Otitis Externa Practice Essentials Otitis externa (OE) is an inflammation or infection of the external auditory canal (EAC), the

auricle, or both.[1, 2, 3] This condition can be found in all age groups.[4] Essential update: AAO-HNSF releases updated diagnosis and management guidelines for acute otitis externa The American Academy of OtolaryngologyHead and Neck Surgery Foundation (AAO-HNSF) has released updated clinical practice guidelines for the diagnosis and treatment of acute OE. Their recommendations include the following[5] : Differentiate diffuse acute OE from other possible causes of otalgia, otorrhea, and inflammation of the EAC. Assess patients with diffuse acute OE for factors that may modify therapeutic management (eg, nonintact tympanic membrane, immunocompromised state). Assess for pain in patients with acute OE; base the analgesia recommendation on the patients pain severity. Administer topical medications as initial therapy for diffuse, uncomplicated acute OE. Do not administer systemic antimicrobial agents as initial therapy for diffuse, uncomplicated acute OE; reserve such treatment for cases in which there is extension outside of the EAC or there are specific host factors that require systemic agents. Instruct patients on how to administer topical drops; perform an aural toilet, place a wick, or both, when the ear canal is obstructed. Use a non-ototoxic topical agent in patients with a known or suspected perforation of the tympanic membrane (eg, tympanostomy tube). Confirm the diagnosis of acute OE and reassess the differential diagnosis within 48-72 hours in cases refractory to the initial therapy. Classification Acute diffuse OE: Most common form of OE, typically seen in swimmers Acute localized OE (furunculosis): Associated with infection of a hair follicle Chronic OE: Same as acute diffuse OE but is of longer duration (>6 wk) Eczematous (eczematoid) OE: Encompasses various dermatologic conditions (eg, atopic dermatitis, psoriasis, systemic lupus erythematosus, and eczema) that may infect the EAC and cause OE Necrotizing (malignant) OE: Infection that extends into the deeper tissues adjacent to the EAC; occurs primarily in immunocompromised adults (eg, diabetics, patients with acquired immunodeficiency syndrome [AIDS]) Otomycosis: Infection of the ear canal from a fungal species (eg, Candida, Aspergillus) Signs and symptoms The key physical finding of OE is pain upon palpation of the tragus (anterior to ear canal) or application of traction to the

pinna (the hallmark of OE). Patients may also have the following signs and symptoms: Otalgia: Ranges from mild to severe, typically progressing over 1-2 days Hearing loss Ear fullness or pressure Erythema, edema, and narrowing of the EAC Tinnitus Fever (occasionally) Itching (especially in fungal OE or chronic OE) Severe deep pain: Immunocompromised patients may have necrotizing (malignant) OE Discharge: Initially, clear; quickly becomes purulent and foul-smelling Cellulitis of the face or neck or lymphadenopathy of the ipsilateral neck (occasionally) Bilateral symptoms (rare) History of exposure to or activities in water (frequently) (eg, swimming, surfing, kayaking) History of preceding ear trauma (usually) (eg, forceful ear cleaning, use of cotton swabs, or water in the ear canal) See Clinical Presentation for more detail. Diagnosis The patients history and physical examination, including otoscopy, usually provide sufficient information for the clinician to make the diagnosis of OE. Note that a patient who is diabetic or immunocompromised with severe pain in the ear should have necrotizing OE excluded by an otolaryngologist.

Laboratory testing

Typically, laboratory studies are not needed, but they may be helpful if the patient is immunocompromised, if the usual treatment measures are ineffective, or if a fungal cause is suspected. Tests may include the following: Gram stain and culture of any discharge from the auditory canal Blood glucose level Urine dipstick

Imaging studies

Imaging studies are not required for most cases of OE. However, radiologic investigation may be helpful if an invasive infection such as necrotizing (malignant) OE is suspected or if the diagnosis of mastoiditis is being considered. Imaging modalities may include the following: High-resolution computed tomography (CT) scanning: Preferred; better depicts bony erosion[6] Radionucleotide bone scanning Gallium scanning Magnetic resonance imaging (MRI): Not used as often as the other modalities; may be considered secondarily or if soft-tissue extension is the predominant concern[7] See Workup for more detail. Management Most persons with OE are treated empirically. Primary treatment involves the following: Pain management

Pharmacotherapy Topical medications (eg, acetic acid in aluminum

Removal of debris from the EAC Administration of topical medications to control edema and infection Avoidance of contributing factors

Surgery Surgical debridement of the ear canal: Usually

acetate, hydrocortisone and acetic acid otic solution, alcohol vinegar otic mix) Analgesic agents (eg, acetaminophen, acetaminophen and codeine) Antibiotics (eg, hydrocortisone/neomycin/polymyxin B, otic ofloxacin, otic ciprofloxacin, gentamicin 0.3%/prednisolone 1% ophthalmic, dexamethasone/tobramycin, otic ciprofloxacin and dexamethasone, otic ciprofloxacin and hydrocortisone suspension) Oral antibiotics (eg, ciprofloxacin) Antifungal agents (eg, otic clotrimazole 1% solution, nystatin powder)

reserved for necrotizing OE or for complications of OE (eg, external canal stenosis); often necessary in more severe cases of OE or in cases where a significant amount of discharge is present in the ear; mainstay of treatment for fungal infections Incision and drainage of an abscess See Treatment and Medication for more detail. Image library

Acute otitis externa. Ear canal is red and edematous, and discharge is present. Background Otitis externa (OE) is an inflammation or infection of the external auditory canal (EAC), the auricle, or both.[1, 2, 3] It is a common disease that can be found in all age groups.[4] OE usually represents an acute bacterial infection of the skin of the ear canal (most commonly attributable to Pseudomonas aeruginosa or Staphylococcus aureus[8] ) but can also be caused by other bacteria, viruses, or a fungal infection (see Pathophysiology and Etiology). Several factors can contribute to EAC infection and the development of OE, including the following[9] : Absence of cerumen High humidity Retained water in ear canal Increased temperature Local trauma (eg, use of cotton swabs or hearing aids)

