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20 Labyrinthitis inChildren andHearing Loss
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[24]. Serous labyrinthitis occurs in association with acute or chronic otitis media. It
is considered amongst the most frequent ways a middle ear infection may be
complicated.
Bacteriotoxins or mediators of inammation enter the tympanic duct and are
deposited at a point slightly medial to the round window. When these molecules
diffuse into the endolymph at the base of the cochlea, auditory impairment results.
This impairment is of sensorineural type and affects high-pitched sounds to a mild
or moderate degree [1].
If an effusion exists within the middle ear cavity, audiometry will show auditory
impairment of mixed type. Problems with balance are possible, but not as frequent.
The therapeutic goal in such cases is to eradicate any pathogen and drain the effusion. Auditory impairment is generally temporary but may become chronic if the ear
infection is not treated [1].
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20.3.4 Autoimmune Labyrinthitis
Rarely autoimmune labyrinthitis occurs, resulting in auditory impairment of sensorineural type. It may be localised to the labyrinth or be part of a systemic autoimmune condition, such as granulomatosis with polyangiitis or polyarteritis nodosa
[25, 26].
20.4 Prognosis
Although vertigo, nausea and vomiting symptoms in cases of labyrinthitis cease
within days or weeks, regardless of cause, the extent to which auditory impairment
resolves is less predictable [1].
Suppurative labyrinthitis virtually invariably causes permanent, almost complete
deafness. However, where deafness is secondary to viral infection, the auditory
impairment may resolve. Derangement of balance and position-related vertigo may
persist for some weeks after the acute infective episode has ended [1].
20.4.1 Morbidity andMortality
There is no association between labyrinthitis and mortality unless the condition is
secondary to meningitis or severe septicaemia. However, labyrinthitis does cause
considerable morbidity, particularly when its cause is bacterial [1].
Bacterial labyrinthitis (irrespective of the pathogen involved) is responsible for
one in three cases of acquired deafness.
It is estimated that between 10 and 20% of children with meningitis will suffer
permanent auditory impairment [22, 27]. According to one study, the risk of vertigo
in cases of meningitis resulting from infection with Streptococcus pneumoniae is
23% [28].
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Around 6% of cases of Ramsay-Hunt syndrome who have deafness at presentation go on to have permanent auditory loss of sensorineural type [23]. Pneumococcal
infection seems to be the most common reason for deafness to occur following
meningitis [29].
M. E. Kaplama et al.
20.5 Diagnosis
20.5.1 History
A detailed patient account encompassing symptomatology, past medical history and
drug history is vital for a diagnosis of labyrinthitis in a case presenting with vertigo
or acquired deafness. The following symptoms should be carefully enquired
about [1]:
• Vertigo—onset and length it persists. Whether its intensity varies when moving
the body or head and its general character
• Deafness. One or two-sided, severity, length of time present and other features
• Feeling the ear is full
• Tinnitus
• Ear discharge
• Earache
• Nausea or vomiting
• Pyrexia
• Paresis of facial muscles or asymmetrical expression
• Nuchal pain or rigidity
• Symptoms suggestive of an upper respiratory tract either before or currently
• Alteration in vision
Items to take particular note of when obtaining the patient’s past medical history include the following [1]
• Vertigo and auditory problems
• Infective episodes
• Contact with sick individuals
• Otological operations
• Blood pressure problems (hyper- or hypo-tension)
• Diabetes mellitus
• Cerebrovascular accident
• Migraine
• Traumatic injury to the head or neck
• History of auditory impairment or otological disorder in a family member
It is also important to check the patient’s drug history, in particular exposure
to [1]
• Aminoglycosides or other agents of known ototoxicity
• Beta-blockers or other blood pressure medications
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• Sedatives, such as benzodiazepines
• Epilepsy drugs
• Alcohol
• Illicit substances
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20.5.1.1 Physical Examination
The patient’s head and neck should be thoroughly examined, paying particular
attention to examining the ears, eyes and cranial nerves. An abbreviated examination of the nervous system is likewise called for. If meningitis is suspected, look for
signs that may conrm the diagnosis [1].
The ears should be examined in the following manner [1]
• Examine the external ear, looking for evidence of mastoiditis, cellulitis and pre-
vious otological procedures.
• Inspection of the external auditory meatus may reveal otitis externa, ear dis-
charge or vesicles.
