CLINICAL STUDY
Malignant Otitis Externa
Emin Karaman, MD, Mehmet Yilmaz, MD, Metin Ibrahimov, MD, Yusuf Haciyev, MD,
and Ozgün Enver, MD
Objective: Malignant external otitis is a severe infection of the
external auditory canal and skull base, which most often affects
elderly patients with diabetes mellitus. This disease is still a seri-
ous disease associated with cranial nerve complications and high
morbidity-mortality rate. Malignant otitis externa requires urgent
diagnosis and treatment. The most effective treatment is to control
the diabetes and to fight infection with the proper antibiotic and
debridement necrotic tissue; sometimes, aggressive surgical man-
agement is done. We present our 5-year institutional experience in
the management of this disease. The aim of this study was to present
our experience with the management of malignant otitis externa.
Methods: All patients’ records with malignant otitis externa during
the last 5 years (2007Y2012) were retrieved and reviewed. Diabetes
mellitus profile, erythrocyte sedimentation rate, ear swab for culture
and sensitivity, computed tomography, and scintigraphy using
technetium 99 and gallium 67 were investigated for all patients.
Results: During the last 5 years (2007Y2012), 10 patients with the
diagnosis of malignant otitis externa were admitted to our clinic for
investigation and treatment. There were 7 men and 3 women, all
between 64 and 83 years of age, with severe persistent otalgia, pu-
rulent otorrhea, granulation tissue in the external auditory canal, and
diffuse external otitis, and there were 4 patients with facial nerve
palsy. Nine patients were confirmed to have a diabetes, and 4 of these
9 cases just had chronic renal failure and underwent dialysis; the
remainder 1 case had no diabetes mellitus, but with chronic renal
failure on dialysis. Ear swabs for culture and sensitivity usually
revealed Pseudomonas aeruginosa. Local debridement and local and
systemic antibiotic treatment were sufficient to control the disease.
Facial nerve decompression was done in facial paralysis. Hyperbaric
oxygen therapy was performed in facial nervy palsy cases.
Conclusions: Malignant otitis externa is still a serious disease
associated with cranial nerve complications and high morbidity-
mortality rate. The most effective treatment is to control the diabetes
and to fight infection with the proper antibiotic, debridement ne-
crotic tissue, and sometimes aggressive surgical management.
Monitoring of therapy response is done through normalization of
From the Otolaryngology Department, Cerrahpasa Medical School, Istanbul
University, Istanbul, Turkey.
Received April 9, 2012.
Accepted for publication May 5, 2012.
Address correspondence and reprint requests to Metin Ibrahimov, MD,
Otolaryngology Department, Cerrahpasa Medical School, Istanbul
University, Istanbul 34098, Turkey; E-mail: metinibrahimov@gmail.com
The authors report no conflicts of interest.
Copyright * 2012 by Mutaz B. Habal, MD
ISSN: 1049-2275
DOI: 10.1097/SCS.0b013e31825e4d9a
1748 The Journal of Craniofacial Surgery
Copyright © 2012 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
erythrocyte sedimentation rate, control of diabetes mellitus, and
improvement of computed tomography and radioisotope scanning.
Key Words: Diabetes mellitus, malignant otitis externa, cranial
nerve paralysis
(J Craniofac Surg 2012;23: 1748Y1751)
M alignant external otitis (MEO) or necrotizing otitis is a life-
threatening, progressive bacterial infection of the external
auditory canal (EAC), mastoid, and skull base. The disease classi-
cally occurs in the elderly patient with diabetes mellitus (DM), al-
though occasional cases have been reported in immunocompetent
and younger individuals. Symptoms and signs may include severe
otalgia, otorrhea, and involvement of various cranial nerves. The
diagnosis is based on a combination of objective findings that in-
clude nearly always recovery of Pseudomonas aeruginosa from the
aural drainage, but also other etiologic agents of MEO may rarely
include other bacteria (Staphylococcus aureus, Proteus mirabilis,
Klebsiella oxytoca, Pseudomonas cepacia) or fungi (Aspergillus,
Pseudallescheria, Candida, Malassezia).1Y11 The presence of granu-
lation tissue in the EAC, an elevated erythrocyte sedimentation rate
(ESR), and abnormalities on imaging studies are also parameters of
diagnosis. It is therefore very important to make the diagnosis of
MEO as early as possible to achieve complete cure. In its early
stages, it is very similar to severe acute external otitis, but MEO
develops into a severe osteomyelitis of the temporal bone, attacking
the adjacent cranial nerves (VIIYXII), blood vessels, and soft tissues,
and finally if untreated, it causes death due to widely expanding
osteomyelitis of the skull and disseminated septic thromboemboli
of the brain. Computed tomography (CT) scan allows the proper
imaging of density reduction of the skull base, opacification of
mastoid, extension of sequesters destruction of temporomandibular
joint, and inflammatory lesions of subtemporal fossa soft tissue.12
In bone scintigraphy, demineralization is not essential to visualize
the lesions; more helpful in monitoring MEO is the scanning with
gallium 67 than with technetium 99.13 Therapy should be conducted
by otolaryngologists in collaboration with the endocrinologist, inter-
nist, neurologist, radiologist, and the microbiologist. Local treatment
(with removal of bony sequesters) and systemic antibiotic therapy
according to results of bacteriologic examinations (aminoglycosides,
semisynthetic penicillins, cephalosporins of third and fourth genera-
tions, fluoroquinolones) are generally accepted. We present 10 cases
of MEO managed in our clinic during the last 5 years.
MATERIALS AND METHODS
Between 2007 and 2012, 10 patients with a preliminary di-
agnosis of MEO were admitted to the Cerrahpasa Medical School
Hospital in Istanbul for investigation and further treatment. The
following examinations were requested for patients: CT of the
mastoid and temporal bones, fasting and random blood sugar anal-
yses, swabs for culture and sensitivity, ESR monitoring during
& Volume 23, Number 6, November 2012
The Journal of Craniofacial Surgery & Volume 23, Number 6, November 2012 Malignant Otitis Externa

