Chondritis, Perichondritis, and Cellulitis of the Auricle
Spectrum of disease from mild superficial skin infection to chondritis.
Cellulitis is an infection of the skin of the auricle.
Perichondritis and chondritis are infections of the auricular perichondrium and cartilage, respectively.
Bacterial infections typically result from blunt or penetrating trauma, or extension of infectious otitis externa (OE).
Superficial infections commonly related to Staphylococcus and Streptococcus.
Deeper infections often involve Pseudomonas.
Trauma—most common cause
Blunt trauma (assault, wrestling) resulting in hematoma and secondary infection
Penetrating trauma—bites, knives, foreign, body, firearms
Ear piercing—transcartilagenous piercings
Extension of OE
Extension of subperiosteal abscess
Relapsing perichondritis—autoimmune condition that involves the cartilage and spares the lobule from inflammation
Pain and erythema common in cellulitis, perichondritis, and chondritis.
Induration and edema typical for chondritis and perichondritis.
Induration usually not seen with cellulitis.
Hematoma with or without abscess formation—fluctuation present with abscess.
Cartilage deformity (“cauliflower ear”) in chronic or recurrent infections and in advanced or untreated cases.
Fever, chills, and elevated white blood cell count can be seen.
Diagnosis made on clinical grounds
Cellulitis of the auricle typically due to Staphylococcus spp
Pseudomonas spp most common cause of perichondritis and chondritis
Most commonly cultured organism from auricular abscess
Incision and drainage with culture when possible
Other rare bacteria—Escherichia coli and Proteus spp
Erysipelas caused by beta-hemolytic Streptococcus
Auricle typically erythematous, indurated, and painful
Infection typically follows a well-demarcated border
Oral anti-staphylococcal and anti-streptococcal antibiotics
Severe infection or immunocompromised patient
IV anti-staphylococcal, anti-streptococcal, and anti-pseudomonal antibiotics
Perichondritis or chondritis
Involvement of cartilage with inflammation or abscess can result in cosmetic deformity (cauliflower ear)
Goal of treatment: rapid diagnosis and initiation of therapy, maximize aesthetic outcome
No abscess—oral antibiotics with anti-pseudomonal coverage (fluoroquinolone)
Abscess—incision and drainage with cartilage debridement as needed
Antibiotic therapy for 2 to 4 weeks
Placement of bolsters as needed
Viral Processes of the Auricle
Thought to occur following viral reactivation within ganglion nerve cells
Can result following insult due to direct trauma, dental work, or upper respiratory infection (URI)
Most commonly seen in the elderly and immunocompromised
Often includes prodrome of otalgia which precedes vesicular eruption.
Vesicles in the external auditory canal (EAC) and conchal bowl.
May included tinnitus, hearing loss, vertigo, decreased lacrimation (associated ganglion).
Facial paralysis with Herpes Zoster Oticus is known as Ramsay Hunt Syndrome.
Other cranial neuropathies (V, IX, X, XI, XII) can be seen.
Tzanck smear to look for multinucleated giant cells at the base of ruptured vesicle
Differential diagnosis includes: herpes zoster, herpes simplex, cytomegalovirus (CMV), and pemphigus vulgaris
Viral antibody titers
Assess for evidence of herpetic keratitis with eye complaints
Prognosis for facial nerve paralysis in Ramsay Hunt Syndrome is worse than Bell palsy (only 60% regain normal function).
High-dose steroids (1 mg/kg/d for 14 days) in cases of facial nerve paralysis and/or sensorineural hearing loss (SNHL).
Antiviral (valacyclovir 1000 mg every 8 hours × 7 days).
Surgical decompression not advocated as neural degeneration widespread rather than localized to geniculate ganglion and labyrinthine segment as in Bell palsy.
Gabapentin can be used for post-herpetic neuralgia.