• When evaluating the eardrum and middle ear, look for a perforated membrane,
cholesteatoma, middle ear effusion or an acute middle ear infection.
The eyes should be examined in the following manner [1]
• Check the eyes’ range of movement and how the pupils respond.
• Use the ophthalmoscope to check for papilloedema.
• Check for nystagmus and how it is provoked (spontaneously, provoked by look-
ing in one direction, related to position). If tolerated, undertake the Dix-Hallpike
manoeuvre.
• If vision is impaired, seek an ophthalmological opinion.
The nervous system should be examined in the following manner [1]
• Test each of the cranial nerves.
• Evaluation of balance uses Romberg testing and hell-to-toe walking.
20.5.2 Audiographic Assessment
Every patient with suspected labyrinthitis should have an audiogram performed.
Assessment of patients who are markedly unwell or suffer severe vertigo can be
undertaken when their condition stabilises and testing is bearable. There are clues to
the type of labyrinthitis revealed by the audiogram. Inammation of the inner ear
secondary to a middle ear infection will probably produce an audiogram showing
impairment of mixed type. A viral cause usually results in audiometric evidence for
sensorineural deafness. If audiometry cannot be undertaken in a particular patient,
alternative investigations of value are otoacoustic emissions testing and auditory
brain stem responses [1].
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Labyrinthitis of viral origin produces sensorineural pattern auditory impairment
on the side of the lesion, with higher-pitched sounds usually, but not invariably,
affected and of mild or moderate severity.
Suppurative labyrinthitis secondary to a bacterial infection causes deafness on
the affected sound that is of severe or profound degree. Where meningitis occurs,
both ears are frequently deaf. Serous labyrinthitis secondary to a bacterial infection
affects one ear and causes impairment in the ability to perceive higher frequencies.
An effusion may result auditory impairment of conductive type on the affected
ear [1].
M. E. Kaplama et al.
20.5.3 Imaging Studies
20.5.3.1 Computed Tomography (CT)
If meningitis is suspected, CT may be advisable prior to performing a lumbar puncture. This investigation is also benecial in excluding a diagnosis of mastoiditis.
Scanning of the temporal bone helps treatment planning for cases where labyrinthitis occurs in conjunction with cholesteatoma.
CT without the use of a contrast agent is the most helpful method to image brosis and calcication within the membranous labyrinth in cases where labyrinthitis
has become chronic or is of the ossicans type [1].
20.5.3.2 Magnetic Resonance Imaging (MRI)
MRI is a helpful investigation where there are certain competing diagnoses to
explain vertigo and deafness, such as acoustic neuroma, cerebrovascular accident,
cerebral abscess or epidural haematoma.
T1-weighting on MRI exhibit enhancement of the cochlea, vestibule and semicircular canals after injection of contrast if the diagnosis is labyrinthitis, whether
acute or subacute [30]. These appearances have high specicity and match the
results of the history and examination. MRI with contrast is being steadily rened,
and this may become the ideal investigation in labyrinthitis in the future [31].
Tumours within the cochlea can be differentiated from other conditions affecting
the labyrinth, such as inammation, on the basis of how intensely they enhance with
gadolinium-based contrast [32].
20.6 Therapy
20.6.1 Viral Labyrinthitis
Viral labyrinthitis patients should be advised to rest in bed and maintain adequate
hydration. The majority of these cases do not require hospital admission. They
should, nonetheless, be warned that if fresh symptoms appear, such as double vision,
unclear speech, problems walking, paresis or paraesthesia, they should urgently
seek medical attention. If patients are severely nauseous or vomit frequently, intravenous hydration and antiemetic agents may be benecial [1].
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20.6.2 Bacterial Labyrinthitis
The choice of antimicrobial therapy is guided by the results of bacteriological culture and susceptibility tests. Therapeutic aims in suppurative labyrinthitis are eradication of the pathogen, support for the patient, drainage of any effusion in the
middle ear or mastoid and ensuring the infection remains contained [1].
20.6.3 Surgical Interventions
For patients where labyrinthitis is secondary to a middle ear infection, myringotomy
should be carried out and any effusion drained. Grommets may need to be inserted.
Aspirated uid should be sent to the laboratory for microscopy, culture and susceptibility testing.
In cases of mastoiditis or cholesteatoma, a mastoidectomy is indicated, which
drains and debrides the area [1].
