Otitis externa

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

Otitis externa is the inflammation of the external auditory canal. It is primarily caused by Pseudomonas aeruginosa and Staphylococcus aureus infection. Less commonly, it is also caused by otomycosis by Candida albicans and Aspergillus niger, as well as the spread of inflammatory dermatoses such as eczema, seborrhea, and psoriasis. The external auditory canal becomes susceptible to infection due to sudden, invasive changes in the conditions of the ear canal epithelium. This includes abrupt changes in humidity, causing epithelial degradation, cerumen decreases, and increased pH levels to increase predisposition to infection from bacterial or fungal pathogens. This can also be caused by localized physical trauma, such as injury or contact with abrasive surfaces (i.e. chemicals or physical cleaning products, such as cotton swabs). Gross pathology for otitis externa will include erythema of the ear canal, along with eczema-esque scaly, shedding of the skin. It also includes visible ear canal swelling, as well as potentially cellulitis of the pinna and otorrhea. Otitis externa is classified as acute, chronic, or malignant based on the duration of the disease, as well as diffusion and severity of infection and symptoms. It must be differentiated from other diseases that cause otalgia, ear itching, otorrhea, erythema and edema of the ear canal, hearing loss, ear pressure, and dermatitis; this includes otitis media, infectious myringitis, sinusitis, and meniere’s disease. The annual incidence of acute otitis externa is usually high, as approximated to be 801 per 100,000 individuals in the U.S. and 140 per 100,000 individuals in the Netherlands. The annual Case Fatality Rate for malignant necrotizing otitis externa is approximately 10-20%. The majority of acute otitis externa cases occur in adults between 65 and 74 years old. The majority of malignant otitis externa patients are aged 50 and older; this is due to the primary cause of immunocompromise resulting in maligant otitis externa being diabetes mellitus. Risk factors for acute and chronic otitis externa include activities and conditions that predispose an individual to ear canal inflammation. They also include being a female between 65 and 74 years old. Risk factors for malignant necrotizing otitis externa include conditions predisposing an individual to immunocompromise, including undergoing chemotherapy or suffering from diabetes mellitus. Symptoms for all forms of otitis externa are primarily pain, itching, and swelling of the ear canal. Symptoms of malignant necrotizing otitis externa include severe ear pain, facial paralysis, difficulty opening mouth, and difficulty swallowing. Laboratory findings consistent with diagnosis of all forms of otitis externa include evidence of bacterial or fungal infection. CT imaging is essential in establishing a diagnosis of malignant necrotizing otitis externa by revealing the extent of infection past the ear canal and spread into temporal and intracranial bones. They reveal the extent of damage and inflammation of the bones and soft tissue, demonstrating the cause for facial palsy due to the inflammatory influence on the cranial nerves. Other imaging findings to facilitate accurate diagnosis of malignant necrotizing otitis externa includes Technetium-99m and Gallium Citrate Ga 67 scintigraphical nuclear imaging. The mainstay of therapy for acute otitis externa (AOE) includes cleaning of the external auditory meatus and treating the infection. Topical therapy is recommended as the initial therapy for diffuse, uncomplicated acute otitis externa. Systemic antimicrobials should be reserved for infections extending outside the external canal or patients with specific host factors. Analgesics such as Acetaminophen or Nonsteroidal anti-inflammatory drugs are administered, either alone or in combination with an opioid. Preventing otitis externa primarily revolves around preventing epithelial damage to the ear canal that predisposes infection or dermatitis. The prognosis of otitis externa varies based on the presence of complications from the spread of the infectious pathogen. Without treatment, the prognosis of acute otitis externa is usually good and it is self-limited. Malignant otitis externa that results in palsies, osteitis of the skull base, and osteomyelitis of the temporal bone have particularly poor prognoses if left untreated. With treatment, acute and chronic otitis externa have good prognoses. The prognosis of malignant necrotizing otitis externa with treatment will vary depending on the severity of resultant complications. Complications of otitis externa include reactions to infection, as well as adverse reactions to the spread of the pathogen past the ear canal. This includes cerebral abscess, osteomyelitis of the skull base, cellulitis of the ear canal, perforated tympanic membrane and Sigmoid sinus thrombosis.

