Pediatric Bacterial Meningitis

8/4/2019 Pediatric Bacterial Meningitis

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Title: BACTERIAL MENIGITIS


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I. BackgroundBacterial meningitis is a life-threatening illness that results from bacterial infection

of the meninges. Beyond the neonatal period, the 3 most common organisms that cause acute

bacterial meningitis areStreptococcus pneumoniae, Neisseria meningitidis,andHaemophilus

influenzaetype b (Hib). Since the routine use of Hib, conjugate pneumococcal, and conjugate

meningococcal vaccines in the United States, the incidence of meningitis has dramatically

decreased.

AlthoughS pneumoniaeis now the leading cause of community-acquired bacterial meningitis

in the United States (1.1 cases per 100,000 population overall), since the introduction of

the conjugate pneumococcal vaccine in 2000, the rate of pneumococcal meningitis has declined

59%. The incidence of disease caused byS pneumoniaeis highest in children aged 1-23 months

and in adults older than 60 years. Predisposing factors include respiratory infection,otitis

media,mastoiditis,head trauma, hemoglobinopathy, human immunodeficiency virus (HIV)

infection, and other immune deficiency states.

The emergence of penicillin-resistantS pneumoniaehas resulted in new challenges in the

treatment of bacterial meningitis. Because bacterial meningitis in the neonatal period has

its own unique epidemiologic and etiologic features, it is described separately in this

article.

II. PathophysiologyBacteria reach the subarachnoid space by a hematogenous route and may directly reach the

meninges in patients with a parameningeal focus of infection.

Once pathogens enter the subarachnoid space, an intense host inflammatory response is

triggered by lipoteichoic acid and other bacterial cell wall products produced as a result of

bacterial lysis. This response is mediated by the stimulation of macrophage-equivalent brain

cells that produce cytokines and other inflammatory mediators. This resultant cytokine
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activation then initiates several processes that ultimately cause damage in the subarachnoid

space, culminating in neuronal injury and apoptosis.

Interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-), and enhanced nitric oxide

production play critical roles in triggering inflammatory response and ensuing neurologic

damage. Infection and inflammatory response later affect penetrating cortical vessels,

resulting in swelling and proliferation of the endothelial cells of arterioles. A similar

process can involve the veins, causing mural thrombi and obstruction of flow. The result is

an increase in intracellular sodium and intracellular water.

The development of brain edema further compromises cerebral circulation, which can result

in increased intracranial pressure and uncal herniation. Increased secretion of antidiuretic

hormone resulting in thesyndrome of inappropriate antidiuretic hormone secretion(SIADH)

occurs in most patients with meningitis and causes further retention of free water. These

factors contribute to the development of focal or generalized seizures.

Severe brain edema also results in a caudal shift of midline structures with their

entrapment in the tentorial notch or foramen magnum. Caudal shifts produce herniation of the

parahippocampal gyri, cerebellum, or both. These intracranial changes appear clinically as an

alteration of consciousness and postural reflexes. Caudal displacement of the brainstem

causes palsy of the third and sixth cranial nerves. If untreated, these changes result in

decortication or decerebration and can progress rapidly to respiratory and cardiac arrest.

III. Pathogenesis of neonatal meningitisBacteria from the maternal genital tract colonize the neonate after rupture of membranes,

and specific bacteria, such as group B streptococci (GBS), enteric gram-negative rods,

andListeria monocytogenes,can reach the fetus transplacentally and cause infection.

Furthermore, newborns can also acquire bacterial pathogens from their surroundings, and

several host factors facilitate a predisposition to bacterial sepsis and meningitis. Bacteria
http://emedicine.medscape.com/article/924829-overviewhttp://emedicine.medscape.com/article/924829-overview


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reach the meninges via the bloodstream and cause inflammation. After reaching the CNS,

bacteria spread from the longitudinal and lateral sinuses to the meninges, the choroid

plexus, and the ventricles.

IL-1 and TNF- also mediate local inflammatory reactions by inducing phospholipase

A2activity, initiating the production of platelet-activating factor and arachidonic acid

pathway. This process results in production of prostaglandins, thromboxanes, and

leukotrienes. By activating adhesion-promoting receptors on endothelial cells, these

cytokines result in attraction of leukocytes, and then release of proteolytic enzymes from

the leukocytes causes alteration of blood-brain permeability, activation of coagulation

cascade, brain edema, and tissue damage.

