135. infections of the external ear

Editors: Bailey, Byron J.; Johnson, Jonas T.; Newlands, Shawn D. Title: Head & Neck Surgery - Otolaryngology, 4th Edition

Copyright Â©2006 Lippincott Williams & Wilkins

> Table of Contents > Volume Two > IX - Otology > 135 - Infections of the External Ear

135

Infections of the External Ear

Christopher J. Linstrom

Frank E. Lucente

Otolaryngologists see many patients with infections of the external ear. The infections may be categorized by location and cause, and classified by time course as acute, subacute, and chronic. Before discussing the individual disease processes, we review the normal anatomy and physiology of the external ear.

Anatomy and Physiology The external ear is composed of the auricle and external auditory canal. Both contain elastic cartilage derived from mesoderm and a small amount of subcutaneous tissue, covered by skin with its adnexal appendages (1,2). There is fat but no cartilage in the lobule. The auricle is derived from six hillocks, three each from branchial arches I and II (Fig. 135.1). During normal gestation, the cartilaginous hillocks merge to form the auricle, and with selective growth of the mandible, the auricle rises from its original position near the lateral commissure of the mouth to the temporal area

The external auditory canal is derived from the first ectodermal branchial groove between the mandibular (I) and hyoid (II) arches (2,3). The epithelium lining this groove contacts the endoderm of the first pharyngeal pouch, thus forming the tympanic membrane, the most medial extent of external auditory canal. Connective tissue of mesodermal origin is found between ectoderm and endoderm and becomes the fibrous layer of the tympanic membrane (2). Because of its origin, the external auditory canal, including the lateral surface of the tympanic membrane, is derived from ectoderm and is lined by squamous epithelium.

The process of canalization is complete by about week 12 of gestation, at which time the canal fills with epithelial tissue. The canal ordinarily recanalizes by about week 28 of fetal life (3).

The external auditory canal may be thought of in two sections. The outer 40% is cartilaginous and contains a thin layer of subcutaneous tissue between the skin and cartilage. The inner 60% is osseous, is formed primarily by the tympanic ring, and contains very scant soft tissue between the skin, periosteum, and bone. The average length of the adult external auditory canal is 2.5 cm. Because of the oblique position of the tympanic membrane, the posterosuperior part of the canal is about 6 mm shorter than the anteroinferior portion (1). The junction of the

of 33Ovid: Head & Neck Surgery - Otolaryngology

3/28/2008mk:@MSITStore:C:\DOCUME~1\Owner\LOCALS~1\Temp\Rar$DI00.141\HNSOTOL....

cartilaginous and bony portions of the canal is a narrowed section termed the isthmus.

The tragus and antitragus form a partial barrier to the entrance of macroscopic foreign bodies. Laterally to medially, the canal curves slightly superiorly and posteriorly in a gentle S shape. The canal can be thought of as pointing toward the nose; thus, the auricle needs to be pulled gently upward, outward, and backward to straighten the canal for examination. Three macroscopic defense mechanisms protect the external auditory canal and lateral surface of the tympanic membrane: the tragus and antitragus, the skin with its cerumen coat, and the isthmus of the canal.

The skin of the cartilaginous canal contains many hair cells and sebaceous and apocrine glands such as cerumen glands (Fig. 135.2). Together, these three adnexal structures provide a protective function and are termed the apopilosebaceous unit. Glandular secretions combine with sloughed squamous epithelium to form an acidic coat of cerumen, one of the primary barriers to infection of the canal. An invagination of the epidermis forms the outer wall of the hair follicle, and the hair shaft forms the inner wall. The follicular canal is the space between these two structures. The alveoli of the sebaceous and apocrine glands empty into short, straight excretory ducts, which drain into follicular canals. Obstruction of any part of the ductal system predisposes to infection.

P.1988



The canal is normally a self-protecting and self-cleansing structure. The cerumen coat gradually works its way past the isthmus to the lateral part of the canal and sloughs externally. Instrumentation and excessive cleansing of the canal disturb this primary protective barrier and may lead to infection. Individual variations in the anatomy of the canal or the consistency of the cerumen produced may predispose some people to wax accumulation.

The canal interfaces on all but its lateral surface. Medially, it is bound by the tympanic membrane and squamosa of the temporal bone, which when intact is a

Figure 135.1 The auricle is formed from six auricular hillocks, three each from branchial archesI and II.



good barrier to the spread of infection. In the presence of a tympanic membrane perforation, infection may spread back and forth from the middle ear cleft to the external auditory canal. The horseshoe-shaped tympanic ring and squamosa separate the canal from the middle cranial fossa. Rarely is this the direct mechanism of intracranial extension of infection. The posterior bony canal serves as the anterior boundary of the mastoid cavity. Several vessels penetrate the canal, especially along the tympanomastoid suture. These may be involved in the hematogenous extension of infection from the canal to the mastoid segment. Posterior to the cartilaginous canal lies dense connective tissue overlying the mastoid, which may become secondarily infected.

Superiorly, the canal is bound by the infratemporal fossa and base of the skull. Infections extending through the roof of the canal may extend into these structures. Anteriorly, the canal is bordered by the temporomandibular joint and the parotid gland.

The lymphatic drainage of the canal is an important channel for the spread of infection. Anteriorly and superiorly, the canal drains to the preauricular lymphatics in the parotid gland and the superior deep cervical nodes. The inferior portion of the canal drains into the infra-auricular nodes near the angle of the mandible. Posteriorly, the lymphatics drain into the postauricular nodes and the superior deep cervical nodes. The auricle and external auditory canal receive

P.1989

Figure 135.2 Microscopic view of the normal apopilosebaceous unit, demonstrating drainage of the secretions of the sebaceous and modified apocrine glands into the follicular canal of the hair follicle.



their arterial supply from the superficial temporal and posterior auricular branches of the external carotid artery (1). Venous drainage from the auricle and meatus is via the superficial temporal and posterior auricular veins. The former joins the retromandibular vein, which usually divides and joins both jugular veins; the latter joins the external jugular but may also drain to the sigmoid sinus through the mastoid emissary vein (1).

Sensation to the auricle and external auditory canal is supplied from cutaneous and cranial nerves, with contributions from the auriculotemporal branches of the trigeminal (V), facial (VII), glossopharyngeal (IX), and vagus (X) nerves and the greater auricular nerve from the cervical plexus (C2â€“3). The vestigial extrinsic muscles of the ear, anterior, superior, and posterior auricular, are supplied by the facial nerve (VII) (1).

Otitis Externa Otitis externa is a spectrum of infection of the external auditory canal. The appearance of the canal varies according to the time course of infection: acute, subacute, or chronic.

