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19.7.1.2 Empirical Treatment
When deciding on the initial antibiotic agent and before culture results are known,
bear in mind if the child has been subject to recurrence in attacks of AOM and what
agents have been administered to the patient recently [3].
In a case where AOM is not recurrent and no antimicrobial therapy has been
administered within the preceding 6 months, a reasonable option is vancomycin
alone, given intravenously at a dose of 15mgkg−1 at 6-h intervals, the maximum
single dose not to exceed 1 g. A second option is linezolid, also intravenously administered, at a dose of 10mgkg−1 8-h if the children is under the age of 12years, or
12-h for older children. The linezolid dose given each time must not exceed 600mg.
These regimes may be changed when culture is complete. The pathogens most likely
to be responsible are S. pneumoniae (some strains of which are insensitive to multiple
agents), S. pyogenes and S. aureus (which also may be insensitive to methicillin) [3].
In paediatric patients where episodes of AOM have been recurrent or an antimicrobial agent has been prescribed within the preceding 6 months, it is recommended
to use agents in combination. One rational empirical approach is combining either
vancomycin or linezolid with an anti-pseudomonal agent initially, then adjusting
treatment if required once the results of microbiological analysis are known [3].
It may be necessary to add in further antibiotics in cases where a complication is
present, such as a cerebral abscess, or where the initial gram staining points towards
a less usual pathogen [3].
Treatment According to Pathogen. Once the microbiological analysis has
shown the pathogen responsible and its sensitivity, the choice of antibiotic may need
to be revised. Frequently occurring pathogens include the following [3]:
• S. pneumoniae
• S. pyogenes
• S. aureus (including strains insensitive to methicillin)
It is usually necessary in treating a patient with acute mastoiditis to drain any
purulent discharge from the middle ear space and mastoid cells. Antibiotic treatment is generally inadequate as monotherapy, especially as the condition develops,
since there may be problems delivering pharmaceutical agents at the necessary concentration within the osseous tissues [22]. Draining the lesion also helps to arrest
further pathological development and may stop the condition becoming complicated [23]. Whilst it has been reported in the literature that acute mastoiditis
responded fully to antibiotics without the need to undertake tympanocentesis or
myringotomy [24], it is generally advisable to obtain a sample of uid from the
middle ear if antibiotic treatment is to avoid being blind.
There is considerable variation between clinics in terms of the optimal approach
used to drain the lesion. Potential methods available are tympanocentesis, myringotomy, myringotomy with grommet insertion or mastoidectomy. The approach
taken may depend on what stage mastoiditis has reached (e.g. with periosteal
involvement or coalescent) and whether a complication is present and of what kind
[4, 25, 26].
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19.7.1.3 Mastoidectomy
This operation results in excision of the cortical bone of the mastoid and removal of
the mastoid air spaces. There are two types. The simple type (which may be referred
to as cortical, complete or canal-wall-up) involves preservation of the posterior portion of the external meatus. The radical procedure (which may be termed canalwall- down) does not permit preservation of the posterior section of the meatus.
The simple procedure aims to clear away any infected material from the mastoid,
allowing opening of the antral entrance and letting any remaining uid drain to the
outside [4]. The radical procedure is conned to cases where a simple mastoidectomy fails to relieve the problem and the patient still has an ear discharge and
otalgia [4].
19.7.2 Chronic Mastoiditis
The approach to treating chronic mastoiditis resembles that taken in chronic suppurative middle ear infections, namely application of antibiotics topically. In cases
of treatment failure, the ear needs to be regularly cleaned and antibiotics administered systemically. The initial agent given is one that targets both aerobes and anaerobes. More than 50% of Gram-negative anaerobes (such as pigment-bearing
Prevotella, Porphyromonas, Bacteroides and Fusobacterium species) are no longer
penicillin-sensitive, since they express a beta-lactamase. The agents that are still
effective against anaerobes are clindamycin, cefoxitin, metronidazole, chloramphenicol, co-amoxiclav and piperacillin-tazobactam [2].