Inflammation of the meninges and ventricles produces a polymorphonuclear response, an

increase in cerebrospinal fluid (CSF) protein content, and utilization of glucose in CSF.

Inflammatory changes and tissue destruction in the form of empyema and abscesses are more

pronounced in gram-negative meningitis. Thick inflammatory exudate causes blockage of the

aqueduct of Sylvius and other CSF pathways, resulting in both obstructive and communicating

hydrocephalus.

IV. EpidemiologyFrequencyUnited StatesPrior to the routine use of the pneumococcal conjugate vaccine, the incidence of bacterial

meningitis in the United States was about 6000 cases per year; roughly half of these were in

pediatric patients (18 y).N meningitidiscauses about 4 cases per 100,000 children (aged

1-23 mo). The rate ofS pneumoniaemeningitis was 6.5 cases per 100,000 children (aged 1-23

mo). This number has since declined given the routine use of conjugate pneumococcal vaccine


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in children. The recent introduction of conjugate meningococcal vaccine in the United States

is expected to reduce the incidence of bacterial meningitis even further.

A study analyzed data on reported cases of bacterial meningitis among residents in 8

surveillance areas of the Emerging Infections Programs Network during 1998-2007. The results

found a 31% decrease in meningitis cases during this period and a median age of patient

increase from 30.3 years in 1998-1999 to 41.9 years in 2006-2007; the case fatality rate did

not change significantly. Overall during 2003-2007, approximately 4100 cases of bacterial

meningitis occurred annually in the United States, with approximately 500 deaths.[1]

Incidence of neonatal bacterial meningitis is 0.25-1 case per 1000 live births. In

addition, incidence is 0.15 case per 1000 full-term births and 2.5 cases per 1000 premature

births. Approximately 30% of newborns with clinical sepsis have associated bacterial

meningitis.

Since the initiation of intrapartum antibiotics in 1996, a decrease has occurred in the

national incidence of early-onset GBS infection from approximately 1.8 cases per 1000 live

births in 1990 to 0.32 case per 1000 live births in 2003.

InternationalThe use ofH influenzaetype B and pneumococcal vaccines is increasing worldwide at a rate

faster than that observed with hepatitis B vaccines.[2]

Mortality/MorbidityIn general, mortality rates vary with age and pathogen, with the highest being forS

pneumoniae. Despite effective antimicrobial and supportive therapy, mortality rates among

neonates remain high, with significant long-term sequelae in survivors. Bacterial meningitis

also causes long-term sequelae and results in significant morbidity beyond the neonatal

period. Mortality rates are highest during the first year of life, decreasing in mid life and

increasing again in elderly persons.


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Despite advances in care for patients with bacterial meningitis, the overall case fatality

remains steady at approximately 10-30%.

RaceIncidence rates are higher in black and Native American populations.

SexMale infants have a higher incidence of gram-negative neonatal meningitis. Female infants

are more susceptible toL monocytogenesinfection.Streptococcus agalactiae(group B

streptococci) affects both sexes equally.

V. HistorySymptoms of neonatal bacterial meningitis are nonspecific and include the following:

Poor feeding Lethargy Irritability Apnea Listlessness Apathy Fever Hypothermia Seizures JaundiceBulging fontanelle

Pallor Shock Hypotonia Shrill cry


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o Cardinal signs of meningitis (eg, fever, vomiting, stiff neck) are rarely present. Forneonatal meningitis, these signs are the exception, rather than the rule.

Infants and childreno Kernig and Brudzinski signs are helpful indicators when present, but they may be absent(along with nuchal rigidity) in the very young, debilitated, or malnourished infants.

o Skin findings range from a nonspecific blanching, erythematous, maculopapular rash to apetechial or purpuric rash, most characteristic of meningococcal meningitis.

o Patients may also have other foci of infection. Presenting symptoms may point toward thosefoci, causing unnecessary delay in diagnosis of bacterial meningitis.

o Approximately 15% of patients have focal neurologic signs upon diagnosis. The presence offocal neurologic signs predicts a complicated hospital course and significant long-term

sequelae.

o Generalized or focal seizures are observed in as many as 33% of patients. Seizures thatoccur during the first 3 days of illness usually have little prognostic significance.

