bacterial central infections in children

Pediatrics

Bacterial Central

Nervous System

Infections

in ChildrenSheldon L. Kaplan, MD

Baylor College of Medicine

Texas Children’s Hospital

Houston, TX

xxx00.#####.ppt 9/9/2021 9:15:10 AMPediatrics

Disclosures

•Pfizer-Grant for Investigator initiated multicenter

pediatric surveillance study of invasive and local

pneumococcal infections.

•Allergan-Investigator initiated study of ceftaroline

for acute osteomyelitis in children

•MeMed-Site PI for Apollo study of MeMed device


Learning Objectives

•Review key ABP 2021 ID Subboard

Infectious Diseases Content for Central

Nervous System Infections


Pathogenesis of Bacterial Meningitis

•Usually is the result of hematogenous dissemination

of organisms

•Bacterial invasion from a contiguous focus of infection,

as in infection of the mastoid or paranasal sinuses, or

as a complication of otitis media.

•Fracture through the paranasal sinuses as a result of

head trauma may precede development of meningitis

caused by S. pneumoniae and H. influenzae

Kim KS Lancet Infect Dis 2010;10:32-42


Pathogenesis of Bacterial Meningitis

•Direct invasion also may occur in individuals with

dermoid sinus tracks or meningomyeloceles, where a

direct communication between the skin and the

meninges is present

•Neurosurgical procedures

and devices

Chen T-M J Pediatr Infect Dis Soc 2021;28:635-640


Clinical Manifestations of Bacterial Meningitis

•Fever generally is present

•Nausea, vomiting, irritability, anorexia, headache,

confusion, back pain, and nuchal rigidity

•Signs of meningeal inflammation (Kernig and

Brudzinski signs) may be minimal in the infant, but

irritability, restlessness, and poor feeding may be

noted


Clinical Manifestations of

Bacterial Meningitis

•Increased intracranial pressure is the rule; it may be reflected by complaints of headache in older children and by a bulging fontanelle and diastasis of sutures in the infant.

•Papilledema is an uncommon finding in acute meningitis, presumably because of the relatively brief duration of increased pressure at the time of diagnosis.

•When papilledema is observed, venous sinus occlusion, subdural empyema, or brain abscess should be sought

•Transient or permanent paralysis of cranial nerves may be noted



Normal Child Greater than Two Months Old

Expected Organisms

Streptococcus pneumoniae

Neisseria meningitidis

Haemophilus influenzae type b

(type a, f, or non-typeable)

Soeters et al. Clin Infect Dis 2020 June 26



Infants less than Two Months Old

Expected Organisms

Group B streptococcus

Gram-negative Enterics (E. coli)


Listeria monocytogenes

Haemophilus influenzae non-typeable



Unusual Organisms

• Dermal sinus- S. aureus, CONS, Gram-negative enterics

• Post neurosurgical procedures- S. aureus, Gram-negative

enterics, CONS

• Renal transplantation- Listeria monocytogenes

• Group A streptococcus*

• In infants-Enterococcus spp, Salmonella spp, Cronobacter

sakazakii, Citrobacter koseri (brain abscess), Pasteurella

multocida (cat or dog)

*Van Veen et al. Transplant Infect Dis 2016;18:674-680


Seizures in Bacterial Meningitis

•20% of patients have seizures prior to admission

•A third of patients have seizures prior to or during 1st 48

hours of hospitalization

•Early, generalized or multifocal seizures of short duration

and minimal frequency are related to “toxic

encephalopathy” associated with bacterial toxins,

hypoperfusion and metabolic derangements; EEG usually

not helpful. Usually controlled easily and have no

prognostic implications

Pomeroy SL et al. N Engl J Med 1990;323:1651-7


Seizures in Bacterial Meningitis

•Persistent focal seizures or recurrent seizures of varying focality imply an underlying complication such as venous or arterial thrombosis with infarction or symptomatic subdural effusion

•Seizures which are difficult to control, which persist beyond the 3rd hospital day or which develop initially after the 3rd hospital day may be associated with permanent sequelae

Pomeroy SL et al. N Engl J Med 1990;323:1651-7


CSF Diagnostic Tests

•Gram stain-60 to 90% positive

•PCR-particularly helpful for N. meningitidis in culture negative patient.

