Otitis externa overview: Difference between revisions
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{{Otitis externa}} | {{Otitis externa}} | ||
{{CMG}} | {{CMG}}{{AE}}{{LRO}} | ||
==Overview== | ==Overview== | ||
''' | 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 [[otalgia|pain]], [[itching]], and [[swelling]] of the [[ear canal]]. Symptoms of malignant necrotizing otitis externa include severe [[ear pain]], facial [[paralysis]], [[Difficulty opening mouth|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]]. | ||
==Historical Perspective== | |||
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 | |||
==Classification== | |||
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. | |||
==Pathophysiology== | |||
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. | |||
==Causes== | |||
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. | |||
==Differentiating Otitis Externa from other Diseases== | |||
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]]. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
The incidence of otitis externa is high | 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== | ||
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]]. | |||
==Natural History, Complications, and Prognosis== | |||
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. | |||
==Diagnosis== | ==Diagnosis== | ||
== | ===History and Symptoms=== | ||
Symptoms for all forms of otitis externa are primarily [[otalgia|pain]], [[itching]], and [[swelling]] of the [[ear canal]]. Symptoms of chronic, recurrent otitis externa include lack of [[earwax]] and buildup of dead skin causing [[stenosis|narrowing of the ear canal]]. Symptoms of malignant necrotizing otitis externa include severe [[ear pain]], facial [[paralysis]], [[Difficulty opening mouth|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=== | |||
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 palsy|facial palsies]]. | |||
===Laboratory Findings=== | |||
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=== | |||
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=== | |||
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. | |||
==Treatment== | |||
===Medical Therapy=== | |||
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]]. | |||
===Prevention=== | |||
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. | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Disease]] | [[Category:Disease]] | ||
[[Category:Inflammations]] | [[Category:Inflammations]] | ||
[[Category:Otolaryngology]] | [[Category:Otolaryngology]] | ||
[[Category:Pediatrics]] | [[Category:Pediatrics]] | ||
[[Category:Emergency mdicine]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Immunology]] | |||
Latest revision as of 23:30, 29 July 2020
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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.
Overview
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.
Historical Perspective
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
Classification
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.
Pathophysiology
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.
Causes
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.
Differentiating Otitis Externa from other Diseases
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.
Epidemiology and Demographics
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
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.
Natural History, Complications, and Prognosis
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.
Diagnosis
History and Symptoms
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
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
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
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
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.
Treatment
Medical Therapy
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.
Prevention
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.