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In gram-negative bacillus meningitis, repeat LP should be performed 2–3 days
after treatment initiation to assess therapy efcacy [29].
E. Yeşil et al.
31.8.3 Treatment inNewborns andPrematures
In cases where clinical and CSF ndings, such as CSF pleocytosis, increased protein level, decreased glucose level, and microorganisms seen in Gram-stained CSF
suggest ABM, empirical antimicrobial therapy should be started immediately.
Treatment for possible pathogens, mostly GBS, E. coli, and other gram-negative
enteric bacilli, is chosen empirically. Ampicillin plus an aminoglycoside (usually
gentamicin) or a (spectrum cephalosporin (e.g., cefotaxime, ceftazidime, or
cefepime) plus an aminoglycoside (usually gentamicin) is recommended for most
newborns. If L. monocytogenes or enterococci are suspected, ampicillin should be
included or added to the treatment. These regimens are suitable for early-onset (rst
72h) and late-onset (>72h) neonatal meningitis. Vancomycin plus an aminoglycoside (usually gentamicin) plus a broad-spectrum cephalosporin (such as cefotaxime,
ceftazidime, or cefepime) is started for the treatment of late-onset meningitis in
hospitalized neonates from birth. The treatment may change according to the reproducing factor and the responses. If multidrug-resistant (MDR) gram-negative bacilli
are suspected based on the current ora of the neonatal intensive care unit (NICU),
meropenem should be used instead of a broad-spectrum cephalosporin.
Acyclovir (60 mg/kg/day, divided into three doses, IV) may be added for herpes
simplex virus (HSV) infection to empirical treatment in cases clinically thought to
have neonatal meningitis with CSF pleocytosis, and no microorganism was detected
on Gram-staining. Treatment is given for at least 21 days in HSV meningitis, and
oral suppressive acyclovir (900 mg/m2/day, divided into three doses, oral) treatment
is continued for 6 months after the newborn is discharged [37].
Empirical broad-spectrum antimicrobial treatment should be continued until the
causative organism and susceptibility of the organism are identied. Treatment coverage should be altered based on antimicrobial susceptibility when the causative
agent is detected.
Ampicillin is used for ampicillin-susceptible strains to treat E. coli and other
gram-negative bacteria. In ampicillin-resistant organisms, a combination of a broadspectrum cephalosporin and an aminoglycoside (such as gentamicin) is used in
most cases. Multidrug-resistant gram-negative bacteria are treated with meropenem. The duration of treatment is at least 21days [28].
Ceftazidime or cefepime may be preferred when cefotaxime is unavailable. In
the neonatal period, ceftriaxone should not be used in neonates, as it may inhibit
bilirubin–albumin binding and cause kernicterus. When used with intravenous calcium, it may precipitate and cause severe reactions [28].
Newborns with ABM should undergo serial neurological examination, evaluation of the general clinical condition, repeated blood cultures, and LP in bacteremic
patients. In neonates with meningitis, repeat LP should be performed 24–48h after
initiation of antimicrobial therapy to conrm CSF sterilization. Repeat LP is
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primarily recommended in neonatal meningitis caused by GBS, gram-negative bac-
with neonatal meningitis. With the sterilization of CSF, combination therapy may be
discontinued in some patients with GBS or Listeria meningitis [28].
Most newborns with uncomplicated ABM show clinical improvement within
24–48 h after receiving appropriate antibiotic therapy. The absence of expected
improvement or clinical deterioration in this time interval should suggest a complication such as obstructive ventriculitis, subdural effusion, brain abscess, intraventricular hemorrhage, or inadequate antimicrobial therapy. In this situation, neuroimaging
should be performed, and pediatric infectious diseases and neurosurgery consultation should be requested. In newborns with ABM, neurological complications may
present with ambiguous ndings. Therefore, MR imaging can be performed 48–72h
before the cessation of treatment, even if there are no obvious neurological ndings
in responding cases. Neonatal neuroimaging with neurological signs should be performed earlier [28]. In addition, delay in CSF sterilization is associated with neurological sequelae and requires a detailed evaluation of the patient [28].