Histopathologic examination of the scrapings from the EAC showed

TABLE 1. Staging
Stage I Necrotizing external otitis (persistent otalgia, bare bone in EAC,
no facial palsy)
Stage II Limited skull base osteomyelitis (lateral to jugular
foramenYfacial palsy)
Stage III Extensive skull base osteomyelitis (jugular foramen and further
medially lower cranial involvement and intracranial extension)
treatment, and scintigraphy (technetium 99 and gallium 67) in pa-
tients with facial nerve palsy. The patients were staged using the
simplified staging of Thakar et al14 (Table 1). Treatment included
local treatment of the EAC, long-term systemic antipseudomonal
therapy, local debridement, and ear surgery in selected patients. All
patients were treated for 6 to 8 weeks, depending on bacterial sen-
sitivity. Intravenous antibiotic treatment and ciprofloxacin eardrops
were given. Diabetes mellitus was controlled with oral hypoglycemic
agents or subcutaneous insulin, in consultation with physicians. Local
debridement was performed in all cases and consisted of removing
all granulation tissue and drilling away the diseased and necrosed
bone. A canal-wall-down modified radical mastoidectomy was per-
formed, starting with a postauricular incision exposing the mastoid
antrum, lowering the posterior canal wall, exposing the facial nerve
up to the stylomastoid foramen, and opening up the latter. Facial
nerve decompression was performed in the patients with facial nerve
paralysis. Hyperbaric oxygen (HBO) therapy was administered in
cases of facial nerve palsy. The patients were followed up for at least
6 months. One patient is still under follow-up. One patient died of a
myocardial infarction after 2 years of follow-up. Patients with facial
nerve palsy were also examined and followed up by neurologists,
ophthalmologists, and physiotherapists.
RESULTS
Seven of the patients were male (70%), and 3 were female
(30%); their ages ranged from 61 to 81 years (mean, 73.5 years)
(Table 2). All of them presented to us after weeks to months of
treatment at a primary care level with oral and local antibiotics. The
patients presented with severe persistent otalgia, purulent otorrhea,
granulation tissue in the EAC, and diffuse external otitis. Four
patients had facial nerve palsies. Nine had DM, and 4 of these
had chronic renal failure and were on dialysis; 1 patient with no DM
had chronic renal failure and was also on dialysis. Six patients had
stage I disease, and 4 patients had stage II disease. Granulation
tissue was found in all patients and polyps in 2 patients, with some
edema, narrowing of the outer ear canal, and purulent discharge.
nonspecific inflammatory changes with necrosis and osteomyelitis.
This was done with the aim of excluding malignancy. Most of the
granulation tissue disappeared, and the discharge stopped after
treatment. Four patients presented with facial nerve palsy: 2 patients
were House-Brackmann grade II, and one each was grades IV and V.
After treatment with antibiotics, HBO therapy, and facial nerve
decompression, the grade II cases showed good improvement, and
the grade IV case regressed to grade II, whereas the grade V case did
not improve. Culture swabs showed P. aeruginosa in 9 patients, and
Enterococcus faecalis was seen in the culture in 1 patient. All 10
patients responded to treatment very well, and their cultures were
negative on discharge. The ESR ranged from 25 to 120 mm/h (mean,
65 mm/h). With treatment, the ESR normalized gradually by the day
of discharge in all patients. In all patients, CT showed osteitis of the
temporal bone, hazy mastoid bone boundaries, and a soft tissue
shadow inside the mastoid air cells, in the middle ear, and in the
EAC causing narrowing. Scintigraphy showed high tissue activity at
the base of skull, temporal, and mastoid bone. On discharge and
during follow-up, the patients improved markedly. On admission,
the 9 patients with DM had fasting blood sugars ranging between
175 and 525 mg/dL. On discharge, all patients had blood sugar levels
within the reference range. Patients were discharged once their pain
disappeared, the DM controlled, the ear swab negative, the ESR nor-
malized, and the CT findings improved.
DISCUSSION
Malignant otitis externa is a necrotizing infection of the EAC
and surrounding tissue affecting usually elderly diabetic patients.
In our study, all 10 cases with MEO were elderly (mean age,
73.5 years), and 9 patients has DM (90%); 1 patient has no DM,
but this case had chronic renal failure on dialysis. Seven (70%) of
the patients were male, and 3 were female (30%). The precise eti-
ology of this condition is unknown, but theories related to altered
host immunity, local tissue microangiopathy, and even altered cerumen
biochemistry have been proposed. Lack of adequate host defenses
leads to spreading cellulites and osteomyelitis. In most cases, this
occurs secondary to DM, in which the host immunity is suppressed
by local microangiopathy and altered leukocyte function. There is also
small but significant group of nondiabetic immunocompromised
patients with malignant otitis externa, such as malignancy, chemo-
therapy, malnutrition and anemia, high-dose steroid administration,
and so on. Etiologic agent of MOE is most commonly P. aeruginosa,
rarely; other bacteria (S. aureus, P. mirabilis, K. oxytoca, P. cepacia) or
fungi (Aspergillus, Pseudallescheria, Candida, Malassezia) are also
found. In our study, 9 patients had documented microbiologic evidence

