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Acute confusion and sudden deterioration in an elderly patient with necrotising otitis externa
European Geriatric Medicine 3 (2012) 242–243
Available online at
www.sciencedirect.com
EGM clinical case
Acute confusion and sudden deterioration in an elderly patient with necrotising otitis externa E. Bellia a,*, R. Galea b, M.-A. Vassallo a a b
Department of Geriatrics, Rehabilitation Hospital Karin Grech, Telghet Guardamangia, Pieta’, PTA 1312, Malta, Europe Mater Dei Hospital, Msida, MSD 2090, Malta, Europe
A R T I C L E I N F O
Article history: Received 7 February 2012 Accepted 13 February 2012 Available online 22 March 2012
1. Introduction Toulmouche reported the first case of malignant otitis externa in 1838, being described as a clinical entity by Chandler in 1968 [1]. Starting as an otitis externa, it eventually progresses to osteomyelitis of the skull base, mainly of the temporal bone. Those over 60 years of age with immuno-suppression and diabetic patients having an increased risk [2,3]. 2. Case History An 80-year old insulin dependent diabetic gentleman was admitted to the rehabilitation hospital following open reduction internal fixation of a transtrochanteric fracture of the right femur. He was improving steadily and was soon to be discharged. He was able to walk with a rollator frame for a good distance under supervision just requiring some assistance with transfers. A few days prior to discharge, his gait deteriorated and he became acutely confused. On examination, he was found to have a purulent discharge from the left ear and was diagnosed with otitis externa. He was otherwise neurologically intact. A swab was sent for culture and sensitivity, and gentamicin eardrops were prescribed. The otitis did not improve, and he was referred to the ENT specialist who advised aural toilet, boric acid wick and oral cefuroxime, since Escherichia coli, Proteus mirabilis and Enterococcus faecalis had been cultured. Unfortunately, his condition deteriorated after a few days with copious purulent discharge and some tenderness over the mastoid process despite the above treatment. He also developed a lower motor neurone left facial * Corresponding author. 13, Mediterranea, Triq il-Fortizza, Pembroke, PBBK 1221, Malta, Europe. Tel.: +21382465. E-mail addresses: [email protected] (E. Bellia), [email protected] (M.-A. Vassallo).
nerve palsy (Grade V on the House-Brackmann classification) (Fig. 1). No other cranial nerves were involved. He was transferred urgently to the ENT ward for further treatment. A complete blood count showed a raised white-cell count, 13.5 109/l, and a raised C-reactive protein (CRP) of 30 mg/l. A repeat swab was taken and this time E. coli ESBL + ve, Proteus mirabilis and Pseudomonas aeruginosa were cultured. Otoscopy examination this time showed a granulation polyp and a computerised tomography (CT) scan of the brain showed fluid in the left mastoid, cavum tympani and external meatus due to otitis media and externa. Diagnosis at this point was changed to necrotising otitis externa (NOE) by the ENT specialist. He was switched to intravenous ciprofloxacin and ceftazidime for 3 weeks. The discharge from the left ear subsided within 2 weeks of treatment. The CRP returned to a normal level of <6 mg/l. The left facial palsy improved and was Grade IV 4 weeks later. With resolution of the NOE, mobility improved and he was able to walk with a rollator frame and supervision for long distances, requiring less assistance for transfers. His confusion improved, but he remained with some weakness of the muscles supplied by the facial nerve at 5-month follow up. 3. Discussion NOE commonly presents with otalgia out of proportion to the physical findings, purulent otorrhea, and more uncommonly dysphasia and hoarseness. Otoscopic examination, looking in particular for granulation tissue at the osseocartilaginous junction is mandatory being virtually pathognomonic for NOE [4]. The involvement of the skull base could involve cranial nerves VII to XII and a lower motor neurone lesions of the facial nerve has been reported in 19.6% in one study [4]. This is due to the proximity of the stylomastoid foramen to the external auditory canal. It was thought that cranial nerve involvement and immune deficiency reflected a more advanced disease and worse prognosis [5], but recent evidence suggests this is not so [6,7]. P. aeuruginosa is isolated in 87% of cases, like in our case, whilst less common organisms included Staphylococcus aureus, Staphylococcus epidermidis, Klebsiella, Proteus mirabilis and various Aspergillus and Candida species. Pseudomonas aeruginosa has a mucoid coating that helps protect against phagocytosis and produces a neurotoxin that is responsible for cranial nerve lesions. In our case Pseudomonas was cultured from the 2nd swab taken a couple of
1878-7649/$ – see front matter ß 2012 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved. doi:10.1016/j.eurger.2012.02.006
E. Bellia et al. / European Geriatric Medicine 3 (2012) 242–243
243
varies between 4.4% and 10% and a poorer diagnosis may be associated with cranial nerve involvement and immune deficiency [4], though other authorities state that this is not so [6]. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. References
Fig. 1. Left facial nerve lower motor neurone lesion. The patient is being asked to close his eyes and show his teeth.