Aquatic athletes are particularly prone to the development of OE because repeated exposure to water results in removal of cerumen and drying of the EAC. Retained water in the ear canal can cause maceration of the skin and a milieu conducive to bacterial or fungal proliferation. OE occurs more often in the summer months, when swimming is more common, [4, 9] and it is also common in tropical areas.[10] Individuals with allergic conditions (eg, eczema, allergic rhinitis, and asthma) are also at significantly higher risk for OE.[11, 12] Although OE rarely causes prolonged problems or serious complications, the infection is responsible for significant pain and acute morbidity (see Presentation). Prompt diagnosis (see DDx and Workup) and appropriate therapy (see Treatment) cure the majority of cases without complications; however, patients who are diabetic, immunocompromised, or untreated may develop necrotizing (malignant) OE, a potentially lifethreatening infection. Classification OE may be classified as follows: Acute diffuse OE This is the most common form of OE, typically seen in swimmers; it is characterized by rapid onset (generally within 48 hours) and symptoms of EAC inflammation (eg, otalgia, itching, or fullness, with or without hearing loss or jaw pain) as well as tenderness of the tragus or pinna or diffuse ear edema or erythema or both, with or without otorrhea, regional lymphadenitis, tympanic membrane erythema, or cellulitis of the pinna[10] Acute localized OE This condition, also known as furunculosis, is associated with infection of a hair follicle Chronic OE This is the same as acute diffuse OE but is of longer duration (>6 weeks) Eczematous (eczematoid) OE This encompasses various dermatologic conditions (eg, atopic dermatitis, psoriasis, systemic lupus erythematosus, and eczema) that may infect the EAC and cause OE Necrotizing (malignant) OE This is an infection that extends into the deeper tissues adjacent to the EAC; it primarily occurs in adult patients who are immunocompromised (eg, as a result of diabetes mellitus or AIDS) and is rarely described in children; it may result in cases of cellulitis and osteomyelitis (see Cellulitis, Osteomyelitis, and Chronic Osteomyelitis Imaging) Otomycosis - Infection of the ear canal secondary to fungus species such as Candida or Aspergillus Anatomy The external ear (see the image below) consists of the auricle and the EAC.

Acute otitis externa. Ear canal is red and edematous, and discharge is present. The auricle is composed of elastic cartilage with the overlying skin attached directly to the perichondrium. It begins to form during week 6 of gestation through consolidation of portions of the mesoderm of the first and second branchial arches, giving rise to the His hillocks. The first 3 hillocks are derived from the first arch, the second 3 from the second arch. The auricle reaches adult shape by the week 20 of gestation, but the adult size is not reached until the age of 9 years. The EAC begins to form during week 8 of gestation, when the surface ectoderm of the first pharyngeal groove thickens and grows toward the middle ear. This core of tissue begins to resorb by week 21 of gestation to form a channel that is complete by week 28. The canal reaches adult size by the age of 9 years and ossifies completely by the age of 3 years. The EAC is related to the mandibular fossa anteriorly, the mastoid air cells posteriorly, the middle cranial fossa superiorly, and the parotid gland inferiorly. The EAC is lined with squamous epithelium and is approximately 2.5 cm long in adults. Its function is to transmit sound to the middle ear while protecting more proximal structures from foreign bodies and any changes in environmental conditions. The outer one third of the canal is primarily cartilaginous and is oriented superiorly and posteriorly; the inner two thirds of the canal is osseous, is covered with thinner skin that adheres tightly, and is oriented inferiorly and anteriorly; this portion of the canal is devoid of any apocrine glands or hair follicles. The thicker skin over the outer (cartilaginous) portion of the EAC contains apopilosebaceous units comprising apocrine and eccrine glands that secrete their products around the base of a hair follicle. These secretions combine with sloughed squamous epithelium (cerumen) to coat the EAC and maintain an acidic pH (4-5). This cerumen coat migrates from the isthmus of the EAC to the lateral part, and its waxy nature protects the underlying epithelium from maceration or skin breakdown. The quantity of cerumen produced varies widely among individuals. The acidity of the cerumen inhibits bacterial or fungal growth. Whereas a paucity of cerumen allows bacterial growth, an excess can create an environment ideal for bacterial invasion by allowing retention of water and debris (as when the EAC is regularly exposed to water). Localized trauma from foreign objects placed in the ear can also lead to direct bacterial invasion in the ear canal. Once an infection becomes established, localized maceration and inflammation occur, which lead to symptoms.

