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S. Belli et al.
14.2 Etiological andEpidemiological Features
Otitis externa occurs frequently worldwide but is more common in the tropics than
in more temperate regions since the tropical climate is warmer and more humid. It
is estimated to affect one in ten people during their lifetime [3]. People who swim
are ve times more likely to develop otitis externa [4], which explains why it is
often referred to as “swimmer’s ear.” Bacterial infections account for at least 90%
of cases [4]. The most frequently isolated pathogen is Pseudomonas aeruginosa
(22–62% of cases), followed by Staphylococcus aureus (between 11 and 34%). The
simultaneous isolation of multiple pathogens occurs frequently [5]. Fungal infections are infrequent reasons for acute otitis externa (10% of cases) but are more
frequently seen where the infection becomes chronic. The usual fungal pathogens
are from the genus Aspergillus (between 60 and 90%) [1, 6] or Candida (between 10
and 40%) [1]. The prolonged use of antibiotics predisposes to otomycosis. Also at
risk are patients who are immunosuppressed or have diabetes mellitus [1].
14.3 Classification
Cases of otitis externa (OE) may be categorized in the following manner [7]
• Acute diffuse OE.This is the most frequently encountered form, with patients
usually being swimmers.
• Acute localized OE (furuncle). This occurs when a hair follicle becomes infected.
• Chronic OE has the same features as acute diffuse OE, although it persists for at
least 6weeks.
• Eczematous/eczematoid OE is an umbrella term for a variety of skin disorders
that may cause an infection of the external auditory meatus and thus provoke
OE.This includes allergic dermatitis, psoriasis, systemic lupus erythematosus,
and eczema.
• Malignant (i.e., necrotic) OE occurs when the site of infection extends deep into
the tissues surrounding the external auditory meatus. This condition mainly affects
patients with immunocompromise (such as those with diabetes mellitus or AIDS).
• Otomycosis refers to an infection of the external auditory meatus caused by
fungi, such as Candida spp. or Aspergillus spp.
14.4 Signs andSymptoms: Otitis Externa
andAuditory Impairment
On physical examination, the main signs to look for are pain when the tragal region
is touched, or the auricle is pulled (a cardinal sign). There are a number of other
potential signs or symptoms to look out for, such as [7]:
• Earache, which may be slight or severe and generally worsens over the course of
one to a couple of days.
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• Auditory impairment.
• Perception of fullness or pressure in the ear.
• The external auditory meatus may be reddened, swollen, and narrower than usual.
• Tinnitus.
• Pyrexia (in a few cases).
• Pruritus, particularly in chronic OE or otomycosis.
• Pain that is severe and deep in a patient with immunocompromise may signal
malignant OE.
• Otorrhea, which begins as a clear uid, after which pus is seen, accompanied by
a foul odor.
• In a few cases, there may be facial or cervical cellulitis, and the lymph nodes of
the same side may be swollen and tender.
• Rarely, there may be symptoms from both ears.
• The history often reveals that the patient has been involved in water-based activi-
ties, such as swimming, surng, or canoeing.
• There may also be a history of injury to the ear, frequently as a result of cleaning
the ears too energetically, inserting a cotton bud in the canal or taking water into
the ears.
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14.5 Signs andSymptoms: Otitis Externa andHearing Loss
OE is typically a clinical diagnosis made on the basis of a matching history and supportive physical ndings, not omitting otoscopy. Any patient with diabetes or some
other source of immunocompromise and who complains of severe otalgia should be
referred to an ENT specialist in case malignant OE is the diagnosis.
14.5.1 Physical Examination
On physical examination, the main signs to look for are pain when the tragal region
is touched, or the auricle is pulled (a cardinal sign). The external auditory meatus
may be reddened, swollen, and narrower than usual. There may be otorrhea, either
clear or containing pus. Auditory impairment of conductive type may be noted. In a
few cases, there may be facial or cervical cellulitis, and the lymph nodes of the same
side may be swollen and tender [8].
Although it is potentially challenging to get a clear view of the ear drum on otoscopy in such cases, it may be possible to see evidence of tympanic inammation.
The drum should move normally when subjected to pneumatic otoscopy. The auricle may show signs of eczema. If there are signs of the cranial nerves being affected
(such as the facial nerve or the ninth to twelfth nerves), the diagnosis cannot be
uncomplicated OE [8].