days before he developed the VII cranial nerve palsy. Treatment is normally with a third-generation cephalosporin together with a fluoroquinolone such as ciprofloxacin or ofloxacin [3]. Optimal duration of treatment is controversial, but a study that used gallium scans to monitor healing found that an average of 8.8 weeks was required for the healing of osteomyelitis to occur [8]. Surgery is occasionally used for local debridement and drainage, whilst hyperbaric oxygen is sometimes used in conjunction with standard treatment but is not yet evidence based [9]. Mortality
[1] Chandler JR. Malignant external otits. Laryngoscope 1968;78(8):1257–94. [2] Doroghazi RM, Nadol JB, Hyslop NE, et al. Invasive external otitis. Report of 21 cases and review of literature. Am J Med 1981;71:603–18. [3] Martel J, Duclos JY, Darrouzet V, Guyot M, Bebear JP. Malignant or necrotizing otitis externa: experience in 22 cases. Ann Otolaryngol Chir Cervicofac 2000;117(5):291. [4] Handzel O, Halperin D. Necrotizing (malignant) external otitis. Am Fam Physician 2003;68(2):309–12. [5] Franco-Vidal V, Blanchet H, Bebear C, Dutronc H, Darrouzet V. Necrotizing external otitis: a report of 46 cases. Otol Neurotol 2007;28(6):771–3. [6] Soudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of malignant external otitis with facial paralysis. Arch Otolaryngol Head Neck Surg 2007;133(10):1002–4. [7] Mani N, Sudhoff H, Rajagopal S, Moffat D, Axon PR. Cranial nerve involvement in malignant otitis externa: implications for clinical outcome. Laryngoscope 2007;117(5):907–10. [8] Benecke Jr JE. Management of osteomyelitis of the skull base. Laryngoscope 1989;99(12):1220–3. [9] Phillips JS, Jones SE. Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa. Cochrane Database Syst Rev 2005;2:CD004617.
Available online at
www.sciencedirect.com
EGM clinical case
Acute confusion and sudden deterioration in an elderly patient with necrotising otitis externa E. Bellia a,*, R. Galea b, M.-A. Vassallo a a b
Department of Geriatrics, Rehabilitation Hospital Karin Grech, Telghet Guardamangia, Pieta’, PTA 1312, Malta, Europe Mater Dei Hospital, Msida, MSD 2090, Malta, Europe
A R T I C L E I N F O
Article history: Received 7 February 2012 Accepted 13 February 2012 Available online 22 March 2012
1. Introduction Toulmouche reported the first case of malignant otitis externa in 1838, being described as a clinical entity by Chandler in 1968 [1]. Starting as an otitis externa, it eventually progresses to osteomyelitis of the skull base, mainly of the temporal bone. Those over 60 years of age with immuno-suppression and diabetic patients having an increased risk [2,3]. 2. Case History An 80-year old insulin dependent diabetic gentleman was admitted to the rehabilitation hospital following open reduction internal fixation of a transtrochanteric fracture of the right femur. He was improving steadily and was soon to be discharged. He was able to walk with a rollator frame for a good distance under supervision just requiring some assistance with transfers. A few days prior to discharge, his gait deteriorated and he became acutely confused. On examination, he was found to have a purulent discharge from the left ear and was diagnosed with otitis externa. He was otherwise neurologically intact. A swab was sent for culture and sensitivity, and gentamicin eardrops were prescribed. The otitis did not improve, and he was referred to the ENT specialist who advised aural toilet, boric acid wick and oral cefuroxime, since Escherichia coli, Proteus mirabilis and Enterococcus faecalis had been cultured. Unfortunately, his condition deteriorated after a few days with copious purulent discharge and some tenderness over the mastoid process despite the above treatment. He also developed a lower motor neurone left facial * Corresponding author. 13, Mediterranea, Triq il-Fortizza, Pembroke, PBBK 1221, Malta, Europe. Tel.: +21382465. E-mail addresses: [email protected] (E. Bellia), [email protected] (M.-A. Vassallo).