•Role of multiplex nucleic acid amplification CSF panels that include bacterial, viral and fungal pathogens is not certain. Most helpful in patients with negative CSF cultures and/or PCR for more common viral etiologies although false positive results are not uncommon.*

Olarte L et al. Clin Infect Dis 2015;61:767-775

*Ekambaram et al. 2020 IDWeek



Normal Child Greater than Two Months Old

Expected Organisms



Haemophilus influenzae type b (a, f, NT)*

Empiric therapy+

Ceftriaxone +

Vancomycin

+Rifampin may be considered if adjunctive

dexamethasone administered

*Ampicillin-resistance can be due to ß-lactamase production or alterations in PBP3

Tsang et al. J Antimicrob Chemother 2017;72:1314


Failure of Broad-Spectrum Cephalosporins

for Pneumococcal Meningitis- USA

MIC

Location Age Therapy mg/kg/day Penicillin Cefotaxime Ceftriaxone

San Diego 2.5 y ceftriaxone (100)* 0.5 2 2Memphis 13 mo

13 mo4 mo11 mo

cefotaxime (200)*cefuroxime (150)cefotaxime (200)cefotaxime

0.254

0.52

3288

16

16

848

Dallas 9 mo ceftriaxone (80) 2 4 4Indianapolis 28 mo ceftriaxone (90)* 4 2 2Ann Arbor 6 mo cefotaxime (200)* 2 >2 >2Providence 33 y ceftriaxone (4 gm)* 1.4 1.4 1.0

*dexamethasone also administered


2021 CLSI Pneumococcal Breakpoints

Antimicrobial

Agent

MIC (µg/mL)

Interpretive Standard

S I R

Penicillin parenteral

(meningitis)

0.06 0.12-1 2

Penicillin parenteral

(nonmeningitis)

2 4 8


2021 CLSI Pneumococcal Breakpoints

Antimicrobial

Agent

MIC (µg/mL)

Interpretive Standard

S I R

ceftriaxone or

cefotaxime

(meningitis)

0.5 1 2

ceftriaxone or

cefotaxime

(nonmeningitis)

1 2 4


Current Antibiotic Susceptibilities of


•In 2018 and 2019, 31% and 6% of IPD

isolates in the Pediatric Multicenter

Pneumococcal Surveillance Study were

non-susceptible to penicillin (MIC > 0.06

µg/mL) and ceftriaxone (MIC > 0.5

µg/mL), respectively, for treating

bacterial meningitis.

Kaplan et al. Abstract #176

IDWeek 2020


Treatment of Pneumococcal Meningitis

Penicillin MIC Ceftriaxone MIC Therapy

(1) < 0.06 µg/ml < 0.5 µg/ml Penicillin

(2 ) > 0.12 /µg/ml < 0.5 µg/ml Ceftriaxone

1 µg/ml Ceftriaxone

+Vancomycin

> 2 µg/ml Ceftriaxone +

Vancomycin+

? Rifampin


Meningococcal Meningitis

Treatment Options•Penicillin

•Ampicillin

•Ceftriaxone/cefotaxime

•Meropenem for patients with anaphylactic reactions

to ß-lactam antibiotics (Chloramphenicol)

•Duration-5-7 days for most cases


•During 2019–2020, 11 meningococcal isolates from U.S. patients had

isolates containing a blaROB-1 β-lactamase gene associated with

penicillin resistance and mutations associated with ciprofloxacin

resistance. An additional 22 cases reported during 2013–2020

contained blaROB-1 but did not have mutations associated with

ciprofloxacin resistance.

What are the implications for public health practice?

•Ceftriaxone and cefotaxime can continue to be used for empiric

bacterial meningitis treatment; meningococcal isolate susceptibility

to penicillin should be determined before switching to penicillin or

ampicillin.* Prophylaxis failures and antimicrobial resistance among

meningococcal isolates should be monitored to inform meningococcal

prophylaxis recommendations.

MMWR June 19, 2020

*2021 Red Book also has this recommendation


Gram-Negative Meningitis

•Combination therapy with cefotaxime (cefepime,

ceftazidime) and an aminoglycoside is used for

empirical therapy and until CSF is sterile.

•For ampicillin-susceptible CSF isolates of E coli,

meningitis can be treated with ampicillin or cefotaxime

(cefepime, ceftazidime)

•Meningitis caused by an ampicillin-resistant,

cefotaxime-susceptible isolate can be treated with

cefotaxime (cefepime, ceftazidime).