The surgical options encompass mastoidectomy, grommet insertion or tympanoplasty, depending on the specic indication. An important factor to consider is
whether there is osteitis or periosteitis present. Any child with a chronic middle ear
infection needs referral to an ENT specialist.
19.8 Complications
The following complications may arise from extracranial extension of mastoid
inammation [27]
• Seventh cranial nerve palsy.
• Auditory impairment, which may be of conductive or sensorineural type.
• Abscess formation within the subperiosteum.
• Osteomyelitis of the cranium, or an erosive process of the bone.
• Formation of a Bezold abscess. This lesion is located deeply within the cervical
soft tissues.
• Inammation of the labyrinth.
• Post-anginal septicaemia.
• Gradenigo syndrome, which consists of the following three features: sixth cra-
nial nerve palsy, deep prosopalgia originating from the fth cranial nerve and
suppurative otitis media. Gradenigo syndrome arises because of inammation of
the petrous temporal bone.
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The following complications may arise from intracranial extension of mastoid
inammation
• Extension of infection to the meninges. Abscess formation within the epidural
space, the temporal lobe or elsewhere in the brain. Empyema formation under
the dura mater. Abscess formation in the subperiosteum.
• Thrombus formation within the sinuses of the dura mater.
References
1. Glynn F, Osman L, Colreavy M, Rowley H, Dwyer TP, Blayney A.Acute mastoiditis in children: presentation and long term consequences. J Laryngol Otol. 2008;122(3):233–7.
2. Brook I.Pediatric mastoiditis. In: Steele RW, editor. Medscape; 2021. https://emedicine.med-
scape.com/article/966099- overview. Accessed 11 Feb 2022.
3. Wald ER.Acute mastoiditis in children: treatment and prevention. In: Kaplan SL, Messner
AH, Armsby C, editors. . UpToDate; 2019.
4. Bluestone CD, Klein JO. Intratemporal complications and sequelae of otitis media. In:
Bluestone CD, Casselbrant ML, Stool SE, et al., editors. Pediatric otolaryngology. 4th ed.
Philadelphia: Saunders; 2003. p.687.
5. Holt GR, Gates GA.Masked mastoiditis. Laryngoscope. 1983;93:1034.
6. Leibovitz E.Complicated otitis media and its implications. Vaccine. 2008;26(Suppl 7):G16–9.
7. Jung TT, Alper CM, Hellstrom SO, Hunter LL, Casselbrant ML, Groth A, et al. Panel 8:
Complications and sequelae. Otolaryngol Head Neck Surg. 2013;148(4 Suppl):E122–43.
8. Laulajainen-Hongisto A, Saat R, Lempinen L, Aarnisalo AA, Jero J. Children hospitalized
due to acute otitis media: how does this condition differ from acute mastoiditis? Int J Pediatr
Otorhinolaryngol. 2015;79(9):1429–35.
9. Kaplan SL, Mason EO, Wald ER, et al. Pneumococcal mastoiditis in children. Pediatrics.
2000;106(4):695–9.
10. Gorphe P, de Barros A, Choussy O, Dehesdin D, Marie JP.Acute mastoiditis in children: 10
years experience in a French tertiary university referral center. Eur Arch Otorhinolaryngol.
2012;269(2):455–60.
11. Brook I.Fusobacterial infections in children. Curr Infect Dis Rep. 2013;15(3):288–94.
12. Brook I.Role of methicillin-resistant Staphylococcus aureus in head and neck infections. J
Laryngol Otol. 2009;123(12):1301–7.
13. Brook I. The role of anaerobic bacteria in acute and chronic mastoiditis. Anaerobe.
2005;11(5):252–7.
14. Shamriz O, Engelhard D, Temper V, Revel-Vilk S, Benenson S, Brooks R, et al. Infections
caused by Fusobacterium in children: a 14-year single-center experience. Infection.
2015;43(6):663–70.
15. Yarden-Bilavsky H, Raveh E, Livni G, Scheuerman O, Amir J, Bilavsky E. Fusobacterium
necrophorum mastoiditis in children—emerging pathogen in an old disease. Int J Pediatr
Otorhinolaryngol. 2013;77(1):92–6.