Pathophysiology OE is a superficial infection of the skin in the EAC. The processes involved in the development of OE can be divided into the following 4 categories: Obstruction (eg, cerumen buildup, surfers exostosis, or a narrow or tortuous canal), resulting in water retention Absence of cerumen, which may occur as a result of repeated water exposure or overcleaning the ear canal Trauma Alteration of the pH of the ear canal If moisture is trapped in the EAC, it may cause maceration of the skin and provide a good breeding ground for bacteria. This may occur after swimming (especially in contaminated water) or bathinghence the common lay term swimmers ear. It may also occur in hot humid weather. Obstruction of the EAC by excessive cerumen, debris, surfers exostosis, or a narrow and tortuous canal may also lead to infection by means of moisture retention. Trauma to the EAC allows invasion of bacteria into the damaged skin. This often occurs after attempts at cleaning the ear with a cotton swab, paper clip, or any other utensil that can fit into the ear. Once infection is established, an inflammatory response occurs with skin edema. Exudate and pus often appear in the EAC as well. If severe, the infection may spread and cause a cellulitis of the face or neck. Necrotizing (malignant) OE is a rare complication that occurs in patients who are immunocompromised or in those who have received radiotherapy to the skull base. In this condition, bacteria invade the deeper underlying structures of the soft tissues and cause osteomyelitis of the temporal bone. This is a life-threatening disorder with an overall mortality that historically has approached 50%. Etiology OE is most often caused by a bacterial pathogen; other varieties include fungal OE (otomycosis) and eczematoid (psoriatic) OE.[13] In one study, 91% of cases of OE were caused by bacteria.[8] Others have found that as many as 40% of cases of OE have no primary identifiable microorganism as a causative agent. The most common causative bacteria are Pseudomonas species (38% of all cases),[13] Staphylococcus species, and anaerobes and gram-negative organisms. Fungal OE may result from overtreatment with topical antibiotics or may arise de novo from moisture trapped in the EAC. It is caused by Aspergillus 80-90% of the time; Candida and other organisms have also been isolated. This condition is characterized by long, white, filamentous hyphae growing from the skin surface. Besides otorrhea, erythema and edema of the EAC are common. In severe cases, soft tissue stenosis may be present. Extension of the infection may manifest as cellulitic skin changes involving the concha of the auricle and the tragus. Eczematoid (psoriatic) OE is associated with the following conditions: Eczema Seborrhea

Neurodermatitis Contact dermatitis from earrings or hearing aid use Purulent otitis media with perforation of the tympanic membrane and drainage; this may mimic OE to an extent, but it is usually painless and does not cause any swelling of the ear canal Sensitivity to topical medications Chronic OE is a fairly common condition that is sometimes the result of incomplete treatment of acute OE.[14] More often, however, chronic OE is caused by overmanipulation of the ear canal as a consequence of cleaning and scratching. Such overmanipulation results in a low-grade inflammatory response that causes further itching of the skin. Eventually, the skin thickens, and canal stenosis may occur. Necrotizing OE occurs in patients who are immunocompromised and represents a true osteomyelitis of the temporal bone. Risk factors for OE include the following: Previous episodes of OE Swimming, diving, or participating in aquatic activities Use of earplugs or probing of the EAC (possibly secondary to trauma to the EAC) Hot, humid weather Use of a hearing aid Coexistence of eczema, allergic rhinitis, or asthma Comorbidities such as diabetes mellitus, AIDS, leukopenia, or malnutrition Epidemiology United States and international statistics OE is found in all regions of the United States, occurring in 4 of every 1000 people annually.[9, 11] The infection is believed to be more prevalent in hot and humid conditions such as prevail during the summer months, presumably because participation in aquatic activities is higher.[4, 9] Acute, chronic, and eczematous OE are also common. Necrotizing OE is rare. The international frequencies of OE have not been fully determined; however, the incidence is increased in tropical countries.[10] Age-, sex-, and race-related demographics Although the infection can affect all age groups, OE appears to be most prevalent in the older pediatric and young adult population, with a peak incidence in children aged 7-12 years.[13] A single epidemiologic study from the United Kingdom found a similar 12-month prevalence for individuals aged 5-64 years and a slight increase in prevalence for those older than 65 years.[4] This was postulated to occur secondary to an increase in comorbidities, as well as an increase in the use of hearing aids, which may cause trauma to the EAC. OE affects both sexes equally. No racial predilection has been established, though people in some racial groups have small ear canals, which may predispose them to obstruction and infection. Prognosis Most incidents of OE resolve without difficulty. The majority of patients improve within 48-72 hours of antibiotic administration. Failure to improve within 2-3 days should call

the diagnosis into question and prompt the physician to reevaluate the patient. OE usually resolves fully in 7-10 days. Resolution of eczematoid OE occurs with control of the primary skin condition. In some patients with OE, the ear must be debrided for full resolution. Surgical incision and drainage are sometimes necessary. In some patients, OE can cause severe otalgia necessitating administration of narcotic pain relievers. Pain usually improves 2-5 days after initiating therapy. Temporary hearing loss is common secondary to canal occlusion. Severe infections may cause lymphadenitis or cellulitis of the face or neck. If left untreated, the infection may invade the deeper adjacent structures and progress to necrotizing (malignant) OE, a serious condition that requires prolonged treatment and often results in severe morbidity or mortality. This complication is almost exclusively seen in immunocompromised patients, such as those with diabetes, AIDS patients, those undergoing chemotherapy, and patients taking immunosuppressant medications (eg, glucocorticoids). Pseudomonas is the inciting organism in the vast majority of cases. When necrotizing OE develops, mortality is in the 20% range among adults, mostly because of the associated comorbidities and the rapid extension of the infection to include sepsis or intracranial extension. If left untreated, necrotizing OE has a mortality approaching 50%. This complication should be suspected if the patients pain and tenderness seem out of proportion to clinical appearance or if granulation tissue is seen in the ear canal. Patient Education OE is a common problem, with risk factors that are easily avoided. Education regarding ways of keeping the ear dry is helpful. Preventive use of acidifying drops is encouraged in patients with recurrent OE. Avoidance of the use of cottontipped swabs to remove ear cerumen should be discussed with patients. Improper use of cotton-tipped applicator sticks simply packs cerumen into the canal and can cause trauma to the tympanic membrane. Patients should be made aware that when OE does strike, it can usually be resolved in a short time, with few if any complications. History Patients with otitis externa (OE) may complain of the following: Otalgia, ranging from mild to severe, typically progressing over 1-2 days Hearing loss Ear fullness or pressure Tinnitus Fever (occasionally) Itching (especially in fungal OE or chronic OE) Severe deep pain If this is experienced by a patient who is immunocompromised or diabetic, be alerted to the possibility of necrotizing (malignant) OE

Discharge Initially, the discharge may be clear and odorless, but it quickly becomes purulent and foulsmelling Bilateral symptoms (rare) Frequently, a history of exposure to or activities in water (eg, swimming, surfing, and kayaking) Usually, a history of preceding ear trauma (eg, forceful ear cleaning, use of cotton swabs, or water in the ear canal) Physical Examination The key physical finding of OE is pain upon palpation of the tragus (anterior to ear canal) or application of traction to the pinna (the hallmark of OE). Examination reveals erythema, edema, and narrowing of the external auditory canal (EAC), and a purulent or serous discharge may be noted (see the image below). Conductive hearing loss may be evident. Cellulitis of the face or neck or lymphadenopathy of the ipsilateral neck occurs in some patients.

