Perichondritis of the Pinna

Infection of the perichondrium of the auricular cartilage, which progresses to chondritis with cartilage necrosis and permanent deformity if treatment is delayed or if the wrong antibiotic is chosen.

Why it destroys the ear

Auricular cartilage has no intrinsic blood supply and depends entirely on the perichondrium. Infection lifts the perichondrium, cuts off nutrition, and produces avascular necrosis. Systemic antibiotics penetrate avascular cartilage poorly, so any collection must be drained.

The organism of greatest concern is Pseudomonas aeruginosa, which is present in 90 percent of post traumatic and post piercing cases and which produces proteolytic enzymes that liquefy cartilage rapidly.

An antibiotic without antipseudomonal cover is a common and avoidable cause of a destroyed ear.

Causes

• High ear piercing through the cartilage, which is now the single commonest cause in young people. Lobule piercing does not carry this risk since the lobule has no cartilage.
• Trauma including lacerations, burns, frostbite and untreated auricular haematoma.
• Surgery, including otoplasty and postauricular incisions.
• Extension from severe otitis externa, particularly necrotising otitis externa.
• Insect bites, acupuncture and contact dermatitis with excoriation.
• Immunosuppression and diabetes, which worsen severity.

Microbiology: Pseudomonas aeruginosa predominates, followed by Staphylococcus aureus including methicillin resistant strains, and less commonly Proteus and Escherichia coli.

• Painful, erythematous, swollen, tender pinna.
• Sparing of the lobule, which is the discriminating physical sign, since the lobule contains no cartilage. Involvement of the lobule indicates cellulitis or erysipelas rather than perichondritis.
• Loss of the normal auricular contours as swelling obscures the antihelix and scaphoid fossa.
• Fluctuance indicating a subperichondrial abscess, which requires drainage.
• Fever and systemic upset in severe cases.
• In late or untreated disease: dusky discolouration, ulceration, purulent discharge and cartilage collapse.

Assessment

• Look for the entry point: a piercing, laceration, burn or surgical incision.
• Examine the canal and drum, since perichondritis may be secondary to otitis externa or, in the elderly diabetic, to necrotising otitis externa.
• Check blood glucose and immune status.
• Photograph the ear to document extent and to track progress.

Differential diagnosis and the discriminating feature

• Cellulitis and erysipelas: lobule involved, sharply demarcated raised border in erysipelas, streptococcal aetiology.
• Relapsing polychondritis: recurrent, often bilateral, non infective inflammation with lobule sparing, associated with nasal chondritis producing a saddle deformity, laryngotracheal involvement, scleritis, arthritis and audiovestibular dysfunction. It does not respond to antibiotics. This diagnosis is missed repeatedly and patients receive multiple antibiotic courses before rheumatology involvement.
• Contact dermatitis to nickel from earrings, with itch, weeping and vesicles rather than deep pain.
• Herpes zoster oticus with vesicles.
• Insect bite reaction.
• Erysipelas versus perichondritis is settled by the lobule.

Clinical, based on a tender erythematous pinna with lobule sparing.

• Swab any discharge or aspirate for culture and sensitivity, specifically requesting Pseudomonas identification.
• Blood cultures if febrile.
• Full blood count, C reactive protein, blood glucose and HbA1c.
• Ultrasound where a collection is suspected but not clinically obvious.
• Computed tomography of the temporal bone where necrotising otitis externa is suspected in a diabetic or immunocompromised patient with associated canal disease, or where deep extension is suspected.
• Investigate for relapsing polychondritis where the presentation is bilateral, recurrent, non traumatic or antibiotic unresponsive: erythrocyte sedimentation rate, C reactive protein, antinuclear antibody, antineutrophil cytoplasmic antibody, and rheumatology referral. Biopsy is occasionally required.

Early, antipseudomonal antibiotics plus drainage of any collection plus removal of any foreign body.

Remove the cause

• Remove all cartilage piercings and jewellery immediately. Leaving jewellery in place perpetuates the infection.
• Debride necrotic tissue.
• Remove any retained foreign material from trauma.

Antibiotics

Mild, early disease without fluctuance, in a reliable patient:

• Ciprofloxacin 500 to 750 mg orally twice daily for 7 to 10 days, which is the key agent because of pseudomonal cover and excellent tissue and cartilage penetration.
• Add flucloxacillin 500 mg orally four times daily where staphylococcal involvement is likely.
• Alternatives in quinolone intolerance are limited, which is one reason quinolones remain first line here despite their general cautions. Discuss with microbiology.

Moderate to severe disease, fluctuance, systemic upset, immunocompromise or failure of oral therapy:

• Admit for intravenous therapy.
• Ciprofloxacin 400 mg intravenously every 8 to 12 hours, or ceftazidime 2 g intravenously every 8 hours, or piperacillin with tazobactam 4.5 g intravenously every 6 to 8 hours.
• Add vancomycin with a target trough of 15 to 20 mg/L where methicillin resistant Staphylococcus aureus is suspected.
• Switch to oral ciprofloxacin once improving, completing a total course of 10 to 14 days, extended where cartilage necrosis is present.
• Quinolone counselling: tendon rupture, aortic risks, QT prolongation, and reduced absorption with calcium, iron, magnesium, zinc and antacids, which must be separated by at least 2 hours.

Surgical drainage

• Indicated for any fluctuant collection, and for failure to improve within 48 hours of appropriate intravenous therapy.
• Incision along the natural contour of the helix or antihelix, evacuation of pus, irrigation, debridement of necrotic cartilage back to bleeding tissue, and culture of tissue rather than surface swab.
• Leave a small drain or a wick for 24 to 48 hours.
• Apply a bolster dressing to prevent dead space and reaccumulation, as for auricular haematoma.
• Repeated debridement may be necessary. Preserve as much viable cartilage as possible, since every millimetre lost worsens the deformity.

Analgesia and supportive care

• Paracetamol 1 g every 6 hours plus ibuprofen 400 mg every 8 hours, with opioids for severe pain.
• Optimise glycaemic control.
• Do not apply topical antibiotic ointment as the sole treatment, which is inadequate.
• Corticosteroids have no place in infective perichondritis and are harmful.

Relapsing polychondritis, when that is the diagnosis

• Prednisolone 0.5 to 1 mg/kg daily for acute flares with a taper.
• Steroid sparing agents including methotrexate, azathioprine and biologic therapy under rheumatology supervision.
• Urgent assessment of the airway, since laryngotracheal chondritis causes life threatening collapse.

Follow up and prevention

• Review at 48 hours and again at 1 week to confirm response and detect a developing collection.
• Photograph serially.
• Counsel young patients firmly against high ear cartilage piercing, and advise those with existing piercings to seek immediate care for any redness or pain.
• Deformity requires delayed reconstruction, no sooner than 6 to 12 months after complete resolution, using cartilage grafting and recontouring, with results that are usually incomplete.