Hearing, vision, and developmental stages should be followed for a duration of
time for all newborns with ABM. Hearing should be evaluated by auditory brainstem response (ABR) test within 4–6 weeks of completion of therapy [28].
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31.8.4 Adjuvant Therapy
Permanent neurological sequelae, such as focal neurological decits and HL, are
common in ABM survivors, especially with pneumococcal and Hib meningitis.
These complications depend on the inammatory state, host response, and bacterial
pathogen. Animal studies show that neurological complications are associated with
the severity of the inammatory process. Therefore, in treating ABM, antiinammatory agents, such as dexamethasone, have come to the fore in addition to
antimicrobial therapy. Anti-inammatory agents can potentially prevent neurological complications of ABM by reducing intracranial pressure and cytokine production. There is less research on other treatments aimed at inhibiting vasogenic edema
(glycerol) and inammatory mediators (e.g., nitric oxide synthase inhibitors), and
they are currently not recommended for routine treatment [38].
In a meta-analysis of 2511 pediatric patients from 18 randomized controlled trials, the mortality rate in children treated with dexamethasone (n=1269) was similar
compared to placebo (n=1242); 13.2% and 14.6%, respectively [39]. However, the
rate of severe HL (usually dened as ≥60 decibels bilateral HL or requiring bilateral
hearing aids) was lower in patients treated with dexamethasone (7% vs. 11.4%)
[39]. The positive effect of dexamethasone was limited to children with Hib meningitis, 3.9% and 11.9% of patients who did and did not receive the drug, respectively.
In comparison, the rates of severe HL for other bacteria were similar in the dexamethasone and placebo groups; 9.6% and 10.2%, respectively. The incidence of
neurological sequelae other than HL was similar (18% vs. 20%) in both groups,
regardless of the causative organism [38, 39].
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E. Yeşil et al.
The results obtained in another meta-analysis (n = 2029 pediatric patients)
included ve studies; dexamethasone was found to reduce HL (24.1% vs. 29.5%)
[40]. However, mortality rates (26.5% vs. 27.2%) and other complications, such as
severe neurological sequelae or bilateral HL, were similar [40]. Variables, such as
the etiologic pathogen, duration of pretreatment symptoms, state of consciousness
at admission, the timing of dexamethasone administration, and human immunodeciency virus (HIV) infection status, did not differ with any of the subgroups evaluated [38, 40].
The benets of dexamethasone therapy vary depending on the etiologic agent.
Dexamethasone is primarily used to prevent HL complications related to meningitis
caused by Hib. Its effects in pneumococcal or meningococcal meningitis have not
been demonstrated, and dexamethasone is not generally recommended, although
there is no consensus among experts.
However, in clinical practice, the causative organism is not known initially. If
CSF Gram-staining or other rapid diagnostic test results suggest Hib meningitis or
if the distinction cannot be made clear, adjuvant treatment with dexamethasone may
be recommended. The initiation time of dexamethasone therapy should be before or
concurrently with empirical antibiotic therapy. The benet of dexamethasone therapy started 1h after antibiotic treatment has not been demonstrated [38]. Therefore,
in practice, the administration of dexamethasone will probably not be benecial
after 1h of the rst dose of antimicrobial therapy. Dexamethasone is not indicated
for treating aseptic, nonbacterial, or suspected gram-negative meningitis. In this
respect, if it is started before the denitive diagnosis, it should be discontinued
when it is conrmed [38]. Dexamethasone is not indicated in infants under 6weeks
of age or those with congenital or acquired abnormalities of the CNS and VPS meningitis. Dexamethasone is not recommended in gram-negative bacterial meningitis
because of insufcient evidence for a benet–harm relationship in treating IIP and
inammation [31, 41].
