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13 Hearing Loss inNeonatal Sepsis andMeningitis
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13.8.3 Supportive Treatment
Newborns with sepsis are closely followed for vital signs, serum glucose, electrolytes, and liver and kidney functions. Enteral or parenteral nutrition, inotropes if
shock is present, and mechanical ventilation in respiratory insufciency are supportive treatments [54].
13.8.4 Adjunctive Treatment
Anticonvulsive therapy, fresh frozen plasma, thrombocyte, and erythrocyte suspensions are given if indicated. Steroids are used only in adrenal insufciency [48]. A
recent Cochrane review showed routine intravenous immunoglobulin (IVIG), or
IgM-enriched IVIG provides no benet in neonatal sepsis [55]. A meta-analysis
evaluating pentoxifylline treatment in sepsis showed a decrease in mortality; however, the quality of evidence was low [56]. Granulocyte stimulating factor (GSF)
treatment is not routinely recommended [54].
13.9 Complications andPrognosis
Neonatal meningitis and sepsis have critical impacts on a child’s life. Long-term
consequences include learning and neuromotor disabilities, HL, seizure disorders,
and visual, speech, language, and behavioral problems [54]. A study evaluating the
outcome of GBS meningitis showed that 26% of cases develop neurologic impairment, such as hypotonia, hypertonia, seizures, clonus, dysphagia, ptosis, cortical
blindness, HL, and temperature instability [57]. A worse neurodevelopmental outcome, including cerebral palsy, low psychomotor developmental index, and HL,
was seen in VLBW infants with a history of sepsis than in those without sepsis [58].
Klinger etal. [41] reported that 19% of term or near-term infants with meningitis
develop a moderate or severe disability at 1year of age. Seizures, coma, leukopenia,
and the need for inotropes were predictors of adverse outcomes. de Louvois etal.
[59] performed a questionnaire survey to identify sequelae of neonatal meningitis
after 5years. Twenty-three percent of children had a severe disability, including
cerebral palsy, hydrocephalus, gross motor delay, and HL.Moderate or severe disability was commonly seen in children with a positive CSF culture, 34% in GBS,
30% in E. coli, and other GNB meningitides.
13.10 Hearing Loss inNeonatal Sepsis andMeningitis
Sensorineural HL (SNHL) is an important complication of meningitis. Persistent
HL develops in 2.5–18% of children with a history of meningitis [60–63]. In
England and Wales, among 1584 children treated for meningitis between 1985 and
1987, HL, with a rate of 25.8%, was the most common long-term disability [56].
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After 11years, a repeat study evaluating children treated for meningitis between
1997 and 1998 showed that the mortality rate decreased from 22 to 6.6% [59].
Among 166 neonatal meningitis cases, ve developed SNHL (one severe, four moderate). The Joint Committee on Infant Hearing (JCIH) in the Netherlands dened
chemotherapy, cholesteatoma, and meningitis as causes of acquired HL [64]. In
Austria, Weichbold et al. [65] assessed the causes of postnatal HL in children.
Among 23 children who passed universal neonatal hearing screening but later
developed permanent HL, two had meningitis.
Of 6093 infants evaluated in a multicenter study investigating the neurodevelopmental and growth impairment among extremely low-birth-weight (ELBW,
<1000g) infants with neonatal infection, 1922 had sepsis, 279 sepsis and necrotizing enterocolitis (NEC), 193 meningitis, and 1536 clinical infections [66]. Adverse
neurodevelopmental outcomes were more common in all four infection groups than
uninfected infants. Among 906 infants with CONS infections, 2% developed
HL.Gram-negative bacterial and fungal sepsis had a signicantly higher risk for HL.
Bielecki etal. [67] evaluated 5282 neonates to identify risk factors for HL.The
research dened 2 groups: the rst group included babies with underlying conditions associated with hearing problems, and the other comprised infants with no risk
factors but failed hearing tests twice. The highest risk was for syndromes already
known to alter hearing capability (15.5%). Mechanical ventilation for more than
5days (11.4%), gestational age under 34weeks (16.2%), and birth weight under
1500g (12%) were other common risk factors. Meningitis was number 9 among
conditions identied to cause HL in infants (6.1%).
Bassler et al. [68] evaluated the relationship between neonatal infection and
visual, hearing, or neurological impairment development among ELBW infants.
Hearing loss was reported in 3.3% (12/359) of babies with sepsis and 4.8% (1/21)
with meningitis. The authors concluded that bronchopulmonary dysplasia, brain
injury, and severe retinopathy were the most signicant factors associated with the
18-month outcome. Meningitis added a considerable risk for poor prognosis.
A multicenter study investigated risk factors for HL among 4478 neonates treated
in NICU [69]. Babies who received ototoxic medications, mechanically ventilated,
were LBW and had low Apgar scores failed hearing tests more commonly than
well babies.
Aminoglycosides, bactericidal, are among the most common antibiotics accused
of causing ototoxicity [70]. After the lysis of bacteria by aminoglycosides, several
more immunogens are released, leading to an exaggeration of inammation, which
can harm the ear. Prolonged therapy with aminoglycosides is known to lead to ototoxicity. Genetic susceptibility to mitochondrial mutations also increases the risk
[71]. The risk is higher if the patient has fever, hypoxia, renal dysfunction, and poor
nutritional or low antioxidant status [72]. Co-administrating other drugs, such as
vancomycin, loop diuretics, and neuromuscular blockers, may increase ototoxicity
[73]. In mice, systemic inammation and endotoxemia increased cochlear uptake of
aminoglycosides and exacerbated ototoxicity [74].