Otitis externa was first identified in 1873 by Adam Politzer, classified and recorded as one of the otological pathologies codified in his otology clinic in Austria. Burow’s solution, a therapeutic application of aqueous aluminium acetate, was invented by Karl August Burow in the mid-19th century. Antibiotic therapy for chronic otitis externa treatment emerged with the invention of mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain. Corticosteroid therapy to relieve pain and itching from otitis externa emerged with the discovery of glucocorticoid dexmethasone in 1957. The current therapy of “ear drops,” or topical application of antibiotics, began to be administered to otitis externa patients in 1987 after the discovery of Ciprofloxacin, a fluoroquinolone-class antibiotic

Otitis externa is classified as acute, chronic, or malignant based on the duration of the disease, as well as diffusion and severity of infection and symptoms.

Otitis externa develops when the external ear canal becomes susceptible to infection due to a variety of causes. The primary pathogens responsible for otitis media are the bacteria Pseudomonas aeruginosa and Staphylococcus aureus. Sudden, invasive changes in humidity from a rapid intake of water into the ear canal can predispose the external ear to bacterial infection: The cerumen quantity in the ear canal decreases, weakening an important protective barrier in the ear; The epithelial surface of the skin begins to degrade, allowing easier infiltration by bacterial; The pH value of the ear canal, usually maintained at 5.0 by a combination of the cerumen and the mechanical construction of the ear, increases and renders the ear more favorable to bacterial reproduction. Increased moisture in the ear canal can also lead to otitis externa caused by otomycosis. The primary fungal causes of otitis externa are Candida albicans and Aspergillus niger. The buildup of fungal debris in the ear canal epithelium leads to increasing pressure and inflammation. Surfer’s ear, or exostosis of the ear canal raises the predisposition to otitis externa by rendering the ear canal more prone to trapping water and water-bourne pathogens. Localized physical trauma can cause Weakening of the ear canal epithelium and the lessening of cerumen, predisposing infection. Otitis externa is associated with infectious, inflammatory ear and head conditions. Gross pathology for otitis externa will include erythema of the ear canal, along with eczema-esque scaly, shedding of the skin. It also includes visible ear canal swelling, as well as potentially cellulitis of the pinna and otorrhea. Laboratory findings consistent with diagnosis of all forms of otitis externa include evidence of bacterial or fungal infection.

The primary cause of otitis externa is bacterial; the majority of cases result from Pseudomonas aeruginosa or Staphylococcus aureus infections. Otomycosis can cause otitis externa, with primary infectious fungi including Candida albicans and Aspergillus niger. Allergy-caused dermatitis can cause non-infectious otitis externa if they spread to the ear canal, including inflammatory dermatoses such as eczema, seborrhea, and psoriasis. Contact dermatitis can cause otitis externa from allergic reactions to cosmetic chemicals and metals. Rarely, psoriasis therapy secukinumab can cause otitis externa as an adverse reaction.

Acute otitis externa must be differentiated from other diseases that cause otalgia, ear itching, otorrhea, erythema and edema of the ear canal, hearing loss, ear pressure, and dermatitis.

The annual incidence of acute otitis externa is usually high, as approximated to be 801 per 100,000 individuals in the U.S. and 140 per 100,000 individuals in the Netherlands. The annual prevalence of acute otitis externa in the United Kingdom is approximately 24 per 100,000 individuals. The annual Case Fatality Rate for malignant necrotizing otitis externa is approximately 10-20%. The majority of acute otitis externa cases occur in adults between 65 and 74 years old. The majority of malignant otitis externa patients are aged 50 and older; this is due to the primary cause of immunocompromise resulting in maligant otitis externa being diabetes mellitus. Acute otitis externa is approximately 1.1 times more likely to occur in females than males of all age groups.