Dexamethasone 0.15 mg/kg/dose may be given intravenously every 6 h for
2–4 days. Two-day treatment is as effective as longer-term treatment and has a
lower risk of toxicity [38].
As a corticosteroid, dexamethasone reduces vomiting and edema and can ameliorate fever. Therefore, it is challenging for the clinician to monitor the patient’s
response to treatment. It may increase the risk of gastrointestinal bleeding in
approximately 1–2% of children [38]. After discontinuing dexamethasone therapy,
secondary fever after a 24-h period without fever may occur. In patients receiving
dexamethasone for pneumococcal meningitis requiring vancomycin treatment,
increased BBB permeability due to inammation may decrease the transmission of
vancomycin to CSF. However, there is no delay in CSF sterilization in patients
receiving dexamethasone treatment as an adjuvant. So, children with S. pneumoniae
meningitis who receive dexamethasone at admission should be carefully monitored
during treatment. The effects of dexamethasone on viral meningitis are not fully
known; there is not enough scientic data on this subject [38].
The use of therapeutic hypothermia is not recommended in children with ABM
at risk for neurological sequelae [38]. Glycerol may be used within its indications if
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it is indicated for the treatment of cerebral edema. There is no other proven adjuvant
therapy, and its use is not recommended [38].
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31.8.5 Duration ofTherapy
The duration of therapy for ABM varies according to the type of causative pathogen. Treatment may also vary and be prolonged by risk factors, complications, and
response to treatment. The duration of treatment in meningitis cases with optimal
response to treatment is 10–14days for S. pneumoniae, 5–7days for N. meningiti-
dis, 7–10days for H. inuenzae, 21days for L. monocytogenes, at least 2weeks for
S. aureus, and 3weeks or a minimum of 2weeks after CSF sterilization, whichever
is longer for gram-negative bacilli [29, 42]. In inadequate response to treatment or
complications, treatment periods may be prolonged. If sterilization in the CSF
(presence of CSF culture positivity at 24–48h and later) is delayed, the treatment
durations are recommended to be longer.
31.9 Prognosis
Acute bacterial meningitis can cause signicant morbidity and mortality despite
effective antimicrobial therapy. The risk of complications or death is related to the
causative pathogen, patient’s age, underlying disease, duration and severity, and
sometimes delays in initiating antibiotic therapy [43].
Mortality in children with ABM ranges from 0% to 15% [29]. However, it has been
higher in some low- and middle-income countries. An ABM study conducted in Angola
of 723 children aged 2 months to 13 years in 2005–2008 reported that the patients were
generally severely ill at hospital admission, and 38% had died [44]. In another study
conducted in the USA of 2780 children between 2001 and 2006, the mortality rate was
4.2% [45]. A meta-analysis of 4920 children between 1955 and 1993 showed that mortality was 4.8% in high-income countries and 8.1% in low- and middle-income countries [46]. The mortality rate in high-income countries was 3.8% for Hib meningitis,
7.5% for meningococcal meningitis, and 15.3% for pneumococcal meningitis [46]. In
a multicenter study of pneumococcal meningitis in the USA from 2007 to 2013, the
mortality rate was 7% [29, 47]. Generally, pneumococcal meningitis has a higher risk
of death or neurologic sequelae than meningococcal or Hib meningitis [29].
Gram-negative bacillary meningitis is less common but has a worse prognosis,
and the mortality rate in adults and children ranges from 40% to 80% [2]. Patients
with spontaneous ABM typically have a higher risk of shock, bacteremia, and death
[2]. In an ABM study of 654 children, the Glasgow Coma Score (GCS) at presentation was the strongest independent predictor of severe neurological sequelae or
death. The risk of death was approximately 10 times higher in the GCS 7–9 range,
and mortality was about 30 times higher if GCS ≤6 [29, 48].