Acute otitis externa is an infection of the canal caused by a break in the normal skin or cerumen protective barrier, often occurring in the milieu of elevated humidity and temperature. Although commonly called swimmer's ear, acute otitis externa may be caused by anything that results in the removal of the protective lipid film from the canal, allowing bacteria or fungal organisms to enter the apopilosebaceous unit. It usually begins with itching in the canal and is commonly caused by instrumenting the canal with a cotton swab or fingernail. This temporarily relieves itching but allows proliferation of bacteria in locally macerated skin and sets up an itch-scratch cycle. The warm, dark, moist setting of the canal is now a perfect medium for rapid bacterial growth. Later, pain ensues as the swollen soft tissues of the canal distract the periosteal lining of the bony canal. As the disease progresses, purulent discharge begins, and the auricle and periauricular soft tissues may become involved.

In patients in whom the disease does not resolve after treatment, a subacute or chronic form may occur. Thiscondition may be likened to eczema and is a spectrum of disease ranging from mild drying and scaling of the canal skin to complete obliteration of the canal by chronically infected hypertrophic skin.

History The history and functional inquiry should include information regarding the length of time, the number of occurrences, the nature and severity of pain, antecedent otologic disease, previous auricular instrumentation or trauma (especially the use of cotton-tipped applicators or forceful aural irrigation), and any predisposing factors such as diabetes or radiotherapy or any condition causing immunosuppression. Any previous otologic or head and neck surgery is noted.

Pain, fullness, itching, and hearing loss are the four major symptoms of external

P.1990



otitis, although not every patient has each symptom (4). Throughout the examination, the examiner should remember the innervation of the external auditory canal and recall that pain from other areas of the upper aerodigestive tract may be referred to the ear.

Physical Examination On initial inspection, look at the ear itself and then at its relation to the head. Is it red, swollen, protruding? Is there obvious discharge? Are the auricle and periauricular tissues normal in appearance or lichenified, with a heaping up of the normal epidermal architecture? Is there erythema or cellulitis spreading to the periauricular tissues, face, and neck? A gentle tug upward and backward will usually confirm the clinical suspicion. Although not an infallible rule, the patient with acute otitis externa usually will not tolerate this maneuver; patients with acute otitis media often will.

To make the correct diagnosis of infections of the external canal and to follow the clinical response to treatment, clean the canal thoroughly and examine it under good illumination. A hand-held otoscope will often suffice for a quick examination, but all instrumentation of the ear is best done under the microscope with the patient lying supine in the chair, in anticipation of a possible vasovagal response mediated by Arnold nerve, a branch of cranial nerve X.

Although topical and local anesthesia may be tried before cleansing, they are usually of little effect in hyperemic macerated tissue and no substitute for

Figure 135.3 Otitis externa, acute inflammatory stage. Mild erythema and edema of the canal skin are seen. Clear secretions may be viewed in the canal. (From Senturia BA, Marcus MD, Lucente FE. Diseases of the external ear, 2nd ed. New York: Grune & Stratton, 1980, with permission.)



reassurance and patience. Using graduated specula will often ease the patient into a complete examination. The canal may be cleaned with suction, a cerumen loop, or alligator forceps. The choice of instruments is unimportant. Gentleness and thoroughness are very important.

Bacteriology The usual pathogens responsible for acute otitis externa are Pseudomonas aeruginosa, Proteus mirabilis, staphylococci, streptococci, and various gram-negative bacilli. For the mild or uncomplicated infection, culture of the canal is ordinarily not taken, because it will usually demonstrate a mixed pattern of growth. For recalcitrant infections, culture may identify a predominant organism and assist in the choice of antibiotic therapy.

Staging Senturia et al. (4) divided the clinical course of external otitis into the following stages: preinflammatory; acute inflammatory, which can be mild, moderate, or severe; and chronic inflammatory. Typically, the preinflammatory stage begins when the stratum corneum becomes edematous because of the removal of the protective lipid layer and acid mantle from the canal, resulting in plugging of the apopilosebaceous unit. As obstruction continues, a sense of fullness and itching begins. The disruption of the epithelial layer allows invasion of bacteria that either reside in the canal or are introduced on foreign objectsinserted into the canal, such as a cotton swab or a dirty fingernail. This produces the acute inflammatory stage, which is accompanied by pain and tenderness of the auricle. In the earliest stage, the skin of the external auditory canal shows mild erythema and minimal edema (Fig. 135.3). A small amount of clear or slightly cloudy secretion may be seen in the canal. As pain and itching increase, the patient progresses to the moderate stage, in which the canal shows more edema and a thicker more profuse exudate (Fig. 135.4).

P.1991



Further progression of the inflammation in the absence of treatment produces the severe inflammatory stage, characterized by increased pain and obliteration of the lumen of the canal. A profuse, purulent exudate and edema of the canal skin may obscure the tympanic membrane. In addition, small white papules are often visible on the surface of the canal skin. P. aeruginosa or another gram-negative bacillus can almost always be cultured at this stage. In the severe stage, the physician often sees evidence of extension of infection beyond the canal to involve the adjacent soft tissues and cervical lymph nodes (Fig. 135.5).

Figure 135.4 Otitis externa, moderate acute inflammatory stage. The external auditory canal is more edematous than in the acute stage, approaching obliteration of the lumen, with a more profuse exudate. (From Senturia BA, Marcus MD, Lucente FE. Diseases of the external ear, 2nd ed. New York: Grune & Stratton, 1980, with permission.)



In the chronic inflammatory stage, the patient experiences less pain but more profound itching. The skin of the external canal is thickened, and superficial flaking may be seen (Fig. 135.6). The auricle and concha often show secondary changes, such as eczematization, lichenification, and superficial ulceration. This condition is likened to eczema and may range from mild drying and thickening of the canal to complete obliteration of the external canal by chronically infected hypertrophic skin (Table 135.1).

Figure 135.5 Otitis externa, severe stage. Infection extends beyond the limits of the canal to involve adjacent soft tissues and cervical lymph nodes. Erythema of the conchal skin and scaliness are secondary to profuse drainage.



Figure 135.6 Otitis externa, chronic inflammatory stage. The skin of the external canal is thickened, and superficial flaking may be seen. The surrounding skin of the auricle may show secondary changes such as eczematization, lichenification, and superficial ulceration.

TABLE 135.1 DIAGNOSIS OTITIS EXTERNA

History Pain Fullness Itching Discharge Physical examination Preinflammatory Mild erythema, edema Acute inflammatory Auricular tenderness Erythema Edema



Differential Diagnosis The differential diagnosis of conditions that are similar to external otitis is large and includes necrotizing otitis externa, bullous external otitis, granular external otitis, perichondritis, chondritis, relapsing polychondritis, furunculosis, and carbunculosis, as well as many dermatoses, such as psoriasis and seborrheic dermatitis. All have features in common with acute and chronic external otitis yet have enough dissimilarities to be considered distinct clinical entities.

Carcinoma involving the external auditory canal may present as infection, and in its earliest stages is often mistaken for infection and treated inappropriately. The most common malignant neoplasm of the external ear is squamous cell carcinoma, although other primary carcinomas, such as basal cell carcinoma, malignant melanoma, ceruminous adenoma or adenocarcinoma, adenoid cystic and metastatic carcinomas to the temporal bone with extension to the external auditory canal such as breast, prostatic, small (oat) cell, and renal cell carcinomas, have been described. The occurrence of pain in an old previously stable mastoid cavity is the hallmark of carcinoma and must be excluded by biopsy and other investigations.

