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Meningococcal Infections inChildren
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andHearing Loss
EnerÇağrıDinleyici, EminSamiArısoy,
andSheldonL.Kaplan
29.1 Introduction
Invasive meningococcal disease (IMD) is one of the leading causes of infectious
disease morbidity and mortality worldwide [1]. With over 1.2 million cases reported
annually, IMD is a foremost global public health concern [2]. Despite improve-
ments in intensive care facilities, 10% of patients die (case fatality rates range from
5% to 20%) and 20% have serious sequelae that can affect their life [1, 3–5]. Factors
such as the host characteristics, the invasiveness of the causative serogroup, availability of treatment, intensive care facilities, and disease follow-up all play a role in
the prognosis and mortality of IMD [3, 4, 6]. Due to the disease’s high mortality,
severe and lifelong sequelae in surviving patients, the sudden onset of the disease,
and its rapid course, it has been highlighted as a vaccine-preventable disease, and
vaccination studies have been recommended [1].
29
E. Ç. Dinleyici (*)
Division of Pediatric Intensive Care, Department of Pediatrics, Faculty of Medicine,
Eskişehir Osmangazi University, Eskişehir, Türkiye
e-mail: enercagri@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_29
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29.2 Etiology andEpidemiology
Humans are the only reservoir for Neisseria meningitidis. Infection is transmitted
through respiratory droplets. The meningococci are colonized on the nasopharyngeal mucosa and then can enter the bloodstream and spread to the meninges (meningitis), the entire body (meningococcemia), or both. The symptoms vary from
moderate nonspecic ones to multi-organ failure [7]. Although N. meningitidis has
12 serogroups based on its capsular polysaccharide antigenic structure, the most
common serogroups are A, B, C, Y, W, and X [1]. Over the years, the serogroup
epidemiology of IMD may differ from country to country and even from region to
region within the same country. The routine use of meningococcal vaccines is
another factor inuencing seroepidemiology [1, 8, 9].
29.3 Risk Factors
The patient’s age has been recognized as the most critical risk factor for
IMD.According to reports, 35–40% of meningococcal disease is seen in children
under the age of 5years old (particularly <1year), mainly due to low serum bactericidal antibodies [4, 9]. Adolescents and young adults between the ages of 15 and
24years old are the second age group at risk for IMD, primarily due to school and
social habits [4]. Although several conditions have been linked to an increased risk
of IMD, in more than 90% of cases, no underlying disease or risk factor exists
[10, 11].
The incidence of IMD (250–600 times higher) and recurrence probability is
increased in people with complement (C)-5-C9 and properdin deciencies in the
complement pathway [12]. In recent years, it has been shown that eculizumab treatment, used to treat many diseases in children and adults, especially in treating atypical hemolytic syndrome and paroxysmal nocturnal hemoglobinuria, causes a
signicant increase in the risk of IMD [1]. Human immunodeciency virus (HIV)
infection increases the IMD risk 10 times [1]. Anatomical or functional asplenia is
another important risk factor for IMD, as it is for all encapsulated bacteria [7].
Staying in dormitories for the rst year at universities, spending time in public areas
such as camps, festivals, and military units, traveling to places where the disease is
endemic, such as Hajj and Umrah, crowded home environments, active or passive
smoking, preceding respiratory tract infections, such as inuenza, respiratory syncytial virus (RSV), and mycoplasma, are among the other risk factors [1, 8, 9, 13].
29.4 Clinical Manifestations
Meningococcal meningitis, meningococcemia, and meningococcemia with meningitis are the most typical clinical presentations of IMD.It is challenging to diagnose
the illness at the initial stage since the early symptoms, including sudden onset of
fever, nausea, vomiting, headache, and muscular aches, are nonspecic and may
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resemble those of an upper respiratory tract infection. In some studies, patients have
been admitted to the hospital within less than 22h when symptoms rst appeared;
in children under 5years, this was 13–14h [7, 14, 15].
Meningococcal meningitis is characterized by abrupt onset of fever, nausea,
vomiting, headache, changes in consciousness, and myalgia as presenting symptoms. The early clinical signs may be mistaken for an inuenza infection if symptoms occur in the nal months of the winter season. Non-blanching rashes may be
present in two-thirds of patients. Fever, headaches, photophobia, nausea, vomiting,
confusion, lethargic behavior, and changes in consciousness are the most typical
symptoms in older children. Twenty percent of cases have been reported to have had
seizures. Most times, there is no history of contact with the meningococcal illness.