The prognosis of ABM in children is related to the level of consciousness at
hospital admission, etiologic pathogen, CSF glucose concentration, presence of
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seizures, delayed sterilization of CSF, and underlying diseases [29]. Seizures after
72h from the start of treatment have been associated with neurological sequelae,
especially in pneumococcal and Hib meningitis [29]. Likewise, children with underlying immunodeciency, malnutrition, malignancy, or preexisting neurological disease are at higher risk of death or neurological sequelae [29]. Cases with baseline
CSF glucose concentration<20mg/dL are associated with adverse outcomes such
as delayed sterilization of CSF (continuing positive culture after 16–18h of initiation of therapy), abnormal neurological ndings, seizures, moderate to severe sensorineural HL (SNHL), and hemiparesis [29].
Worldwide, 12–35% of survivors of ABM have sequelae. In Africa, this gure
may double [49]. Permanent neurological sequelae are common in children with
ABM.The most common sequelae are HL, seizures, intellectual disability, spasticity, and paresis [29]. Hearing loss occurs in 31% of children with S. pneumoniae
meningitis, 10.5% with N. meningitidis meningitis, and 6% with Hib meningitis [50].
In young children treated for meningitis, developmental steps should be followed
throughout the growth and development process [29]. The hearing examination
should be done at the hospital or immediately after discharge. Hearing can be evaluated with pure tone audiometry. The ABR test can be used in young children or
children who cannot cooperate with pure tone audiometry. The hearing evaluation
should be repeated if the initial assessment results show more than a mild HL [29].
E. Yeşil et al.
31.9.1 Neonatal Meningitis Prognosis
Neonatal meningitis is a devastating disease. Neonatal intensive care follow-up
decreases mortality, but morbidity remains high. Neonatal ABM mortality is
approximately 10%, which may cause moderate to severe disability in about
15–20% of survivors and mild disability in 30–35% [28]. Long-term hearing, vision,
and developmental stages should be followed-up in infants with neonatal meningitis.
Poor prognostic factors in newborns with ABM are low-birth-weight (LBW,
<2500g), preterm birth (<37weeks of gestation), history of clinical signs more than
24h before hospitalization, leukopenia (white blood cell, <5000/mm3) and neutropenia, very high CSF protein level (>3g/dL) and/or very low CSF glucose (<10%
of blood glucose value), seizures occurring 72h after hospitalization, focal neurological disorders recorded during acute illness, need for mechanical ventilation or
inotropes, and delayed sterilization of CSF [28].
In neuroimaging ndings of meningeal inammation, the presence and size of
parenchymal lesions, such as thrombus, and encephalomalacia, have prognostic
importance. Mainly, abscess formation is associated with neurological sequelae that
may develop in the future. The overall prognosis is worse, especially in preterms
compared to term neonates [28].
In neonatal meningitis, the causative GBS mortality is around 6–11%, and the
long-term sequelae rate is about 20–40% [28]. The mean mortality in E. coli meningitis in newborns is 9%, and mortality in preterms is 3 times higher than in term
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neonates. The most common short-term morbidities among newborns are seizures,
empyema, intraventricular hemorrhage, hydrocephalus, cerebral venous thrombosis, and stroke [28].
Between 1977 and 1995, in 64 very-low-birth-weight (VLBW <1500g) newborns with 67 culture-positive meningitis, etiologically, 43% coagulase-negative
staphylococci, 19% other gram-positive bacteria, 17% gram-negative bacteria, and
20% Candida spp. were observed. In surviving cases, culture-proven meningitis
compared without meningitis (sepsis); the rate of major neurologic sequelae (41%
vs. 11%, respectively) and subnormal Mental Development Index (<70) (38% vs.
14%, respectively) were higher. However, no difference was found between neurological sequelae according to the pathogen [51].
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31.10 Prevention
The best way to eliminate the neurological complications of ABM is to prevent
infections. Acute bacterial meningitis can be controlled mainly by vaccines, such as
conjugate Hib, 13-valent pneumococcal, 4-valent meningococcal, and meningococcal B vaccines, and antibiotic chemoprophylaxis in risky exposure situations [38].