Natural History The natural history of untreated acute otitis externa is one of increasing pain, swelling, and discharge from the canal. The infection may spread to the adjacent periauricular soft tissues, face, and neck. In an immunocompromised patient, what began as an isolated superficial infection of the apopilosebaceous unit of the external auditory canal may progress to perichondritis, chondritis, cellulitis, and erysipelas. Rich lymphatic and hematogenous drainage pathways favor the spread of infection to local and regional sites in the head and neck. Few patients progress to such an advanced stage before seeking medical attention.

Discharge Chronic inflammatory Thickening, flaking of canal skin Eczematization Ulceration Laboratory Culture P. aeruginosa P. mirabilis Staphylococcus sp. Streptococcus sp. Radiology Rarely indicated

P.1992



The natural history of chronic otitis externa is far less dramatic than its acute counterpart. The chronic scaling and itching in the canal predispose to manipulation of the canal, excoriation, and repeated episodes of acute otitis externa. With time, the canal skin may become lichenified, and ultimately the canal may become completely obliterated.

Medical Treatment The four fundamental principles in the treatment of external otitis in all stages (5) are frequent and thorough cleaning, judicious use of appropriate antibiotics, treatment of associated inflammation and pain, and recommendations regarding the prevention of future infections. In any stage of infection, thorough cleaning is a priority. Meticulous debridement of exfoliated debris, purulence, and cerumen will do as much if not more than simply placing the patient on ear drops. In the preinflammatory stage, a complete cleaning may be all that is required. In the absence of purulence, a brief course of an acidifying drop such as aluminum sulfateâ€“calcium sulfate (Domeboro) is efficacious in discouraging bacterial or fungal growth.

Treatment of the acute inflammatory stage varies with the extent of disease. In the mildest form, cleaning as described previously is indicated. An antibiotic otic drop is recommended to cover what is probably a Pseudomonas infection. There is an emerging body of evidence that the fluoroquinolone preparations with or without steroids (ciprofloxacin, ofloxacin, dexamethasone, hydrocortisone (Cipro HC, Ciprodex, Floxin)] may have advantages over the neomycin/polymyxin/hydrocortisone preparations (Cortisporin or Coly-Mycin S Otic) (6,7).

At this time, no significant antibiotic resistance has been shown to emerge due to the use of the fluoroquinalone ototopic medications (8).

At this stage, edema of the external auditory canal should not be severe, and the patient should be able to instill drops into the ear by tilting the head to the side or by lying down with the involved ear upright.

Moderate Stage In the moderate stage of inflammation, edema of the canal may interfere with the instillation of drops. The physician should then insert a wick into the canal and instill drops on it. Often the canal may accommodate two or even three wicks. As the wick expands, it presses the soft tissues and periosteum toward the nondistended position; this alone may relieve pain. All instrumentation of the ear is best done under the microscope. The wick is removed by the physician at the time of reexamination. If the edema has not been significantly reduced, repacking is indicated. Antibiotic drops should be continued for at least 2 to 3 days after the cessation of pain, itching, and drainage, so that complete eradication of infection may be ensured.

In the moderate stage, an oral analgesic is often prescribed because pain can be pronounced. Caution the patient to avoid manipulation of the canal. Teach

P.1993



swimmers to towel dry the concha and lateral canal, to shake water out of the canal, or to instill an acidifying drop after swimming. If the infection has not spread beyond the boundaries of the external canal, the use of oral antibiotics will be of little if any value. A final office visit is important to ensure that the infection has completely resolved and the canal is back to its normal state.

Severe Stage In the severe stage, infection usually extends beyond the limit of the canal. In addition to the cleaning, packing, and use of antibiotic drops as discussed previously, attend to any soft-tissue involvement by using an oral antibiotic with broad-spectrum coverage. Successive generations of the cephalosporins widen gram-negative coverage at the expense of gram-positive coverage.

In addition to anti-Pseudomonas eardrops, common choices of oral antibiotics are antistaphylococcal penicillins, first-generation cephalosporins, or one of the antipseudomonal fluoroquinolones such as ciprofloxacin or levofloxacin. The fluoroquinolone antibiotics are effective against Pseudomonas species but at present are not approved for use in patients under age 18 because of the risk of arthropathy formation (6). Multiple reports over the last 10 years have indicated the safe use of ciprofloxacin in the pediatric patient with little if any increased development of arthopathy over adults. The fluoroquinolones remain contra-indicated, however, except in extraordinary circumstances, such as in the treatment of respiratory disease in children with cystic fibrosis. (9)

Warm soaks (normal saline or diluted aluminumsulfateâ€“calcium acetate solution) are also useful in the treatment of the crusting and edema involving the auricle and surrounding skin. Culture of the canal is indicated only for the severe stage or for patients who have previously been treated without resolution. Treatment is generally continued for 10 to 14 days if there is a good response. In rare patients who do not respond to this regimen, hospitalization, vigorous daily local care, repeat culturing, and intravenous antibiotics are indicated.

Chronic Stage The chronic stage of external otitis is manifested by marked thickening of the skin of the external auditory canal caused by long-standing infection. Examinationreveals flakes of dry scaly skin in the canal. Although removal of debris is recommended, this may be difficult due to the narrowing of the lumen of the canal. Repeatedcleaning and instillation of antibiotics and steroids are indicated. Triamcinalone acetonide 0.25% cream or ointment (Kenalog) or dexamethasone sodium phosphate 0.1% (Decadron, Pred Forte 1%) ophthalmic drops may be used.

In all cases of acute or chronic external otitis, instruct the patient to avoid future infections by not placing any object or instrument into the canal. These often excoriate the canal skin and push debris further into the canal rather than remove it. Patients who have repeated infections despite adhering to these measures are best advised to use an acidifying drop composed of equal measures of vinegar and water, or ethyl alcohol and water, when exposed to high humidity.



Alternatively, an acidifying power such as boric acid may be used. Custom-made ear molds are useful for these patients.

Recalcitrant Otitis Externa The physician will be able to judge very quickly which patients are responding. If no progress is made in the office, the rare patient may have to be admitted as an inpatient. Toilet of the ear should be performed under the microscope, frequently (at least daily) and carefully. Look for subtle signs of chronic middle ear diseaseâ€”granulation tissue or the opening of a tiny perforation. The latter may be obscured by a swollen tympanic membrane, giving a â€œfish-mouthâ€� appearance to the perforation. A â€œsewer capâ€� of crust on the drum may

reveal a cholesteatoma underneath. Examine every part of the auricle. Look for signs of underlying chondritis or perichondritis, especially diffuse crusting or exudative weeping. Culture the ear. Examine the periauricular tissues carefully to look for signs of spreading infection. Computed tomography of the temporal bones may give additional information. Look for opacification of the mastoid and signs of bony erosion.