16. Brook I.The role of beta-lactamase-producing-bacteria in mixed infections. BMC Infect Dis.
2009;14(9):202.
17. Nguyen JT, Challapalli M, McElheny K, Fridirici Z. Blastomycosis presenting as isolated
otitis and otomastoiditis. Pediatr Infect Dis J. 2013;32(3):301–2.
18. Mongkolrattanothai K, Oram R, Redleaf M, Bova J, Englund JA.Tuberculous otitis media with
mastoiditis and central nervous system involvement. Pediatr Infect Dis J. 2003;22(5):453–6.
19. Bal ZS, Sen S, Yildiz KB, Ciftdogan DY, Vardar F.Tuberculous otomastoiditis complicated by
sinus vein thrombosis. Braz J Infect Dis. 2012;16(6):608–9.
20. van den Aardweg MT, Rovers MM, de Ru JA, Albers FW, Schilder AG.A systematic review of
diagnostic criteria for acute mastoiditis in children. Otol Neurotol. 2008;29(6):751–7.
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21. Vazquez E, Castellote A, Piqueras J, etal. Imaging of complications of acute mastoiditis in
children. Radiographics. 2003;23(2):359–72.
22. Luntz M, Brodsky A, Nusem S, etal. Acute mastoiditis—the antibiotic era: a multicenter
study. Int J Pediatr Otorhinolaryngol. 2001;57:1.
23. Geva A, Oestreicher-Kedem Y, Fishman G, etal. Conservative management of acute mastoiditis in children. Int J Pediatr Otorhinolaryngol. 2008;72:629.
24. Lin HW, Shargorodsky J, Gopen Q.Clinical strategies for the management of acute mastoiditis
in the pediatric population. Clin Pediatr (Phila). 2010;49:110.
25. Zanetti D, Nassif N.Indications for surgery in acute mastoiditis and their complications in
children. Int J Pediatr Otorhinolaryngol. 2006;70:1175.
26. Cincinnati Children’s Hospital Medical Center. (Guideline) Evidence based clinical practice
guideline for medical management of acute otitis media in children 2 months to 13 years of
age. 2004.
27. Fischer JB, Prout A, Blackwood RA, Warrier K.Lemierre syndrome presenting as acute mastoiditis in a 2-year-old girl with congenital dwarsm. Infect Dis Rep. 2015;7(2):5922.
A. Karaogullarindan et al.
Labyrinthitis inChildren andHearing
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Loss
MehmetErkanKaplama, NurayBayar Muluk,
andMarioMilkov
20.1 Introduction
Labyrinthitis refers to inammation occurring in the labyrinth/inner ear. The clinical presentation involves symptoms of disordered balance and auditory impairment,
which may vary in severity. It may be uni- or bilateral. Labyrinthitis may be triggered by bacterial or viral pathogens and occurs in the context of a local or systemic
infection. Another potential cause is autoimmunity. Interruption to the blood supply
of the labyrinth may cause symptoms that closely resemble labyrinthitis [1].
20.2 Aetiology
20
To appreciate the pathophysiological mechanism of labyrinthitis, it is vital to know
the anatomy of the labyrinth and adjoining structures, namely the middle ear cavity,
mastoid and subarachnoid space. The inner ear consists of an external bony framework that protects the fragile arrangement of membranes constituting the sense
organs that allow for auditory perception and equilibrioception [1].
M. E. Kaplama (*)
Department of Otorhinolaryngology, Private Sanmed Hospital, Sanliurfa, Türkiye
e-mail: drmehmeterkan@yahoo.com
N. Bayar Muluk
Department of Otorhinolaryngology, Faculty of Medicine, Kırıkkale University,
Kırıkkale, Türkiye
e-mail: nbayarmuluk@yahoo.com
M. Milkov
Department of Otorhinolaryngology, Faculty of Medicine, Varna University, Varna, Bulgaria
e-mail: mario.milkov@gmail.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_20
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The organs of perception consist of the utricle, saccule, semicircular canals and
cochlea. Inammation within the labyrinth results from invasion by pathogenic
microbes or mediators of inammation into the labyrinthine membranes. This then
causes injury to the vestibular and auditory organs [1].