nerve palsy (Grade V on the House-Brackmann classification) (Fig. 1). No other cranial nerves were involved. He was transferred urgently to the ENT ward for further treatment. A complete blood count showed a raised white-cell count, 13.5 109/l, and a raised C-reactive protein (CRP) of 30 mg/l. A repeat swab was taken and this time E. coli ESBL + ve, Proteus mirabilis and Pseudomonas aeruginosa were cultured. Otoscopy examination this time showed a granulation polyp and a computerised tomography (CT) scan of the brain showed fluid in the left mastoid, cavum tympani and external meatus due to otitis media and externa. Diagnosis at this point was changed to necrotising otitis externa (NOE) by the ENT specialist. He was switched to intravenous ciprofloxacin and ceftazidime for 3 weeks. The discharge from the left ear subsided within 2 weeks of treatment. The CRP returned to a normal level of <6 mg/l. The left facial palsy improved and was Grade IV 4 weeks later. With resolution of the NOE, mobility improved and he was able to walk with a rollator frame and supervision for long distances, requiring less assistance for transfers. His confusion improved, but he remained with some weakness of the muscles supplied by the facial nerve at 5-month follow up. 3. Discussion NOE commonly presents with otalgia out of proportion to the physical findings, purulent otorrhea, and more uncommonly dysphasia and hoarseness. Otoscopic examination, looking in particular for granulation tissue at the osseocartilaginous junction is mandatory being virtually pathognomonic for NOE [4]. The involvement of the skull base could involve cranial nerves VII to XII and a lower motor neurone lesions of the facial nerve has been reported in 19.6% in one study [4]. This is due to the proximity of the stylomastoid foramen to the external auditory canal. It was thought that cranial nerve involvement and immune deficiency reflected a more advanced disease and worse prognosis [5], but recent evidence suggests this is not so [6,7]. P. aeuruginosa is isolated in 87% of cases, like in our case, whilst less common organisms included Staphylococcus aureus, Staphylococcus epidermidis, Klebsiella, Proteus mirabilis and various Aspergillus and Candida species. Pseudomonas aeruginosa has a mucoid coating that helps protect against phagocytosis and produces a neurotoxin that is responsible for cranial nerve lesions. In our case Pseudomonas was cultured from the 2nd swab taken a couple of
1878-7649/$ – see front matter ß 2012 Elsevier Masson SAS and European Union Geriatric Medicine Society. All rights reserved. doi:10.1016/j.eurger.2012.02.006
E. Bellia et al. / European Geriatric Medicine 3 (2012) 242–243
243
varies between 4.4% and 10% and a poorer diagnosis may be associated with cranial nerve involvement and immune deficiency [4], though other authorities state that this is not so [6]. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. References
Fig. 1. Left facial nerve lower motor neurone lesion. The patient is being asked to close his eyes and show his teeth.
days before he developed the VII cranial nerve palsy. Treatment is normally with a third-generation cephalosporin together with a fluoroquinolone such as ciprofloxacin or ofloxacin [3]. Optimal duration of treatment is controversial, but a study that used gallium scans to monitor healing found that an average of 8.8 weeks was required for the healing of osteomyelitis to occur [8]. Surgery is occasionally used for local debridement and drainage, whilst hyperbaric oxygen is sometimes used in conjunction with standard treatment but is not yet evidence based [9]. Mortality
[1] Chandler JR. Malignant external otits. Laryngoscope 1968;78(8):1257–94. [2] Doroghazi RM, Nadol JB, Hyslop NE, et al. Invasive external otitis. Report of 21 cases and review of literature. Am J Med 1981;71:603–18. [3] Martel J, Duclos JY, Darrouzet V, Guyot M, Bebear JP. Malignant or necrotizing otitis externa: experience in 22 cases. Ann Otolaryngol Chir Cervicofac 2000;117(5):291. [4] Handzel O, Halperin D. Necrotizing (malignant) external otitis. Am Fam Physician 2003;68(2):309–12. [5] Franco-Vidal V, Blanchet H, Bebear C, Dutronc H, Darrouzet V. Necrotizing external otitis: a report of 46 cases. Otol Neurotol 2007;28(6):771–3. [6] Soudry E, Joshua BZ, Sulkes J, Nageris BI. Characteristics and prognosis of malignant external otitis with facial paralysis. Arch Otolaryngol Head Neck Surg 2007;133(10):1002–4. [7] Mani N, Sudhoff H, Rajagopal S, Moffat D, Axon PR. Cranial nerve involvement in malignant otitis externa: implications for clinical outcome. Laryngoscope 2007;117(5):907–10. [8] Benecke Jr JE. Management of osteomyelitis of the skull base. Laryngoscope 1989;99(12):1220–3. [9] Phillips JS, Jones SE. Hyperbaric oxygen as an adjuvant treatment for malignant otitis externa. Cochrane Database Syst Rev 2005;2:CD004617.