However, prolonged or difficult-to-control seizures, especially when observed beyond the

fourth hospital day, are predictors of a complicated hospital course with serious

sequelae.

o In later stages of the disease, a few patients develop focal CNS symptoms and othersystemic signs (eg, fever) indicating a significant collection of fluid in the subdural

space. Incidence of subdural effusion is independent of the bacterial organism causing

meningitis.

o Approximately 6% of affected infants and children show signs of disseminated intravascularcoagulopathy and endotoxic shock. These signs are indicative of a poor prognosis


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VI. CausesThe causes are as follows:

Etiology of neonatal meningitiso Bacteria are often acquired from the maternal vaginal flora. Gram-negative enteric floraand group B streptococci are predominant pathogens. In premature newborns who receive

multiple antibiotics, hyperalimentation, and who undergo various surgical

procedures,Staphylococcus epidermidisandCandidaspecies are uncommon etiologies but are

reported in greater frequency in neonates.L monocytogenesis another well known but

fairly uncommon etiologic pathogen.

o Early onset group B streptococcal meningitis occurs during the first 7 days of life, aconsequence of maternal colonization and the absence of protective antibody in the

neonate; it is often associated with obstetric complications. The disease is seen most

often in premature or low birth weight babies. Pathogens are acquired before or during the

birth process.

o Late-onset meningitis is defined as disease occurring after 7 days of life. Etiologicagents include perinatally acquired and nosocomial pathogens.S agalactiae(group B

streptococci) are classified into 5 distinct serotypes: Ia, Ib, Ic, II, and III. Although

these serotypes occur with almost equal frequency in the early onset of disease, serotype

III causes 90% of late-onset disease.

o Use of respiratory equipment in the nursery increases the risk of infection causedbySerratia marcescens,Pseudomonas aeruginosa,andProteusspecies. Invasive devices

predispose infants to the infections caused byStaphylococcus epidermidisandPseudomonas,

Citrobacter,andBacteroidesspecies.

o Infection withCitrobacter diversus, Citrobacter koseri, Salmonellaspecies,andProteusspecies though uncommon, carries a high mortality rate. These patients often


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develop brain abscesses, particularlyCitrobacterwhere meningitis produces brain

abscesses in 80-90% of cases.

Etiology of meningitis in infants and children: In children older than 4 weeks,SpneumoniaeandN meningitidisare the most common etiologic agents.H influenzaetype b has

essentially disappeared in countries where the conjugate vaccine is routinely used.

S pneumoniaemeningitiso S pneumoniaeare lancet-shaped, gram-positive diplococci and are the leading cause ofmeningitis. Of the 84 serotypes, numbers 1, 3, 6, 7, 14, 19, and 23 are the ones most

often associated with bacteremia and meningitis.

o Children of any age may be affected, but incidence and severity are highest in very youngand elderly persons.

o In patients with recurrent meningitis, predisposing factors are anatomic defects,asplenia, and primary immune deficiency. Often history includes recent or remote head

trauma.

o This organism also has a predilection for causing meningitis in patients with sickle celldisease, other hemoglobinopathies, and functional asplenia. Immunity is type specific and

long lasting.

o S pneumoniaecolonizes the upper respiratory tract of healthy individuals; however,disease often is caused by a recently acquired isolate. Transmission is person-to-person,

usually by direct contact, and secondary cases are rare. The incubation period varies from

1-7 days, and infections are more prevalent during the winter when viral respiratory

disease is prevalent. The disease often results in sensorineural hearing loss,

hydrocephalus, and other CNS sequelae. Prolonged fever despite adequate therapy is common

in patients with meningitis caused by this organism.