TABLE 2. Details of Patients

Patient Age Sex Immunosuppression Stage Affected Cranial Nerves Polyp and Granulation Germs Treatment

1 77 M DM + CRF(D) 1 Polyp + granulation P. aeruginosa Piperacillin + fluoroquinolone

2 82 M DM + CRF(D) 2 VII (grade IV) Granulation P. aeruginosa Tazobactam + fluoroquinolone + HBO
3 65 F DM 1 Granulation P. aeruginosa Piperacillin + fluoroquinolone
4 73 M DM 1 Granulation P. aeruginosa Tazobactam + fluoroquinolone
5 76 M DM + CRF(D) 2 VII (grade V) Polyp + granulation P. aeruginosa Imipenem + fluoroquinolone + HBO
6 70 F DM 1 Granulation E. faecalis Imipenem + fluoroquinolone
7 78 M CRF(D) 1 Granulation P. aeruginosa Tazobactam + fluoroquinolone
8 67 F DM 1 Granulation P. aeruginosa Imipenem + fluoroquinolone
9 64 M DM 2 VII (grade II) Granulation P. aeruginosa Ceftazidime + fluoroquinolone + HBO
10 83 M DM + CRF(D) 2 VII (grade II) Granulation P. aeruginosa Piperacillin + fluoroquinolone + HBO
M indicates male; F, female; CRF(D), chronic renal failure(dialysis).