Otomycosis generally causes severe pruritus but is not normally as painful as
infection with bacteria. There is frequently an accompanying viscous otorrhea of
gray or white color. Infections caused by Pseudomonas generally provoke a
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green- or yellow-colored discharge of pus, whereas a fungal infection caused by
Aspergillus resembles a ne mat of white with black spheres resting on top. When
the fungal discharge is examined microscopically, spores or hyphae may be seen, or
there may be indistinct areas [8].
If the ear is viewed under magnication, the presence of granulation tissue may
be apparent within the meatus. Infection may extend into the adjoining soft tissues,
including the parotid gland. If the infection tracks into the bone, the mastoid, temporomandibular joint, or basal skull may be invaded, resulting in involvement of CN
VII and IX–XII [8].
S. Belli et al.
14.5.2 Laboratory Tests
Generally speaking, the diagnosis does not call for laboratory investigations,
although these may be of value where there is immunocompromise, treatment failure, or features suggestive of otomycosis. Potentially useful investigations include
the following [7]:
• Gram staining and microscopy of discharge from the ear
• Serum glucose estimation
• Urinalysis
14.5.3 Imaging Investigations
In the majority of patients with suspected OE, imaging is not appropriate.
Nonetheless, imaging studies may be required in specic cases, where, for example,
malignant OE or mastoiditis is the putative diagnosis.
The following imaging methods may be of value
• High denition computed tomography (CT) is the investigation of choice as it
reveals osseous erosion.
• Bone scan utilizing radionucleotides.
• Gallium scan.
• Magnetic resonance imaging (MRI) is less commonly employed than other
methods but may be helpful as a second line investigation if there is a suspicion
the infection has spread to the soft tissues [9, 10].
14.6 Treatment
The rst line in treating OE is to provide analgesia, debride the external auditory
meatus, provide topical treatments to counter infection and reduce swelling, and
prevent factors that are complicating the situation [8].
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The majority of cases resolve with over-the-counter painkillers and ear drops
applied to the canal. The ear drops usually employed for this purpose are ones containing ethanoic acid (to manipulate the acidity of the meatus), antibiotics (for bacterial causes), and antifungals. Although OE of eczematous or psoriatic type is
frequently responsive to topically applied steroids, such cases may recur or become
persistent. There may be a need for regular debridement using suction and under
microscopic guidance. If the meatus is very swollen, a wick may be placed in the
canal to carry topical treatments deeper into the meatus [8].
Clinical improvement is observed within 7–10days in 65–90% of treated cases
of OE, irrespective of the agent employed [5]. A meta-analysis of randomized controlled trials, conducted by the Cochrane Collaboration, found that equal benet
occurred when either antiseptic or antibiotic medications were used. Monotherapy
was as effective as combination treatments and the addition of steroids did not affect
the outcome [11]. When corticosteroids were applied topically, however, it was
noted that there was a reduction in erythema and ear discharge. Some of the trials
included did purport to indicate varying outcomes, depending on whether a single
or multiple agents were employed in treatment. The wide variety of different agents
employed means that meaningful conclusions about best practice were difcult to
draw [11].
In a systematic review that compared topical antibiotic agents with placebo, the
active agent was associated with a 46% increase in resolution as assessed clinically,
or 61% when assessed bacteriologically [12]. In cases of tympanic perforation,
agents with known ototoxicity should not be used. The use of a gauze wick impregnated with medication as monotherapy appears to increase the efcacy of topically
applied agents and to reduce swelling from inammation, but no randomized trial
of this method has yet been reported [11].
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14.6.1 Antibiotics
Since the majority of patients with OE have a supercially located bacterial infection of the ear canal, a topically applied antibiotic solution is generally appropriate.
Sometimes the antibiotic is combined with a corticosteroid. The dose of corticosteroid involved is low, but sufcient to reduce otalgia and swelling in the canal [8].
14.6.1.1 Hydrocortisone/Neomycin/Polymyxin B
(Cortisporin, Cortomycin)
This agent is a combination of antibiotic and anti-inammatory intended to be
applied to the ear. It comes in solution or suspension forms. The indication is where
OE is caused by a condition susceptible to treatment by corticosteroid and either a
bacterial infection already exists or there is a danger of one occurring [8].
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S. Belli et al.
14.6.1.2 Ofloxacin Ear Drops
This antibiotic is a broad-spectrum quinolone that prevents bacterial multiplication
through inhibition of DNA gyrase. It is supplied as a solution containing ooxacin
3mg/mL (i.e. 0.3%) [8].