Meningococcemia may accompany meningitis.
Meningococcal meningitis and meningococcemia are characterized by a rapid
progression of symptoms, a decline in general health, and the potential for shock.
Leg pain, numbness in the hands and feet, abrupt changes in skin color, and the
appearance of a rash are all considered warning signs of meningococcemia in children with meningococcal meningitis [7, 14, 16].
Fever and a non-blanching rash are the most typical meningococcemia presenting symptoms in children. Although the rash initially looks like maculopapular
rashes, it has the potential to develop into petechiae and ecchymosis within minutes
to hours. It has been seen that initially, sparse petechiae quickly increase in number
within minutes or hours to become ecchymoses. The degree of thrombocytopenia
and the emergence of disseminated intravascular coagulation are directly correlated
with petechiae occurrence. Additionally, the conjunctiva and soft palate may bleed.
Initial clinical symptoms of meningococcemia include leg pain, numbness in the
hands and feet, and skin discoloration (mottled appearance with signs of circulatory
dysfunction). The patient may experience nonspecic symptoms at the onset of the
illness, such as fever, headache, myalgia, and signs of an upper respiratory infection
that looks like the u; shock could occur within hours.
Patients with IMD due to serogroup W present gastrointestinal symptoms, particularly diarrhea, abdominal pain, and in some cases, an acute abdomen. Rapidly
developing symptoms are commonly reported, including tachypnea, sweating,
tachycardia, hypotension, extended capillary lling time, and oliguria related to
shock. Unconsciousness and coma might be seen depending on the decline in cerebral perfusion. The development of hypotension not responsive to uids or vasoactive agents and multiple organ failure are risk factors for mortality.
Purpura fulminans occurs in 15–25% of patients with meningococcemia.
Necrosis may spread to the deep tissues and then to the muscles and bones, resulting
in signicant loss of tissue and organs. Most fatality occurrences have been reported
to occur within the rst 12–48h after the onset of illness [7, 14, 17, 18].
Pneumonia, arthritis, purulent pericarditis, endophthalmitis, primary peritonitis,
urethritis, and osteomyelitis are other illnesses linked to meningococcal infections.
Ten percent of meningococcal infections result in meningococcal arthritis, which
frequently affects the knee joint. Immune complex arthritis brought on by
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meningococcal infection typically affects multiple joints and has onset later in the
course of illness compared with true septic arthritis caused by N. meningitidis [7].
E. Ç. Dinleyici et al.
29.5 Diagnosis andLaboratory Findings
Early diagnosis of IMD is attainable with suspicion based on the history and clinical
ndings. Because of the disease’s potential effects on the general public’s health,
detection or isolation of N. meningitidis is also crucial. Leukopenia or leukocytosis,
anemia, thrombocytopenia, proteinuria, and hematuria might be detected in IMD
with routine laboratory testing. Even when the disease progresses quickly in the
beginning, the erythrocyte sedimentation rate and serum C-reactive protein levels
may be high. Hypoalbuminemia, hypocalcemia, hypokalemia, hypomagnesemia,
hypophosphatemia, hypoglycemia, metabolic acidosis, and lactate elevation might
be observed. The majority of cases have coagulation problems related to disseminated intravascular coagulation. Computed cranial tomography can detect cerebral
bleeding and/or high intracranial pressure syndrome in meningococcal infections,
followed by loss of consciousness [7, 14, 16, 18].
The gold standard for diagnosis of IMD is the presence of the N. meningitidis in
blood, cerebrospinal uid (CSF), or other sterile bodily uids, such as joint uid,
pleural or pericardial uid, or samples taken from petechiae or purpura lesions.
Gram staining in samples collected from skin lesions or buffy-coat can show gramnegative diplococci. Patients who have taken antibiotics have a lesser chance of the
agent being isolated in blood culture samples, and negative ndings are frequently
obtained. In these situations, a polymerase chain reaction (PCR) test can be used to
demonstrate N. meningitidis within 4–8h and determine the serogroup. Syndromic
test panels (meningitis or sepsis) have been popular in recent years as tools for the
early detection of disease [7, 19]. Analysis and culture of CSF are required to conrm the diagnosis of meningococcal meningitis. Thus, lumbar puncture (LP) should
be performed in patients for whom a diagnosis of meningococcal meningitis is suspected as long as there are no contraindications for this procedure. Gram staining of
the CSF may reveal gram-negative diplococci along with cytochemical results
(increased neutrophil count in CSF, increased CSF protein concentration, and
reduced CSF glucose concentration), supporting the diagnosis of bacterial meningitis. Cerebrospinal uid Gram staining yields a positive result in 75–80% of untreated
cases; the test’s specicity is 97%. Rarely, CSF results are within normal limits in a
patient with meningococcal meningitis; in such instances, CSF cultures may be
positive, or diplococci might be found on CSF Gram stain in cases where CSF culture is negative [7, 15].