The inner ear is contained by the petrous temporal bone and lies next to the mastoid air cells. The communication with the middle ear cavity is via the round and
oval windows. The internal acoustic meatus and canaliculus provide communication with the brain and the leptomeningeal space. Bacterial pathogens may invade
the membranous labyrinth by this route or via a defect in the osseous labyrinth,
which may have been present since birth or formed later. Viral pathogens reach the
inner ear either via the bloodstream or through the canaliculus and internal acoustic
meatus [1].
M. E. Kaplama et al.
20.2.1 Causative Viral andBacterial Pathogens
There is a lack of direct experimental conrmation that viruses cause labyrinthitis.
Nonetheless, epidemiological data point towards several viral pathogens as likely
causes of labyrinthitis. Viral labyrinthitis frequently follows an infection of the
upper respiratory tract and may occur in outbreaks. On histopathological examination, the axons are degenerated within the vestibular nerve, and this implies that
vestibular neuritis results from a virus [2].
Bacterial pathogens implicated in cases of labyrinthitis are identical with those
causing meningitis and ear infections. If cholesteatoma is present, the pathogen
involved is frequently a Gram-negative bacterium [1].
There are a number of viruses that may be responsible for labyrinthitis, namely [1]
• Cytomegalovirus
• Mumps virus
• Varicella-zoster virus
• Rubeola virus
• Inuenza virus
• Parainuenza virus
• Rubella virus
• Herpes simplex virus 1
• Adenovirus
• Coxsackievirus
• Respiratory syncytial virus
There are also a number of bacteria that may be responsible for labyrinthitis,
namely [1]
• Streptococcus pneumoniae
• Haemophilus inuenzae
• Moraxella catarrhalis
• Neisseria meningitidis
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• Streptococcus species
• Staphylococcus species
• Proteus species
• Bacteroides species
• Escherichia coli
• Mycobacterium tuberculosis
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20.3 Classification
20.3.1 Viral Labyrinthitis
Both congenital and acquired deafness may result from a viral infection. The most
well-documented viruses responsible for congenital deafness are rubella and cytomegalovirus. If deafness occurs after birth, it is typically caused by mumps or measles. Viruses also appear likely to cause sudden sensorineural hearing loss (SNHL)
in idiopathic cases. Molecules expressed in inammation have been shown experimentally to feature signicantly in the pathological mechanism by which cytomegalovirus causes deafness [3].
Herpes zoster oticus, also termed Ramsay-Hunt syndrome, is a distinctive subtype of labyrinthitis occurring secondary to a viral infection. In this syndrome,
varicella- zoster virus, which has persisted from an earlier primary episode of infection, becomes active once more. It appears that the vestibulocochlear nerve is not
the only region affected, since the spiral and vestibular ganglia are also affected [4].
This viral reactivation causes paralysis of facial muscles, the eruption of vesicles
and, in around a quarter of cases, symptoms affecting hearing and balance [5].
20.3.1.1 Vestibular Neuritis
There are several synonyms used for vestibular neuritis, namely vestibular neuronitis, labyrinthitis, neurolabyrinthitis and acute peripheral vestibulopathy [6]. This
condition resolves spontaneously and entirely in the majority of cases. However,
patients with this condition may suffer briey from limitations caused by the
unpleasant symptoms. Patients complain of vertigo, feeling they are about to vomit
or actual vomiting and difculty in walking [7].
There is an overlap between the presentation of vestibular neuritis and other
conditions with a graver prognosis, especially ischaemic events affecting the brain.
It is vital that these more serious conditions are not misdiagnosed as vestibular neuritis, since failure to recognise them may lead to excessive morbidity or patient
death [7].