Vaccination is more effective, long-lasting, and reliable.
Antibiotic prophylaxis may be required for close and risky contact with patients
with Hib and invasive meningococcal diseases. Antibiotic prophylaxis against other
bacterial pathogens of meningitis is not recommended.
31.10.1 Meningococcal Chemoprophylaxis
The infection rate in close contact with patients with meningococcal disease is
0.4%, which is 500–800 times higher than the general population. Close contacts
should be given chemoprophylaxis. Close contact refers to persons with exposure
less than 1 meter close to the patient and >8 h of direct exposure to the patient's oral
secretions. The chemoprophylactic agent should be administered before 7 days and
up to 24 h after the appropriate antibiotic therapy onset of the patient's symptoms
[42]. All household contacts, contacts staying in the same room with the index case
for more than 8h, or traveling or sleeping in the same room are considered in this
group [52].
Nasopharyngeal or oropharyngeal cultures are not recommended and have no
place in deciding the need for chemoprophylaxis as they may unduly delay
administration [42]. Antimicrobial chemoprophylaxis should ideally be administered within 24h after the index case diagnosis. After 14days of exposure to the
index case, chemoprophylaxis is not recommended by the USA Centers for
Disease Control and Prevention (CDC) because its efcacy is controversial [42,
53]. Postexposure infection is usually seen in the rst 10days on contact per-
sons; however, cases occurring in a more extended period have also been
reported rarely.
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The preferred agents for antimicrobial chemoprophylaxis against meningococcal
infection are rifampin, ceftriaxone, ciprooxacin, and azithromycin [45, 52]. For
meningococcal prophylaxis, rifampin (20mg/kg/day, maximum 600mg/day, in neonates 10mg/kg/day, in equal 2 doses, orally, 2days), ceftriaxone (125mg for <15-yearold, 250 mg for >15-year-old, intramuscular [IM], as a single dose), ciprooxacin
(20mg/kg for >1month-old, maximum 500mg, orally, as a single dose) or azithromycin (10mg/kg, maximum 500 mg, orally, as a single dose) may be administered
[52]. However, rifampin and ciprooxacin are not given to pregnant women [52].
If treated with an antibiotic other than a third-generation cephalosporin, the
nasopharyngeal carriage of N. meningitidis may not be resolved in patients with
invasive meningococcal disease. Therefore, these patients should receive appropriate chemoprophylaxis for the eradication of nasopharyngeal carriage before discharge from the hospital. Chemoprophylaxis regimens for such patients are the
same as postexposure prophylaxis [29, 42].
E. Yeşil et al.
31.10.2 Haemophilus influenzae Type b Chemoprophylaxis
Rifampin is recommended for Hib prophylaxis. Rifampin is given once daily
(20 mg/kg, maximum 600 mg, in newborns 10 mg/kg, orally) for 4 days [54].
Prophylaxis is given to household contacts of children with Hib meningitis if an
unvaccinated or incompletely vaccinated child exists under 4years of age at home
or an immunocompromised child regardless of age. In addition, chemoprophylaxis
is applied to children in preschool nurseries or nursing homes if there are ≥2 children with invasive Hib disease. Chemoprophylaxis is also used for a sick child
receiving treatment other than cefotaxime or ceftriaxone if there is contact with a
child younger than 2years old or immunocompromised at home [54].
31.11 Complications
Complications of ABM may be classied as neurological and non-neurological
complications. Non-neurological systemic complications such as uid–electrolyte
disturbances, cerebral edema, septic shock, acute respiratory distress syndrome
(ARDS), disseminated intravascular coagulation (DIC), and septic or reactive
arthritis are usually the results of bacteremia, which often accompanies meningitis
[43]. Neurological complications, however, are sequela-related complications that
tend to be longer-lasting. Complications of meningitis are usually neurological.