Risk factors for acute otitis externa include activities and conditions that predispose an individual to ear canal inflammation. They also include being a female between 65 and 74 years old. Risk factors for malignant necrotizing otitis externa include conditions predisposing an individual to immunocompromise, including undergoing chemotherapy or suffering from diabetes mellitus.

The prognosis of otitis externa varies based on the presence of complications from the spread of the infectious pathogen. Without treatment, the prognosis of acute otitis externa is usually good and it is self-limited. It usually develops up to 7 days after infection. Initial symptoms include an odorless discharge from otorrhea, as well as mild otalgia and pruritus with signs of mild erythema of the ear canal. Without treatment, acute otitis externa will usually resolve without treatment within 4 days of onset. Otitis externa considered “chronic” – cases lasting more than 3 months with or without treatment – will usually persist indefinitely and will require treatment for resolution. Recurrent otitis externa usually results from otomycosis or dermatoses that do not resolve without treatment. Malignant necrotizing otitis externa usually develops when an infectiously-caused case of acute otitis externa spreads to the temporal bones, as well as bones in the ear adjacent to the canal. Without treatment, the prognosis of maligant otitis externa is usually poor due to resultant intracranial complications. Malignant otitis externa that results in palsies, osteitis of the skull base, and osteomyelitis of the temporal bone have particularly poor prognoses if left untreated. With treatment, acute and chronic otitis externa have good prognoses. The prognosis of malignant necrotizing otitis externa with treatment will vary depending on the severity of resultant complications.

Symptoms for all forms of otitis externa are primarily pain, itching, and swelling of the ear canal. Symptoms of chronic, recurrent otitis externa include lack of earwax and buildup of dead skin causing narrowing of the ear canal. Symptoms of malignant necrotizing otitis externa include severe ear pain, facial paralysis, difficulty opening mouth, and difficulty swallowing. History of allergies, aquatic-based occupations, or exposure to sources of immunocompromise, including chemotherapy and diabetes mellitus should be considered in otitis externa patients.

Physical examination of the ear canal will reveal findings indicative of acute, chronic, and malignant necrotizing otitis externa. For acute otitis externa, the patient can appear ill if the cause is infectious and is accompanied by fever. Patients with chronic otitis externa are usually well-appearing. Malignant necrotizing otitis externa patients are usually ill-appearing due to the accompanying fever and facial palsies.

Laboratory findings consistent with diagnosis of all forms of otitis externa include evidence of bacterial or fungal infection. They also include markers of inflammation, such as an elevated Erythrocyte sedimentation rate and C-reactive protein, as well as elevated white blood cell count.

CT imaging is essential in establishing a diagnosis of malignant necrotizing otitis externa by revealing the extent of infection past the ear canal and spread into temporal and intracranial bones. They reveal the extent of damage and inflammation of the bones and soft tissue, demonstrating the cause for facial palsy due to the inflammatory influence on the cranial nerves.

Other imaging findings to facilitate accurate diagnosis of malignant necrotizing otitis externa includes Technetium-99m and Gallium Citrate Ga 67 scintigraphical nuclear imaging. Tc-99m analysis will display findings of activity of osteoblast cells that are indicative of infection from malignant otitis externa. Gallium Citrate Ga 67 scans will reveal extent of the spread of malignant otitis externa infection by measuring the response by macrophages and reticular endothelial cells in the areas of inflammation in the temporal and intracranial bones. Gallium Citrate Ga 67 is preferred to Technetium-99m for scintigraphic scans due to the tendency of Tc-99m to be overly sensitive to osteoblast activity, often resulting in positive malignant otitis externa results prematurely, as well as displaying lingering positive results after the infection is treated.

The mainstay of therapy for acute otitis externa (AOE) includes cleaning of the external auditory meatus and treating the infection. Topical therapy is recommended as the initial therapy for diffuse, uncomplicated acute otitis externa. Systemic antimicrobials should be reserved for infections extending outside the external canal or patients with specific host factors. Analgesics such as Acetaminophen or Nonsteroidal anti-inflammatory drugs are administered, either alone or in combination with an opioid.