The clinical picture of vestibular neuritis is a condition that occurs suddenly,
without warning and affects the peripheral vestibular nerve. The patient suffers sudden vertigo, which is severe and accompanied by nausea, vomiting and difculty
walking without falling. Although vertigo in adults is often attributable to vestibular
neuritis, this is not so for children. Patients demonstrate a preference for lying
motionless on the opposite side from the lesion. Auditory impairment does not
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M. E. Kaplama et al.
result from vestibular neuritis. The aetiology has been hypothesised to involve a
post-viral inammatory response or an infection of the vestibular nerve caused by
mumps, measles, Epstein-Barr virus or herpesvirus. One problem with this hypothesis is that under 50% of cases are found in patients where a recent infection with a
virus has occurred. The duration of symptoms is between weeks and months [8].
Labyrinthitis is a subtype of vestibular neuritis, which appears as acute deafness
accompanied by vertigo. The aetiology is infection affecting the inner ear due to a
pathogenic virus or bacterium. Labyrinthitis may be seen in isolation or following a
middle ear infection or meningitis. Auditory impairment in some cases does not
recover [8].
Pathophysiology
Although vestibular neuritis is typically described as inammation, which involves
the vestibular division of the vestibulocochlear nerve [6], there is little evidence
available to conrm this is what actually occurs in patients. Indeed, below 50% of
cases can be linked to a viral infection before symptoms began [9–12]. A study that
used magnetic resonance imaging scans as evidence found that 20 out of 29 cases
diagnosed as vestibular neuritis exhibited enhanced lesions consistent with the putative pathogenetic mechanism [13].
Clinical Presentation
Symptoms of vestibular neuritis include an abruptly beginning vertigo of high
severity that leaves patients unstable when walking and is accompanied by nausea
and vomiting. It is an acute syndrome that occurs without warning and affects
peripheral balance [7].
On physical examination, a picture of acutely disturbed balance is noted,
namely [7]
• Unprovoked vestibular nystagmus that occurs to one side, in a horizontal direc-
tion, or horizontal plus rotary nystagmus. If the gaze is xed, nystagmus disap-
pears. The direction of nystagmus is not affected by where the patient is looking.
The rapid phase of nystagmus is towards the unaffected ear.
• Positivity of head impulse testing. The physician turns the head swiftly in the
direction of the affected ear, and the patient cannot keep their gaze xed on one
spot. A cases series found positivity of the test in 82% of cases [14]. Positivity of
this test correlated with symptoms that endured for longer than average. Although
positivity of the sign does correlate with vestibular neuritis, it may also occur
with other conditions affecting the central nervous system [15].
• Patients can walk, albeit they are highly unstable. Any swaying or tendency to
fall is on the side of the lesion, hence also in the direction of the rapid phase of
nystagmus [7].
• There should be no other signs or symptoms indicating a nervous system disorder.
Thus, the patient should not be dysarthric; unable to swallow; have weakness of the
limbs, perceptual decits and drooping of the face; or exhibit limb dysmetria.
Although some patients do have double vision in a vertical direction or skew devia-
tion, this nding should make the clinician suspect a cerebrovascular accident [7].
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Diagnosis
Diagnosis is clinical, with no test that can rule vestibular neuritis out or in. The
patient should present with features of an abrupt onset vestibular syndrome. The
ndings on physical examination have been discussed in the preceding section.
Where physical examination suggests features that are not consistent with a
peripheral syndrome, imaging of the central nervous system is warranted. This
applies where the patient is at an elevated likelihood of suffering a cerebrovascular
accident, focal neurology is present or a new onset headache occurs with vertigo
[10, 16]. Thus, the diagnosis is most likely in a young individual whose examination
reveals a peripheral nervous disorder, exhibits nystagmus, has no other features of a
nervous system lesion, and describes vertigo that begins suddenly and persists [10].
The ideal investigation is magnetic resonance imaging (MRI) with diffusion
weighting (DWI) or MR angiography. Diffusion-weighted MRI is able to identify
infarcted brain in the posterior fossa within 24h of the triggering event. MR angiography is excellent for detecting vascular lesions within the posterior circulation,
such as stenotic or occluded vessels. It is more than 95% sensitive and specic for
this purpose [17]. Diffusion-weighted MRI may not at rst reveal a cerebrovascular
accident in the brain stem or cerebellum, if it is small and the investigation may
need to be performed again 3days after symptoms began, should a central lesion
still seem likely. This second study should have perfusion-weighted sequences
where feasible [18, 19].
