ear canal changes, alter cerumen production and epithelial migration, and predispose to otitis externa.
MICROBIOLOGY —
The most common pathogenic organisms responsible for AOE are Pseudomonas aeruginosa (41 percent) and Staphylococcus aureus (15 percent) (table 1). However, there are several other gram-positive and -negative bacteria that can also cause AOE. Anaerobic pathogens are present in 17 percent of patients; bacteroides and peptostreptococci are the most frequently encountered anaerobic organisms [5,8-10]. Some patients may have mixed aerobic and anaerobic infection.
Fungal infection accounts for 2 to 10 percent of cases of AOE and most frequently occurs after treatment of bacterial infection. Candidal infection occurs more commonly in patients who use hearing aids [11]. Polymicrobial disease occurs in up to one-third of cases [8,9]. (See 'Otomycosis' below.)
CLINICAL FEATURES —
The most common symptoms of AOE are ear pain, pruritus, discharge, and hearing loss [2]. In addition to symptoms, patients should be asked about any known tympanic membrane perforation, previous ear infections, any prior ear surgery or radiation, chronic skin conditions, recent ear instrumentation, use of devices in the ear canal, and water exposure.
On physical examination, the auricle and tragus should be examined for erythema or signs of trauma (figure 1). Tenderness with tragal pressure or when the auricle is manipulated or pulled are indicative findings of otitis externa. However, these signs may be absent in mild cases.
Otoscopy is critical for distinguishing between otitis externa, otitis media, and other ear pathology. The ear canal usually appears edematous and erythematous in otitis externa. Debris or cerumen is typically yellow, brown, white, or gray. Otomycosis, a fungal infection of the external canal, may take on different appearances (eg, fine, dark coating with Aspergillus; white, sebaceous-like material with Candida) (see 'Otomycosis' below). The tympanic membrane may be erythematous in otitis externa and only partially visible due to canal edema. The presence of an air-fluid level along the tympanic membrane is indicative of a middle ear effusion and underlying otitis media (picture 1).
The examination is aided with a pneumatic otoscope that allows for insufflation (picture 2). The tympanic membrane in patients with otitis externa should be mobile with pneumatic insufflation. With gentle application of positive then negative pressure by the pneumatic otoscope, the normal tympanic membrane moves inwards then outwards, respectively (movie 1). The movement of the tympanic membrane is most evident posterosuperiorly. A fluid-filled middle ear will minimize any tympanic membrane excursions with insufflation (movie 2). There should be no evidence of middle ear fluid in isolated otitis externa. (See "Acute otitis media in adults", section on 'Presentation and diagnosis' and "Acute otitis media in children: Clinical manifestations and diagnosis", section on 'Otoscopic evaluation'.)
The diagnosis of AOE should also be questioned when the patient has a perforated tympanic membrane. It is likely that the primary focus of disease in these patients is the middle ear, with secondary inflammation of the ear canal. (See "Evaluation and management of middle ear trauma" and "Acute otitis media in adults", section on 'Management of acute tympanic membrane rupture in acute otitis media' and "Evaluation of earache in children", section on 'Blunt or penetrating trauma'.)
The patient should be evaluated for findings that might indicate malignant otitis externa. Granulation tissue at the bony cartilaginous junction of the ear canal floor is a classic finding. Frank necrosis of ear canal skin may be evident. (See 'Malignant otitis externa' below.)
Severity — The spectrum of AOE ranges from mild to severe, based on the presenting symptoms and physical examination [7].
●Mild disease is characterized by minor discomfort and pruritus (picture 3). There is minimal canal edema.
●Moderate disease is characterized by an intermediate degree of pain and pruritus. The canal is partially occluded (picture 4).
●Severe disease is characterized by intense pain, and the canal is completely occluded from edema. There may be periauricular erythema, lymphadenopathy, and fever (picture 5).
DIAGNOSIS —
The diagnosis of AOE is clinical, based on a characteristic history and physical examination. (See 'Clinical features' above.)
Guidelines from the American Academy of Otolaryngology-Head and Neck Surgery define diffuse acute otitis externa as occurring with rapid onset (generally within 48 hours) in the previous three weeks with signs and symptoms of ear canal inflammation (tender tragus and/or pinna), or diffuse edema or erythema of the ear canal, with or without otorrhea, regional adenopathy, erythema of the tympanic membrane, or cellulitis of the pinna and adjacent skin [12].
Cultures — Cultures are generally reserved for patients with severe cases of AOE. Performing culture is usually more costly than simply starting empiric treatment, which is usually very effective. Thus, patients with mild and moderate AOE do not need culture of the ear canal prior to starting therapy. However, cultures should be performed in those with severe AOE, recurrent AOE, chronic otitis externa, immunosuppressed patients (eg, posttransplant, HIV, receiving chemotherapy or radiation therapy), infections in patients after ear surgery, and patients who do not respond to initial therapy [13]. Culture is performed using a small cotton swab within the external canal.