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29.6 Treatment
In cases with clinical suspicion of IMD, if possible, empirical third generation cephalosporin treatment, primarily ceftriaxone or cefotaxime, should be initiated after
culture samples are taken. Considering that N. meningitidis is transmitted by droplets, it is crucial to take isolation precautions. In regions where pneumococcal meningitis cannot be excluded, and penicillin and ceftriaxone resistance have been
reported in regional pneumococcal isolates, it is recommended to add vancomycin
to the treatment. Antibiotic treatment is usually recommended for 7 days.
Vancomycin therapy should be discontinued in proven cases with N. meningitidis
[7, 15, 18].
Rapid evaluation of shock in meningococcemia cases, follow-up, and treatment
in the intensive care unit are required. Intubation should be planned for follow-up
on mechanical ventilators in necessary cases. Fluid support treatments and inotropic
support should be provided quickly for the shock treatment. Hematological, coagulation, blood gas, and biochemical parameters should be closely monitored.
Anticoagulant or brinolytic treatments, plasmapheresis, and extracorporeal membranous oxygenation (ECMO) treatment approaches can be applied on a case-bycase basis. No data exists on steroid use’s benet in meningococcal meningitis
cases. In meningococcemia, steroid treatment may be benecial in patients with
severe septic shock with resistant hypotension or secondary adrenal insufciency
(Waterhouse–Friderichsen syndrome) [7, 14, 18].
29.7 Prognosis
Invasive meningococcal disease is still a signicant public health concern worldwide, not only because of its high mortality rate but also because of its severe disabling sequelae, such as hearing loss (HL). Despite being relatively uncommon,
IMD is a serious public health problem because of its rapid onset and potentially
severe and sometimes lifelong sequelae, including neurologic, physical, and psychological complications [5, 20, 21]. Disabling long-term sequelae in survivors
have potentially devastating effects on survivors’ quality of life (QoL), particularly
in children and adolescents [22].
29.8 Bacterial Meningitis, Invasive Meningococcal Disease,
andHearing Loss
Acute bacterial meningitis (ABM) is the most prevalent bacterial central nervous
system (CNS) infection, with a high case-fatality rate and potential neurological
complications [23, 24]. Children with ABM had a 3.1-fold higher risk of disabilities, and 8.5% had serious sequelae such as severe HL, mental retardation, and
epilepsy in some studies [25, 26]. Outcomes are highly dependent on the patient’s
age (signicantly below 1 year), the infecting organism (sequelae are higher in
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ABM due to Streptococcus pneumoniae than Haemophilus inuenzae type b and
N. meningitidis), and the time it takes to start antibiotics [27, 28]. Hearing loss is a
typical complication of ABM, ranging from mild to severe [23, 28–32]. According
to a retrospective database research in Spain, the total deafness rate was 2.6%; however, the rate was 6.1% among meningitis survivors compared to 1% in the general
pediatric population [22].
Hearing loss may be conductive or sensorineural, and it is characterized as mild
(hearing threshold 20–40 decibels [dB]), moderate (40–70dB), severe (70–90dB),
or profound (deep) (>90dB) based on severity [33]. The most common cause of
acquired sensorineural HL (SNHL) in children is ABM, which accounts for 60–90%
of all cases [34]. Sensorineural HL can be unilateral after ABM, but a bilateral HL
is signicantly more likely [29]. The frequency of some degree of HL after ABM
ranges from 2% to 33.6%; 5% to 25% of children experience bilateral severe or
profound HL [31, 35].
Edmond etal. [31] evaluated the chances of major and minor sequelae induced
by ABM, with HL being the most prevalent major sequelae (33.6%). The most prevalent combination of multiple impairments was cognitive decit plus HL (39.1%).
Changes in hearing testing methodology, parameters used to dene hearing impairment, and interpretation of results account for most of the variation in reported HL
[33]. In high-income countries, improved immunization practices, a consequent fall
in susceptibility to fatal disease, better health-seeking habits, and early hospital
admission could all contribute to the large discrepancy in prevalence rates [32].