31.11.1 Non-Neurological Complications
In ABM, septicemia in children and organ failure such as kidneys, liver, lungs, and
heart failure may be seen depending on the severity of septicemia. As in meningococcemia, extremity losses due to purpura fulminans may be seen.
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31.11.2 Neurological Complications
General neurological complications are mainly mental status changes, brain edema,
seizures, IIP, HL, quadriparesis, hemiparesis, ataxia, cranial nerve palsies, cerebrovascular abnormalities, developmental disorder, neuropsychological disorders,
hydrocephalus, subdural effusion or empyema, rarely brain abscess and hypothalamic dysfunction. Neurological complications of meningitis can occur any time
after the onset of symptoms. Impaired mental status is seen in most patients at the
presentation time, and seizures are mostly seen in the acute period. These are also
counted among the clinical ndings of the disease. Complications may also be of an
acute or chronic nature [43]. Although many neurological complications are readily
and severely apparent, such as HL, they may occur in the early stages of infection.
Although SNHL occurs early, it may not be noticed in young children until a hearing assessment is performed [43].
31.11.2.1 Cerebral Edema
Cerebral edema occurs due to cytotoxic, vasogenic, or interstitial mechanisms and
leads to IIP.Vasogenic cerebral edema is usually caused by increased permeability
of the BBB, particularly in the choroid plexus and cerebral microvascular endothelia. Cytotoxic factors released from neutrophils, microglia, and astrocytes can cause
brain edema. Inammation due to infection may interfere with the normal absorption of CSF from the subarachnoid space through the arachnoid villi. Cerebral
edema and IIP are initially manifested by headache, confusion, irritability, nausea,
and vomiting. Papilledema may be detected on physical examination. More severe
intracranial hypertension is characterized by severe impairment of consciousness;
coma. In addition, cranial nerve palsies, primarily the sixth nerve, hypertension,
bradycardia, Cushing’s reex, or triad may occur. In severe cases, cerebral edema
can cause death by cerebellar herniation. In critically ill patients with meningitis,
the possibility of cerebral edema should be kept in mind, particularly those with
severely impaired consciousness, asymmetric pupillary reexes, or other cranial
nerve palsies. Neuroimaging conrms the diagnosis, but urgent empirical treatment
may be required if there is high clinical suspicion. In children with ABM, uid volume balance should be carefully adjusted, considering cerebral edema [43].
31.11.2.2 Subdural Effusion
Subdural effusion occurs in 10–33% of children with ABM [43]. In young children,
the bulging fontanel may signify subdural effusion, whereas, in older children, subdural effusions may rarely cause IIP and shift in intracranial structures. Most children are asymptomatic and do not require treatment. However, drainage is required
if a compression-related neurologic nding or subdural empyema exists [43].
31.11.2.3 Seizures
Seizures occur in 20–30% of children with ABM.The pathogenesis of seizures in
meningitis is not clear. Although fever can be a risk factor in very young children,
most seizures are likely caused by cerebrovascular inammation or secondary
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neurochemical changes [43]. Seizures occurring before or at admission are usually
generalized, but seizures occurring after 72h are generally focal. Early and easily
controlled seizures are rarely associated with permanent neurological sequelae. In
contrast, seizures that begin more than 72h after hospitalization are challenging to
manage or are prolonged and more likely associated with neurological sequelae,
suggesting that a cerebrovascular complication may have occurred [43].
E. Yeşil et al.
31.11.2.4 Cranial Nerve Palsy
Cranial nerve palsies may result from nerve compression due to cerebral edema or
perineuritis due to adjacent meningeal inammation. The sixth cranial nerve is the
cranial nerve most affected by IIP due to the length of its intracranial part. The third,
fourth, and seventh cranial nerves may also be affected. Cranial nerve disorders due
to meningitis are usually temporary. Acute bacterial meningitis can cause arachnoiditis around the optic nerve, resulting in temporary or permanent vision loss.
Irreversible complete blindness is a rare complication of severe meningitis due to
optic atrophy [55].