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9. Rujescu D, Hartmann AM, Giegling I, etal. Genome-wide association study in vestibular neuritis: involvement of the host factor for HSV-1 replication. Front Neurol. 2018;9:591.
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11. Dix MR, Hallpike CS.The pathology symptomatology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med. 1952;45:341.
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13. Byun H, Chung JH, Lee SH, etal. Clinical value of 4-h delayed gadolinium-enhanced 3D
FLAIR MR images in acute vestibular neuritis. Laryngoscope. 2018;128:1946.
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15. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ.Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008;70:2378.
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16. Lee DH, Kim WY, Shim BS, etal. Characteristics of central lesions in patients with dizziness
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18. Choi JH, Park MG, Choi SY, etal. Acute transient vestibular syndrome: prevalence of stroke
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19. Saber Tehrani AS, Kattah JC, Mantokoudis G, etal. Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms. Neurology. 2014;83:169.
20. McDonnell MN, Hillier SL.Vestibular rehabilitation for unilateral peripheral vestibular dysfunction. Cochrane Database Syst Rev. 2015;1:CD005397.
21. Wu JF, Jin Z, Yang JM, Liu YH, Duan ML.Extracranial and intracranial complications of otitis
media: 22-year clinical experience and analysis. Acta Otolaryngol. 2012;132(3):261–5.
22. Nadol JB Jr. Hearing loss as a sequela of meningitis. Laryngoscope. 1978;88(5):739–55.
23. Gulya AJ.Infections of the labyrinth. In: Bailey BJ, Johnson JT, Pillsbury HC, Tardy ME,
Kohut RI, editors. Head and neck surgery-otolaryngology, vol. 2. Philadelphia: JB Lippincott;
1993. p.1769–81.
24. Jang CH, Park SY, Wang PC.A case of tympanogenic labyrinthitis complicated by acute otitis
media. Yonsei Med J. 2005;46(1):161–5.
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26. Broughton SS, Meyerhoff WE, Cohen SB.Immune-mediated inner ear disease: 10-year experience. Semin Arthritis Rheum. 2004;34(2):544–8.
27. Woolley AL, Kirk KA, Neumann AM Jr, McWilliams SM, Murray J, Freind D.Risk factors for
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28. Bohr V, Paulson OB, Rasmussen N.Pneumococcal meningitis. Late neurologic sequelae and
features of prognostic impact. Arch Neurol. 1984;41(10):1045–9.
29. Kutz JW, Simon LM, Chennupati SK, Giannoni CM, Manolidis S. Clinical predictors for
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Laryngol. 1992;101(6):459–64.
31. Kopelovich JC, Germiller JA, Laury AM, Shah SS, Pollock AN.Early prediction of postmeningitic hearing loss in children using magnetic resonance imaging. Arch Otolaryngol Head
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Bacterial Meningitis inChildren
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andHearing Loss
ZümrütŞahbudak Bal, EminSamiArısoy,
andSheldonL.Kaplan
21.1 Introduction
Acute bacterial meningitis (ABM) is inammation of the meninges caused by bacteria or bacterial products. It is still one of the primary concerns for pediatricians
due to high morbidity and mortality in childhood [1, 2]. The World Health
Organization (WHO) estimates 170,000 deaths due to ABM annually [2]. Despite
appropriate and immediate antibiotic treatment, signicant morbidities such as neuropsychological decits, particularly hearing loss (HL), can occur.
Haemophilus inuenzae type b (Hib) was one of the most common microorganisms as the cause of ABM worldwide before the introduction of the conjugate Hib
vaccine into routine infant immunization globally. Streptococcus pneumoniae
became the most common causative pathogen in global invasive bacterial vaccinepreventable disease surveillance by WHO between 2014 and 2019 [2]. The highest
attributable mortality rate was also determined in patients with S. pneumoniae
21
Z. Şahbudak Bal (*)
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine, Ege
University, İzmir, Türkiye
e-mail: z.sahbudak@gmail.com
E. S. Arısoy
Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine,
Kocaeli University, Kocaeli, Türkiye
e-mail: emin.sami.arisoy@gmail.com
S. L. Kaplan
Division of Infectious Diseases, Department of Pediatrics, Baylor College of Medicine,
Houston, TX, USA
Infectious Disease Service, Texas Children’s Hospital, Houston, TX, USA
e-mail: slkaplan@texaschildrens.org
© 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_21
273
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meningitis. The pneumococcal conjugate vaccine (PCV)-7 has been available since
2000, followed by PCV-13 in 2010. Furthermore, a dramatic decline occurred in
ABM incidence after implementing conjugate Hib and pneumococcal vaccines into
infant immunization programs in many countries [3–10].