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o Effective antimicrobial therapy can eradicate the organism from nasopharyngeal secretionswithin 24 hours. Over the past decade, pneumococci have developed resistance to a variety

of antibiotics. Although this development is seen worldwide, resistance rates to

penicillin vary from 10-60%. Recent multicenter surveillance results of pneumococci

isolated from the cerebrospinal fluid (CSF) show resistance rates of 20% and 7% to

penicillin and ceftriaxone, respectively. Penicillin resistance in pneumococci is due to

alterations in enzymes necessary for growth and repair of the penicillin-binding proteins;

thus, beta-lactamase inhibitors offer no advantage. Penicillin-resistant pneumococci often

demonstrate resistance to sulfamethoxazole/trimethoprim, tetracyclines, chloramphenicol,

and macrolides. However, selected third-generation cephalosporins (eg, cefotaxime,

ceftriaxone) do exhibit activity against most penicillin-resistant isolates.

o To date, all isolates remain susceptible to vancomycin and various oxazolidinones. Severalof the new fluoroquinolones (eg, levofloxacin), although contraindicated in children, have

excellent activity against most pneumococci and achieve adequate CNS penetration.

o Tolerance, a trait distinct from resistance, was first described in 1970 to characterizebacteria that stop growing in the presence of antibiotic, yet do not lyse and die.

Pneumococci tolerant to penicillin and vancomycin have been previously described in

literature and a subsequent link to recrudescence in meningitis described in one child.

The overall incidence and clinical impact of such bacterial strains is unknown. However,

this characteristic should be kept in mind in cases of recurrent pneumococcal meningitis.

N meningitidismeningitiso N meningitidisare gram-negative, kidney beanshaped organisms and frequently are foundintracellularly. Organisms are grouped serologically on the basis of capsular

polysaccharide; A, B, C, D, X, Y, Z, 29E, and W-135 are the pathogenic serotypes. In

developed countries, serotypes B, C, Y, and W-135 account for most childhood cases. Group


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A strains are most prevalent in developing countries and have resulted in epidemics of

meningococcal meningitis throughout the world and in outbreaks in military barracks. The

upper respiratory tract frequently is colonized with meningococci, and transmission is

person-to-person by direct contact through infected droplets of respiratory secretions,

often from asymptomatic carriers. The incubation period is generally less than 4 days,

with a range of 1-7 days.

o Most cases occur in infants aged 6-12 months; a second lower peak occurs amongadolescents. A petechial or purpuric rash frequently is seen. Mortality rates are

significant in patients who have a rapidly progressive fulminant form of the disease.

Normocellular CSF also has been reported in patients with meningococcal meningitis. Most

deaths occur within 24 hours of hospital admission in patients who have features

associated with poor prognosis (eg, hypotension, shock, neutropenia, extremes of ages,

petechiae and purpura of < 12 h duration, disseminated intravascular coagulopathy,

acidosis, presence of organism in WBC on peripheral smear, low erythrocyte sedimentation

rate [ESR] or C-reactive protein [CRP], serogroup C disease).

o Higher rates of fatality and physical sequelae such as scarring and amputation arereported in survivors of serogroup C disease. Long-term sequelae are rare in patients who

have an uneventful hospital course.

H influenzaetype b meningitiso H influenzaetype b is a pleomorphic gram-negative rod whose shape varies from acoccobacillary form to a long curved rod.H influenzaemeningitis occurs primarily in

children who have not been immunized withH influenzaetype b vaccine, with 80-90% of the

cases occurring in children aged 1 month to 3 years. By age 3 years, a significant number

of nonimmunized children acquire antibodies against the capsular polyribophosphate ofH

influenzaetype b, which are protective.


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o Mode of transmission is person-to-person by direct contact through infected droplets ofrespiratory secretions. The incubation period generally is less than 10 days.

o Current mortality rates are less than 5%. Most fatalities occur during the first few daysof the illness.

o Plasmid-mediated resistance to ampicillin due to the production of beta-lactamase enzymesby bacterium is being reported increasingly, and now 30-35% of the isolates are ampicillin

resistant. As many as 30% of cases may have subtle long-term sequelae. Administration of

dexamethasone early in treatment reduces the morbidity and sequelae.

L monocytogenesmeningitis:L monocytogenescauses meningitis in newborns,immunocompromised children, and pregnant women. The disease also has been associated with

the consumption of contaminated foods (eg, milk, cheese). Most cases are caused by

serotypes Ia, Ib, and IVb. Signs and symptoms in patients with listerial meningitis tend to

be subtle, and diagnosis often is delayed. In the laboratory, this pathogen can be

misidentified as a diphtheroid or as hemolytic streptococci.