Fungal Infections of the Auricle
Can be primary or secondary (manifestation of disseminated fungal infection)
Geographic location, particular hobbies (rose handling, etc.) may aid in diagnosis
More common in immunocompromised patients
Often difficult to distinguish from bacterial cellulitis
Otalgia (often dull and mild)
Erythematous and edematous skin similar to bacterial cellulitis
Multisystem disease present in disseminated disease
High index of suspicion—consider if cellulitis unresponsive to antibiotics
Fungal smear and culture—may require tissue biopsy to identify organism
Fungal serologic titers and chest X-ray if systemic disease suspected
Most common are Aspergillus and Candida species
Topical antifungals for mild infection
IV therapy for severe or disseminated disease
Consider infectious disease consultation
Rare Pinna Infections
External Auditory Canal
Furuncle is a localized abscess of the apopilosebaceous unit.
Rupture of furuncle may result in more diffuse cellulitis and AOE.
Associated with warm, humid climates.
Common in swimmers.
Most common in children 5 to 10 years old.
Maceration of EAC skin allows invasion of skin commensal bacteria to the apopilosebaceous unit.
Trauma to skin from cotton tip applicators or other instrumentation.
Chronic skin conditions (eczema, psoriasis, seborrhea dermatitis).
Devices that occlude EAC (hearing aids, earbuds)
Congenitally narrow EAC with poor self-cleaning ability
Lack of cerumen
Antibacterial properties (acidic, lysozymes, antibodies)
History of external beam radiation
Rapid onset (< 48 hours)
Pain—often severe, extreme tenderness to manipulation
“Tragal sign”—pressure on the tragus induces extreme pain
Fever is rare unless significant periauricular cellulitis
Edema—may result in near complete occlusion of EAC
Tympanic membrane (TM) mobility normal (vs suppurative otitis media)
Lymphadenopathy of the preauricular or cervical lymph nodes
Bacterial infections account for 90% of AOE (see later for fungal AOE)
Most commonly Pseudomonas aeruginosa
Also Staphylococcus aureus, Staphylococcus epidermidis, and other gram-negative rods
Goals include pain control, aural toilet, and topical therapy.
Debridement of EAC allows penetration of ototopical therapy.
Otowick may be necessary in cases with obstructive edema.
Allows ototopical drops to penetrate to medial EAC tissue
Replaced every 3 to 5 days to avoid toxic shock syndrome
Maintain dry ear precautions with bathing.
Mild disease—irrigation with acidifying agent (dilute vinegar, acetic acid) may be sufficient.
Moderate to severe disease—topical antibiotics with or without steroid.
Provides high concentration of medication without systemic absorption.
Examples include neomycin, ciprofloxacin, ofloxacin, and tobramycin.
Frequently effective in treatment of periauricular cellulitis.
Neomycin can cause dermatitis in some patients—consider switching agents with lack of response.
Not effective in uncomplicated AOE.
May be considered for severe periauricular cellulitis or immunocompromised patients.
Incision and drainage
Used for furuncles or carbuncles.
Treat similar to AOE after I&D.
Inflammation involving lateral surface of TM and medial portion of EAC wall
Typically associated with upper respiratory infections
More common in winter months
Can occur alone (primary) or with serous otitis media (secondary) in 30% to 40%
Severe pain lasting 3 to 4 days, then subsiding
Hallmark finding—bullae over the TM and medial canal filled with serous or serosanguinous fluid
Rupture of bullae can cause serosanguinous discharge
60% can demonstrate mixed or SNHL that typically resolves
Mycoplasma pneumoniae used to be considered offending agent—not proven
Others—Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
Dry ear precautions
Lancing bullae for pain relief
Topical antibiotic/steroid drops to prevent bacterial superinfection
If associated with acute otitis media (AOM), treat accordingly
Uncommon, prolonged, infection of the squamous surface of TM.
Characterized by loss of epithelium of TM and replacement with granulation tissue.
Relapsing and recurring symptoms are common.
Difficult to treat.
