Complications of Acute Otitis Externa

RED FLAGS

  • Complete acute stenosis of the ear canal – you cannot insert a speculum at all

  • Cellulitis of the pinna or peri-auricular area

  • Ipsilateral cranial nerve palsy

  • Ipsilateral severe deep otalgia (eg causing insomnia)

 

WHY IS THIS IMPORTANT?

Complications of acute otitis externa (AOE) require urgent identification and treatment as they can potentially be life threatening.

 

WHEN TO INVOLVE THE ENT REGISTRAR

The ENT registrar should be informed soon if you suspect a complication of AOE, particularly if the patient has any red flags.

Discuss patients immediately if they have central neurological signs such as meningism and reduction in GCS. 

 

WHO TO ADMIT

Admit patients where you have clinical suspicion of necrotising otitis externa (NOE), abscess collection or pinna/facial cellulitis. 

Patients with complete acute stenosis of the ear canal alone should be seen urgently as outpatients or in the treatment room but rarely need admission; an otowick should be inserted to keep the inflamed canal open.

 

ASSESSMENT AND RECOGNITION

Complications of AOE are uncommon but can be serious and therefore should be suspected in patients who do not respond to treatment.

 

Complications

Necrotising otitis externa (NOE; previously known as malignant otitis externa)

  • Infection spreads through soft tissue resulting in osteomyelitis of the temporal bone and skull base

  • Older male patients with diabetes are at high risk (classical presentation); but all immunocompromised patients are at risk

  • Pseudomonas aeruginosa is the most common causative organism

  • Characterised by non-resolving AOE despite adequate topical treatment; deep severe pain which is out of proportion to general status (patient patients are apyrexial) and which can cause insomnia; purulent otorrhoea; evidence of granulation and necrotic tissue within the ear canal

  • Some patients may appear to have non-resolving AOE but, on closer questioning, they turn out never to have been prescribed topical treatment; the vast majority will not have NOE and will get better once they start the correct treatment

  • In more severe cases, there may be evidence of conductive hearing loss and lower cranial neuropathies (CN VII, IX, X, XI and XII) as the disease becomes more erosive and spreads along the skull base. This may become life threatening if this extends as far as the jugular foramen.

  • More rarely, NOE may involve the petrous apex leading to CN V and VI nerve palsies (Gradenigo’s syndrome).

 

Abscess formation

  • AOE can lead to localised abscess formation; this is usually as a result of Staphylococcus aureus

  • This presents with localised fluctuant swelling, which may form in or around the affected ear

  • Occlusion of the ear canal may lead to a conductive hearing deficit; If the abscess ruptures, there may be evidence of purulent discharge

 

Peri-auricular or pinna cellulitis

  • This presents with erythema, swelling and warmth of the pinna or around the ear, which may extend to surrounding tissues overlying the parotid gland, mastoid and sternomastoid. Pain is present, particularly on manipulation of the pinna, but is usually moderate in comparison to NOE

  • There may be systemic symptoms including fever, generalised illness and regional lymphadenopathy

 

Chronic stenosis of the ear canal or false fundus

In patients with recurrent AOE, fibrosis within the canal can lead to chronic stenosis or complete obstruction of the ear canal (formation of a false fundus covering the tympanic membrane). This is distinct from acute stenosis due to inflammation, which is reversible.

 

IMMEDIATE AND OVERNIGHT MANAGEMENT

This depends on the complication. In general, the following would be appropriate in most cases with an acute complication.

 

Investigations

  • Microbiology swabs of any discharge prior to initiating management

  • IV access and FBC, U&E, serum glucose, CRP, ESR

  • Blood cultures if pyrexial

  • Don't forget the Sepsis Six bundle

  • CT Temporal bone (fine slice) if NOE is suspected

 

Treatment

Treatment should always be based on topical antibiotics, good analgesia and water precautions

 

NOE

  • Antibiotic treatment usually consists of a combination of IV ceftazidine or tazocin with oral ciprofloxacin, however you should seek local microbiology guidance

  • Prolonged courses of IV antibiotics (six weeks) are frequently needed

 

Abscess or cellulitis

  • Can often be treated initially with IV or oral antibiotics; antibiotic choice will vary according to local guidance though penicillins are often recommended

 

Diabetic patients should have meticulous blood glucose monitoring and control, which may necessitate use of sliding scale insulin.

 

FURTHER MANAGEMENT

NOE

  • Progress can be monitored with bi-weekly CRP/ESR

  • Progress can also be ascertained with Isotope scans every 4 to 6 weeks

  • MRI of ears and skull base if progression/severe disease suspected

  • Discussion at skull base MDT is useful

  • Baseline audiogram

  • Biopsy of granulation tissue will help to exclude possible squamous cell carcinoma (this can wait until working hours if you have not done it before)

  • Surgical debridement of granulation tissue and bony sequestra may be required

  • Hyperbaric oxygen therapy is often reserved for refractory or recurrent cases or for patients with extensive skull base and intracranial involvement

 

Abscess or cellulitis

  • Incision and drainage will be required (aspiration if small) - discuss with the ENT registrar

 

Ear canal stenosis

  • If acute and due to inflammation, the use of an otowick may be required to help delivery of topical therapy

  • Where recurrent infection causes permanent fibrotic stenosis and even more infections, surgery can be performed to improve patency (but see below)

  • Sometimes, recurrent infection leads to formation of a false fundus and patients tend to find that they suffer little or no further AOE; they may choose to live with the hearing deficit

 

PROGNOSIS of noe

NOE is potentially curable if recognised and treated early and aggressively: mortality rate can still be up to 15% in these cases. If, however, diagnosis and treatment is delayed, mortality can be up to 75%. Facial nerve palsy is a poor prognostic factor and its presence indicates a need for a longer course of antibiotics. Facial nerve function may never fully recover.

 

 

Page last reviewed: 15 December 2019