* 2012 Mutaz B. Habal, MD 1749

Copyright © 2012 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
Karaman et al The Journal of Craniofacial Surgery
of P. aeruginosa, and 1 patient had E. faecalis in ear swab culture.
The disease originates in the EAC and spreads through the osteo-
cartilaginous junction to involve the soft tissues beneath the temporal
bone. Granulation tissue is usually present in the EAC. Further
spread of the infection can lead to thrombosis of lateral sinus and
superior and inferior petrosal sinuses. Initially osteomyelitis of the
skull base ensues. Progressive skull base osteomyelitis can result in
cranial polyneuropathy, facial nerve paralysis being the most com-
mon; cranial nerves IX, X, and XI nerves (jugular foramen syn-
drome) and cranial nerve XII (hypoglossal canal) are less often
involved. Further spread of the infection can lead to thrombosis of
the lateral sinus and superior and inferior petrosal sinuses. Secondary
osteomyelitis at the petrous apex can spread to the floor of the middle
cranial fossa or the basisphenoid with the development of sphenoidal
sinusitis. In our study, 6 patients had stage I disease, and 4 patients
had stage II disease. Four patients (60%) had facial nerve palsy,
2 patients had grade II, 1 patient had grade IV, and 1 patient had grade
V facial nerve palsy. We exposed patients with facial paralysis to
HBO and facial decompression, which did not benefit from medical
treatment, and at the conclusion, there are 3 patients who take utility
from HBO, and in 1 patient, there was no progress. Al-Doussary
et al15 reported a case of MEO with facial palsy that showed good
improvement under HBO treatment. Bath et al16 reported a case of
MEO with optic neuritis that improved only after the use of HBO.
The diagnosis is based on a combination of objective findings that
include recovery of P. aeruginosa from the aural drainage, the
presence of granulation tissue in the EAC, an elevated ESR, and ab-
normalities on imaging studies. Erythrocyte sedimentation rate has
been noted to be markedly elevated in association with MOE, often
exceeding of 100 mm/h, and it is helpful not only in supporting
the diagnosis, but also in monitoring the therapeutic response.16,17 In
the current study, ESR ranged from 25 to 120 mm/h (mean, 65 mm/h).
Under treatment, ESR gradually reached reference value at the day
of discharge in all patients. Computed tomography scan is the cur-
rent modality of choice for defining the anatomic extent of the dis-
ease in MOE, and not only is it useful to support the diagnosis, but
it also have been proven to be accurate to monitor therapy.18Y20 It was
demonstrated that radioisotope scan of technetium 99 and gallium 67
could support the diagnosis, showing extension of the disease more
precisely and monitoring the effectiveness of treatment.16,17 The
most effective treatment is to control the diabetes and to fight in-
fection with the proper antibiotic, debridement necrotic tissue, and
sometimes aggressive surgical management. Hyperbaric oxygen ther-
apy is gradually gaining acceptance as beneficial adjunctive ther-
apy.21Y23 Gaining control of diabetes should be considered the first
line of treatment and the first step toward the total management of
the patient.5 The patient should, if possible, not leave the hospital
without the control of his/her diabetes as suggested by Driss et al.24
Achieving control over diabetes is the first sign of response to
therapy.25 In our study, diabetic control was established by oral hy-
poglycemic agents or subcutaneously administered insulin, in con-
sultation with physicians, and intravenous antibiotic treatment and
ciprofloxacin eardrops were given, and intravenous treatment was
shifted to oral treatment before discharge. Hyperbaric oxygen therapy
and facial nerve decompression were done in facial nerve palsy cases.
The mortality for this condition has been reported to be as high oc-
casionally in initial studies,26 but when cranial nerves are affected, it
may be as high. Early diagnosis and proper treatment decreased
mortality rate. There was no mortality in our cases due to the disease
process. One of the patients died because of myocardial infarction
after 2 years of follow-up.
In conclusion, MEO is an invasive, potentially life-threatening
infection of the external ear and skull base that requires urgent di-
agnosis and treatment, which most often affects elderly patients with
DM. Malignant external otitis is still a serious disease associated
1750