Late-onset HL has always been a concern, although it is usually recognized
promptly after infection [24]. Hearing loss is most common in the rst 48h of illness, and many children have reversible HL in the rst 2 days of illness [33].
According to Smyth etal. [36], the frequency decreased from 44% (48h after diagnosis) to 29% (6 weeks post-admission) and 21% (12 weeks post-admission).
Patients with normal hearing initially kept their normal hearing after meningitis. On
the other hand, meningitis-related HL may improve or deteriorate with time. The
average rate of deterioration of a rst-time HL is 14% [24].
The frequency and severity of HL linked with IMD and/or meningococcal meningitis have been studied extensively. Strier et al. [37] systematically reviewed
health outcomes in IMD cases and found that the most common sequelae related to
IMD were hearing and cognitive impairments and psychosocial difculties. While
meningococcal meningitis was associated with a lower rate of HL than pneumococcal meningitis, HL was the most common long-term outcome of meningococcal
meningitis in particular [33]. According to a meta-analysis of long-term consequences of meningococcal meningitis, unilateral or bilateral SNHL is the most
common complication, necessitating cochlear implantation in just 0.4% of patients
[20, 30].
The incidence of HL associated with meningococcal meningitis varies [22, 30].
In a large nationwide cohort study in the Netherlands, HL occurred in 20 of 495
children (4%) after meningococcal meningitis among 578 children who survived
ABM [38]. A retrospective examination of Dutch IMD hospital cases from 1999 to
2011 revealed 5.6% of HL events, with 2.5% occurring in children aged 0–4, 1.3%
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in children aged 5–19, and 1.7% in adults aged 20–64years [39]. At 21 months,
11.9% of adolescent IMD survivors (73% meningitis with or without septicemia)
experienced hearing impairments, compared to 4% (1/25) of college students [40,
41]. Thirteen percent of meningococcal meningitis patients (68% serogroup B) had
neurologic decits at discharge, with 8% having HL [42].
In 159 occurrences of IMD treated in 10 pediatric hospitals in the United States
of America (USA) between 2001 and 2005, unilateral or bilateral HL occurred in
12.5% of 112 children with meningitis, a proportion quite similar to in studies from
over 25years ago [43]. Another study in the USA found that 11% of children with
meningococcal meningitis had severe HL at discharge, whereas 13% had mild or
moderate HL [44]. A follow-up study in the United Kingdom (UK) reported SNHL
in 15 of 232 survivors with serogroup B meningococcal disease (32% with meningitis with or without septicemia), with 2% having severe bilateral SNHL and 5%
having moderately severe bilateral SNHL [45]. A retrospective assessment of
national IMD cases in Canada from 2002 to 2011 found 46 HL occurrences out of
868 cases (58% with meningitis with or without septicemia), with 7.4% in children
and 3.3% in adults [27].
Davis etal. [46] analyzed healthcare use and expenses between individuals with
and without IMD-related complications. They found 173 individuals with IMD;
41.0% had one or more sequelae during the follow-up, and 9.3% had HL.Hearing
loss was more prevalent following meningococcal meningitis in two African studies
[30]. Hearing loss was found in 19% of 351 meningococcal meningitis patients in
an Angolan research on day 7 of hospitalization [47]. An investigation on HL in
children with meningococcal meningitis in Malawi revealed that 23% of the 67
children who participated in the study had HL [48].
Gil Prieto etal. [49] examined medical data from 1997 to 2008in Spain for all
11,611 meningococcal infections (median age 5years) linked to hospital discharges
and deaths (846 deaths for IMD, 235 for meningococcal meningitis, and 605 for
meningococcemia). In the 30 days after discharge, they reported that 3% of the
subjects were readmitted, with HL being one of the causes for readmission.
Children with more severe IMD are more likely to develop serious neurological
sequelae and HL.On follow-up 4–10years after being discharged from the pediatric
intensive care unit, 35% of 120 children who survived meningococcal septic shock
showed neurological impairments in one study [50]. Two to four percent of IMD
survivors, including those who have experienced meningococcal septic shock and
those who have experienced meningitis, are found to suffer HL [50].