14.6.1.3 Ciprofloxacin Otic (Cetraxal)
Ciprooxacin is another agent that interferes with bacterial DNA replication through
inhibition of DNA gyrase. It is classed as a uoroquinolone. Bacterial species with
sensitivity to this agent include Pseudomonas spp., Streptococcus spp., methicillinresistant Staphylococcus aureus (MRSA), S. epidermidis, and the majority of Gram
negatives. It is not effective against anaerobic bacteria. Preparations are available
alone or in combination with hydrocortisone. Cetraxal is an ear drop that is supplied
as 14 single-use applicators, each of which carries 0.25mL of a 0.2% solution of the
antibiotic.
Ciloxan is an eye drop that is also suitable for use in cases of OE [8].
14.6.1.4 Dexamethasone/Tobramycin (TobraDex)
Tobramycin works by disrupting the bacterial outer membrane. It prevents the bacterium from manufacturing proteins by forming a bond to the 30S and 50S subunits
of the bacterial ribosome. Dexamethasone exerts an anti-inammatory effect
through preventing recruitment of polymorphonuclear leucocytes and decreasing
the permeability of the vascular endothelium.
TobraDex is an eye drop that is of value in treating OE.
14.6.1.5 Gentamicin Ophthalmic (Garamycin, Gentak)
Gentamicin is classied as an aminoglycoside. It has activity against Gram negative
organisms. This agent is an eye drop that is suitable for treating OE.The preparation
is a mixture in which 1mL contains both gentamicin sulphate 3mg and betamethasone sodium phosphate 1mg [8].
14.6.1.6 Ciprofloxacin andDexamethasone Otic (Ciprodex)
As stated earlier, ciprooxacin is classied as a uoroquinolone. Its mode of action
is inhibition of DNA gyrase and DNA topoisomerase. Thus, it prevents bacteria
from replicating and manufacturing gene products. Bacterial species with sensitivity to this agent include Pseudomonas spp., Streptococcus spp., methicillin-resistant
Staphylococcus aureus (MRSA), S. epidermidis, and the majority of Gram negatives. It is ineffective against anaerobic bacteria. Dexamethasone exerts an antiinammatory effect through preventing recruitment of polymorphonuclear
leucocytes and decreasing the permeability of the vascular endothelium. It also lessens otalgia [8].
Ciprodex has an indication for OE, and may be used for cases of otitis media in
patients with grommets in situ.
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14.6.1.7 Ciprofloxacin andHydrocortisone Ear Drops (Cipro
HC Otic)
Ciprooxacin is classied as a uoroquinolone. Its mode of action is inhibition of
DNA gyrase and DNA topoisomerase. Thus it prevents bacteria from replicating
and manufacturing gene products. Bacterial species with sensitivity to this agent
include Pseudomonas spp., Streptoccus spp., methicillin-resistant Staphylococcus
aureus (MRSA), S. epidermidis and the majority of Gram negatives. It is ineffective
against anaerobic bacteria. Hydrocortisone exerts an anti-inammatory effect
through preventing recruitment of polymorphonuclear leucocytes and decreasing
the permeability of the vascular endothelium [8].
14.6.2 Debriding andDraining theEar Canal
The external auditory meatus is generally only debrided in cases of malignant OE
or if complications occur, such as stenosis of the meatus. Debridement is frequently
indicated if OE is highly severe or if there is a high level of otorrhea. This procedure
is usually undertaken by an ENT specialist utilizing the operating microscope and
suction equipment. For otomycosis, debridement is a key component in treatment.
Abscess formation within the external auditory meatus is unusual but may result
from infection with S. aureus. The abscess can be treated straightforwardly by incising the lesion and draining it. Typically, an ENT surgeon uses a small bladed scalpel
or needle to achieve this [8].
14.6.3 Complications
Although complications seldom occur, potential complicating factors include
the following [8]
• Malignant OE, development of which heralds an emergency
• Mastoiditis
• Inammation of the collagenous tissue in the pinna, by extension, especially in
individuals whose ears have recently undergone piercing
• Osteomyelitis of the basal skull, causing osseous erosion [13]
• Invasion of the brain or spinal cord
• Cellulitis or lymphadenitis
Diabetic patients with these complications frequently also have diabetic
ketoacidosis.
Herpes zoster may resemble OE at the start, with blisters erupting 1 or 2 days
later. An infrequently occurring complication of herpes zoster is the Ramsay Hunt
syndrome, in which patients develop a one-sided palsy of the seventh cranial nerve
peripherally. Patients with herpes zoster should be informed about this potential
complication and be instructed to consult a physician if symptoms develop [14].