The United Kingdom (UK) licensed the rst meningococcal conjugate vaccine in 1999 [10]. In the following years, remarkable progress has been observed
with meningococcal vaccines worldwide, including in the meningitis belt of
Africa [11]. Today, a few quadrivalent meningococcal conjugate vaccines in
which the capsular polysaccharides from Neisseria meningitidis serogroups A,
C, W, and Y are conjugated to different carrier proteins are available, mainly in
middle- and high-income countries [12]. Neisseria meningitidis serogroup B
(MenB) has also been the leading cause of invasive meningococcal disease
(IMD) in several European countries [13]. Two meningococcal vaccines developed against serogroup B are widely available in several countries, and one of
them has been in use for infants and young children [12]. Various meningococcal
serogroup C conjugate vaccine formulations have also been available in Europe,
Canada, and other countries [12].
Acute bacterial meningitis still contributes to morbidities such as neuropsychological decits and mortality. Meanwhile, ABM is still one of the signicant causes
of HL during childhood. Therefore, it is crucial to implement vaccines against
S. pneumoniae, H. inuenzae type b, and N. meningitidis into national immunization programs worldwide to develop herd immunity and reduce ABM incidence.
Z. Şahbudak Bal et al.
21.2 Etiology andEpidemiology
The causative microorganisms of ABM vary according to the patient’s age, immunization status, socioeconomical factors, geographic region, and underlying conditions such as immunodeciency. In the neonatal period, the most common
etiologic pathogens are Streptococcus agalactiae (group B Streptococcus; GBS),
contributing to about half of the cases (50%), and Escherichia coli (20%) [13].
Screening and intrapartum antibiotic prophylaxis (IAP) have been implemented
for pregnant women with high-risk factors for GBS in several countries [14].
Other strategies, including mother GBS vaccination, have also been studied to
reduce bacterial translocation in mouse models [15]. A recent study using wholegenome sequencing showed that S. agalactiae serotype 1b sequence type 10
(ST10) carried a higher risk for neonatal meningitis [16]. The remaining rare
pathogens are Klebsiella spp., Enterococcus spp., Staphylococcus aureus, Listeria
monocytogenes, Streptococcus pyogenes (group A Streptococcus; GAS), and nontypeable H. inuenzae. Gram- negative pathogens, including E. coli and Klebsiella,
have been more common in low- and middle-income countries [17, 18]. A 7-year
retrospective study from Ethiopia showed that Klebsiella pneumoniae and E. coli
contributed nearly 60% of the causative pathogens, and S. agalactiae was the third
most common [18].
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275
Streptococcus pneumoniae (PCV and non-PCV serotypes), N. meningitidis,
rarely non-typeable H. inuenzae, and other rare bacterial pathogens are the leading
causes of ABM beyond the neonatal period [2]. After implementing the PCV-7
(serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F), a shift toward non-PCV serotypes was
observed. Following this shift, a 13-valent (additional serotypes 1, 3, 5, 6A, 7F,
19A) PCV (PCV-13) was implemented in 2010. However, despite the administration of PCV13, breakthrough cases were reported most frequently due to 3, 19A,
and 19F [19]. Pediatric meningitis surveillance in Southern and East African countries from 2008 to 2017 evaluated pathogens by using the polymerase chain reaction
(PCR) test, which determined a pathogen in 10% of 11,626 samples; S. pneumoniae
(7%) was the most common, followed by H. inuenzae (2%) and N. meningitidis
(1.5%) [20].
In high-income countries, S. pneumoniae and H. inuenzae meningitis have been
dramatically reduced through conjugate vaccines; N. meningitidis has become the
most common pathogen in some. The highest incidence of invasive meningococcal
disease (IMD) has been observed in the African meningitis belt [21]. Of 13N. men-
ingitis serogroups, six serogroups (A, B, C, W, X, Y, and Z) predominantly cause
IMD and show geographic and temporal variation [22]. Neisseria meningitis serogroup B has been the most common cause of IMD in the United States of America
(USA) and European countries. Six college outbreaks were observed in the USA
due to MenB between 2014 and 2016; a nearly four-fold increased risk was determined for college students versus non-college students [23]. Therefore, college students have been included in the risk group for MenB infection. Meningococcus
serogroup A (MenA) was predominant before the MenA conjugate vaccine was
developed for the African meningitis belt countries [24].