Acute otitis externa. Ear canal is red and edematous, and discharge is present. The tympanic membrane may be difficult to visualize and may be mildly inflamed, but it should be normally mobile on insufflation. Eczema of the pinna may be present. By definition, cranial nerve (CN) involvement (ie, of CNs VII and IX-XII) is not associated with simple OE. Fungal OE results in severe itching but typically causes less pain than bacterial OE does. A thick discharge that may be white or gray is often present. Whereas pseudomonal infection produces purulent otorrhea that may be green or yellow, Aspergillus otomycosis looks like a fine white mat topped by black spheres. Upon close examination, the discharge may contain visible fungal elements (eg, spores or hyphae) or have a fuzzy appearance. The sine qua non of necrotizing OE is pain that is out of proportion to the clinical findings. Upon close examination, granulation tissue may be present in the ear canal. In severe cases, the infection may spread to the surrounding soft tissues, including the parotid gland. Bony extension may also occur into the mastoid bone, temporomandibular joint, and base of the skull, in which case cranial nerves VII (facial), IX (glossopharyngeal), X (vagus), XI (accessory), or XII (hypoglossal) may be affected. Complications Complications of OE are rare and may include the following: Necrotizing OE (the most significant complication) Mastoiditis Chondritis of the auricle (from spread of acute OE to the pinna, particularly in patients with newly pierced ears)

Bony erosion of the base of the skull (skull base osteomyelitis[15] ) Central nervous system (CNS) infection Cellulitis or lymphadenitis Diabetic ketoacidosis is often present in diabetics with this condition. Herpes zoster may initially present with symptoms similar to those of OE, and vesicular eruption may occur 1-2 days after the initial symptoms. Ramsey Hunt syndrome is a rare complication of herpes zoster and presents with peripheral unilateral facial palsy. Patients should be counseled on this possible presentation and advised to seek medical care if it occurs.[16] Diagnostic Considerations Failure to recognize necrotizing (ie, malignant) otitis externa (OE) is a significant pitfall. A patient who is diabetic or immunocompromised with severe pain in the ear should have necrotizing OE excluded by an otolaryngologist. Problems to be considered include the following: Ear canal trauma Ear canal carcinoma Otitis media with a perforation or ventilation tube present Chondritis Cranial nerve palsy Hearing loss Wisdom tooth eruption Intracranial abscess Cavernous sinus thrombosis Ramsay Hunt syndrome Furuncle Skull base osteomyelitis Preauricular cyst and fistula Lacerations Atopic dermatitis Cerumen impaction Exostosis and osteoma Foreign body Acute (bullous) and chronic (granular) myringitis Although malignant tumors of the ear canal are rare, they do occur and sometimes are misdiagnosed as OE.[17] If the condition does not respond to treatment as expected, an otolaryngologist should evaluate the patient. Ramsay Hunt syndrome, more accurately known as herpes zoster oticus, is caused by varicella-zoster virus (VZV) infection. It is characterized by facial nerve paralysis and sensorineural hearing loss, with bullous myringitis and a vesicular eruption of the concha of the pinna and the external auditory canal (EAC). Painful OE may be present as well. Treatment includes use of an antiviral agent (eg, valacyclovir) and systemic steroids. The role of facial nerve decompression remains controversial. A furuncle is usually caused by staphylococcal infection of a hair follicle. This infection occurs in the lateral cartilaginous hair-bearing portion of the EAC. On otoscopic examination, a furuncle appears as a localized process, which may develop into an abscess, rather than as a diffuse inflammatory process, as is characteristic of OE.

Skull base osteomyelitis occurs most often in patients who are diabetic or immunocompromised. The usual bacterial pathogen is Pseudomonas aeruginosa. Other predisposing conditions include arteriosclerosis, immunosuppression, chemotherapy, steroid use, and other immunodeficient states. The diagnosis is strongly suggested by a history of diabetes mellitus, severe otalgia, cranial neuropathies, and characteristic EAC findings. The EAC may be filled with friable granulation tissue, which is primarily found inferiorly. Because this presentation may be identical to that of a soft tissue malignancy, prudence dictates a tissue biopsy even if a history of diabetes mellitus is present. Bare bone of the EAC floor may be exposed; small bony sequestra may be observed as well. Computed tomography (CT) demonstrates bone erosion, and gallium scanning can be performed at points throughout treatment to monitor resolution. Treatment consists of administration of an antipseudomonal intravenous (IV) antibiotic such as ceftazidime (in some cases) or oral ciprofloxacin (in less dramatic cases). Extended treatment for at least 6 weeks is most appropriate. Hyperbaric oxygen therapy may also be effective. Surgical debridement is reserved for granulation tissue and bony sequestra. A preauricular cyst or fistula may form as the result of abnormal development of the first and second branchial arch and may manifest as persistent discharge or recurrent infection. A draining sinus may be present anterior to the tragus; when infected, the cyst distends with pus, and the overlying skin is erythematous. Complete excision is indicated if these lesions become repeatedly infected. The facial nerve is at risk for injury during excision because of the close relation of the cyst or fistula to the superior branches of the nerve within the parotid gland. First branchial cleft anomalies have a more complex embryologic origin than preauricular cysts and fistulas do. These lesions may not have an obvious sinus tract on the skin and may manifest as an abscess extending deeply into the EAC, the parotid, or the neck. Full-thickness auricular lacerations may be observed after blunt or sharp trauma. These injuries are managed surgically by closing both the perichondrium and the skin. In contrast, external canal lacerations may occur after attempts to clean the ear canal with cotton-tipped applicators. These lacerations are usually managed by microscopically placing any skin flaps in their normal position, packing the ear canal, and administering topical antibiotic drops. Atopic dermatitis resulting from sensitivity to topical antibiotic solutions is well known. Neomycin allergy occurs in as many as 5% of patients treated with the medication. Suspect drug sensitivity if worsening of symptoms associated with skin excoriation and weeping occurs in the distribution of the topical medication exposure after the application of drops. Metal sensitivity also manifests as excoriation, erythema, and edema around the exposure site (eg, a piercing hole). A common allergen is nickel, an impurity that may be present in precious metals. Atopic dermatitis is managed by removal of the allergen (eg, an earring) and beginning topical steroids