2021 Red Book


Gram-Negative Meningitis

A carbapenem is the drug of choice for treatment of

infections caused by ESBL-producing organisms, especially

some Klebsiella pneumoniae isolates. Of the

aminoglycosides, amikacin retains the most activity against

ESBL-producing strains.

2021 Red Book


Causes of Prolonged or Recurrent Fever

in Children with Bacterial Meningitis

•Inadequate Treatment

•Nosocomial Infection

•Dexamethasone D/CD

•Phlebitis

•Immune mediated arthritis

•Drug Fever

•Suppurative complication

-Pericarditis

-Pneumonia

-Pyogenic arthritis

-Subdural empyema

•Unknown

Lin Ty et al. Pediatr Infect Dis J 1984;3:319-22


Indications for Repeat Lumbar

Puncture

•Patient not responding clinically after

48 h of appropriate therapy.

•Pneumococcal isolate resistant to

ceftriaxone (MIC > 2 µg/ml)

•Patient with Gram-negative meningitis


Indications for Neuroimaging

in Bacterial meningitis

•Neonatal bacterial meningitis

•Persistent focal neurologic findings

•Persistently positive CSF cultures despite appropriate therapy

•Recurrent meningitis

* In general neuroimaging does not elucidate the cause of prolonged fever

Klein JO et al. Pediatrics 78:959-82

Kralik et al. AJNR Am J Neuroradiol 2019;40:1413-1417


•H. influenzae 43%

•S. pneumoniae 30%

•N. meningitidis 22%

•No difference in duration of fever or outcome

between children with or without an effusion.

Snedeker et al. Pediatrics 1990;86:163-170


Neurologic Sequelae of Bacterial Meningitis

•intellectual disabilities

-language delay

-learning disorders

•behavior disorders

•delayed or abnormal motor

development

•hemiparesis

•hearing handicap

•ataxia

•seizure disorder

•blindness

•hydrocephalus

•hypothalamic dysfunction

Olarte L et al. Clin Infect Dis 2015;61:767-775


Sensorineural Hearing Loss in


•Unilateral or bilateral loss

S. pneumoniae 30%

H. influenzae type b 6-15%

N. meningitidis 5-10%

•Ataxia commonly associated with deafness#

•Hearing loss appears to occur early-present at or near

time of admission*Dodge PR et al. N Engl J Med 1984;311:869-874

#Kaplan SL et al. Pediatrics 1981;68:8-13

*Wald ER et al. Pediatrics 1995;95:21-28


Pathogenesis of Deafness in

Bacterial Meningitis•labyrinthitis develops following bacterial invasion of the cochlea presumably via the cochlear aqueduct from CSF

•bacteria may also reach the cochlea hematogenously via the stria vascularis, a highly vascularized wall of the scalamedia

•direct damage to auditory nerve by inflammatory response or bacteria reaching the nerve through the internal auditory canal


Brain Abscess-Location and Origin

•Ear and mastoid sources are associated with abscess formation at the temporal or cerebellar locations

• Sinus and dental infections give rise to purulent collections in the frontal lobe

• Metastatic spread from distant foci in children with congenital cardiac or pulmonary right-to-left shunts commonly results in involvement of any parenchyma area, including parietal or occipital regions


Usual Location of Lesion, and Associated Neurologic

Findings in Children with Brain Abscess

•Headache in older children and adolescents,

irritability in infants and younger children

•Behavioral changes if abscess in the frontal or

temporal lobes

•CN palsy, gait disturbance, headache or altered

mental status if abscess in the cerebellum

•Seizures occur in up to 25% of patients

Textbook of Pediatric Infectious Diseases 2019


Brain Abscess-Neuroimaging

•MRI scanning is superior to CT for soft-tissue resolution and imaging detail. It is more sensitive for detecting cerebritis and edema formation than CT.

•MRI scanning is also more accurate than CT for diagnosis of cerebellar and brainstem purulent collections.

•Serial CT or MRI scanning, performed weekly or biweekly, provides evaluation on the response to therapy and on the need for a repeat surgical procedure.