Unclear, no predisposing factors identified
Painless, usually foul smelling otorrhea
Conductive hearing loss due to thickening and blunting of the TM
Many patients can be asymptomatic
Replacement of epithelium with granulation tissue (most commonly posterior superior quadrant)
Late stages—scarring of anterior EAC angle resulting in blunting or acquired EAC stenosis or obliteration
TM perforation common and frequently heals spontaneously
Middle ear (ME) normal
Diagnosis based on history and physical examination
May require computed tomography (CT) of temporal bone to rule out COM
Numerous treatment options have been described
Drying agents (desiccation)
Chemical cautery (silver nitrate or trichloroacetic acid)
Laser ablation (CO2)
Acidification with dilute vinegar irrigation
Surgical removal of granulation tissue
Two most effective treatments: irrigation with dilute vinegar, surgical removal
Tympanoplasty with canalplasty reserved for severe obliterative disease
High rate of recurrence or exacerbation with surgery
Several mechanisms have been proposed
Allergen exposure (allergic reaction to topical agents, contact dermatitis)
Systemic disease (ie, amyloid, sarcoid, psoriasis, Wegener)
Local factors (seborrheic dermatitis, elevated pH, chronic moisture)
Leads to chronic inflammation within dermis and surrounding apocrine glands
Results in increased depth of rete pegs and loss of normal sebaceous glands
Mild discomfort but usually no otalgia
Thickened skin in cartilaginous canal
Mild to moderate erythema with clear, scant drainage
Keratosis—adherent skin debris
Canal obliteration in late stage—medal canal fibrosis
Biopsy chronic granulation tissue to rule out malignancy
Gram-negative species (ie, Proteus)
Fungus common (see below) (Aspergillus, Candida)
Focused on reducing inflammation
Dry ear precautions
Avoidance of Q-tips
Frequent, microscopic debridement of debris and dead skin
Acidification of EAC (vinegar and alcohol solution, acetic acid)
Antifungal preparations (see later)
Topical steroids when infection ruled out
Topical immunosuppressant (ie, tacrolimus) described, not widely used
Elimination of underlying skin condition
Canalplasty with skin grafting
Primarily seen in immunocompromised patients (diabetic, HIV, transplant)
Infection begins in soft tissues of EAC
Spreads via fissures of Santorini and to stylomastoid and jugular foramen via tympanomastoid suture line
High morbidity due to typical delay in treatment from symptom onset
Must have high index of suspicion
Mortality between 5% to 20% even in antibiotic era
Microangiopathy and increased EAC pH leads to bacterial invasion of vessel walls
Causes vascular thrombosis
Coagulative necrosis of surrounding tissue
Severe, deep-seated and long-standing aural pain often worse at night
Otalgia often “out of proportion to examination findings”
Ear canal edema
Hallmark—granulation tissue at isthmus of EAC (bony-cartilaginous junction)
Occasionally can involve lower cranial nerves (VII-XII)
Facial nerve most commonly affected (stylomastoid foramen involvement)
Multiple cranial neuropathies imply a worse prognosis
Septic thrombophlebitis of sigmoid sinus can occur resulting in “picket fence” pattern of fevers
Meningeal signs as infection moves intracranial
Must biopsy granulation tissue to rule out malignancy
ESR typically elevated—nonspecific but can be used to follow treatment response and possible recurrence
Bacterial and fungal cultures
Technetium (Tc-99) scintigraphy imaging of choice to confirm diagnosis
Concentrates in areas of osteoblastic activity
High sensitivity for bone infection
Test positive before CT visibly abnormal
Single-photon emission computed tomography (SPECT) more sensitive than planar imaging
Tc-99 remains in bone long after acute infection resolves—not used to track disease progress
Gallium-67 or Indium-111 labeled leukocyte scan
Shows areas of inflammatory cell activity
Sensitivity increased with Tc-99 scan
Used to follow treatment response as tests return to normal quickly
Scan every 4 weeks during treatment
Findings include bony erosion and soft tissue abnormalities around EAC
Unable to distinguish infection from malignancy
Significant bony erosion must occur before grossly abnormal on imaging
Contrast not necessary unless concern for abscess
Not useful in following response to treatment
Useful in detecting soft tissue changes and dural involvement
Pseudomonas aeruginosa accounts for more than 90% of cases
Staphyloccocus aureus, S. epidermidis, Proteus mirabilis, Klebsiella spp. also reported
Fluoroquinolone-resistant Pseudomonas increasing in incidence
Fungal MOE less common
Associated with HIV+ patients
Usually Aspergillus fumigatus
Aggressive blood glucose control in diabetic patients.
Correct other causes of immunodeficiency if possible.
Surgical intervention warranted only for abscess drainage or debridement of bony sequestrum.
More heroic surgical measures necessary with recalcitrant disease.
Role of hyperbaric oxygen therapy is unproven for MOE.