Preventing otitis externa primarily revolves around preventing epithelial damage to the ear canal that predisposes infection or dermatitis. This includes avoiding exposure to water contaminated by otitis externa bacteria or fungal pathogens, as well as limiting prolonged exposure to excessively humid conditions. Preventing recurrence of otitis externa revolves around identifying the cause (infectious or dermatologic) and ensuring appropriate topical or systemic therapy is administered.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

Otitis externa was first identified in 1873 by Adam Politzer, classified and recorded as one of the otological pathologies codified in his otology clinic in Austria. Burow’s solution, a therapeutic application of aqueous aluminium acetate, was invented by Karl August Burow in the mid-19th century. Antibiotic therapy for chronic otitis externa treatment emerged with the invention of mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain. Corticosteroid therapy to relieve pain and itching from otitis externa emerged with the discovery of the glucocorticoid dexamethasone in 1957. The current therapy of “ear drops,” or topical application of antibiotics, began to be administered to otitis externa patients in 1987 after the discovery of ciprofloxacin, a fluoroquinolone-class antibiotic.

• German physicians Hermann Schwartze, Anton von Troltsch, and Adam Politzer advanced the discourse of clinicial study of otitis externa by publishing the first journal dedicated to ear pathology and treatment in 1865.^[1]
• Adam Politzer founded the first otology clinic in 1873 in Austria, beginning the codification and standardization of ear disease treatment, such as otitis externa.
• Burow’s solution, a therapeutic application of aqueous aluminium acetate, was invented by Karl August Burow in the mid-19th century that is still used presently as a topical remedy for otitis externa.^[2]
• Antibiotic therapy for chronic otitis externa treatment emerged with the invention of mass production of penicillin in 1940 by Alexander Fleming, Howard Florey, and Ernst Chain.^[3]
  • This was the first instance of the modern use of antibiotic therapy for otitis externa treatment.
• Corticosteroid therapy to relieve pain and itching from otitis externa emerged with the discovery of the glucocorticoid dexamethasone in 1957.^[4]
• The “tektite solution” therapy of 15% tannic acid, 15% acetic acid, and 50% isopropanol or ethanol, emerged in 1969 in response to high incidence of otitis externa in biologists involved in the Tektite I diving mission.^[5]
• The current therapy of “ear drops,” or topical application of antibiotics, began to be administered to otitis externa patients in 1987 after the discovery of Ciprofloxacin, a fluoroquinolone-class antibiotic.^[6][7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

Otitis externa is classified as acute, chronic, or malignant based on the duration of the disease, diffusion of the infection, and the severity of symptoms.

Otitis externa is classified by duration, diffusion, and symptom severity.

• Onset within 48 hours.^[1]
• Acute otitis externa is localized to the [[ear canal]..

• Otitis externa is considered chronic in cases that persist greater than 3 months with treatment.^[1]

• Acute otitis externa becomes reclassified as malignant and necrotizing when the infectious pathogen diffuses from the ear canal and infects the temporal bones, as well as bones in the ear adjacent to the canal, leading to damage and degradation.^[2][3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

Otitis externa develops when the external ear canal becomes susceptible to bacterial or fungal infection by various mechanisms. Sudden invasive changes in humidity from a rapid intake of water into the ear canal can predispose the external ear to bacterial infection. This occurs by thinning of the cerumen in the ear canal and weakening an important protective barrier in the ear. The epithelial surface of the skin begins to degrade, allowing easier infiltration by bacteria. The pH of the ear canal is usually maintained at 5.0 by a combination of the cerumen and the mechanical construction of the ear; when this increases it renders the ear more favorable to bacterial reproduction. Increased moisture in the ear canal can also lead to otitis externa caused by otomycosis. The buildup of fungal debris in the ear canal epithelium leads to increasing pressure and inflammation. Surfer’s ear or exostosis of the ear canal predisposes to otitis externa by rendering the ear canal more prone water-bourne pathogens. Localized trauma can cause weakening of the ear canal epithelium and thinning of cerumen, predisposing infection. Otitis externa is associated with infectious, inflammatory ear and head conditions. Gross pathology for otitis externa will include erythema of the ear canal, along with eczema-like scaly, shedding of the skin. It also includes visible ear canal swelling, as well as potentially cellulitis of the pinna and otorrhea.