Place the patient on daily aural drops, preferably one covering P. aeruginosa, and intravenous antibiotics with gram-positive and gram-negative coverage. A cephalosporin together with an aminoglycoside is a logical combination. Therapy should be tapered according to culture and sensitivities. Severely swollen ears may calm down with steroids.

Many recalcitrant infections occur because of noncompliance or chronic instrumentation of the canal skin. The patient should be counseled to amend bad habits. Treat these patients exactly as those with severe otitis externa, but as inpatients. This will allow intravenous antibiotics to be given and will ensure local care (Tables 135.2 and 135.3).



Surgical Management of Hypertrophic Chronic Otitis Externa When such local measures are insufficient to eradicate infection and reestablish the lumen of the canal, it is necessary to remove the involved canal skin and any adjacent involved cutaneous or cartilaginous tissue. This is very rarely required and may be performed through the canal but is better done through a postauricular incision, which allows visualization of the involved tissues. A

TABLE 135.2 COMPLICATIONS OTITIS EXTERNA

Cellulitis Erysipelas Perichondritis Chondritis Chronic nonresolving infection

TABLE 135.3 EMERGENCIES OTITIS EXTERNA

Unresolving pain, despite local care Admit to hospital Analgesia Control inflammation

Cranial neuropathy with external otitis Consider necrotizing external otitis

P.1994



generous amount of conchal cartilage is removed to effect a wide meatoplasty. The bony canal is enlarged with a drill. Take care to protect the facial nerve in its vertical segment; the use of an intraoperative facial nerve monitor facilitates this. The canal is resurfaced with a split-thickness (8:1,000 inch) skin graft that is temporarily held in place with stents or packing.

It is the experience of many otolaryngologists that even the most recalcitrant infection can be managed if the four basic principlesâ€”thorough cleaning, antibiotic treatment, pain control, and instruction of the patientâ€”are meticulously followed. There is no substitute for thorough and repeated local care (Table 135.4).

Necrotizing (Malignant) External Otitis This potentially life-threatening disease should be viewed within the larger context of osteomyelitis of the temporal bone and skull base. Thanks in large part to newer anti-Pseudomonas antibiotics, chief among them the fluoroquinolones, necrotizing external otitis (NEO) is not as prevalent as it was even a decade ago. By no means is it a disease of the past, especially among diabetics; the immunocompromised, especially HIV+ patients; and the elderly. The otolaryngologist must still keep NEO within the differential diagnosis of a refractory external ear infection in the patient at risk.

Toulmouche (10) described a case of progressive osteomyelitis of the temporal bone in 1838 that was probably the first reported case of NEO. In 1959 Melzer and Kelleman (11) described a case of progressive Pseudomonas osteomyelitis of the temporal bone and skull base. Chandler (12,13,14,15,16) is credited with the

TABLE 135.4 TREATMENT OTITIS EXTERNA

Medical Frequent thorough cleaning Antibiotic coverage Drops Oral Intravenous as needed Treat inflammation, pain Recommendations for prevention

Surgical Excise involved canal skin Perform wide meatoplasty Resurface canal with split-thickness skin graft



clinical description of what he termed malignant otitis externa in 1968 and thereafter. He believed that radical surgical debridement of the ear and adnexal structures offered the only hope of a cure. Although many early cases ended in the death of the patient, the entity does not involve carcinoma and thus the more appropriate term used today is NEO. Advances in both early radiological imaging and, more importantly, antiPseudomonas medications have significantly altered the natural history of this disease.

Diagnosis The diagnosis of NEO is made in a patient with the appropriate history, physical examination, and supporting laboratory findings. Four salient features are found (17): persistent otalgia for longer than 1 month; persistent purulent otorrhea with granulation tissue for several weeks; diabetes mellitus, another immunocompromised state, or advanced age; and cranial nerve involvement. The disease that begins in the external auditory canal may pass through preformed channels: anteriorly through the fissures of Santorini and posteroinferiorly through the stylomastoid foramen to the jugular bulb and skull base. The disease may pass through thrombosed veins and along the route of the facial nerve anteriorly and inferiorly toward both the petrous apex and the skull base.

Other diseases to be included in the differential diagnosis include severe acute otitis externa, squamous cell carcinoma, glomus jugulare tumor, cholesteatoma, nasopharyngeal carcinoma, Hans-SchÃ¼ller-Christian disease, eosinophilic granuloma, Wegener granulomatosis, clival chordoma, and meningeal carcinoma (18). The physician's index of suspicion should be high so that no patient is denied aggressive treatment when appropriate (Table 135.5).

Clinical and Radiographic Findings NEO usually begins as an acute external otitis that does not resolve despite medical therapy, as described previously. The history is significant for a long-standing infection of the external canal accompanied by aural discharge and severe deep-seated pain. The disease is usually found in elderly diabetic patients in poor metabolic control, although it may be found in any chronically ill, debilitated, or immunocompromised patient (19). The HIV status of the patient should be known.

P.1995

TABLE 135.5 DIAGNOSIS NECROTIZING EXTERNAL OTITIS

History Persistent otalgia



On physical examination, most patients with NEO usually but not invariably have granulation tissue visible in the inferior aspect of the canal or even extruding from it. This may obscure the tympanic membrane. It is rare to see granulation tissue in patients with routine otitis externa; however, granulations are common in an acute exacerbation of chronic otitis media with perforation of the tympanic membrane. The skin of the canal is often erythematous, indurated, and sometimes macerated. Purulent secretions are common.

The causative organism is almost always P. aeruginosa, although other organisms such as P. mirabilis, Aspergillus fumigatus, Proteus sp., Klebsiella sp., and Staphylococcus sp. have been isolated (13,20,21,22,23). Fungal infections causing NEO are less commonly associated with diabetes but are found more commonly in patients who are immunocompromised in other ways, especially by HIV disease (24).

The natural history of NEO is one of relentless progression to involve the cranial nerves, especially the facial nerve. Pain is inexorable and is deep seated. Damiani et al. (25) reported that the most commonly involved cranial nerves were VII (75%), X (70%), and XI (56%). More recent reports have estimated the facial nerve to be involved in at least one fourth of patients, with less frequent involvement of cranial nerves IX, X and XI (24).

Persistent purulent otorrhea, granulations Diabetes mellitus, advanced age, immunocompromised state Cranial neuropathy(ies)

Physical examination Granulations in external canal Purulent discharge seen +/- cranial neuropathy, especially cranial nerve VII

Culture Pseudomonas sp.a

Pseudomonas aeruginosaa

Radiology Nuclear (gallium, technetium) CT with contrast MRI with contrast

CT, computed tomography; MRI, magnetic resonance imaging. aAlmost always.



CT of the temporal bone with contrast is the initial radiograph to be done, yielding excellent bony detail with less precise information about soft tissue. It may define subtle bony changes such as erosion of the anterior canal wall with involvement of the temporomandibular joint and erosion of the tympanic ring and base of the skull. It may demonstrate soft tissue thickening and mastoid clouding. An important radiological feature on coronal CT of thetemporal bone is effacement of the tympanic ring (Fig. 135.7). The fat plane in the subtemporal triangle near the stylomastoid foramen may be effaced (26).