and antibiotics if the wound is secondarily infected. The diagnosis of metal sensitivity is confirmed by performing a skin patch test. Cerumen impaction is the most common abnormality found on otoscopic examination, yet only a small proportion of the general population requires regular disimpaction because the EAC has the innate ability both to produce and to clear itself of cerumen. Cerumen may vary in color and consistency, and cerumen impaction may coexist with other pathologic conditions. Debris in the EAC from cholesteatoma or tumors may be confused with cerumen; accordingly, considerable care is required when debridement of the EAC is attempted. Debridement may be accomplished by using microinstruments or by aspirating ear canal contents with a No. 5 or No. 7 Barton suction device under direct vision through the otoscope or microscope. Irrigation of the ear canal is another option, but use of a pressurized irrigation system entails the risk of trauma. Exostoses and osteomas, the 2 most common bony lesions of the EAC, differ both histologically and clinically. Exostoses tend to arise from the anterior or posterior floor of the medial EAC (or from both simultaneously), have a sessile base, and are covered with normal-appearing skin. Osteomas may arise from any region of the bony EAC, are often pedunculated, may be single or multiple, and are covered by normal skin. Exostosis and osteomas require surgical treatment only if they are so large that they lead to a conductive hearing loss or intractable OE. Foreign bodies in the EAC are not infrequently encountered. In children, the appearance of these foreign bodies is variable; parts of toys or even food may be found in the EAC. In adults, fragments of cotton swabs are the most common finding. Erythema and edema surrounding the foreign body are commonly present. Depending on the patients ability to cooperate, the foreign body may be removed under a microscope with the aid of microinstruments. Acute myringitis is usually caused by a mycoplasmal or viral infection and has been observed in both adults and children. It is characterized by hemorrhagic bullae involving the tympanic membrane and a flulike syndrome. It is self-limiting; treatment involves pain control and fever management. Chronic myringitis is defined as deepithelization of the tympanic membrane, granulation tissue formation, and discharge. Treatment includes topical application of eardrops, a caustic solution in unresponsive cases, and mechanical removal of polypoidal granulations. Differential Diagnoses Otitis Media Approach Considerations The patients history and physical examination usually provide sufficient information to allow the clinician to make the diagnosis of otitis externa (OE). Most persons with OE are treated empirically. Thus, laboratory studies typically are not needed. However, Gram staining and culture of any discharge from the auditory canal may be helpful if the patient is immunocompromised, if the usual treatment measures are ineffective, or if a fungal

cause is suspected. However, as many as 40% of all cases of OE do not produce a dominant pathogen. Adults with OE may benefit from a blood glucose check or a urine dipstick test to evaluate for occult diabetes. Histologic examination of the skin of the external canal shows acute inflammation with exudate. CT, MRI, Bone Scan, and Gallium Scan Imaging studies are not required for most cases of OE. However, radiologic investigation may be helpful if an invasive infection such as necrotizing (malignant) OE is suspected or if the diagnosis of mastoiditis is being considered. High-resolution computed tomography (CT) is preferred and better depicts bony erosion.[6] Radionucleotide bone scanning and gallium scanning have been used to make the diagnosis. Magnetic resonance imaging (MRI), though not used as often, may be considered secondarily or if soft tissue extension is the predominant concern.[7] Otoscopy In cases of external ear infection, otoscopic examination must be performed in conjunction with evaluation of related structures (eg, the external ear and the head and neck). For example, the auricle should be examined for swelling, deformity, and erythema; the face, for evidence of facial nerve paresis or other cranial neuropathy; and the neck, for masses. An otoscope consists of a head and a handle and is used to examine the external auditory canal (EAC), the tympanic membrane, and the middle ear. A magnifying lens enhances the clinicians view. The following 2 types of head are available for the otoscope: Diagnostic head This head is fixed to the otoscope and does not allow the use of microinstruments through the scope Working (operating head) This head has a magnifying lens that can slide to the side, enabling passage of microinstruments through the speculum into the EAC and the middle ear A pneumatic attachment on the diagnostic head allows assessment of tympanic membrane motion by generating positive pressure in the EAC, causing the tympanic membrane to deflect medially. When pressure is released, the tympanic membrane expands laterally. This technique is an important tool in the diagnosis of middle ear effusions, vascular lesions, and inner ear fistulas. For optimal viewing of the tympanic membrane in an adult, retract the auricle posteriorly and superiorly to straighten the EAC; for optimal viewing in a child, pull the auricle posteriorly. Remove any debris or cerumen to allow an adequate examination. Proceed with the examination as follows: First, examine the EAC for masses, skin changes, and otorrhea Next, examine all parts of the tympanic membrane (eg, pars tensa and pars flaccida) Next, assess the motion of the tympanic membrane by means of pneumatic otoscopy Finally, attempt a thorough examination of the middle ear contents through the tympanic