Other causeso S epidermidisand other coagulase-negative staphylococci frequently cause meningitis andCSF shunt infection in patients with hydrocephalus or following neurosurgical procedures.

o Immunocompromised children can develop meningitis caused by species ofPseudomonas,Serratia,Proteus,and diphtheroids


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VII. Imaging StudiesCT scanning and MRI may reveal ventriculomegaly and sulcal effacement, as in the images

below.

Acute bacterial meningitis (same patient as in the other two images). This axial nonenhanced

CT scan shows mild ventriculomegaly and sulcal effacement.

Acute bacterial meningitis (same patient as in the other two images). This axial T2-weighted

MRI shows only mild ventriculomegaly.
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Acute bacterial meningitis (same patient as in the other two images). This contrast-enhanced,

axial T1-weighted MRI shows leptomeningeal enhancement (arrows)

VIII. Medical CareTreatment for bacterial meningitis includes the following:

Neonatalo Initiate treatment as soon as bacterial meningitis is suspected. Ideally, blood andcerebrospinal fluid (CSF) cultures should be obtained before antibiotics are administered.

If a newborn is on a ventilator and clinical judgment dictates that a spinal tap may be

hazardous, it can be deferred until the infant is stable. A spinal tap performed a few

days following initial treatment still reveals cellular and chemical abnormalities but

culture results may be negative.

o Establish intravenous access, and meticulously monitor fluid administration. Neonates withmeningitis are prone to develop hyponatremia due to syndrome of inappropriate antidiuretic

hormone secretion (SIADH). These electrolyte changes also contribute to the development of

seizures, especially during the first 72 hours of disease.

o Increased intracranial pressure secondary to cerebral edema is rarely a management problemin infants. Monitor blood gas levels closely to ensure adequate oxygenation and metabolic

stability.
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o MRI with gadoteridol, ultrasonography, or CT scanning with contrast is needed to delineateintracranial pathology. A Pediatric Academic Societies meeting in resulted in the

recommendation that MRIs with contrast should be performed for neonates with uncomplicated

meningitis 7-10 days after treatment initiation to ensure that no complicating pathology

is present. All newborns recovering from meningitis should have auditory evoked potential

studies to screen for hearing impairment.

Infants and children: Management of acute bacterial meningitis involves both appropriateantimicrobial therapy and supportive measures. All patients should have an audiologic

evaluation upon completion of therapy.

Fluid and electrolyte managemento Closely monitor patients by checking vital signs and neurologic status and by ensuring anaccurate record of intake and output.

o By prescribing the correct type and volume of fluid, the risk of development of brainedema can be minimized. The child should receive fluids sufficient to maintain systolic

blood pressure at around 80 mm Hg, urinary output of 500 mL/m2/d, and adequate tissue

perfusion. Although care to avoid SIADH is important, underhydrating the patient and risk

of decreased cerebral perfusion are equally concerning as well.

o Dopamine and other inotropic agents may be necessary to maintain blood pressure andadequate circulation.

IX. Deterrence/PreventionPrevention is an important aspect of care in bacterial meningitis because it has been

shown to reduce mortality and morbidity. It can be divided into 2 categories:

chemoprophylaxis and immunization.

H influenzae type b Chemoprophylaxis


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Risk of invasive disease is increased among unimmunized household contacts younger than 4years. Rifampin eradicates the organism from the pharynx of approximately 95% of carriers.

The efficacy of rifampin in preventing disease in childcare groups is not established.

Recommendations for rifampin chemoprophylaxis for contacts of index cases of invasiveHinfluenzaetype b disease include the following:

All household contacts with at least one contact younger than 4 years who is unimmunizedor partially immunized; those with a child younger than 12 months who has not received the

primary series; and those with an immunocompromised child (even if aged > 4 y), regardless

of immunization status

Nursery and childcare center contacts regardless of age, when 2 or more cases of invasivedisease have occurred within 60 days

For index case if younger than 2 years old or with a susceptible household contact andtreated with ampicillin or chloramphenicol

Immunization: Immunizations should be administered as per American Academy of Pediatricsguidelines.

[10]Universal immunization againstH influenzaetype b infection has led to a

dramatic decline in the incidence of invasiveH influenzaedisease.

N meningitidis Chemoprophylaxis Antimicrobial administration to contacts is divided into high- and low-risk categories.Only those stratified as high risk require prophylaxis.

