30
Epidemiology
Otitis externa is a common disease affecting all age groups and is usually infective in etiology. Though bacterial infections of the skin of the external auditory canal are the commonest cause, fungal infection can also occur (otomycosis). Infections are more prevalent in hot and humid climate conditions, and are often associated with trauma to the skin of the external auditory canal, such as during mechanical removal of cerumen. Swimming is considered a risk factor, hence the term swimmer’s ear . Malignant (necrotizing) otitis externa is a particularly aggressive form of infection occurring in a select patient population and is responsible for considerable morbidity and mortality.
Clinical Features
Otitis externa can cause a variable amount of pain (otalgia) and discharge (otorrhea), but it seldom causes signifi cant morbidity. Bacterial infections are usually more symptomatic. Depending on the degree of swelling and debris in the external auditory canal, there may be conductive hearing loss.
Systemic signs such as fever and (pretragal) lymphadenopathy may be present.
Malignant (necrotizing) otitis externa is a particularly aggressive life-threatening form of infec- tion caused by Pseudomonas aeruginosa infection typically in elderly diabetics and individuals with other immunosuppressed states, such as HIV patients or those who have undergone chemotherapy.
Clinically, a high index of suspicion in the susceptible patient population is required for diagnosis.
Nonspecifi c granulation tissue may be seen along the inferior wall of the external auditory canal (at the bony–cartilaginous junction) with exquisitely painful otorrhea. Cranial nerve palsies may result in advanced cases.
7 EXTERNAL OTITIS 31
CT
Bone destruction and invasion of the temporal bone and mastoid are the hallmark of malignant otitis externa. CT is sensitive in detection of early bone erosions. Contrast-enhanced studies are useful in detection of foci of frank pus in the deep facial spaces. Abnormal soft tissue is seen in the external audi- tory canal and the infratemporal fossa. Facial nerve involvement can occur with infratemporal spread.
Other common routes of spread include posterior spread to the mastoid and middle ear, and anteriorly to the temporomandibular joint. Posteromedial spread to the jugular fossa may result in multiple lower cranial nerve palsies. Intracranial spread may result in meningitis, abscess formation, and sigmoid si- nus thrombosis. Diffuse skull base osteomyelitis represents an advanced stage of disease ( Fig. 7–1 ).
MRI
MRI is superior to CT for the detection of bone marrow edema in skull base involvement and in the eval- uation of intracranial complications such as dural, vascular, and cranial nerve involvement ( Fig. 7–2 ).
M
A B
10.1055/978-2-58890-647-2c007_f001
Figure 7–1 Computed tomography (CT) of malignant otitis externa. (A) Axial and (B) coronal CT of the right temporal bone reveals an abnormal soft tissue ( large arrow ) mass with destruction of the cortical margins of the external auditory canal ( small arrows ). The internal areas of high attenuation
are likely due to adjacent bony destruction. There is opaci- fi cation of the mastoid air cells (M) identifi ed on the axial images, which may due to direct extension or obstructed secretions.
A
M
10.1055/978-2-58890-647-2c007_f002 B
Figure 7–2 Magnetic resonance (MR) of otitis externa. (A) Non- contrast T1-weighted (T1W) image demonstrates a low signal le- sion replacing the normal fascial spaces of the lateral masticator space ( arrows ). (B) Fat-suppressed postcontrast T1W image shows
diffuse enhancement of the infl ammatory process, which involves the masticator space ( arrows ) and surrounds the mandible (M).
Note the involvement and enlargement of cranial nerve V 3 ( curved arrow ).
32 II EXTERNAL AUDITORY CANAL
Radionuclide Imaging
It has been suggested that anatomic imaging with CT or MR should be supported by routine single photon emission computed tomography (SPECT) bone imaging for initial diagnosis of malignant otitis externa. Technetium-99m (Tc-99m)-methylene diphosphonate (MDP) SPECT imaging, and gallium-67 (Ga-67) scintigraphy or more recently SPECT Indium-111 (In-111) white blood cell (WBC) scanning have been used for the detection and follow-up of disease. Furthermore, these also appear to be the investi- gations of choice for posttherapeutic assessment.
PE ARL S
•
Imaging is warranted in suspected cases of malignant (necrotizing) otitis externa.•
CT of the temporal bone is the most useful investigation and demonstrates osseous destruction of the temporal bone or the mastoid with enhancing soft tissue in the external ear and adjacent deep neck.•
MR is useful in the evaluation of intracranial complications or nerve involvement.•
CT and MR are excellent in demonstrating the resolution of the soft tissue component but may not be as useful in assessment of the success of osteomyelitis treatment.•
Radionuclide imaging may play a role in the detection of disease and in posttherapeutic assess- ment of these patients.
Suggested Readings
Davidson HC . Imaging of the temporal bone. Magn Reson Imaging Clin North Am 2002 ; 10 : 573 – 613 Harnsberger HR. The temporal bone. In: Harnsberger HR, ed.Handbook of Head and Neck Imaging, 2nd
ed. St. Louis: Mosby, 1995:438
Okpala NCE , Siraj QH , Nilssen E , Pringle M . Radiological and radionuclide investigation of malignant otitis externa. J Laryngol Otol 2005 ; 119 : 71 – 75
Remley KB, Swartz JD, Harnsberger HR. The external auditory canal. In: Swartz JD, Harnsberger HR, eds.
Imaging of the Temporal Bone, 3rd ed. New York: Thieme, 1997:16–46
33
CHAPTER 8 Cholesteatoma of the External Auditory Canal
Ellen G. HoeffnerEpidemiology
External auditory canal cholesteatomas (EACC) are rare, with an incidence of 1 in 1000 new otologic patients. Their exact etiology is unknown, and many may occur spontaneously, although prior infl am- mation, trauma, or surgery have all been associated with EACC. EACC may be caused by loss of normal lateral epithelial migration from the tympanic membrane and external auditory canal (EAC); or in- creased cellular proliferation induced by accumulation of keratin debris may play a role in the develop- ment of these lesions. EAC stenosis or obstruction may also result in EACC. Although EACC can develop in any portion of the canal, the posterior-inferior wall is most common.
Clinical Features
Most patients are adults presenting between 40 and 75 years of age with otorrhea and dull otalgia.
Rarely, hearing loss may occur secondary to obstruction of the canal by the EACC. Facial nerve paralysis is even less common. Examination reveals squamous debris protruding from the involved canal wall, which unlike keratosis obturans, does not form a plug. Purulent drainage may be present deeper in the