Magnetic resonance imaging (MRI) yields very little information about bone, which appears as a silhouette. MRI without and with gadolinium enhancement may be advantageous in defining the medial extent of soft tissue disease at the skull base. Dural enhancement and involvement of the medullary bone spaces are seen with central-skull-base invasion (24). Underlying cerebral involvement is easily visualized with gadolinium-enhanced MRI. The patency of the dural sinuses and great vessels of the neck may be assessed in a noninvasive fashion with magnetic resonance angiography or venography. Changes seen on MRI do not resolve with clinical improvement. Thus, MRI is a useful diagnostic tool to assess the extent of disease but is not a useful tool in following the clinical course of NEO (27).

Technetium-99m bone scanning and gallium-67 scanning have been advocated in the evaluation of NEO (21,24). Their sensitivity for the presence of infection is far greater than their specificity for the cause (Fig. 135.8).

Figure 135.7 Coronal computed tomography scan of a patient with left necrotizing otitis externa.



Tc-99m scanning gives excellent information about bone function but poor information about bone structure. A positive scan is thought to represent osteoblastic activity as little as 10% above normal (21). The scan is positive in acute and chronic osteomyelitis and in areas of active bone repair without infection, as in trauma. Increases in Tc-99m uptake between 4 and 24 hours postinjection is the most sensitive indicator of temporal bone osteomyelitis (28). Its use in the evaluation of NEO is complementary to that of Ga-67 scanning. Ga-67 is thought to be incorporated into proteins and polymorphonucleocytes at sites of active infection as a Ga-67â€“lactoferrin complex (21). It will highlight an acute infective focus but not the full extent of an osteomyelitic process. As treatment progresses, the Ga-67 scan will revert to normal (negative). The Tc-99m scan will lag behind for many months. Baseline studies of both are thus recommended, and sequential imaging is used to monitor the response to therapy. Indium-111â€“labeled leukocyte (In-WBC) planar scintigraphy has been demonstrated to yield better results for the detection of osteomyelitis than either planar or tomographic Ga-67 and/or Tc-99mâ€“methyline diphosphonate and may replace the former two radionuclide modalities in the evaluation of NEO-suspected patients (22). It is best to consult with whomever will be performing the radionuclide study, though, to determine which of these choices will be best.

Medical Treatment Swab and/or tissue cultures of the external auditory canal should be obtained. If present, granulations should be biopsied and sent to rule out carcinoma or another pathological entity. P. aeruginosa is almost always cultured. Pseudomas

Figure 135.8 Bone scan of a patient with necrotizing otitisexterna.

P.1996



is frequently the predominant organism, so the patient is treated with anti-Pseudomonas antibiotics for an extended period, often for 6 weeks or more. Because of the synergy achieved with the use of 2 antibiotics, one an anti-pseudomonal antibiotic and the other an aminoglycoside, monotherapy is discouraged in the treatment of NEO. Usually two anti-Pseudomonas antibiotics are chosen from several alternatives, including gentamicin or tobramycin with or without ticarcillin or piperacillin. Alternative antibiotics include mezlocillin or azlocillin, ceftazidime, imipenem, aztreonam, amikacin, norfloxacin, and ciprofloxacin or any of the other appropriate anti-Pseudomonas fluoroquinolones. If an aminoglycoside is chosen, peak and trough levels and hearing must be carefully monitored. It is wise to treat in concert with an infectious disease colleague to help select those medications that will be of greatest benefit with the least toxicity.

Because of the high tissue levels seen with oral fluoroquinolones, the apparent incidence of NEO has fallen. The physician should not be lulled into a false sense of security, however. Many patients with poor microvasculature, especially diabetics, may achieve cidal concentrations of an antibiotic solely with intravenous administration.Patients refractory to intravenous administration of antibiotic may require surgical control of the infected site. Emergence of resistance to ciprofloxacin has been reported in 20% of long-term (6 weeks or more) therapy for osteomyelitis (29). Outside of cystic fibrosis and severe infections in which no other treatment is possible, the only pediatric situations where fluoroquinolones are superior to standard treatments for children are typhoid fever, severe shigella dysenteries and enterobacteria meningitis. Thus, fluoroquinolones should still be reserved for second-line use in pediatrics because of the potential emergence of resistant strains and because they have been shown to cause arthropathy in the weight-bearing joints of immature animals (9).

An early clinical feature of success in treatment is the cessation of pain, and patients may be tempted to discontinue therapy once this occurs. Regardless of the choice of medication or mode of delivery, patients must understand that they will require meticulous aural toilet and antibiotic treatment for at least 6 weeks and vigorous management of diabetes.

Either in the hospital or in the office, the ear is debrided carefully under the microscope on a regular basis until granulations have subsided. The patient is placed on anti-Pseudomonas otic drops and appropriate systemic antibiotics. Diabetes is aggressively managed, usually with the aid of an internist or endocrinologist. The diet is carefully monitored with the aid of the nutritionist.

Hyperbaric oxygen has been advocated by Shupak et al. (30), but Chandler et al. (15) were unsure of its value. Hyperbaric oxygen is thought to facilitate osteoneogenesis and to promote repair of diseased bone. The cost and inconvenience of hyperbaric oxygen therapy have limited its availability. Its use is recommended for advanced disease with significant skull base or intracranial involvement, recurrent disease, and infections refractory to antibiotic treatment (24).



Surgical Treatment Most patients can be managed medically, and the role of surgery in NEO remains controversial. Surgical debridement of tissue and osteomyelitic bone is usually reserved for patients who do not respond to conventional therapy. Progression of pain despite aggressive medical therapy, persistence of granulations, and the development of cranial nerve involvement are all ominous signs that call for more aggressive medical therapy and possibly surgical intervention.

With the onset of clinical facial weakness, early surgical removal of granulations and, when necessary, decompression of the descending facial nerve have given excellent return of function. The primary surgical goal is to excise the underlying necrosis and to replace it with vascularized tissue. Serial electroneuronography (ENOG) has been used to determine the electrical degeneration of the VII nerve in patients with clinical facial paralysis. An ENOG showing more than 90% electrical degeneration of the clinically involved facial nerve may support surgical decompression of the involved segment of the nerve.

John and Cheesman (31) have advocated wide local excision of infected cartilage and soft tissues if pain persists after medical treatment or if facial palsy occurs. Reines and Schindler (32) have reported three cases in which subtotal temporal bone resection was performed to gain access to the primary focus of infection and provide adequate drainage. Surgical treatment including abscess drainage, debridement of sequestra, and more extensive resection should be individualized depending upon the patient's overall health status and response to more conservative measures (33).