Candidates for prophylaxis include the following: All household contacts Childcare or nursery school contact during 7 days before illness onset Direct exposure to index case secretions through kissing or sharing toothbrushes or eatingutensils, markers of close social contact during 7 days before illness onset


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Mouth-to-mouth resuscitation, unprotected contact during endotracheal intubation during 7days before illness onset

Frequently slept or ate in the same dwelling as index patient during 7 days before illnessonset

Outbreaks or clusters need to be managed as per local public health authorities. Immunization: A quadrivalent (ie, A, C, Y, W-135) meningococcal conjugate vaccine isrecommended for high-risk groups, including patients with immunodeficiency, patients with

functional or anatomic asplenia, and patients with deficiencies of terminal components of

complement. The vaccine is also valuable in controlling the epidemics of meningococcal

disease. The Advisory Committee on Immunization Practices (ACIP) has recommended this vaccine

for all children aged 11-12 years and first-year college students who will be living in a

dormitory or dormitorylike setting, and other high-risk groups.[11]

S pneumoniae Chemoprophylaxis: Routine chemoprophylactic measures for invasive disease secondary to thisorganism are limited to people with specific medical conditions.

Immunizations: The heptavalent pneumococcal conjugate vaccine has been introduced into theprimary childhood vaccination schedule. Immunizations should be administered as per American

Academy of Pediatrics guidelines. The polysaccharide vaccine is generally used for those with

specific medical conditions.

Table 4. Chemoprophylaxis for Contacts of Patients and Index (Case ofH influenzaetype b

and contacts of meningococcal disease)(Open Table in a new window)

Drug Name Age ofContact

Dosage


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H influenzaedisease

Rifampin Adults 600 mg PO qd for 4

d

1 month 20 mg/kg PO qd for 4

d;

not to exceed 600 mg/dose

< 1 month 10 mg/kg PO qd for

4 d

N meningitidisdisease

Rifampin Adults 600 mg PO q12h for 2

d

>1 month 10 mg/kg PO q12h for

2 d;


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not to exceed 600 mg/dose

1 month 5 mg/kg PO q12h for 2

d

Ceftriaxone >15 years 250 mg IM once

15

years125 mg IM once

Ciprofloxacin 18

years

500 mg PO once

X. ComplicationsComplications of bacterial meningitis include the following:

Seizures: These are a common complication of bacterial meningitis, affecting almost onethird of the patients. Persistent seizures, seizures late in the course of disease, and

focal seizures are more likely to be associated with neurologic sequelae.

Other complications: Numerous other complications that can be seen during the course ofbacterial meningitis include syndrome of inappropriate antidiuretic hormone secretion

(SIADH), subdural effusions, and brain abscesses. Subdural effusions are generally

asymptomatic and resolve without neurologic sequelae.


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Long-term sequelae: These are seen in as many as 30% of children and vary with etiologicagent, patient's age, presenting features, and hospital course. Long-term, close follow-up

care of children is crucial for the early detection of sequelae.

CNS sequelae: Although most patients have subtle CNS changes, serious complicationsoccasionally are observed. These complications include nerve deafness, cortical blindness,

hemiparesis, quadriparesis, muscular hypertonia, ataxia, complex seizure disorders, mental

motor retardation, learning disabilities, obstructive hydrocephalus, and cerebral atrophy.

Hearing impairmento Mild-to-severe impairment of hearing is noted in as many as 20-30% of affected childrenwithH influenzaedisease but is less common with other pathogens.

o Early administration of dexamethasone reduces the incidence of audiologic complicationsinH influenzaetype b meningitis.

o Severe hearing impairment interferes with the development of normal speech; thus, frequentaudiologic evaluation and developmental assessment must be performed during healthcare

visits.

Motor sequelae: Whenever motor sequelae are detected, physical, occupational, andrehabilitation services should evaluate the patient to prevent further damage and to provide

optimal functional status

XI. PrognosisProlonged or difficult-to-control seizures, especially after the fourth hospital day, are

predictors of a complicated hospital course with serious sequelae. On the other hand,

seizures that occur during the first 3 days of illness usually have little prognostic

significance.

Approximately 6% of affected infants and children show signs of disseminated intravascular

coagulopathy and endotoxic shock. These signs are indicative of a poor prognosis

Documents

Pediatric Bacterial Meningitis