Otitis Externa - what a pain in the neck!

Yaeeun Suh1 Shahzad Ilyas1 Nithin K Bejjanki2, Shafic S Al-Nammari2

1St Thomas’ Hospital, London, 2York District Hospital   

Corresponding Author Mr Shafic S Al-Nammari e-mail: shafic2@hotmail.com

SMJ 2007 52(4): 53

 

Abstract

We report on the first case of pyogenic spondylodiscitis caused by otitis externa, which arose by haematogenous spread. Pyogenic spondylodiscitis is a serious condition and it is imperative to have a high index of suspicion for this condition in any patient that has back or neck pain, systemic upset and raised inflammatory markers.

Keywords: otitis externa, pyogenic spondylodiscitis

 

Introduction

Pyogenic spondylodiscitis is a rare condition although its incidence is increasing.1  It is imperative to have a high index of suspicion for this condition in any patient that has back pain, systemic upset and raised inflammatory markers. We report here on the first case of pyogenic spondylodiscitis as a complication of otitis externa.

 

Case Report

A sixty-six year old lady presented to her GP with a one week history of left sided otalgia, otorrhoea and decreased hearing.  Her only past medical history consisted of mild asthma for which she was on salbutamol and becatide inhalers and osteoarthritis of her knees and wrists.  She was noted to have a normal tympanic membrane on examination by her GP and was diagnosed with otitis externa.  The ear was swabbed and she was commenced on empirical oral amoxicillin and gentamycin eardrops.  Malignant otitis externa, which is an osteomyelitis of the skull base typically, caused by Pseudomonas aeruginosa, which carries a high morbidity, and mortality was thought unlikely as it tends to occur only in elderly diabetics and immunosuppressed individuals.  Furthermore the patient’s ear symptoms resolved entirely within two weeks and the swab grew Streptococcus agalactiae.  However the patient did notice a gradual onset of neck pain radiating to both shoulders that was exacerbated by movement but with no neurological symptoms, systemic upset or history of trauma.  She was seen by her GP who felt that taking into account her known osteoarthritis, the patients’ current symptoms most likely represented new onset cervical spondylosis and the patient was started on ibuprofen.  This had minimal effect and two weeks later she was brought in to our Hospital with an non-steroidal anti-inflammatory drug induced upper gastrointestinal haemorrhage secondary to multiple gastric and duodenal erosions. 

 

During her admission the patient complained of persistent and worsening neck pain.  She was referred to the rheumatologists who noted that her symptoms now included occipital headache, jaw claudication and malaise.  Examination at that time revealed that she was afebrile with point tenderness over C5 and C6 with a decreased range of neck movement and no neurology.  She was also tender over her temporal arteries; although the pulses were palpable.  Bloods showed a White Cell Count (WCC) of 12.4x10-9/L, Erythrocyte Sedimentation Rate (ESR) of 116 mm/hr and a C-reactive Protein (CRP) of 197 mg/dL and a negative myeloma screen.  At this stage the differential diagnosis consisted of giant cell arteritis, polymyalgia rheumatica and spinal sepsis.  She was started on empirical prednisolone and sent for urgent plain X-ray of her cervical spine and temporal artery biopsy.  Plain X- Ray’s showed severe degenerative changes at C4/5 and temporal artery biopsy was subsequently found to be normal.  Her inflammatory markers remained elevated despite an improvement of her symptoms following the introduction of corticosteroids and on the seventh day of admission she spiked a Temperature of 39.2C.  Three sets of blood cultures grew Streptococcus agalactiae, which were fully sensitive to penicillin.  There were no other identifiable focuses of infection other than the spine.  MRI C-spine was performed and showed odontoid destruction, in keeping with osteomyelitis, with mild posterior odontoid peg thecal impingement and a C4/5 spondylodiscitis.  At this point steroids were stopped, the Spinal Team was contacted and the patient was started on intravenous penicillin.  This was continued for one month at which point her symptoms had improved and her inflammatory markers had normalised.  Oral penicillin was continued for a further two months.  At follow up at two years she was complaining only of occasional occipital neck stiffness with headaches.  Examination revealed a mild torticollis with her head tilting to the right a decreased range of motion throughout the cervical spine without neurology.  MRI showed burned out spondylodiscitis with fusion of C5/6 and widening of the odontoid processes.

 

Discussion

Pyogenic spondylodiscitis is rare especially in otherwise well individuals; although its incidence is increasing.1 It is a serious infection which had a death rate ranging from 40% to 70% in the pre-antibiotic era.2  Spondylodiscitis occurs by three routes haematogenous spread, contiguous spread and direct inoculation.3  Haematogenous spread and direct inoculation are the two most common routes while contiguous spread is rare.  The most common causative organism of spondylodiscitis is Staphylococcus aureus, which accounts for about 45% of cases.4   Streptococcus agalactiae is traditionally considered to be a rare cause of any infection in adults other than urinary tract infection in pregnant women.  However its incidence is increasing as the causative agent in a range of conditions including urinary tract infection, respiratory tract infections, soft tissue infection and osteomyelitis.  In the neonatal period bone and joint infections caused by this organism are well documented.5  Spondylodiscitis caused by Streptococcus agalactiae is normally associated with a very good outcome.  It most commonly occurs in the lumbar and thoracic spine and is commonly associated with diabetes mellitus, alcoholism, intravenous drug abuse and steroids.  This is the only reported case of Streptococcus agalactiae spondylodiscitis resulting in chronic pain and spinal instability as is common in other causes of spondylodiscitis and vertebral osteomyelitis6 and it occurred in an unusual location in a patient without risk factors.  This is the first reported case of spondylodiscitis secondary to otitis externa and serves to highlight the importance of having a high index of suspicion for this condition in anyone presenting with new onset neck or back pain, systemic upset and raised inflammatory markers.

 

References:

1.  Krogsgaard MR, Wagn P, Bengtsson J. Epidemiology of acute vertebral osteomyelitis in Denmark: 137 cases in Denmark 1970–1982, compared to cases reported to the National Patient Register 1991–1993. Acta Orthop Scand 1998; 69: 513–517.

2.  Wood GW. Infections of the spine. In: Crenshaw AH, ed. Campbell's operative orthopedics, vol. 4. St. Louis: Mosby; 1987: 3323–45.

3.  McCutchen TM, Cuddy BG.  Intervertebral Disk Space Infection.  Neurosurgery Quarterly 2001; 11(3): 209-219.

4.  Priest DH; Peacock JE.  Hematogenous Vertebral Osteomyelitis Due to Staphylococcus aureus in the Adult: Clinical Features and Therapeutic Outcomes.  Southern Medical Journal 2005; 98(9): 854-862.

5.  Baxter MP, Finnegan MA. Skeletal infection by group B beta-haemolytic streptococci in neonates. A case report and review of the literature. J Bone Joint Surg Br 70: 812-14, 1988.

6.  Garcia-Lechuz JM, Bachiller P; Vasallo FJ, et al.  Group B Streptococcal Osteomyelitis in Adults.  Medicine 1999; 78(3): 191-199.

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