Primary Source Usual Etiologic MicroorganismsUpper Respiratory Infection

Sinusitis/dental infection Viridans and anaerobic streptococci, Haemophilus spp., Fusobacterium spp., Bacteroides spp. (non-fragilis)

Chronic otitis/mastoiditis Aerobic and anaerobic streptococci, gram-negative enteric bacilli, Bacteroides spp. (including B. fragilis), Pseudomonas aeruginosa

Head trauma Staphylococcus aureus, aerobic streptococci, gram-negative enteric bacilli

Postoperative Staphylococcus epidermidis, S. aureus, gram-negative rods, P. aeruginosa

Endocarditis S. aureus, viridans streptococci

Pulmonary infection Aerobic streptococci, Actinomyces, Fusobacterium

Congenital heart disease Viridans streptococci, Haemophilus spp., Haemophilus aphrophilus

Bacterial meningitis S. pneumoniae, Haemophilus influenzae, Salmonella spp., Citrobacter (neonates)

Cryptogenic source and immunosuppression Any type of microorganisms

Nocardia, fungi, Mycobacterium tuberculosis

Primary Source, Usual Etiologic Pathogens in Children with Brain Abscess


Dou Z-Z et al. Pediatr Infect Dis J 2021;40:109-115


Brain Abscess-Empiric Antibiotics

•Sinusitis/Otitis media/Mastoiditis/Dental infection

Vancomycin + Ceftriaxone/Cefotaxime +

Metronidazole

•Head trauma

Vancomycin/nafcillin + Ceftriaxone/cefotaxime

•Post-operative

Vancomycin + Ceftazidime or cefepime


Brain Abscess-Operative Treatment•Prompt surgical intervention is critical in most

cases

•By removing purulent material, reduction of

intracranial pressure and relief of the mass effect

caused by the abscess are rapidly achieved.

•By providing a specimen for bacteriologic analysis

and antibiotic susceptibility testing, specific

antimicrobial therapy can be promptly

administered.


Brain Abscess

Non-Operative Treatment•May be appropriate for clinically stable patients who are poor candidates for surgery or have inaccessible lesions.

•Small collections (<2 cm) located in well-vascularized cortical areas are more likely to respond to antibiotics alone.

•Cases treated in this manner may require a more prolonged duration of treatment and close clinical and radiographic follow-up.

•Repeat CT and MRI (some experts discourage MRI for follow up) imaging will eventually show a decrease in size of the abscess, disappearing of surrounding edema, and lessening of the enhancement ring. These improvements are usually observed within 1 to 4 weeks but complete radiographic resolution often extends to several months of follow-up.


Brain Abscess

•The appropriate duration of antimicrobial therapy

for brain abscess is unclear.

•A 4- to 8-week course of parenteral antibiotics has

been recommended traditionally, provided that the

etiologic organisms are susceptible and adequate

surgical drainage is achieved. Also resolution or

substantial improvement of neuroimaging findings

help determine duration.


UpToDate


Cranial Epidural Abscess

•Localized collection of pus between the dura mater and the overlying skull or vertebral column

•Pathogenesis of cranial epidural abscess is usually spread from a focus in the paranasal sinuses, middle ear, or mastoid cells via phlebitic bridging veins, hematogenous spread, or direct extension from adjacent structures.

•Etiology-streptococci (Streptococcus anginosusgroup) including S. pneumoniae and GAS, anaerobes and microaerophilic streptococci, S. aureus, polymicrobial; gram-negative bacilli (chronic sinusitis)

Otto et al. JPIDS 2021;10:309-316

McNeil et al. PIDJ 2020;39:108-113


Cranial Epidural Abscess Treatment

•The management of cranial epidural abscess requires a combined medical and surgical approach. Empirical antimicrobial therapy for cranial epidural abscess usually vancomycin, ceftriaxone/cefotaxime plus metronidazole if secondary to sinusitis or mastoiditis pending cultures.

•Surgical drainage typically required; craniotomy or craniectomy is generally preferred over burr hole placement or aspiration of purulent material through the scalp. Endoscopic sinus surgery (EES) generally also performed if complication of sinusitis.

• If abscess associated with minimal mass effect, EES plus antibiotics may suffice.

