Necrotising otitis externa: an unusual cause of cranial nerve palsy in a diabetic haemodialysis patient

Abstract

A 77-year-old South Asian man presented to the acute admissions service with a one-month history of progressive, left-sided facial weakness and left-sided mandibular and pre-auricular pain. A diagnosis of Bell's palsy was made. He was receiving ongoing treatment for ipsilateral otitis externa with topical tri-adcortyl ointment. His medical history included end-stage renal disease (ESRD) of uncertain cause, treated with hospital haemodialysis; poorly controlled insulin-treated type 2 diabetes mellitus; ischaemic heart disease; and gout.Unfortunately, the patient's symptoms continued to deteriorate and he was admitted to renal services from the haemodialysis unit. On examination he had periauricular tenderness and purulent discharge from the left auditory canal and associated conductive hearing loss. There was a left lower motor neurone facial palsy, with grade III upper division involvement and grade IV lower division involvement (House-Brackmann classification).1 Other cranial nerves were spared. Inflammatory markers were mildly elevated with a C-reactive protein of 71 mg/l. Glycosylated haemoglobin (HbA1c) of 10.7% reflected recent poor glycaemic control. Left-sided otoscopy revealed posteroinferior perforations of the tympanic membrane, with debris and mucopurulent discharge on the left, and pure-tone audiometry confirmed conductive deafness. A contrast-enhanced computerised tomography (CT) scan demonstrated soft tissue thickening in the external auditory canal and a 2.7 x 1.3 cm mass below the left skull base, engulfing the carotid artery and severely compressing the internal jugular vein. The mass extended through the parapharyngeal space onto the lateral pterygoid and deep temporalis muscles (Figure 1). Auricular swabs grew Aspergillus flavus and Proteus mirabilis.A diagnosis of necrotising (malignant) otitis externa (NOE) was made. The patient was treated for a total of six weeks with systemic agents and localised intraauricular ribbon gauze. He completed four weeks of intravenous meropenem (1 g once daily), combined with oral ciprofloxacin (250 mg twice daily) and voriconazole (400 mg mane, 200 mg nocte). Thereafter he continued with a further two weeks of oral ciprofloxacin and voriconazole. Doses were adjusted for the renal impairment and haemodialysis requirements. Topical ribbon gauze soaked with amphotericin and nystatin was administered daily over this period. The initial treatment was based upon the likelihood that Pseudomonas is the usual causative agent, and that resistant strains of Pseudomonas are increasingly prevalent. Culture results guided treatment thereafter.Two months later the facial nerve palsy was improving so that the lower division involvement had reduced to grade II weakness. Otoscopy confirmed reduced suppurative discharge with ongoing dry perforation of the tympanic membrane. Follow-up CT scans at three months and then seven months from diagnosis showed continuing improvement (Figure 2). DISCUSSIONThis case highlights a number of key learning points. The ESRD and diabetic populat...

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