Mortality remains significant, especially in the immunocompromised patient. Progression of disease results in severe unremitting pain within the ear and at

P.1997

TABLE 135.6 TREATMENT NECROTIZING EXTERNAL OTITIS

Medical Hospital admission Intravenous antibiotics Daily cleaning, debridement

Surgical Excise granulations +/- middle ear exploration +/- mastoidectomy +/- facial nerve decompression +/- temporal bone resection if no response



the base of the skull and extension of infection to the mastoid, parotid, lower cranial nerves, and transverse and sigmoid sinuses. Osteomyelitis of the skull base may lead to meningitis, brain abscess, and death. Meyerhoff et al. (34) reported an overall mortality of 37% before the introduction of combined carbenicillin and gentamicin and 23% afterward. With multiple cranial neuropathies, Babiatzki and SadÃ© (18) and Damiani et al. (25) have reported mortality rates of 60% and 61%, respectively. Poor prognostic factors include facial paralysis, polyneuropathy, and intracranial extension (35).

The diagnosis and management of patients with NEO remains an otoloryngologic challenge. Perhaps the greatest advance in its treatment has been the recognition of NEO as a distinct entity and a clear understanding of its pathophysiology. A team approach involving the cooperation of otolaryngology, endocrinology, and infectious disease may enhance the overall outcome (Tables 135.6 to 135.8). The devastating disease reported by Chandler (12) in his classic 1968 article has significantly changed. The advent of the fluoroquinolones and other anti-Pseudomonas antibiotics has significantly lowered the morbidity and mortality associated with NEO.

TABLE 135.7 COMPLICATIONS NECROTIZING EXTERNAL OTITIS

Cranial neuropathy (VII and lower) Progression despite aggressive local care, including hyperbaric oxygen therapy (to mastoid, parotid, lower cranial nerves, base of skull, dural venous sinuses, brain) Meningitis Brain abscess Death

TABLE 135.8 EMERGENCIES NECROTIZING EXTERNAL OTITIS

Any complications in Table 135.7 (in living patient) Change antibiotic Increase level of daily care



Conditions Related Toexternal Otitis Several other infectious and inflammatory diseases are included in the differential diagnosis of otitis externa.

Radiation-Induced Otitis Externa Another form of otitis externa occasionally occurs after radiotherapy of the region of the external ear. The predominant symptoms result from the inflammation and infection that occur when radiotherapy weakens local defense mechanisms and resident bacteria flourish. When limited to the skin of the external auditory canal, treatment measures with particular attention to water avoidance are appropriate. In its worst form of osteoradionecrosis, sequestra of devitalized tissue must be removed and replaced with vascularized tissue.

Bullous External Otitis Bullous external otitis is a very painful condition in which vesicles or bullae are noted in the bony portion of the external canal. The vesicles are commonly hemorrhagic and should not be ruptured, because secondary infection may ensue. Because Pseudomonas may be one of the causative organisms, appropriate otic drops are recommended. Packing and irrigation of the canal should be avoided, because they tend to prolong the course of this disease.

Granular External Otitis Granular external otitis often resembles the earliest stage of NEO in that there may be small granular plaques or pedunculated granulations in the external canal. This condition may occur in patients who have not been fully treated for a previous episode of external otitis. After topical or local anesthesia, removal of granulation tissue, placement of a wick in the canal, and the instillation of antibiotic drops will usually resolve the problem. Oral antibiotics should be given if the infection extends beyond the canal. If the

Consider surgery

P.1998



patient is diabetic or debilitated, the diagnosis of NEO is entertained and treated appropriately.

Perichondritis and Chondritis Perichondritis, inflammation of the perichondrium, and chondritis, inflammation of cartilage, may follow or complicate infections of the external auditory canal or result from accidental or surgical trauma to the auricle. The condition is painful, and the patient often complains of severe itching deep within the canal. With time, the skin over the affected area becomes crusted with squamous debris, and the involved cartilage begins to weep. The ear is indurated and erythematous; often the canal swells shut. The surrounding soft tissues of the face and neck may become involved.

In the mildest stages, thorough debridement and treatment with topical and oral antibiotics are generally sufficient. If these measures do not succeed, the ear is debrided again, and cultures are taken. Appropriate treatment for common pathogens, especially Pseudomonas, is begun and tapered according to culture results. Ciprofloxacin is a logical choice for moderate stages, combined with an anti-Pseudomonas drop such as gentamicin or a fluoroquinolone drop.

If the infection spreads to involve regional soft tissues and lymphatics, the patient should be hospitalized and parenteral treatment with adequate coverage for Pseudomonas begun. In difficult cases, the ear should be cultured before starting treatment. With recalcitrant infections, ask the help of an infectious disease consultant. At every stage of the disease, frequent and thorough debridement of the canal is essential. The metabolic requirements of cartilage are low, and its blood supply is appropriately diminished. Once infection has become established in the perichondrium or cartilage, it is extremely difficult to treat. If subacute or chronic infection evidenced by inexorable weeping continues, surgical intervention is indicated. This is best done in the operating room under controlled conditions.

The affected area is cleansed and injected with local anesthetic containing epinephrine. Skin flaps are appropriately planned and the dissection taken down to the affected cartilage. If it has lost its normal â€œpearly whiteâ€� appearance, it is most likely necrotic and should be excised. Often necrosis extends farther than can be grossly visualized. Small irrigation drains are placed beneath the flaps and sutured to the skin. The skin flaps are closed. The drainage ports are irrigated with antibiotic irrigation such as bacitracin (50,000 U of bacitracin dissolved in 250 mL of normal saline). The drains are advanced as the condition resolves. Parenteral antibiotics, otic drops, and aggressive local care continue until the infection has resolved.

Relapsing Polychondritis Relapsing polychondritis is an intermittently progressive disease marked by inflammatory destruction of cartilage. Although thought to be an autoimmune disorder, the exact cause is unknown. Cartilage of the external ear, larynx, trachea, bronchi, and nose may be involved. Symptoms are episodic, with fever,



anemia, erythema, swelling, pain, and an elevated sedimentation rate during acute episodes. As the disease progresses, symptoms of increasing respiratory obstruction become apparent. Labyrinthine disturbances are rarely present. The diagnosis is made on the basis of the history and physical examination, supported by an elevated sedimentation rate. Biopsy of involved cartilage may show necrosis, inflammation, and fibrosis. Treatment is with oral corticosteroids.

Furunculosis and Carbunculosis Furunculosis and carbunculosis are conditions resulting from gram-positive infections, usually staphylococcal, of the hair follicles. The primary lesion is usually a small well-circumscribed pustule that may enlarge to become a furuncle or merge with several similar lesions to form a carbuncle. The infection occurs most commonly at the junction of the concha and canal skin.

For treatment to be successful, any accumulated infectious material must be removed. Spontaneous drainage can often be encouraged by the use of warm soaks, supplemented by topical and oral antibiotics. If this fails to relieve obstruction of the canal, incision and drainage under local anesthesia are indicated.

Infectious Eczematoid Dermatitis Infectious eczematoid dermatitis results from the drainage of contaminated or purulent material from the middle ear into the floor of the external ear and adjacent infra-auricular skin (Fig. 135.9). This drainage causes a secondary infection or an autosensitization phenomenon manifested by crusted plaques in the canal. Treatment is directed at control of the underlying middle ear infection. Supportive treatment of the external canal reaction consists of removal of accumulated debris, application of sterile saline soaks to the crusted areas, and application of an antibiotic cream or ointment.