Also, a difference between the meningococcal serogroups exists. A matchedcohort study of adolescent survivors of IMD in the UK found that 57% had severe
physical sequelae, such as mobility, speech, and hearing impairments. These
sequelae were more severe in meningococcal serogroup C (MenC) disease survivors than in meningococcal serogroup B (MenB) disease [13]. The MOSAIC study
enlisted children who had MenB disease in the UK between May 2008 and
September 2010 and evaluated their physical, psychological, and neurocognitive
outcomes 3years later [45]. The majority of children with MenB disease recovered
without serious complications. Approximately a tenth of those with signicant
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sequelae had major physical or neurological disabilities, such as HL.Compared to
controls, children with MenB disease had a 4.8-fold higher incidence of bilateral
SNHL of 40dB or more. This research demonstrated a higher prevalence of SNHL
in IMD than previously reported, both in terms of profound HL requiring a cochlear
implant and less severe HL [45].
Richardson etal. [23] aimed to nd out more about the natural history and pathophysiology of HL in 124 children with ABM in England and Wales (74% of whom
had meningococcal meningitis). Children were subjected to audiological examinations, the rst of which, otoacoustic emissions, was done within 6h after diagnosis.
Children who had been sick for more than 24h were more likely to have HL.This
study adds to the growing body of evidence showing HL occurs early in the course
of ABM, with a reversible HL rate of 10.5%, with most instances resolving within
48h. The absence of otoacoustic emissions and normal tympanogram in all of these
children indicated cochlear dysfunction. The cochlea was identied as the source of
the lesion in both permanent and reversible sensorineural decits. The administration of dexamethasone did not appear to impact the audiological outcome in this
investigation [23].
In Canada, with proven IMD among children and adults (55% MenB), Sadaranghi
et al. [27] discovered risk factors related to mortality and the development of
sequelae. There were 73 deaths (8.4%) and 157 complications (18%) among the 868
people admitted to the hospital with IMD (21% in children and 15%in adults).
Hearing loss (5.4%) was the most prevalent complication. Children under the age of
1year were most likely to suffer from HL and seizures, while children between the
ages of 1 and 4years were most likely to suffer from skin scarring and amputation.
Monitoring of the circulatory condition and early and vigorous shock care are critical since shock is the most signicant predictor of death in adults and children and
a major predictor of complication rates.
The etiology of HL after ABM is linked to abnormalities in the cochlea and auditory nerve that develop during ABM. Hearing loss can occur as a result of both
direct bacterial product dissemination and the host’s inammatory reaction to the
invasion of the meninges and CSF.The auditory lesion in meningitis occurs in the
inner ear. Severe labyrinthitis develops when bacteria migrate from the subarachnoid area to the cochlear aqueduct, resulting in blood–labyrinth barrier breakdown
and, eventually, meningitis-associated HL. Serobrinous exudate, inammatory
cell inltration, and granulation cell formation are all indicators of cochlear disease.
In untreated labyrinthitis ossicans, the infectious process in the cochlea creates an
endosteal response, most typically involving the basal scala tympani. It could also
be caused by bacterial toxins or inammatory mediators acting on the hair cells of
the Corti organ. Alternatively, the same mechanisms could disturb the endocochlear
potential.
According to growing data, toll-like receptors (TLRs) appear to mediate cochlear
damage in meningitis. A metabolic deciency caused by insufcient CSF uid glucose and the inuence of variations in intracranial pressure conveyed by the cochlear
aqueduct are further possibilities. Other reasons include cochlear nerve injury or
vascular damage caused by septic emboli or thrombotic occlusions of the cochlear
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artery and/or vein. Although retrocochlear disease is uncommon, bacterial meningitis can cause direct injury to the auditory nerve and central brain circuits. The
absence of otoacoustic emissions has been observed in children with bacterial meningitis and SNHL, and this observation shows that the cochlea is the site of the damage in deafness after ABM since emission production is independent of the nervous
system [23]. Indeed, the fact that the aqueduct is more likely to be patent in childhood than in maturity could explain why HL after ABM is more common in children. For H. inuenzae type b, pneumococcus, and meningococcus, the distribution
of different sequelae appeared similar, implying that the organisms may produce
similar cerebral pathogenic processes [23, 30, 32–34, 51].
Genetic diversity in innate immune response genes inuences interindividual
disparities in illness appearance and infection consequences. Some associations
between TLR single nucleotide polymorphisms (SNPs) and HL exist in patients
with ABM.The immune response to ABM and subsequent neuronal damage, as
well as cochlear inammation, appear to be mediated by the TLR system. Toll-like
receptor-9 SNPs have previously been associated with meningococcal meningitis
risk. Toll-like receptor-4+896 mutant alleles were found to be strongly linked to HL
after ABM, particularly meningococcal meningitis. According to a multigene analysis, combining the TLR2+2477 wild type (WT) and TLR4+896 mutant alleles
enhances the likelihood of HL.Genetic markers may be utilized to identify highrisk patients by developing prediction criteria for HL after ABM and other complications and a better understanding of the complicated immune response in the CNS,
perhaps leading to new treatment options [51].