•Therapy is usually continued for 3 to 6 weeks after surgical drainage, or longer (6 to 8 weeks) if osteomyelitis is present. Transition to oral levofloxacin successful in completing therapy for purulent S. anginosisintracranial infections in a preliminary pediatric report. (Dodson et al. 2020 IDWeek)

Bonfield et al. J Infect 2015;71:S42-S46

Pediatrics

Thank You


Supplemental Material


2004 IDSA Bacterial Meningitis Guidelines

Suspected Bacterial Meningitis in a Child

•If patient is immunocompromised, has a history of

selected CNS diseases (ie mass lesion,

hydrocephalus), has papilledema, or selected focal

neurologic deficits (facial palsy)

Delay LP

Obtain blood cultures

Administer empiric antibiotics

Head CT scan, if negative proceed with LP

IDSA Bacterial Meningitis Practice Guidelines

Clin Infect Dis 2004;39:1267-84


Bacterial meningitis

Differential Diagnosis

•Tuberculous meningitis

•Fungal meningitis

•Aseptic meningitis

•Brain abscess

•Intracranial or spinal epidural abscesses

•Bacterial endocarditis with embolism

•Subdural empyema with

or without

thrombophlebitis

•Ruptured dermoid cysts

•Ruptured spinal

ependymomas

• Brain tumors


https://www.cdc.gov/pneumococcal/surveillance.html


https://www.cdc.gov/meningococcal/images/meningococcal-disease-incidence.jpg


https://www.cdc.gov/meningococcal/images/meningococcal-incidence-serogroup.jpg?noicon


https://www.cdc.gov/meningococcal/images/meningococcal-

graph.jpg?noicon



Antimicrobial Susceptibility•Susceptible

penicillin MIC < 0.06 μg/ml

ceftriaxone MIC < 0.12 μg/ml

• Intermediate

penicillin MIC 0.12-0.25 μg/ml

ceftriaxone MIC not defined

• Resistant

penicillin MIC > 0.5 μg/ml

ceftriaxone MIC not defined

CLSI


Meningococcal Disease

Clinical Manifestations•Fever

•Muscle Aches

•Headache (stiff neck with meningitis)

•Nausea and vomiting

•Hypotension

•Rash

-macular papular rash initially in 25%‐petechiae-50-60%; primarily on trunk and extremities) -purpura-15-25%


United States Pediatric

Meningococcal Surveillance StudySelected Clinical and Laboratory Features in Children with

Meningococcal Infections by Age at Admission to Hospital

Features < 5 yo

N=105

6-10 yo

N=21

>10 yo

N=33

Petechiae 57 13 17

Purpura 36 11 13

Hypotension 13 0 3

Platelet Ct <

100,000/mm3

5 1 3

ANC < 1500/mm3 8

P=0.007

0 0

Kaplan et al Pediatrics

2006;118:e979-984.

Kaplan et al Pediatrics 2006;118:e979-984


United States Pediatric Meningococcal

Surveillance Study: Outcome

• The mortality rate for all patients with invasive infections was 8% (13/159).

• The mortality rate was greater for children > 11 years old [7/33 (21.2%)] than for children < 11 years old [6/126 (4.8%)] (RR-3.0, 95% CI 1.6-5.6; P<0.001).

• Mortality in the three age groups < 5 years, 6-10 years and > 10 years old was 4/105 (3.8%), 2/21 (9.5%) and 7/33 (21.2%), respectively (P= 0.01).

Kaplan et al Pediatrics 2006;118:e979-984.




• Of the 13 patients who died, 9 had meningitis

including one associated with fulminant bacteremia

and 4 had fulminant bacteremia alone. There was no

significant difference in mortality rates for children

with meningitis (9/112) versus those with bacteremia

alone (4/43).





•Hearing loss occurred in 14 children (all < 10 years old; 8 < 2 years old) or 12.5% of those with meningitis.

•Skin necrosis (n = 13; 9 < 4 years old) with some requirements for grafting was the second most common sequela.

•2 children suffered amputations.

•3 children had vasculitis and one had pericarditis



Dexamethasone for Bacterial Meningitis

•For infants and children 6 weeks and older, adjunctive

therapy with dexamethasone may be considered after

weighing the potential benefits and risks. Some experts

recommend use of corticosteroids in pneumococcal

meningitis, but this issue is controversial and data are

not sufficient to make a routine recommendation for

children. The Infectious Diseases Society of America

recommends use of dexamethasone in adults with

suspected or proven pneumococcal meningitis. If used,

dexamethasone should be administered before or

concurrently with the first dose of antimicrobial agents.