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S. Belli et al.
References
1. Wiegand S, Berner R, Schneider A, Lundershausen E, Dietz A.Otitis externa—investigation
and evidence-based treatment. Dtsch Arztebl Int. 2019;116:224–34.
2. Neher A, Nagl M, Scholtz AW.Otitis externa. HNO. 2008;56:1067–80.
3. Raza SA, Denholm SW, Wong JC. An audit of the management of otitis externa in an ENT
casualty clinic. J Laryngol Otol. 1995;109:130–3.
4. Roland PS, Stroman DW. Microbiology of acute otitis externa. Laryngoscope.
2002;112:1166–77.
5. Rosenfeld RM, Schwartz SR, Cannon CR, et al. Clinical practice guideline: acute otitis
externa. Otolaryngol Head Neck Surg. 2014;150(1 Suppl):S1–S24.
6. Sander R.Otitis externa: a practical guide to treatment and prevention. Am Fam Physician.
2001;63:927–37.
7. Waitzman AA.Otitis externa. In: Elluru RG, editor. Medscape; 2020. https://emedicine.med-
scape.com/article/994550- overview. Accessed 10 Feb 2022.
8. Waitzman AA.Otitis externa clinical presentation. In: Elluru RG, editor. Medscape; 2020.
https://emedicine.medscape.com/article/994550- clinical#b2. Accessed 10 Feb 2022.
9. Grandis JR, Curtin HD, Yu VL.Necrotizing (malignant) external otitis: prospective comparison of CT and MR imaging in diagnosis and follow-up. Radiology. 1995;196(2):499–504.
10. Hegde AN, Mohan S, Pandya A, Shah GV. Imaging in infections of the head and neck.
Neuroimaging Clin N Am. 2012;22(4):727–54.
11. Kaushik V, Malik T, Saeed SR.Interventions for acute otitis externa. Cochrane Database Syst
Rev. 2010;1:CD004740.
12. Rosenfeld RM, Singer M, Wasserman JM, Stinnett SS.Systematic review of topical antimicrobial therapy for acute otitis externa. Otolaryngol Head Neck Surg. 2006;134(4 Suppl):24–48.
13. Alva B, Prasad KC, Prasad SC, Pallavi S.Temporal bone osteomyelitis and temporoparietal
abscess secondary to malignant otitis externa. J Laryngol Otol. 2009;123(11):1288–91.
14. Kim D, Bhimani M. Ramsay hunt syndrome presenting as simple otitis externa.
CJEM. 2008;10(3):247–50.
Necrotising (Malignant) Otitis Externa
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andAuditory Impairment inChildren
NeslihanSarı, SongülDemir, andNurayBayar Muluk
15.1 Introduction
Malignant otitis externa, also referred to as necrotising otitis externa (NOE), results
from infection of the external auditory meatus and the temporal bone. The most
frequent pathogen responsible is Pseudomonas aeruginosa, with elderly, diabetic
individuals those most at risk of developing the condition. NOE develops from otitis
externa when osteomyelitis of the temporal bone develops. The infection can track
into the bone via the ssures of Santorini and the junction between the cartilage and
bone [1].
It seems that the rst reported case of NOE dates from 1838, when Toulmouche
described its occurrence. There is a report from 1959in which Meltzer describes
osteomyelitis of the temporal bone secondary to P. aeruginosa. Chandler argued in
1968 for the existence of NOE as a distinct clinical entity [2]. Chandler attached the
term ‘malignant’ to his description on account of the aggressive nature of the condition, the low response to treatment, and the large number of associated deaths in
patients with the condition [3].
15
N. Sarı (*)
Department of Otorhinolaryngology, Faculty of Medicine, Mardin Artuklu University,
Mardin, Türkiye
e-mail: neslihansari@hotmail.com
S. Demir
Section of Otorhinolaryngology, Mardin Training and Research Hospital, Mardin, Türkiye
e-mail: s.gule@hotmail.com
N. Bayar Muluk
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, Türkiye
e-mail: nbayarmuluk@yahoo.com
© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood
Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_15
203
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Since Chandler was writing, antibiotics with activity against P. aeruginosa have
been developed, and this has meant an improvement in the prognosis. Accordingly,
some experts favour discontinuing the use of the epithet ‘malignant’ as it no longer
accords with a realistic picture of the usual clinical situation [3]. Throughout this
chapter, the term necrotising otitis externa (NOE) will be used.