Otomycosis Otomycosis is a fungal infection of the skin of the external canal. Although fungi may be the primary pathogens, they are usually superimposed on chronic bacterial infection of the external canal or middle ear. Secondary otomycosis tends to recur if the underlying primary infection is not controlled. All fungi have three basic growth requirements: moisture, warmth, and darkness. Altering moisture will discourage fungal growth. Aspergillus species are the most common, and pruritus is the primary clinical manifestation. Physical examination commonly shows a white, black, or dotted gray membrane. Thorough cleaning with removal of the matted fungal debris is supplemented by the topical application of an acidifying solution such as aluminum sulfateâ€“calcium acetate (Domeboro) or by a drying powder such as boric acid. Clotrimazole cream or solution (Lotrimin) may also be used. In the presence of a tympanic membrane perforation or pressure-equalizing tube, clotrimazole drops or lotion may be very painful. Thorough cleaning and drying therapies such as powders are best. Metacresyl acetate (Cresylate) may be

P.1999



painted on the margin of a perforation or an infected ventilation tube. This is best done under the microscope. Be careful not to allow this medication to enter the middle ear cleft, because it is quite irritating. In recalcitrant infections, a foreign body such as a ventilation tube acts as the nidus for infection and should be removed. Tympanoplasty is best performed to close a perforation that intermittently drains with a superimposed fungal infection.

Gentian violet is usually well tolerated in patients with mastoid cavities, although it is best left out of the middle ear cleft in the presence of a perforation. Because it will permanently stain skin and clothing, small amounts are used with adequate protection of the surrounding area.

Many patients with refractory otomycotic infections may have had previous mastoid surgery. Often the canal wall is down. Because of moderate to severe hearing loss, the patient must wear a hearing aid with a closed mold. This is a significant problem, because the patient relies on the aid virtually all day and is reluctant to leave the instrument out. Carefully explain the problem to the patient, meticulously debride the ear, and use a drying agent such as boric acid powder, chloromycetin-sulfanilamide-fungizone (amphotericin B) powder or

Figure 135.9 Infectious eczematoid dermatitis with inflammation and crusting of the skin of the canal and auricle secondary to drainage of purulent material through a tympanic membrane perforation in a patient with chronic otitis media.



chloromycetin-sulfanilamide-tinactin (tolnaftate) powder; this will often help clean up the cavity. Ointments in cavities with closed hearing aids may promote fungal growth because of the accumulation of moisture. In refractory cases, gentian violet or metacresyl acetate (Cresylate) is used topically.

Herpes Zoster and Herpes Simplex Herpes zoster and herpes simplex are viruses known to affect the external auditory canal. The patient initially experiences a period of burning, pain, or localized headache, and vesicles usually appear within several days. When vesicles coalesce and rupture, crusts are formed. Herpes zoster tends to appear unilaterally in a dermatomic distribution. Involvement of the facial nerve may produce paresis or paralysis (herpes zoster oticus or Ramsay Hunt syndrome). Treatment is supportive, with topical application of a drying agent, such as hydrogen peroxide for crusts. The status of the facial nerve is carefully followed; surgical decompression of the facial nerve may be a consideration. Many patients excoriate the blisters, and bacitracin ointment or a suitable substitute should be applied to prevent superinfection. Acyclovir, famcyclovir and valacyclovir have been shown to ameliorate herpetic infections, especially herpes zoster oticus. The latter two have easier dosing schedules and are better absorbed orally than acyclovir. Also, famcyclovir reduces the duration of postherpetic neuralgia. However, it will cause a transitory rise in hepatic enzyme production and must be used with caution.

Dermatoses Allergic and irritant contact dermatoses may mimic diffuse external otitis. These result when the susceptible patient comes in contact with any type of agent that can produce a cutaneous response. Irritants may be absolute, so noxious that a reaction occurs in everyone exposed (e.g., strong acids or alkalis), or relative, noxious to susceptible individuals, usually after repeated exposures (e.g., soaps and the plastic mold of a hearing aid). Allergic contact dermatitis refers to delayed hypersensitivity reactions resulting from substances such as poison ivy, nickel compounds (earrings), and rubber compounds (headphones). The typical reaction presents as erythema, weeping, and vesiculation accompanied by itching. The patient may produce a secondary infection by scratching. Treatment consists of removal of the causative agent and the use of topical steroids and astringents. Topical or systemic antibiotics are indicated for the treatment of infection. Systemic steroids may be indicated for severe cases. In rare cases, for example, the patient with a cochlear implant and hypersensitivity to plastic, the external, ear-level receiver/stimulator may be painted with a different material or covered with a cloth casing to separate it from the skin.

External Ear Disease in the Human Immunodeficiency Virusâ€“Infected Patient Among the external ear manifestations in HIV disease is Kaposi sarcoma, which

P.2000



presents with reddish-blue lesions typically described as hemorrhagic nodules (36). The lesions may be discrete or confluent. Although chemotherapy, radiotherapy, and interferon-Î± have been used for therapy, treatment of auricular and canal lesions is rarely necessary.

Infections of the external ear in HIV-infected patients include both typical and atypical pathogens. Recurrent herpetic infections and Pneumocystis cariniiâ€“infected aural polyps have been reported in the external auditory canal as a result of chronic otitis media (37).

Another external ear manifestation of HIV disease is seborrheic dermatitis, which tends to be more widespread and refractory to treatment than the same condition in noninfected patients. Necrotizing external otitis in the HIV+ patient adds another level of concern regarding its treatment. An infectious disease consultant should be involved in the overall care of the HIV+ patient.

Conclusion With a thorough knowledge of the normal embryology, anatomy, and physiology of the external ear, together with an understanding of the natural history of the various common disease processes that occur in this location, treatment of the patient with external ear disease becomes logical. However, it is not always easy. Most conditions can be managed with the recommendations outlined in this chapter. There is no substitute for patience and thoroughness.

Highlights

An understanding of the various disease entities occurring in the external ear is predicated on a knowledge of the embryology, anatomy, and physiology of the canal.

Infection and blockage of the apopilosebaceous unit are the precursors of infectious otitis externa.

Otitis externa presents as a spectrum of disease and may be classified into preinflammatory, acute inflam-matory, and chronic inflammatory stages.

Four principles form the basis of treatment for all stages of infection of the external ear: thorough cleaning, antibiotic therapy, control of inflammation and pain, and recommendations to prevent infection. Of these, thorough cleaning is the cornerstone of therapy.

Recalcitrant and recurrent otitis externa must be treated aggressively with daily local care and antibiotics, often in the hospital. Patience and thoroughness are needed for successful treatment.

Surgery is rarely indicated for infections of the external canal but may be required to reverse the natural course of chronic disease.

NEO is a disease occurring in immunosuppressed patients. It must enter the differential diagnosis of any patient with nonresolving acute external otitis.