membrane, though this examination may be limited by the opacity of the membrane itself Approach Considerations Primary treatment of otitis externa (OE) involves management of pain, removal of debris from the external auditory canal (EAC), administration of topical medications to control edema and infection, and avoidance of contributing factors. Most cases can be treated with over-the-counter analgesics and topical eardrops. Commonly used eardrops include acetic acid drops, which change the pH of the ear canal; antibacterial drops, which control bacterial growth; and antifungal preparations. Eczematoid (psoriatic) OE often responds to topical steroid drops but may be chronic or recurrent. The ear may require frequent suction debridement under a microscope. If significant canal edema develops, an ear wick may be used to facilitate delivery of topical medications into the medial canal. In severe cases, oral or intravenous (IV) antibiotic therapy and narcotic analgesics may be required.[18] In the case of necrotizing (malignant) OE, the patient must be admitted to a hospital for IV antibiotic therapy at the discretion of the consulting otorhinolaryngologist. The treatment that is rendered depends on the likely organism, which is best determined by means of Gram staining of the affected area. Clinical guidelines are available from the American Academy of Otolaryngology - Head and Neck Surgery Foundation.[3] Removal of Debris From Ear Canal Removal of debris from the ear canal improves the effectiveness of the topical medication. Gentle cleaning with a soft plastic curette or a small Frazier suction tip under direct vision is appropriate. Irrigation with a mix of peroxide and warm water may be useful for removing debris from the canal, but only if the tympanic membrane is intact. Any water instilled must be removed to keep from exacerbating the condition. Not uncommonly, children insert a foreign body in their ear canal and do not mention it to their parents. If any pain accompanies purulent drainage, the possibility of a foreign body in the ear canal should be considered. A patient with a foreign body in place will not improve until it is removed. Pharmacologic Therapy Before antibiotic treatment was recommended for OE, astringents and acetic acid solutions were commonly used to treat this condition. These solutions can be painful to inflamed ear canals and are not generally used today. An aminoglycoside combined with a second antibiotic and a topical steroid (eg, neomycinpolymyxin Bhydrocortisone) used to be the most commonly prescribed topical preparation; however, the neomycin component led to hypersensitivity reactions and ototoxicity in some patients. Most physicians prescribe topical antibiotic-containing preparations. Otic antibiotic and steroid combinations have shown to be highly successful in treatment, with cure rates of 87-97%.[19] Other agents used include analgesics for pain relief, acidifying solutions, and, in some instances, antipruritics or antihistamines. Topical medications

Most cases of acute OE respond well to topical treatment. Antibiotic eardrops, with or without a corticosteroid (given to decrease inflammation), are the mainstay of therapy. Topical acidifying and drying agents (given to alter the pH and to inhibit the growth of microorganisms) may be used in mild or resolving cases and are useful in fungal infections. An antifungal agent may be included as necessary. Mild OE usually responds to the use of an acidifying agent and a corticosteroid. As an alternative, a 2:1 ratio mixture of 70% isopropyl alcohol and acetic acid may be used. For moderate OE, consideration should be given to adding antibacterial and antifungal agents to the acidifying agent and the corticosteroid. In a systematic review of therapy for OE, Rosenfeld et al demonstrated little overall difference among the various topical agents used to treat this condition[20, 21] ; however, they found that use of a topical steroid alone increased cure rates by 20% as compared with a steroid-antibiotic combination. The combination of oral antibiotics with otic antibiotic solutions has not been shown to improve treatment success rates.[22] Use of aminoglycoside antibiotic eardrops in the presence of a perforation or ventilation tube may cause problems. Although this is controversial, many otolaryngologists believe that aminoglycoside eardrops may be ototoxic if they enter the middle ear. In these situations, using an alternative, nonototoxic topical preparation (eg, a fluoroquinolone, with or without a steroid) may be safer. Fluoroquinolones are not associated with ototoxicity, and ofloxacin is safe in cases of a perforated tympanic membrane. One literature review concluded that OE can be safely treated with an otic suspension containing 0.3% ciprofloxacin and 0.1% dexamethasone and that the inclusion of dexamethasone improves treatment success rates.[19] A German meta-analysis found a trend suggesting the superiority of quinolone monotherapy to classic combination regimens comprising a nonquinolone antibiotic plus a steroid.[23] Mild fungal infections can usually be treated with an acetic acid solution, whereas more severe cases may have to be treated with a topical antifungal agent, such as 1% clotrimazole. In the setting of chronic, noninfectious, therapy-resistant OE, a prospective study by Caffier et al demonstrated that daily use of 0.1% tacrolimus cream (administered via an ear wick [see below] that was changed every second to third day) resulted in high rates of resolution (46% through 1-2 years of follow-up) after 9-12 days of therapy.[24] The study also demonstrated longer periods of symptom-free intervals for those who experienced a recurrence.

Ear wick

If the ear canal is severely swollen, an ear wick may be inserted to facilitate the delivery of topical medications (see the image below). The wick may be commercially prepared from a hard sponge material that expands when wet (eg, the Merocel ear wick or the Pope Oto-Wick), cut from a bigger sponge by the physician, or made from narrow gauze (0.25-in. packing works well).