In a literature review covering 1970–2010, approximately half of 1433 postneonatal ABM survivors had at least one neurologic sequela at ≥5 years of follow-up
[56]. Of the reported sequelae, 78% were mental/behavioral defects, such as academic difculties, cognitive impairment, and attention decit hyperactivity disorder; 14% were neurological defects, including seizures, motor defects, and cerebral
palsy, 7% were HL, and 3% were visual impairment. Considering the bacterial
agents of children with sequelae, 37% were H. inuenzae, 4% were S. pneumoniae,
and 3% were N. meningitidis.
Risk factors for neurological complications of ABM in children vary according
to the following characteristics [43]:
• Patient age: The younger the child, the worsening the prognosis.
• The type of etiologic pathogen: Streptococcus pneumoniae infection has a worse
prognosis than others.
• The disease duration before effective antibiotic therapy: ≥2days post-symptom
hospital admission.
• Severe CSF ndings at admission: Very low CSF glucose concentration, bacte-
rial growth; ≥107 (colony-forming unit [CFU]/mL), delayed CSF sterilization.
• Seizures starting 72h after admission.
• Focal neurologic decit in non-postictal patients.
• Inadequate host response to infection.
Gram-negative bacillus meningitis has a worse prognostic outcome than other
bacterial pathogens in all age groups [43].
31.11.2.5 Ataxia
Among all neurological sequelae, ataxia is considered a minor complication. Ataxia
was observed in 1–5% of patients with H. inuenzae or meningococcal meningitis
and 18% with S. pneumoniae meningitis [44]. It is usually transient, but cases of
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ataxia lasting for months have rarely been identied. This nding suggested that
ataxia may be of vestibular origin, rather than cerebellar origin, as in most cases of
acquired postinfectious ataxia in childhood.
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31.11.2.6 Motor Deficits
Hemiparesis, quadriparesis, and other motor decits may be seen as complications
of ABM.Most motor decits are temporary with successful treatment, but longterm sequelae may occur. The paresis is typically caused by an intracranial abnormality such as a cerebral artery spasm, cortical or sagittal vein thrombosis, subdural
effusion or empyema, cerebral infarction or abscess, hydrocephalus, or cerebral
edema. Paralysis from meningitis usually resolves over time. In a study of 235 children with ABM, quadriparesis or hemiparesis was found in 12% of patients immediately after discharge [20]. However, paresis persisted in only 2% of cases at
follow-up, 1 year after discharge.
31.11.2.7 Cerebrovascular Complications
Thrombosis, vasculitis, intracranial hemorrhage, acute infarction, and aneurysm
formation are potential complications of ABM.These ndings may present as focal
abnormalities such as hemiparesis or focal seizures [43].
31.11.2.8 Mental andBehavioral Disabilities
Survivors of ABM are at increased risk for learning difculties, developmental
delays, and behavioral problems [43]. This is true even for those who do not have
acute neurological complications during the acute illness. Caregivers and teachers
should be aware of possible language problems and problems understanding
language- based materials. Early diagnosis and intervention can help to alter the
long-term effect of these problems.
31.11.2.9 Intellectual Disability
Intellectual disability is a well-known complication of ABM in children and can
range from mild to severe. A meta-analysis of 19 prospective studies of ABM in
children in developed countries reported that 4% of survivors had intellectual disability (intelligence level IQ ≤70) [43, 46]. Compared with the healthy control
group, children with ABM in infancy were found to have lower school performance
and were about four times more likely to attend special needs schools [57].
31.11.2.10 Behavioral Problems
Survivors of childhood ABM may have behavioral problems such as increasing
somatic complaints, mood disorders, social problems, and thought and attention
disorders. It is unclear whether behavioral problems vary by the pathogen.
31.11.2.11 Hearing Loss
The most common cause of acquired HL in childhood is ABM.Hearing loss after
meningitis can be temporary or permanent. In many affected patients, transient HL
may occur due to conduction disturbance. However, SNHL (temporary or
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