There are four hallmarks of NEO: persistent otalgia; persistent otorrhea and granulation tissue; diabetes mellitus, advanced age, or immunocompromised



state; and cranial nerve involvement.

NEO must be treated aggressively with proper radiographic imaging to map the extent of disease, meticulous local care control of diabetes or immunodeficiencies (when possible), and antibiotics. Surgery is rarely required. Mortality remains significant with cranial nerve involvement.

Many infectious and inflammatory conditions related to external otitis occur in the ear. Therapy is based on treatment of the underlying condition.

References

1. Hollinshead WH. Anatomy for surgeons: the head and neck, 3rd ed. Vol. 1. Philadelphia: Harper & Row, 1982:159â€“163.

2. Anson BJ, Donaldson JA. Surgical anatomy of the temporal bone, 3rd ed. Philadelphia: W.B. Saunders, 1981:28.

3. Hughes GB, Pensak ML. Textbook of clinical otology. New York: Thieme-Stratton, 1997.

4. Senturia BA, Marcus MD, Lucent FE. Diseases of the external ear, 2nd ed. New York: Grune & Stratton, 1980.

5. Lucente FE. External otitis. In: Gates GA, ed. Current therapy inotolaryngologyâ€”head and neck surgery, 6th ed. New York: Elsevier

Science, 1997.

6. Roland PS, Pien FD, Henry DC, et al. Efficacy and safety of topical ciprofloxacin/dexamethasone versus neomycin/polymyxin B/ hydrocortisone for otitis externa. Curr Med Res Opin 2004;8: 1175â€“1183.

7. Myer CM III. Ear Nose Throat J. 2004;83(Suppl):9â€“11.

8. Weber PC, Roland PS, Hannley M, et al. The development of antibiotic resistant organisms with the use of ototopical medications. Otolaryngol Head Neck Surg. 2004;130(3 Suppl)S89â€“S94.

9. Gendrel D, Chalumeau M, Moulin F, et al. Fluoroquinolones in paediatrics: a risk for the patient or for the community? Lancet Infect Dis 2003;9:537â€“546.

10. Toulmouche MA. Observations d'otorrhee cÃ©rÃ©brate suivis des



reflexions. Gazette Med Paris 1838;6:422â€“426.

11. Meltzer PE, Kellemen G. Pyocyaneus osteomyelitis of the temporal bone, mandible and zygoma. Laryngoscope 1959;60:1300â€“1316.

12. Chandler JR. Malignant external otitis. Laryngoscope 1968;78: 1257â€“1294.

13. Chandler JR. Malignant external otitis: further considerations. Ann Otol Rhinol Laryngol 1977;86:417â€“428.

14. Chandler JR. Pathogenesis and treatment of facial paralysis due to malignant otitis externa. Ann Otol Rhinol Laryngol 1972;81: 648â€“656.

15. Chandler JR, Grobman L, Quencer R, et al. Osteomyelitis of the base of the skull. Laryngoscope 1986;96:245â€“251.

16. Chandler JR. Malignant external otitis and osteomyelitis of the base of the skull. Am J Otol 1989;10:108.

17. Kimmelman CP, Lucente FE. Use of ceftazidime for malignant external otitis. Ann Otol Rhinol Laryngol 1989;98:721.

18. Babiatzki A, SadÃ© J. Malignant external otitis. J Laryngol Otol 1987;101:205â€“210.

19. Geerlings SE, Hoepelman AM. Immune dysfunction in patients with diabetes mellitus (DM). FEMS Immunol Med Microbiol 1999; 28:259â€“265.

20. Strauss M, Aber RC, Conner GH, et al. Malignant external otitis: long-term (months) antimicrobial therapy. Laryngoscope 1982;92: 397â€“406.

21. Weber PC, Seabold JE, Graham SM, et al. Evaluation of temporal and facial osteomyelitis by simultaneous In-WBC/Tc-99m-MDP bone SPECT scintigraphy and computed tomography scan. Otolaryngol Head Neck Surg 1995;113:36â€“41.

22. Cunningham M, Yu LY, Turner J, et al. Necrotizing otitis externa due to aspergillus in an immunocompromised patient. Arch Otolaryngol Head Neck

P.2001



Surg 1988;114:554â€“556.

23. Cohen D, Friedman P. The diagnostic criteria of malignant external otitis. J Laryngol Otol 1987;101:216â€“221.

24. Gangadar SS, Kwartler JA. Skull base osteomyelitis secondary to maliganant otitis externa. Current Opin Otol HN Surg 2003;1:316â€“323.

25. Damiani JM, Damiani KK, Kinney FE. Malignant external otitis with multiple cranial nerve involvement. Am J Otol 1979;2:115.

26. Murray ME, Britton L: Osteomyelitis of the skull base: the role of high resolution CT in diagnosis. Clin Radiol 1994;49:408â€“411.

27. Grandis JR, Curton HD, Yu VL. Necrotizing (malignant) external otitis: prosective comparison of CT and MR imaging and follow-up. Radiology 1995;196:499â€“504.

28. Hardoff R, Gipa S, Uri N, et al. Semiquantitative skull planar and SPECT bone scintigraphy in diabetic patients: differentiation of necrotizing (malignant) external otitis from severe external otitis. J Nucl Med 1994;35:411â€“415.

29. Gilbert D, Tice AD, Marsh PK, et al. Oral ciprofloxacin therapy for chronic contiguous osteomyelitis caused by aerobic gram-negative bacilli. Am J Med 1987;82:254.

30. Shupak A, Greenberg E, Hardoff R, et al. Hyperbaric oxygenation for necrotizing (malignant) otitis externa. Arch Otolaryngol Head Neck Surg 1989;115:1470.

31. John AC, Cheesman AD. Malignant otitis externa. Hosp Update 1979;5:589.

32. Reines JM, Schindler RA. The surgical management of recalcitrant malignant external otitis. Laryngoscope 1980;90:369.

33. Pedersen HB, Rosborg J: Necrotizing external otitis: aminoglycoside and Î²-lactam antibiotic treatment combined with surgical treatment. Clin Otolaryngol 1997,22:271â€“274.



34. Meyerhoff WL, Gates GA, Montalbot PJ. Pseudomonas mastoiditis. Laryngoscope 1977;87:483.

35. Amorosa L, Modugno GC, Pirodda A. Malignant external otitis: review and personal experience. Acta Otolaryngol Suppl 1996;521: 3â€“16.

36. Gherman CR, Ward RR, Bassis ML. Pneumocystis carinii otitis media and mastoiditis as the initial manifestation of the acquired immuno-deficiency syndrome. Am J Med 1988;85:250.

37. Lucente FE. Acquired immunodeficiency syndrome (AIDS) In: Lucente FE, Lawson W, Novick N, eds. The external ear. Philadelphia: W.B. Saunders, 1995:95.



135. infections of the external ear

Documents

docume 1ownerlocals 1temprardi00

magnetic resonance

elevated sedimentation

cervical lymph

chronic otitis

herpes zoster

malignant

chronic external