Otitis externa with ear wick in place. Note discharge from canal and swelling of canal. After the placement of the wick in the ear canal (a process that, unfortunately, causes brief but significant discomfort), the topical antibiotic drops are placed on the external end of the wick to be carried into the recesses of the ear canal. This is done 2-4 times daily, depending on the recommended dosing frequency for the medication. The wick may fall out as the edema decreases. In any case, it should be removed after 2-3 days. Analgesics Pain control is essential to quality patient care. OE can be quite painful, and patients frequently request analgesics. These agents ensure patient comfort and may have sedating properties. Inexpensive, simple nonsteroidal antiinflammatory drugs (NSAIDs) reduce inflammation and irritation and can be paired with opiates to improve pain symptoms Over-the-counter acetaminophen is appropriate for most patients. In some cases, systemic analgesics are helpful before ear cleaning or wick placement. Oral and intravenous antibiotics Most persons with OE do not require oral medications. Oral antibiotics are generally reserved for patients with fever, immunosuppression, diabetes, adenopathy, or an infection extending outside the ear canal. They should be given to individuals with cellulitis of the face or neck skin or to persons in whom severe edema of the ear canal limits penetration of topical agents. IV antibiotics are used in individuals with necrotizing (malignant) OE; they may also be appropriate for patients with severe cellulitis or persons whose symptoms do not respond to topical and oral antibiotics. A prolonged course of IV antibiotics, lasting for up to 6 weeks, may be required. If the patient is stable, IV antibiotics may be administered at home. Begin treatment with antibiotics to cover pseudomonads, and alter the regimen as necessary on the basis of culture results. Surgical Debridement and Drainage Surgical debridement of the ear canal is usually reserved for necrotizing OE or for complications of OE (eg, external canal stenosis). It is often necessary in more severe cases of OE or in cases where a significant amount of discharge is present in the ear. An otolaryngologist usually performs debridement using magnification and suction equipment. Debridement is the mainstay of treatment for fungal infections. Occasionally, an abscess forms in the ear canal; this usually occurs in cases of OE caused by S aureus. Treatment of the abscess is often accomplished by means of a simple incision and drainage procedure that is usually performed by an otolaryngologist using a needle or a small blade.

Activity During treatment of OE and for 1-2 weeks after its resolution, advise the patient to keep the ear canal dry. During bathing or showering, advise the patient to place an earplug or cotton ball lightly coated with petroleum jelly in the ear canal to prevent water penetration. Patients involved in aquatic activities may resume these activities once the infection has been eradicated, generally within 4-5 days. Aquatic athletes may return to the pool earlier than 4-5 days; generally, after 2-3 days of refraining from any water activity, they can return to their usual activities. However, the head must be kept dry until the infection has been eradicated. The best way of keeping the ear dry, obviously, is to avoid aquatic activities altogether, but the more common practice is simply to limit such activities to those that do not expose the ear to the water (eg, kicking while using a foam floatation board to keep the head above water). Prevention Some patients experience multiple recurrences of OE and thus benefit from the adoption of a preventive strategy. The following recommendations related to ear hygiene may help prevent recurrent OE: Eliminate any self-inflicted trauma to the ear canal, such as may occur with the use of cotton swabs or the insertion of objects (eg, bobby pins) into the EAC Avoid frequent washing of the ears with soap; this leaves an alkaline residue that neutralizes the acidic pH of the EAC Avoid swimming in polluted waters Ensure that the ear canals are emptied of water after swimming or bathing; the use of a blow dryer on a low setting after swimming to dry the ear canal has been suggested as a preventive measure, though no studies have demonstrated this suggestion to be effective Instill prophylactic eardrops after each exposure to water to assist in drying and acidifying the ear canal; a combination of 70% isopropyl alcohol and acetic acid in a 2:1 ratio may be used Some have recommended wearing earplugs for swimming and bathing. If worn, earplugs should be wiped with rubbing alcohol after use. Others have argued that the use of earplugs should be avoided, on the grounds that they may cause trauma to the ear canal and thereby predispose to the development of OE. Consultations For simple OE, consultation with an otorhinolaryngologist generally is not necessary. However, such consultation is appropriate if the patient has severe OE, is not responding to treatment as expected, has a suppurative complication or a perforated tympanic membrane, or is suspected of having necrotizing (malignant) OE. Debridement of the ear canal is often necessary for resolution of the infection. Necrotizing OE necessitates consultation with an otorhinolaryngologist, an infectious disease specialist, and, in some instances, a neurosurgeon.

Long-Term Monitoring Suctioning of the EAC on a weekly basis is required until debris has been removed. Patients must be monitored to ensure complete resolution of OE. Even in mild cases, follow-up is important for evaluating the response to treatment. In the view of some physicians, a follow-up visit 1 week after starting treatment is usually adequate; some prefer a shorter interval (eg, 2-3 days after the initiation of therapy). Medication Summary Most cases of otitis externa (OE) are caused by superficial bacterial infections and can be treated with over-thecounter analgesics and topical eardrops. Commonly used topical eardrops are acetic acid drops, which change the pH of the ear canal; antibacterial drops, which control bacterial growth; and antifungal preparations. Oral or parenteral antibiotics are reserved for severe cases. Otic antibiotic and steroid combinations have shown to be highly successful in treatment. The corticosteroid ingredient decreases inflammation and can help to ease the pain. These eardrops treat bacterial infection and reduce canal edema. The agents commonly prescribed for treating otitis externa are associated with cure rates between 87% and 97%.[19] In severe cases, oral or intravenous (IV) antibiotic therapy and narcotic analgesics may be required. Antibiotics Class Summary Most cases of OE are caused by superficial bacterial infections. Accordingly, most individuals with this condition may be treated with topical antibiotic preparations. Some preparations also contain a corticosteroid ingredient. The small amount of steroid that is present in the solution can help to ease the pain and edema associated with OE. Hydrocortisone/neomycin/polymyxin B (Cortisporin, Cortomycin) Hydrocortisone/neomycin/polymyxin is an antibacterial and anti-inflammatory agent for otic use, available as a solution or a suspension. It is used to treat steroid-responsive inflammatory conditions for which a corticosteroid is indicated and in which bacterial infection or a risk of bacterial infection exists. View full drug information Ofloxacin otic Otic ofloxacin is a pyridine carboxylic acid derivative with broad-spectrum effect that inhibits bacterial growth by inhibiting DNA gyrase. It is available as a 0.3% (3 mg/mL) solution. View full drug information Ciprofloxacin otic (Cetraxal) Otic ciprofloxacin is a fluoroquinolone that inhibits bacterial synthesis (and thus growth) by inhibiting DNA gyrase. It has activity against pseudomonads, streptococci, methicillinresistant Staphylococcus aureus (MRSA), Staphylococcus epidermidis, and most gram-negative organisms but has no activity against anaerobes. It is available with or without