Otitis externa develops when the external ear canal becomes susceptible to infection due to a variety of causes.

• Sudden invasive changes in humidity from a rapid intake of water into the ear canal can predispose the external ear to infection.^[1]
  • Prolonged exposure to moisture causes swelling of the stratum corneum.
  • The cerumen quantity in the ear canal decreases, weakening an important protective barrier in the ear.
  • The epithelial surface of the skin begins to degrade allowing increased access for bacterial infection.
  • The pH value of the ear canal, usually maintained at 5.0 by a combination of the cerumen and the mechanical construction of the ear, increases and renders the ear more favorable to bacterial infection and otomycosis.^[2]
• Increased moisture in the ear canal can also lead to otitis externa caused by otomycosis.^[3]
  • Spread of fungi results in inflammation in the ear canal.^[3]
  • The buildup of fungal debris in the ear canal epithelium leads to increasing pressure and inflammation.
  • Extensive use of topical antibiotic ear drops to treat bacterial otitis externa increases predisposition to otomycosis.
• For immunocompromised individuals, chronic or recurrent otitis externa from bacterial infection results from the spread of infection to the temporal bone.^[4]
  • Spread of infection may proceed through the temporal bone to the cranium.

• Surfer’s ear or exostosis of the ear canal raises the predisposition to otitis externa by rendering the ear canal more prone to trapping water and water-bourne pathogens.^[5]

• Localized trauma can lead to otitis externa from the following dermatoses. Weakening of the ear canal epithelium and thinning of cerumen predisposes infection in the following dermatoses:^[6]
  • Eczema
  • Seborrhea
  • Psoriasis
  • Contact dermatitis

• Otitis externa is associated with the following infectious, inflammatory ear and head conditions:
  • Otitis media
  • Osteitis
  • Osteomyelitis^[7]
  • Otorrhea^[8]
  • Otalgia

• Gross pathology for otitis externa will include erythema of the ear canal, along with eczema-esque scaly, shedding of the skin.^[9]
• Ear canal swelling will be visible.
• Cellulitis of the pinna and otorrhea may also be present upon physical examination.^[10]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

The primary cause of otitis externa is bacterial; the majority of cases result from Pseudomonas aeruginosa or Staphylococcus aureus infections. Otomycosis can cause otitis externa with primary infectious fungi including Candida albicans and Aspergillus niger. Allergy-caused dermatitis can cause non-infectious otitis externa if it spreads to the ear canal; this includes inflammatory dermatoses such as eczema, seborrhea, and psoriasis. Contact dermatitis can cause otitis externa from allergic reactions to cosmetic chemicals and metals. Rarely, psoriasis therapy secukinumab can cause otitis externa as an adverse reaction.

Causes of otitis externa include all sources of inflammation of the external ear canal.^[1]

• The most common bacterial causes of otitis externa include:^[2]
  • Pseudomonas aeruginosa^[2]
  • Staphylococcus aureus
• Additional bacterial causes of otitis externa include:^[3]
  • Staphylococcus epidermidis
  • Microbacterium otitidis
  • Microbacterium alconae
  • Staphylococcus caprae
  • Staphylococcus auricularis
  • Enterococcus faecalis
  • Enterobacter cloacae
  • Staphylococcus capitis
  • Staphylococcus haemolyticus
• Infectious bacteria that thrive in water can cause otitis externa due to facilitated transport to the ear canal.^[4]

• Otomycosis can cause otitis externa. The most common causes of fungal otitis externa include:^[5]
  • Candida albicans
  • Aspergillus niger
• Otomycosis-caused otitis externa is common after prolonged antibiotic therapy.^[1]