DIFFERENTIAL DIAGNOSIS —
A number of disorders can mimic bacterial AOE.
Otomycosis — Otomycosis is a fungal infection of the external auditory canal. Otomycosis can occur as the primary infection or can develop along with bacterial AOE, usually as a result of antibiotic therapy. Fungal infections are responsible for approximately 9 percent of ear canal infections [14]. Aspergillus niger and Candida are the most common organisms, although the dominant organism varies according to geographic location. The incidence of otomycosis is higher in tropical and subtropical locations, probably because of the humidity [15]. Swimming and ear canal scratching or cleaning also predispose to otomycosis. Concern has been raised that excessive use of antibiotic ear drops might allow fungal proliferation. However, the incidence and types of fungal infections have not changed significantly despite several decades of topical antibiotic use.
Patients with otomycosis most commonly report ear itching, discomfort, discharge, and/or a feeling that something is in the ear canal [16]. Deep-seated itching is the most troublesome symptom; pain is less intense than with bacterial AOE.
Fungal infections are often located in the medial aspect of the ear canal. This may be due in part to the location of the inferior tympanic recess (figure 1), which facilitates accumulation of debris in this area. In addition, the medial aspect of the ear canal is darker and warmer, features that promote fungal growth.
Edema of the ear canal is less severe than with bacterial AOE. Fungal organisms have a very characteristic appearance in the ear canal, especially under magnified vision (picture 6). Fine fungal filaments and spores may be seen that resemble mold growing on spoiled food. A. niger spores look like a fine coal dust sprinkled in the ear canal. Aspergillus may also resemble wet newspaper or blotting paper. Candidal infections typically are associated with soft, white, sebaceous-like material that may fill the ear canal in severe cases. A pseudomembrane often lines the ear canal that, when removed, reveals an underlying friable granular membrane.
The treatment of otomycosis is discussed elsewhere. (See "Acute otitis externa in adults: Treatment", section on 'Otomycosis'.)
Contact dermatitis — Patients with persistent edema and erythema of the ear canal and auricle despite appropriate AOE treatment may be experiencing an allergic reaction. Contact dermatitis can be commonly caused by ototopical medication, cosmetics, or shampoos. These are Gell and Coombs type IV delayed hypersensitivity reactions; secondary exposure to the allergen initiates an inflammatory response.
Contact dermatitis should be considered if there has been a lack of response to AOE treatment over a one-week period. Pruritus is the dominant symptom. Erythema intensifies and classically extends to the inferior aspect of the conchal cartilage where drops often collect after application (picture 7). Vesicles may be seen, and there are often extensive secondary changes from rubbing and itching.
Common ototopical agents causing allergic reactions are neomycin, benzocaine, and propylene glycol [17,18]:
●Neomycin allergy occurs in 35 percent of chronically treated patients [19]. Cross-reactivity among other aminoglycosides, including tobramycin and gentamicin, is common.
●Benzocaine is the topical anesthetic present in many topical anesthetic otic solutions. Benzocaine is an allergic sensitizer, particularly in the presence of skin breakdown. It is no longer available in the United States. Pain from otitis externa should be managed with oral nonsteroidal antiinflammatory agents or acetaminophen to avoid sensitization by topical anesthetics. (See "Allergic reactions to local anesthetics", section on 'Rare: Delayed reactions (contact dermatitis or local swelling)'.)
●Propylene glycol is a common solvent and preservative in ototopical agents. It can act as a primary irritant or an allergic sensitizer.
If the causative agent is not readily apparent by history alone, patch testing can help identify the allergen.
The treatment of contact dermatitis of the ear canal is discussed elsewhere. (See "Acute otitis externa in adults: Treatment", section on 'Contact dermatitis'.)
Chronic suppurative otitis media — Patients with chronic suppurative otitis media (CSOM) may also present with a draining ear and can be mistakenly thought to have AOE. CSOM is usually associated with a long history of ear disease. Symptoms of CSOM include otorrhea and possibly otalgia, hearing loss, tinnitus, or vertigo. (See "Chronic suppurative otitis media (CSOM): Clinical features and diagnosis" and "Chronic otitis media and cholesteatoma in adults", section on 'Chronic otitis media'.)
Ear canal symptoms and signs are usually mild compared with bacterial AOE. Swelling typically does not completely occlude the canal. Ear canal findings are focused medially near the tympanic membrane where polyps or granulation tissue may be seen. The tympanic membrane is usually at least partly visible and frequently not mobile on insufflation. A tympanic membrane perforation or retraction pocket may be evident. The pocket can be filled with white, cheesy-looking, keratin debris consistent with a cholesteatoma (picture 8). Patients with these findings should be referred to an otolaryngologist. (See "Acute otitis media in adults", section on 'Management of acute tympanic membrane rupture in acute otitis media' and "Chronic otitis media and cholesteatoma in adults", section on 'Chronic otitis media'.)