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29.9 Meningococcal Meningitis Follow-Up forHearing Loss
In infants and toddlers, a critical period exists in which language and speech developments occur. To avoid long-term repercussions such as speech and language
delays, poor academic performance, behavioral difculties, and poorer psychosocial integration, early identication of SNHL in children is crucial. Serious language development and academic achievement impairments arise even when only a
mild-to-moderate bilateral SNHL is present in neonates and young children [24, 30,
34]. Compared to children with SNHL discovered later, those identied earlier
showed more remarkable development in language and vocal skills, age-appropriate
language retention, and superior language skills [34]. Children who survive meningococcal meningitis have a greater rate of behavioral and psychiatric issues and
lower academic achievement, which may be linked to HL.Hearing loss and other
neurological sequelae can have long-term effects on the development of children
and on their ability to reintegrate into society [30].
As a result, all surviving patients should have their hearing tested as part of the
usual follow-up after ABM.Hearing tests are performed on all people with bacterial
meningitis after the acute phase has passed. Testing during the acute phase is ineffective: even in the case of severe HL and cochlear ossication, the patient’s physical condition must be addressed before a cochlear implant may be implanted [24].
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Even if HL is not clinically suspected, all children aficted with meningitis should
have their hearing tested before release or 4–6weeks after discharge. Because up to
90% of children’s cochleae with HL due to meningitis can ossify, preventing effective treatment with cochlear implants, it is crucial to get an audiology evaluation a
month following diagnosis, or sooner if possible. The chance of developing HL in
people who do not have HL immediately after infection is extremely low, and audiological follow-up is not required. Patients who incur an HL during ABM require
long-term and detailed audiological monitoring [24, 28].
Bozzola etal. [33] looked for factors that could predict long-term audiological
difculties in children with meningitis, including meningococcal meningitis,
between 2017 and 2019. If the results were normal, the tests were redone at discharge, and if the results were normal again, the patients were dropped from the
follow-up program. Regular hearing tests were performed if a unilateral SNHL was
found. If bilateral SNHL was found, high-resolution temporal computed tomography (CT) scans and magnetic resonance (MR) imaging with gadolinium for the
inner ear were conducted quickly to look for signs of labyrinthine brosis or ossication. In severe or substantial SNHL, immediate bilateral simultaneous cochlear
implantation was recommended if ossication was discovered. Otherwise, imaging
and audiological tests were repeated after 15 days; if no progress was seen, the
patient received appropriate therapy with cochlear implantation or hearing aid tting within 6weeks [33].
No uniform recommendation exists for follow-up for children with ABM for HL
[24]. The UK’s National Health System (NHS) states that little evidence exists to
support the need for additional testing if the initial hearing test after meningitis is
satisfactory. In the USA and Australia, ABM is recognized as a risk factor for lateonset HL, albeit the timing and frequency of hearing reevaluations are not specied
[24]. The French Infectious Diseases Society published the most recent recommendations for pediatric ABM follow-up. According to these recommendations, follow up appointments should be scheduled at the end of treatment or within 15 days
(neurological exam and hearing test based on the patient’s age), 1 month after diagnosis (neurological exam, head circumference measurement, hearing test), and then
every 3 months for the next year (clinical monitoring of the patient’s hearing abilities, school adjustment monitoring). An otorhinolaryngology visit is advised for
severe HL to assess for early cochlear ossication [26].
Cochlear implantation surgery should be considered in children as young as
1year old who have severe or profound bilateral deafness (hearing threshold >75dB
HL) as evidenced by both subjective and objective audiometric techniques and
cases where hearing and communication skills have not improved after 3–6months
of hearing aids and speech therapy, according to Italian guidelines [33]. Even if the
patient is under the age of 12months, bilateral simultaneous cochlear implantation
surgery is essential in cases of profound SNHL caused by meningitis [33].
In addition to HL, IMD survivors should be tested for cognitive abnormalities
and developmental delays on a regular basis. In order to reintegrate an IMD survivor
back into society, extensive follow-up treatment and adaptive measures may be
required. Hearing aids, physiotherapy, and specialized schooling are among the
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