Copyright © 2012 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.
& Volume 23, Number 6, November 2012
with cranial nerve complications and high morbidity-mortality rate.
The most effective treatment is to control diabetes and to fight in-
fection with the proper antibiotic, debridement necrotic tissue, and
sometimes aggressive surgical management. Monitoring of therapy
response is done through normalization of ESR, control of DM, and
improvement of CT and radioisotope scanning. The study highlights
the need for increasing the awareness regarding the condition es-
pecially among gerontologists.
REFERENCES
1. Chandler JR. Malignant external otitis. Laryngoscope
1968;78:1257Y1294
2. Meltzer PE, Kelemen G. Pyocyaneous osteomyelitis of the
temporal bone, mandible and zygoma. Laryngoscope
1959;69:1300Y1316
3. Shelton JC, Antonelli PJ, Hackett R. Skull base fungal osteomyelitis
in an immunocompetent host. Otolaryngol Head Neck Surg
2002;126:76Y78
4. Sreepada GS, Kwartler JA. Skull base osteomyelitis secondary to
malignant otitis externa. Curr Opin Otolaryngol Head Neck Surg
2003;11:316Y323
5. Granström G, Hanner P, Edebo L, et al. Malignant external otitis
caused by Pseudoallescheria boydii. Treatment with hyperbaric
oxygenation. In: Proceedings 1st EUBS Congress. Amsterdam.
1990;41Y49
6. Menchof MR, Jackler RK. Otogenic skull base osteomyelitis caused
by invasive fungal infection. Otolaryngol Head Neck Surg
1990;102:285Y289
7. Kountakis SE, Kemper JV, Chang CYJ, et al. Osteomyelitis of
the base of the skull secondary to Aspergillus. Am J Otolaryngol
1997;18:19Y22
8. Yao M, Messner AH. Fungal malignant otitis externa due to
Scedosporium apiospermum. Ann Otol Rhinol Laryngol
2001;110:377Y380
9. Petrak RM, Pottage JC, Levin S. Invasive external otitis caused by
Aspergillus fumigatus in an immunocompromised host. J Infect Dis
1985;151:196
10. Finer G, Greenberg D, Leibovitz E, et al. Conservative treatment of
malignant (invasive) external otitis caused by Aspergillus flavus with oral
itraconazole solution in neutropenic patient. Scand J Infect Dis
2002;34:227Y229
11. Bellini C, Antonini P, Ermanni S, et al. Malignant otitis externa due
Aspergillus niger. Scand J Infect Dis 2003;35:284Y288
12. Grandis JR, Curton HD, Yu VL. Necrotizing (malignant) external otitis:
prospective comparison of CT and MRI imaging in diagnosis and
follow-up. Radiology 1995;196:499Y504
13. Sreepada GS, Kwartler JA. Skull base osteomyelitis secondary
to malignant otitis externa. Curr Opin Otolaryngol Head Neck Surg
2003;11:316Y332
14. Thakar A, Kacker SK, Bahadur S. Malignant external otitis.
Ind J Otolaryngol Head Neck Surg 1996;48:114Y120
15. Al-Doussary S, Attalah M., Al Rahab A, et al. Otitis externa
malignant. A case report and review of literature. Otolaryngol Pol
1998;52:19Y22
16. Bath AP, Rowe JR, Innes AJ. Clinical records malignant otitis externa
with optic neuritis. J Laryngol Otol 1998;112:274Y277
17. Combacchio F, D’ Eredita R, Biron E, et al. Follow up of
necrotizing external otitis. Acta Otorhinolaryngol
1993;13:517Y524
18. Mendelson DS, Som PM, Mendelron MH, et al. Malignant otitis externa:
the role of computed tomography and radionuclides in evaluation.
Radiology 1983;149:745Y749
19. Gold, Som PM, Lucente FE, et al. Radiographic findings in
progressive necrotizing malignant external otitis. Laryngoscope
1984;94:363Y366
20. Munoz A, Chamorro ME. Radiology in focus; necrotizing external
otitis caused by Aspergilllus fumigatus: computed tomography and
* 2012 Mutaz B. Habal, MD
The Journal of Craniofacial Surgery & Volume 23, Number 6, November 2012 Malignant Otitis Externa

high resolution magnetic resonance imaging in an AIDS patient.
JLO 1998;112:98Y102
21. Davis JC, Gates GA, Lerner C, et al. Adjuvant hyperbaric oxygen in
malignant external otitis. Arch Otolaryngol Head Neck Surg
1992;118:89Y93
22. Shupak A, Greenberg E, Hardoff R, et al. Hyperbaric oxygenation
for necrotizing (malignant) otitis externa. Arch Otolaryngol Head
Neck Surg 1989;115:1470Y1475
23. Tisch M, Lorenz M, Lampl L, et al. Otitis externa necroticans. HNO
2003;51:315Y320
24. Driss N, Mighrik K, Hassine M, et al. Malignant otitis externa (2 cases).
Tunis Med 1993;71:541Y545
25. Meyerhoff W, Caruso VG. Trauma and infection of external canal. In:
Paparella MM, Shumrick DA, eds. Otolaryngology. Philadelphia, PA:
WB Saunders, 1991;2792Y2793
26. Chandler J R. Malignant external otitis. Laryngoscope 1968;78:1257Y1294

* 2012 Mutaz B. Habal, MD 1751

Copyright © 2012 Mutaz B. Habal, MD. Unauthorized reproduction of this article is prohibited.