hydrocortisone. Cetraxal is an otic solution available as 14 single-use applicators containing 0.25 mL of 0.2% solution each. Ciloxan is an ophthalmic solution that may be used for OE. Dexamethasone/tobramycin (TobraDex) Tobramycin interferes with bacterial protein synthesis by binding to 30S and 50S ribosomal subunits, thereby causing defects in the bacterial cell membrane. Dexamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reducing capillary permeability. TobraDex is an ophthalmic solution that may be used for OE. View full drug information Gentamicin ophthalmic (Garamycin, Gentak) Gentamicin is an aminoglycoside antibiotic used for gramnegative bacterial coverage. It is available as an ophthalmic solution that may be used for OE. This solution is a compounded medication, with each 1 mL containing 3 mg of gentamicin sulfate and 1 mg of betamethasone sodium phosphate. View full drug information Ciprofloxacin and dexamethasone otic (Ciprodex) Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA synthesis (and thus growth) by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. It has activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms but not against anaerobes. Dexamethasone decreases external auditory canal (EAC) inflammation by suppressing migration of PMNs and reducing capillary permeability; it also relieves pain symptoms. This otic suspension is indicated for use in OE, as well as for use in otitis media in individuals with tympanostomy tubes. View full drug information Ciprofloxacin and hydrocortisone otic suspension (Cipro HC Otic) Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA synthesis (and thus growth) by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. It has activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms but not against anaerobes. Hydrocortisone decreases inflammation by suppressing migration of PMNs and reducing capillary permeability. Otic, Other Class Summary Inflammation and accumulated debris allow the growth of bacterial species. This growth is counteracted by the use of mild acidifying medications, such as acetic acid solutions. These agents are useful for fungal OE or for mild OE believed to be of bacterial origin. They can also be useful for prevention.

Acetic acid in aluminum acetate (Borofair) Aluminum acetate has a drying effect. Acetic acid works well in superficial bacterial infections of OE. View full drug information Hydrocortisone and acetic acid otic solution (VoSoL HC) Acetic acid is antibacterial and antifungal; hydrocortisone is anti-inflammatory, antiallergic, and antipruritic. The combination of the 2 agents is inexpensive and works well in treating superficial bacterial infections of OE. Alcohol vinegar otic mix A homemade mix of 50% rubbing alcohol, 25% white vinegar, and 25% distilled water is as effective as pharmaceutical acidifying agents and less expensive. It is very useful for prevention and can be used as a flushing solution for fungal infections. Oral Antibiotics Class Summary Oral antibiotics are used to treat severe infection or cellulitis. Fluoroquinolones are the drugs of choice by virtue of their coverage of Pseudomonas species. View full drug information Ciprofloxacin (Cipro) Ciprofloxacin is a fluoroquinolone that inhibits bacterial DNA synthesis (and thus growth) by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. It has activity against pseudomonads, streptococci, MRSA, S epidermidis, and most gram-negative organisms but not against anaerobes. Analgesics Class Summary OE can be quite painful, and control of this pain is essential to quality patient care. Analgesics ensure patient comfort and may have sedating properties. Inexpensive, simple nonsteroidal anti-inflammatory drugs (NSAIDs) reduce inflammation and irritation and can be paired with opiates to improve pain symptoms. View full drug information Acetaminophen (Tylenol, FeverAll, Aspirin-Free Anacin, Tylenol Children) Over-the-counter acetaminophen is appropriate for most patients. It is the drug of choice for pain in patients who are known to be hypersensitive to aspirin or NSAIDs, who have upper GI gastrointestinal (GI) disease, or who are taking oral anticoagulants. View full drug information Acetaminophen and codeine (Tylenol #3) The combination of acetaminophen and codeine is indicated for the treatment of mild to moderate pain. Antifungals, Other Class Summary

A small but significant percentage of OE cases are due to Aspergillus species or other yeasts and fungi (otomycosis). Some cases of fungal OE can be treated with acidifying drops; topical antifungal agents are used to treat otomycosis refractory to these drops. The mechanism of action of topical antifungal agents usually involves inhibition of the pathways (eg, enzymes, substrates, and transport) necessary for sterol/cell membrane synthesis or those involved in altering the permeability of the fungal cell membrane (eg, polyenes). View full drug information Clotrimazole 1% otic solution (Lotrimin AF) Otic clotrimazole solution is a compounded medication. Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing the death of fungal cells. View full drug information Nystatin powder (Nystop, Nyamic, Pedi-Dri) Nystatin is a fungicidal and fungistatic antimicrobial obtained from Streptomyces noursei; it is effective against various yeasts and yeastlike fungi. It changes the permeability of the fungal cell membrane after binding to cell membrane sterols, causing the cellular contents to leak. Treatment should continue until 48 hours after the disappearance of symptoms. Topical application of nystatin reduces fungal growth.