• Allergy-caused dermatitis can cause non-infectious otitis externa if they spread to the ear canal and include the following:^[5]
  • Eczema
  • Seborrhea
  • Psoriasis^[6]
  • Contact dermatitis as a reaction to the following:
    • Metals such as nickel or silver
    • Hearing aids
    • Chemical irritants, including shampoos, soaps, cosmetics etc.,

• Rarely, psoriasis therapy secukinumab can cause otitis externa as an adverse reaction.^[7]

• Chronic otitis externa is most commonly caused by the following:
  • Otomycosis, particularly by Candida albicans and Aspergillus niger
  • Allergic rhinitis
  • Underlying dermatoses:
    • Eczema
    • Seborrhea
    • Psoriasis
    • Contact dermatitis

• • Primarily caused by bacterial infection of Pseudomonas aeruginosa and Staphylococcus aureus.^[8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

Acute otitis externa must be differentiated from other diseases that cause otalgia, ear itching, otorrhea, erythema and edema of the ear canal, hearing loss, ear pressure, and dermatitis.

Acute otitis externa must be differentiated from other diseases that cause otalgia, ear itching, otorrhea, erythema and edema of the ear canal, hearing loss, ear pressure, and dermatitis.^[1][2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

The annual incidence of acute otitis externa is approximated to be 801 per 100,000 individuals in the U.S. and 140 per 100,000 individuals in the Netherlands. The annual prevalence of acute otitis externa in the United Kingdom is approximately 24 per 100,000 individuals. The annual case fatality rate for malignant necrotizing otitis externa is approximately 10-20%. The majority of acute otitis externa cases occur in adults between 65 and 74 years old. The majority of malignant otitis externa patients are aged 50 and older; this is due to the primary cause of immunocompromise resulting in maligant otitis externa being diabetes mellitus. Acute otitis externa is approximately 1.1 times more likely to occur in females than males of all age groups.

• The incidence of acute otitis externa is usually high:
  • In the U.S. the incidence is approximately 801 per 100,000 individuals.^[1]
  • In the Netherlands the incidence is approximately 140 per 100,000 individuals.^[2]
• The incidence of acute otitis externa is greater in climates that experience more year-round humidity which is more conducive to bacterial and fungal colonization.^[3][4]

• A study of acute otitis externa patients in the United Kingdom revealed that the disease prevailed for 12-months in approximately 24 per 100,000 individuals.^[5][6]

• The annual case fatality rate for malignant necrotizing otitis externa is approximately 10-20%.^[7]

• The majority of acute otitis externa cases occur in adults between 65 and 74 years old.^[6]
• There is an increase in acute otitis externa among children between 5 and 14 years old.^[8]
• The majority of malignant otitis externa patients are aged 50 and older; this is due to the primary cause of immunocompromise resulting in maligant otitis externa being diabetes mellitus.^[9][10]

• Acute otitis externa is approximately 1.1 times more likely to occur in females than males of all age groups.^[6]
  • Males are more likely to have a recurrent acute otitis externa episode after initial infection.

• There is no racial predisposition to otitis externa.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

Risk factors for acute otitis externa include activities and conditions that predispose an individual to ear canal inflammation. Risk factors also include being a female between 65 and 74 years old. Risk factors for malignant necrotizing otitis externa include conditions predisposing an individual to immunocompromise including undergoing chemotherapy or suffering from diabetes mellitus.