Monotherapy with oral fluoroquinolone is first-line therapy.
Culture directed therapy when possible.
Advanced cases may require primary parenteral therapy.
Parenteral antipseudomonal aminopenicillins if unable to take fluoroquinolones.
Typical treatment duration of 6 weeks.
Treatment should continue until clinical examination normal.
Can treat until Gallium-67 scan normalizes but may result in prolonged treatment
Parenteral antifungal therapy for culture positive disease
Amphotericin B commonly used, significant side effects
Voriconazole first-line therapy for invasive Aspergillosis
10% of all AOE
Warm, wet ear canal (swimmers, surfers, divers, tropical environments)
Chronic moisture of ear canal (hearing aid users)
Fungal overgrowth in modified radical mastoid cavities
Same as acute bacterial OE.
Pruritus is more common than bacterial OE.
Fungal hyphae or fungal ball (“wet newspaper”) may be visible.
Otalgia and otorrhea may be present.
Cultures not typically helpful
Biopsy in immunocompromised patients or atypical presentations
Aspergillus most common
Candida and Penicillium also seen
Frequent aural toilet
Dry ear precautions
Acidifying and drying agents (ie, gentian violet, boric acid)
Topical antifungal agents first-line pharmacologic treatment
CSF powder (chloromycetin, amphotericin B [Fungizone], sulfanilamide)
Systemic therapy reserved for refractory disease, immunocompromised patients with suspicion of invasive fungal disease
Abnormal accumulation of keratin in EAC.
Primarily seen in adults (30-60 years).
Theories for disease include abnormal epithelial migration and excessive production of epithelial cells in the EAC and on the TM.
Involves entire circumference of skin of the medial EAC.
Dense keratin plug forms in the EAC.
Can lead to conductive hearing loss from mechanical obstruction and/or thickening of TM and blunting of the annulus.
Often associated with secondary AOE and otorrhea.
Most often involves both ears.
Disease progression can cause bony widening of the EAC and in severe cases auto-mastoidectomy.
Frequent aural toilet and debridement
Lifelong cleanings may be necessary
Ulceration of EAC skin and necrosis of underlying bone most often at posteroinferior EAC.
Physical examination involves focal findings (vs keratosis obturans).
Theories for disease include invasion of bone by epithelium and secondary necrosis versus focal bone injury with secondary invasion of epithelium.
Physical examination often shows EAC defect filled with desquamated epithelium and surrounding granulation tissue.
Mechanical removal of keratin
Silver nitrate for granulation tissue
Frequent microscopic cleanings
Surgery for refractory cases
Removal of necrotic bone with coverage of the cavity (fascia)
Infections of the Middle Ear (ME) and Mastoid
Most common reason for pediatrician visit in the United States
Day care attendance
Tobacco smoke exposure
Presence of siblings
Supine bottle feeding
Lack of breast-feeding in first 6 months
Eustachian tube dysfunction
Craniofacial syndromes (ie, Treacher Collins)
Genetic predisposition (Down syndrome)
Indigenous populations (Native American, Inuit, Native Australians)
Low socioeconomic status
Association with upper respiratory infections implicates Eustachian tube (ET).
Inflammation of Gerlach tonsil compromising ET function.
Adenoid pad harbors bacteria that can reflux into the ME.
ET is shorter and more horizontal in children resulting in impaired clearance and drainage.
Recurrent AOM may be due to functional obstruction of ET (ie, adenoid hypertrophy).
Combination of poor ME clearance and refluxed bacteria leads to inflammation of ME.
Otalgia (often rapid onset < 48 hours)
Signs and symptoms are not specific to AOM
Bulging and erythematous TM.
Limited or absence of movement on pneumatic otoscopy.
Pneumatic otoscopy is the key diagnostic tool and required to make diagnosis.
Air-fluid level in ME.
Purulent otorrhea if TM ruptured (suppurative otitis media).
Tympanometry can be used in equivocal cases.
Streptococcus pneumoniae most common organism
Introduction of PCV7 and Prevnar 13 vaccinations have altered prevalence of certain serotypes.
Decreased absolute number of invasive complications.
Serotype 19A is a highly multidrug-resistant strain increasing in prevalence.
Penicillin (PCN) resistance due to alterations of PCN-binding proteins in cell wall.