N. Sarı et al.
15.2 Pathophysiology
Necrotic otitis externa results from infection of the external auditory meatus and
temporal bone. The pathogen responsible is typically P. aeruginosa, and the condi-
tion frequently affects elderly, diabetic individuals. Otitis externa becomes NOE
when it invades the temporal bone, setting off an osteomyelitic reaction. The path
taken by the pathogen is through the ssures of Santorini and the junction between
the bony and cartilaginous canal [1].
The pathogen may invade other tissues, leading to osseous erosions and distant
spread via the planes of fascia and venous sinuses. It may affect the basal skull and
the adjacent structures, causing damage to the cranial nerves and entering into the
cranial cavity [4].
If the pathogen spreads to the temporal bone via the ssures of Santorini, it may
pass through the stylomastoid foramen and jugular foramen, through which cranial
nerves VII, IX, X and XI pass. Where the infection tracks through the junction of the
bone and cartilage of the external auditory meatus, it passes subtemporally to the
retrocondylar and parapharyngeal adipose tissues, the temporomandibular joint,
and the masticator muscle [5].
The routes followed by pathogens in NOE can be classied in the following way [4]
• Anterior route. The infection tracks to the masticator, the interior of the man-
dibular condyle, the parotid gland, seventh cranial nerve, fossa of the temporal
bone, temporomandibular joint and the stylomastoid opening.
• Medial or crossed route. The infection invades the adipose tissue surrounding
the pharynx, the musculature of the nasopharynx, cranial nerves IX–XI, the
sphenoid, clivus, jugular foramen and the apical portion of the petrous tempo-
ral bone.
• Intracranial. If the dura mater is thickened, the infection may track to the signoid
sinus, jugular vein, internal carotid artery, jugular fossa and the dura.
• Posterior. The pathogen may spread to the bony mastoid, but no soft tissues are
invaded by this route [6].
In addition to the above, infection may spread intravascularly, especially where
the causative pathogen is a fungus. Nonetheless, otomycosis rarely affects the temporal bone [7].
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15.3 Mortality andMorbidity
15.3.1 Cranial Nerve Palsies
Inammation around the basal skull may directly affect the cranial nerves, or a
palsy may result from toxins secreted by Pseudomonal organisms. The seventh cranial nerve is the most frequently affected in this way, with the site usually being the
stylomastoid foramen. Continuing spread of the infection leads to the glossopharyngeal, vagal and accessory nerves developing a neuropathy at the site of the jugular
foramen. Finally, the 12th cranial nerve is affected within its canal. If the infection
spreads to the apical portion of the petrous temporal bone, the trigeminal and abducens nerves may be affected [3].
Chandler stated that a seventh cranial nerve paralysis was present in 32% of
cases in 1977 [8], but this now seems to have gone down with the advent of antibiotic treatment effective against Pseudomonas. Franco-Vidal etal. [9] noted that
only 20% of a group of 46 cases undergoing treatment had paralysis of the seventh
cranial nerve. Cranial neuropathies other than facial palsy are rarer. It was previously considered that the development of a cranial nerve palsy heralded severe otitis
externa and meant a poor clinical outlook, but it has now been proposed by both
Soudry etal. and Mani etal. that the clinical outcome is not affected by whether a
seventh nerve palsy is present or not [10, 11]. Resolution of a seventh cranial nerve
palsy can be problematic, and unexpected outcomes do occur; hence, clinicians
should not consider that cure has been achieved if the symptoms fully resolve. For
the other cranial nerve palsies, resolution is generally more frequent than for the
facial nerve [3].
15.3.2 Intracranial Extension
Intracranial spread is seldom seen without there being present a cranial neuropathy.
Spread into the cranial cavity may cause meningitis, a cerebral abscess or thrombus
formation in the cranial sinuses. A cranial nerve palsy suggesting the jugular foramen is affected ought to prompt a search for thrombus formation in the sigmoid
sinus. A trigeminal or abducens palsy should raise suspicion of thrombus within the
cavernous sinus. Spread into the cranial cavity indicates high severity of NOE and
often results in death [3].
15.3.3 Comorbidities
It is virtually invariably the case that a patient with NOE is also diabetic, and there
may well be other comorbidities in addition [12]. In Chandler’s study, mortality
occurred due to pneumonia, uraemia, myocardial infarction, cerebrovascular accidents, and hepatic failure. Cases where systemic immunodeciency is present fare
less well, as Franco-Vidal has demonstrated [9].
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