• Risk factors for acute otitis externa include activities and conditions that predispose an individual to ear canal inflammation:^[1]
  • Scuba-diving increases the risk of trapped water in the ear canal.^[2]
  • Swimming in public pools or other unclean bodies of water increases the chance of bacterial or fungal infection.
  • Living in a humid or tropical climate^[3]
  • Developing dermatoses such as eczema, seborrhea, and psoriasis^[4]
  • Loss of cerumen in the ear canal thins the ear canal protective coating
  • Introduction of foreign objects in the ear canal such as hearing aids, or ear plugs can cause irritation and inflammation
  • Ear canal obstruction such as sebaceous cysts
  • Suppuration from other ear diseases such as otitis media
  • Undergoing prolonged treatment with topical antibiotics raises the risk of otomycosis.^[4]
  • Trauma to the ear canal
  • Repeated exposure to irritants such as soaps, shampoos, or related cosmetic chemicals
  • Having a narrow ear canal more prone to retaining water
• Being a female between age 65 and 74^[5]
• For malignant necrotizing otitis externa, contributors to immunocompromise include:^[6]
  • Chemotherapy
  • Diabetes mellitus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.; Tarek Nafee, M.D. [2]

The prognosis of otitis externa varies based on the associated complications. Without treatment, the prognosis of acute otitis externa is usually good and it is self-limited. Otitis externa will usually resolve without treatment within 4 days of onset. Patients usually develop symptoms up to 7 days after infection. Initial symptoms include an odorless discharge from otorrhea, mild otalgia, and pruritus with signs of mild erythema of the ear canal. Chronic otitis externa may persist indefinitely and will require treatment for resolution. Recurrent otitis externa commonly results from otomycosis or dermatoses and require treatment. Malignant necrotizing otitis externa may develop when an infectious case of acute otitis externa extends to the temporal bones and to bones in the ear adjacent to the ear canal. Without treatment, the prognosis of maligant otitis externa is poor due to subsequent intracranial complications. Malignant otitis externa that results in cranial nerve palsies, osteitis of the skull base, and osteomyelitis of the temporal bone have particularly poor prognoses if left untreated. With treatment, acute and chronic otitis externa have good prognoses. The prognosis of malignant necrotizing otitis externa with treatment will vary depending on the severity of associated complications.

• Acute otitis externa usually develops up to 7 days after infection from the causative pathogen.^[1]
• Without treatment, acute otitis externa will usually resolve within 4 days of onset.^[2]
• Patients that are immunocompromised may experience a longer duration and escalation of symptoms.^[1]
• Chronic otitis externa lasting greater than 3 months with or without treatment, will usually persist indefinitely.^[3]
  • This is usually the case when it is caused by a form of dermatitis as a chronic reaction to recurrent exposure to cosmetological chemical irritants.
• Malignant necrotizing otitis externa usually develops when an infectiously-caused case of acute otitis externa spreads to the temporal bones and bones in the ear adjacent to the canal leading to damage and degradation.^[4]
  • Without treatment, malignant otitis externa will usually result in severe intra and extra cranial manifestations.

Complications of otitis externa may include:^[1]

• Abscesses in the ear canal^[5]
• Cellulitis from bacterial or fungal epithelial penetration in the damaged ear canal
• Perforated ear drum may manifest with the following complications:^[5]
  • Hearing loss
  • Otalgia
  • Otorrhea
  • Tinnitus
• Surfer’s ear from cold water exposure and irritation
• In severe cases of acute otitis externa complicationsparotitis, adenopathy, and auricular cellulitis
• Osteomyelitis of the temporal bone^[6]
• Malignant otitis externa
• Sigmoid sinus thrombosis may occur as a complication of malignant otitis externa due to intracranial spread of bacterial infection^[4]
• Cerebral abscess^[7]

• The prognosis of acute and chronic otitis externa is usually good, without treatment, due to its self-limited nature.
• Chronic otitis externa will require treatment to relieve symptoms.^[3]
  • Recurrent otitis externa usually results from otomycosis or dermatoses that do not resolve without treatment.
• Without treatment, the prognosis of maligant otitis externa is usually poor due to resultant intracranial complications.
  • Malignant otitis externa that results in cranial nerve palsies, osteitis of the skull base, and osteomyelitis of the temporal bone have particularly poor prognoses if left untreated.^[6]
  • The prognosis of malignant necrotizing otitis externa with treatment will vary depending on the severity of resultant complications.

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