Carcinoma of the ear canal — Cancer of the external auditory canal is a rare disease that should always be considered any time there is an abnormal tissue growth in the ear canal or a lack of response to prolonged AOE treatment [20]. Ear canal cancer occurs far less frequently than auricular cancer. In the early stages, it is often indistinguishable from AOE. The diagnosis of carcinoma of the external auditory canal is often delayed secondary to misdiagnosis as AOE.
Mild pain and bloody otorrhea are common symptoms. A friable ear canal lesion with surrounding purulence is a typical finding on otoscopy. Hearing loss and facial paralysis may develop as late signs. The definitive diagnosis is made with biopsy of the lesion or affected area.
Psoriasis — Psoriasis can commonly involve the external ear canal, causing redness and scaling often extending to the conchal bowl and auricle. The clinical appearance of psoriasis in the external canal may vary. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)
COMPLICATIONS —
Complications of AOE include periauricular cellulitis and malignant otitis externa.
Periauricular cellulitis — Periauricular cellulitis presents with erythema, edema, and warmth of the skin around the auricle (picture 9).
Pain may be mild or severe. Fever is sometimes present, but other systemic manifestations are usually absent, which helps distinguish cellulitis from malignant otitis externa. Periauricular cellulitis should be differentiated from relapsing polychondritis, which usually spares the earlobe.
Malignant otitis externa — Malignant otitis externa (also termed necrotizing external otitis) is a severe, potentially fatal complication of bacterial AOE. Most common in older adult diabetic patients or other immunocompromised individuals, it occurs when the infection spreads from the skin to bone and marrow spaces of the skull base (also involving soft tissue and cartilage of the temporal region).
Patients typically have severe otalgia and otorrhea with pain that appears out of proportion to examination findings. Granulation tissue at the bony cartilaginous junction of the ear canal floor is a classic finding. Edema, erythema, and frank necrosis of ear canal skin may be evident. Cranial nerve palsies are a poor prognostic sign. Patients generally have a markedly elevated erythrocyte sedimentation rate (ESR). Diagnosis is aided with an abnormal magnetic resonance imaging (MRI) or computed tomography (CT) scan showing extension of infection into bony structures. Patients who may have malignant otitis externa should be promptly referred to an otolaryngologist.
Malignant otitis externa is discussed in detail elsewhere. (See "Necrotizing (malignant) external otitis".)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acute otitis media, otitis media with effusion, and external otitis".)
INFORMATION FOR PATIENTS —
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Outer ear infection (The Basics)")
●Beyond the Basics topics (see "Patient education: External otitis (including swimmer's ear) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition – The term otitis externa (also known as external otitisor swimmer's ear) refers to inflammation of the external auditory canal or auricle, usually from infection.
●Risk factors – Risk factors for developing AOE include swimming (or other water exposure), trauma (eg, ear scratching, cotton swabs), occlusive ear devices (eg, hearing aids, ear phones), allergic contact dermatitis (eg, due to shampoos, cosmetics), and dermatologic conditions (eg, psoriasis). (See 'Pathogenesis and risk factors' above.)
●Clinical features – AOE usually presents with ear pain, pruritus, and discharge. Examination findings of AOE include tenderness when the tragus is pushed or the auricle is pulled, as well as erythema and swelling of the external auditory canal. The otoscopic examination should also assess for otitis media, tympanic membrane perforation, and signs of other disease. (See 'Clinical features' above.)
●Levels of severity – AOE is categorized by severity as mild, moderate, or severe (see 'Severity' above):
•Mild disease is characterized by pruritus, minor discomfort, and minimal canal edema (picture 3).
•Moderate disease is characterized by pruritus, an intermediate degree of pain, and a partially occluded canal (picture 4).
•Severe disease is characterized by complete canal obstruction and intense pain. There may be periauricular erythema, adenopathy, and fever (picture 5).
●Diagnosis – The diagnosis of AOE is clinical, based on a characteristic history and physical examination. Cultures are reserved for patients with severe AOE, immunocompromised patients, and those who do not respond to initial therapy. (See 'Diagnosis' above.)
●Differential diagnosis – The differential diagnosis for AOE includes otomycosis, contact dermatitis, chronic suppurative otitis media, and ear canal carcinoma. Carcinoma of the ear canal is a rare, aggressive disease that is suggested by blood otorrhea, a friable ear canal, and failure to respond to treatment for AOE. (See 'Differential diagnosis' above.)
●Malignant (necrotizing) otitis externa – Malignant (necrotizing) otitis externa occurs when AOE spreads to the skull base (soft tissue, cartilage, and bone of the temporal region and skull). Malignant otitis externa most commonly develops in older adult with diabetes mellitus or other immunocompromised individuals. Severe pain, otorrhea, presence of granulation tissue in the canal floor, and cranial nerve palsies may be present. These patients should be promptly referred to an otolaryngologist. (See "Necrotizing (malignant) external otitis".)