The global incidence of ABM declined after implementing Hib, PCV, and meningococcal vaccines into infant immunization programs, while deaths decreased by
21.0% from 1990 to 2016 [9]. The incidence of ABM signicantly decreased in the
USA, Greenland, European, high-income West Asian, and Latin American countries [25]. Invasive pneumococcal diseases, in general, also declined; however, the
decrease was not as remarkable as the infections caused by Hib due in part to an
increase in the incidence of non-PCV13 serotypes [19, 25]. Sub-Saharan African
countries in the meningitis belt still battle with ABM that meningococci cause seasonal meningitis outbreaks every 8–12years [26, 27].
The median age of patients with bacterial meningitis rose to 30–40years from
<5years, while the highest incidence of ABM is still in the neonatal period (81 per
100,000 population) [1, 13]. The leading causative pathogens of ABM are transmitted via respiratory droplets, and isolation procedures can alter transmission rates. A
recent prospective analysis of the effect of coronavirus disease 2019 (COVID-19)
containment measures showed a dramatic decline in invasive diseases due to
S. pneumoniae, H. inuenzae, and N. meningitidis in 26 countries in early 2020
(January 1 to May 31, 2020) [28]. However, pandemic restriction implementations
did not alter the incidence of S. agalactiae infections.
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Z. Şahbudak Bal et al.
21.3 Pathogenesis andPredisposing Risk Factors
Acute bacterial meningitis can occur from hematogenous spread, direct invasion
from adjacent sites, or rarely secondary to epidural and subdural spaces. Bacterial
entry induces the blood–brain barrier (BBB) to lead to a robust inammatory
response, including releasing cytokines, mainly tumor necrosis factor-alpha (TNFα), interleukin-1-beta (IL-1-β), and IL-6, and polymorphonuclear leukocyte (PMN)
transendothelial migration across the BBB [29, 30]. Several factors, such as capsule, cell-wall anchored proteins, neuraminidase A of S. pneumoniae and capsule,
type IV pili, and outer membrane proteins of N. meningitidis, are thought to contribute to leptomeningeal bacterial invasion by these pathogens [31].
Acute bacterial meningitis develops most commonly by two main routes of bacteria invading the central nervous system (CNS): (1) hematogenous, which can result
from (a) nasopharyngeal colonization followed by bacterial translocation to the bloodstream and CNS invasion, (b) another localized source causing bacteremia such as
translocation of enteric bacteria to the bloodstream and then CNS invasion, (c) transplacentally; (2) direct entry from adjacent sites (sinusitis, mastoiditis), trauma, or surgery resulting in cerebrospinal uid (CSF) leak or via medical devices (CSF shunts,
cochlear implants), via dermoid sinus tracts and meningomyelocele [1, 30].
Well-described predisposing risk factors for specic pathogens are as follows
[1, 32]:
Streptococcus pneumoniae: Splenectomy or with a hyposplenic state, chronic kid-
ney or liver disease, human immunodeciency virus (HIV) infection, hypogam-
maglobulinemia, anatomic defects resulting CSF leak (surgery or fracture),
presence of a cochlear implant.
Neisseria meningitidis: Complement system deciencies, a recent visit to an
endemic country (African meningitis belt countries).
Haemophilus inuenzae: Hypogammaglobulinemia, splenectomy, or with a
hyposplenic state.
21.4 Clinical Manifestations
Clinical manifestations are nonspecic in the neonatal period, including poor feeding, vomiting, hypothermia, hyperthermia, abdominal distension, respiratory distress, bulging fontanel, and lethargy [1, 30]. Fever and seizure are the most frequent
manifestations in neonates [30].
Beyond the neonatal period, the classic triad of bacterial meningitis includes
fever, neck stiffness, and altered mental status (e.g., confusion, lethargy, and irritability). However, the classic triad occurs in 40–50% of the patients [30]. Other
symptoms may include headache, photophobia, nausea, and vomiting. Meningeal
irritation signs include neck stiffness, Kerning, and Brudzinski signs, which may be
present in 60–80% of the children with ABM [1]. Neck stiffness is the most common meningeal sign, particularly in younger children.
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