Periventricular leukomalacia (PVL) and severe intraventricular hemorrhage
(IVH) are the most common causes of adverse neurodevelopmental outcomes in
13 Hearing Loss inNeonatal Sepsis andMeningitis
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preterm babies [75]. Infection-induced inammation leads to astrocytosis and
microglial reactivity. Inammatory cytokines interleukin (IL)-1, IL-6, and IL-8 and
tumor necrosis factor-alpha (TNF-α) increase. Free radical production and oxidative injury add to the necrosis of oligodendrocyte precursors and axonal death.
The pathogenesis of HL in meningitis is multifactorial, including direct labyrinth
involvement, cochlear neuroepithelial damage, eighth cranial nerve damage, and
vascular insult [76]. Hearing loss following meningitis results in speech and language disabilities and the inability to participate in school activities [77]. Bedford
etal. [56] identied that 9.4% of children with meningitis had speech or language
delay at 5years of follow-up.
Otoacoustic emission (OAE), brain stem auditory evoked response (BAER), and
behavioral audiometry are recommended tests performed in children with meningitis [78, 79]. Children should be tested before discharge to diagnose any degree of
HL with a high level of accuracy [78]. In a large cohort of 578 children with meningitis, 68% were checked for HL during routine follow-up, and 32 were found to
have [80]. An additional 11 cases of HL were detected among children tested after
the follow-up period had ended since they had complaints, of which ten were
detected after 6months of meningitis. The authors suggested that if all children with
predicted risk factors had been evaluated during routine follow-up, all cases with
HL would have been identied.
Turel etal. [81] evaluated children under 5years of age diagnosed with bacterial
meningitis at 11 hospitals in İstanbul. Sensorineural HL was detected in 7.6% of
patients, and speech or language problems were the most common (14.5%) sequelae.
Other affected abilities included ne and gross motor skills and social contact. Most
patients whose hearing was affected also had delays in neuromotor or developmental functions. Seventy-ve percent of the cases had not been referred for audiological services at discharge.
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13.11 Prevention andControl
13.11.1 Prevention ofEarly-Onset Sepsis
All pregnant women should be searched for GBS colonization at 35–37weeks, and
those colonized should be given prophylaxis [82]. However, IAP does not prevent
GBS-associated LOS [83]. Since most LOS cases are acquired after birth from the
environment, hospital infection control strategies effectively reduce the incidence.
13.11.2 Isolation andProphylactic Measures Against
Nursery Outbreaks
Effective programs can prevent one-third of healthcare-associated infections [84].
Every NICU should have rules for providing good hand hygiene to prevent LOS
[85]. Environmental disinfection systems and advances in cleaning practices of
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medical devices aid in preventing healthcare-associated infections [86]. Removing
catheters when no longer necessary is also recommended [87].
13.11.3 Breastfeeding
Breastfeeding has been shown to decrease sepsis and necrotizing enterocolitis
(NEC) in premature babies [88].
13.11.4 Chemoprophylaxis andImmunoprophylaxis
Every NICU should have programs for the judicious use of antibiotics and antibiotic
stewardship programs [89, 90]. Fluconazole prophylaxis given to ELBW infants
decreases colonization and invasive infection due to Candida spp. [91]. Loss of
intestinal microbial diversity is accused of a predisposing factor to sepsis [92]. In a
randomized controlled trial, Bidobacterium and Lactobacillus probiotics were
given to VLBW infants for 6weeks [93]. The incidence of NEC and mortality were
signicantly lower in infants who received probiotics. Enteral lactoferrin has been
shown to decrease culture-conrmed LOS [94]. However, studies evaluating this
subject are not adequate yet.
13.12 Conclusion
Neonates with meningitis and sepsis have an increased risk of developing
HL.Permanent HL is a devastating sequela that can inuence speech, cognitive, and
developmental issues. Every infant with neonatal sepsis and/or meningitis should be
checked and followed up routinely for hearing problems.
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Part III
https://t.me/medicina_free
Focal and Systemic Infectious Diseases
Otitis Externa inChildren andAuditory
https://t.me/medicina_free
Impairment
SeydaBelli, CemalCingi, andSuelaSallavaci
14.1 Introduction
Otitis externa refers to any condition in which the epidermis, dermis, or hypodermis
of the external auditory meatus becomes infected. Infection may also affect the ear
drum or auricle. Otitis externa may occur in various forms, such as acute diffuse,
circumscribed, chronic otitis, or malignant (where necrosis is a feature). A number
of conditions may be responsible, such as perichondrial inammation, erysipelas, a
fungal infection, herpes zoster of the ear, bullous and hemorrhagic forms, otitis
media with a perforated tympanic membrane, eczema, cholesteatoma, or a malignant neoplasm involving the external auditory meatus [1, 2].
14
S. Belli (*)
Section of Otorhinolaryngology, Bağcılar Training and Research Hospital, University of
Health Sciences, İstanbul, Türkiye
e-mail: drseydabelli@gmail.com
C. Cingi
Department of Otorhinolaryngology, Faculty of Medicine, Eskişehir Osmangazi University,
Eskişehir, Türkiye
e-mail: cemal@ogu.edu.tr; ccingi@gmail.com
S. Sallavaci
Department of Otorhinolaryngology, University Hospital Centre “Mother Teresa”,
Tirana, Albania
e-mail: sallavacis@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_14
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