Haemophilus influenzae and M. catarrhalis also common
Haemophilus influenzae strains largely nontypeable since introduction of HIB vaccine.
50% of H. influenza and 100% of M. catarrhalis are beta-lactamase positive.
RSV, rhinovirus, coronavirus, parainfluenza virus, enterovirus, adenovirus
Virus isolated in up to 75% of AOM aspirates
Original guidelines published in 2004 by American Academy of Pediatrics (AAP), American Academy of Family Practice (AAFP), and American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS)
Revised guidelines for children 6 months to 12 years published in 2013
Guidelines written for children without underlying immunodeficiency, genetic conditions, cochlear implants, recurrent AOM, or AOM with underlying chronic otitis media with effusion (COME)
Cannot be overlooked
Narcotics—risk of respiratory depression; use sparingly
Myringotomy with or without tympanostomy tube
Relives pressure within ME space
Requires sedation in children
Risk of chronic perforation
Children more than 2 years, option to observe for 48 to 72 hours without antibiotic intervention.
May be advised since natural history of AOM is for resolution of symptoms and effusion over time.
Observation feasible if diagnosis uncertain or symptoms mild in children more than 2 years.
Pain control should still be initiated.
Initiate antibiotic therapy with failure to improve.
Requires compliant parents with ready access to health care provider.
Observation does not increase rates of complications (ie, mastoiditis).
Unilateral or bilateral AOM in children at least 6 months old with severe signs or symptoms (moderate to severe otalgia > 48 hours or temperature > 39°C).
Nonsevere, bilateral AOM in children 6 to 23 months.
Children less than 2 years have prolonged symptoms and higher recurrence rates without treatment.
Antibiotic therapy decreases symptomatic infection by 1 day compared to observation.
80% with AOM improve within 3 days without antibiotics
92% more improve within 3 days with antibiotics
3 out of 10 develop rash, 8 out of 10 develop diarrhea
Amoxicillin 90 mg/kg/d divided tid
Provides tissue concentrations to overcome bacterial resistance in most intermediate-resistant (> 0.1-1 µg/mL minimal inhibitory concentration [MIC]) pneumococcal, H. influenza, and M. catarrhalis strains.
Length of treatment controversial
7-day therapy increases rate of recurrence but lowers side effects.
10-day therapy lowers rate of recurrence but increases side effects.
Therapy more than 10 days has no advantage in reducing failure rates or duration of middle ear effusion (MEE) vs 10-day course.
Children less than 2 years: 10 days
Children 2 to 5 years: 10 days
Children less than 6 years: 5 to 7 days
Highly resistant Pneumococcal strains (MIC > 2 µg/mL) will not respond.
Day care attendees and children with older siblings at risk for resistant strains.
Amoxicillin should not be used in patients receiving amoxicillin in the past 30 days, cases of AOM with concurrent purulent conjunctivitis, or PCN allergic patients.
Amoxicillin-clavulanic acid (amox-clav)
Recommended for children receiving amoxicillin in past 30 days, concurrent purulent conjunctivitis, or history of recurrent AOM unresponsive to amoxicillin.
Patients with severe illness (fever > 39°C, severe otalgia) or if H. influenzae or M. catarrhalis suspected.
90 mg/kg/d of amoxicillin and 6.4 mg/kg/d clavulanate
Type 1 hypersensitivity (ie, urticaria and anaphylaxis)
Azithromycin 10 mg/kg for 1 day, then 5 mg/kg for 4 days
Clindamycin 30 to 40 mg/kg/d divided tid for known resistant Pneumococcus
Patients unable to take oral medications or with mild-delayed hypersensitivity to amoxicillin
50 mg/kg IM per day for 1 to 3 days (higher failure rate with 1 day vs 3 days)
Failure of symptoms to improve within 48 to 72 hours after initiation of treatment
If on amoxicillin, switch to amox-clav
If on amox-clav, initiate 3-day course of ceftriaxone IM
If on erythromycin or trimethoprim-sulfamethoxazole, start parenteral therapy with third-generation cephalosporin for pneumococcal resistance
Tympanocentesis with cultures
Considered in patients who fail second-line therapy
Treatment failure higher in younger patients, day care attendees, regions with highly resistant bacteria