If MRI is not an option (e.g. in a patient with a metal implanted device), CT may
be used, with slices placed close to each other. If CT is performed within 60min of
infarction, the appearances do not reveal any abnormality. If there has been bleeding
into the parenchyma or a degree of swelling sufcient to cause fourth ventricular
compression, this abnormality is generally visible from an early stage. In a case
where a scan of the CNS is called for, if MRI will be delayed, CT imaging should
be undertaken without delay [7].
Therapy
There are several therapeutic options in cases of vestibular neuritis, such as direct
treatment of the disorder using steroids and antiviral medication, treatment aiming
to mitigate symptoms and vestibular rehabilitation therapy. There is limited trial
evidence to conrm the efcacy of such approaches in vestibular neuritis [7].
Direct Treatment of Vestibular Neuritis Steroids administered during the acute
phase of labyrinthitis have proven benet in restoring peripheral balance, according
to the results of a single trial. Nonetheless, several studies have since failed to replicate this nding. These more recent studies, however, suffered from several weaknesses [7].
Although the evidence base does not permit a denite conclusion on the clinical
efcacy of steroids in acute vestibular neuritis of presumed viral aetiology, this
approach appears defensible, provided the treatment is not contraindicated.
Similarly, if there is a heightened risk of side effects, withholding this treatment also
seems appropriate [7].
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Palliative Treatment It is common to employ palliative methods to lessen vertigo,
nausea and vomiting within the initial days after the onset of vestibular neuritis.
Palliative agents suitable for this purpose are antiemetics and antihistamines. It is
usually best not to supply oral agents, due to vomiting. Start at a minimal dose and
increase until the desired effect is achieved [7].
Vestibular Rehabilitation Based on the scores used to measure symptomatic
severity and functional balance in cases where peripheral damage to the vestibular
system has occurred on one side, vestibular rehabilitation may be considered benecial [20]. There is considerable clinical experience, too, showing that this treatment
results in signicant benet.
M. E. Kaplama et al.
20.3.2 Bacterial Labyrinthitis
Bacterial labyrinthitis may be a complication of infection of the meninges or middle
ear and occurs by two mechanisms: in suppurative cases, the pathogens themselves
enter the inner ear; in serous cases, it is the entry of toxins synthesised by the bacterium or inammatory signalling molecules that trigger the condition. The most frequently occurring complication of a middle ear infection is actually labyrinthitis,
which may represent 32% of all complications, whether intra- or extracranial,
according to a single study [21].
Whilst bacterial labyrinthitis is seldom seen since antibiotics have become
widely available, deafness is still often the outcome following meningitis [21]. Up
to 20% of paediatric cases of meningitis feature symptoms related to balance and
hearing [22]. In cases of meningitis, the symptoms are usually bilateral, in contrast
to ear infections, which usually only affect one side [1].
20.3.2.1 Suppurative Labyrinthitis
Bacterial infection can track into the membranous labyrinth via the internal acoustic
meatus or cochlear aqueduct from the cerebrospinal uid when meningitis is present. For bacteria causing otitis media or mastoiditis to reach the inner ear, there is
usually dehiscence of the horizontal semicircular canal [23]. This crack in the bone
typically occurs because of encroachment by cholesteatoma. Suppurative infection
of the labyrinth occurring as a complication of middle ear infection is rare now that
efcient antimicrobial treatments are available. Indeed, when seen, it is virtually
invariably accompanied by cholesteatoma. Bacterial labyrinthitis frequently causes
almost complete deafness, vertigo of high severity, ataxia, nausea and vomiting [1].
20.3.3 Serous Labyrinthitis
In cases of serous labyrinthitis, there are no actual pathogens within the inner ear.
Instead, bacteriotoxins, inammatory signalling molecules or complement proteins
traverse the round window, setting up an inammatory reaction in the labyrinth
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