2021 Red Book


Dexamethasone for Bacterial Meningitis

• Dexamethasone is beneficial for treatment of infants

and children with Hib meningitis to diminish the risk of

hearing loss, if administered before or concurrently

with the first dose of antimicrobial agent(s)

2021 Red Book


Eosinophilic Meningitis•Angiostrongylus

•Gnathostoma

•Baylisacscaris

•Coccidiodes

•Schistosoma spp.

•M. tuberculosis

•T. pallidum

•Toxocariasis

•Toxoplasmosis

•Neurocysticercosis

•Chemical

•Drug hypersensitivity

•Neoplastic



Chronic Meningitis-Selected Causes

•M. tuberculosis

•Spirochetal: B. burgdorferi,

T. pallidum

•Bacterial: Brucella spp, Whipple’s

Disease, F. tularensis

•Viral: EBV, CMV, HIV, Enterovirus,

Herpes, Varicella

•Fungal: Cryptococcus,

Histoplasma, Coccidioides,

Blastomyces

•Parasitic: T. solium,

Angiostrongylus, Toxoplasma,

Acanthamoeba

•Non-infectious: neoplastic,

sarcoidosis, SLE, Vasculitis

•Drugs: TMP-SMX, IVIG, NSAIDS,

intrathecal chemotherapy

UpToDate


Symptoms Percent Signs Percent

Headache 60-70% Focal Neurologic Deficits 35-50%

Fever 50-80% Papilledema 30-40%

Vomiting 35-55% Meningeal Signs 25-35%

Seizures 30-45% Hemiparesis 20-30%

Mental changes 30-40% Cranial nerve palsy 10-20%

Coma 15-20% Ataxia 5-15%

Frequency of Presenting Signs and Symptoms in

Children with Brain Abscess



Primary Source Location of Abscess Associated Neurologic Findings

Sinusitis Frontal lobe Headache, behavioral changes, motor speech disorders, depressed consciousness, forced grasping and sucking, hemiparesis

Chronic otitis/mastoiditis Temporal lobe Dyspraxia and aphasia (dominant hemisphere), ipsilateral third cranial nerve palsy, ipsilateral headache, upper homonymous hemianopsia, motor dysfunction of face and arm

Cerebellum Dizziness, vomiting, ipsilateral ataxia and tremor, sixth cranial nerve palsy, nystagmus (toward lesion)

Dental infection Frontal lobe

Head trauma Related to injured site Variable by region involved

Postoperative At operative site Variable by region involved

Metastatic spread Multiple lesions Variable by region involved

If parietal lobe involved Visual field defects in inferior quadrant, homonymous hemianopsia, dysphasia (dominant hemisphere), dyspraxia and contralateral spatial neglect

Primary Source, Usual Location of Lesion, and Associated

Neurologic Findings in Children with Brain Abscess



Brain Abscess

•Steroid treatment of brain abscess is controversial. These agents are usually indicated to control life-threatening intracranial hypertension that is associated with risk of herniation or when significant symptoms and signs are presumed to be the result of cerebral edema.

•Severe brain edema may necessitate the additional administration of intravenous mannitol.

•Anticonvulsants are recommended in children who have developed seizures to potentially prevent further episodes


Brain Abscess

•Mortality associated with brain abscess in infantsand children is < 20%, reflecting earlier, moreaccurate diagnosis, appropriate antimicrobialtherapy, and novel surgical modalities.

• Focal residual deficits may persist, depending onthe location of the abscess and the underlyingpathologic process of affected patients.

•The mortality is higher among pediatric patientswith severe mental status changes onpresentation, multiple collections, and rapidlyprogressing neurological impairment


Cranial Epidural Abscess

Clinical Manifestations

•Most common in adolescent males

•Facial or eye swelling (associated with sinusitis); Pott’s puffy tumor or frontal bone osteomyelitis

•Headache, nausea, vomiting

•Altered mental status

•Papilledema, focal neurologic signs

•New onset seizures

Otto et al. JPIDS 2021;10:309-316


Cranial or Spinal Epidural Abscess

Diagnosis

•Head CT usually obtained initially

•MRI with gadolinium enhancement is

the diagnostic procedure of choice


Subdural Empyema

•A collection of purulent material in the space

between the dura and arachnoid membranes.

•Most common predisposing conditions to cranial

subdural empyema are ENT infections, especially

of the paranasal sinuses, which are affected in

50% to 80% of cases.

•Complication of bacterial meningitis


Subdural Empyema-Pathogenesis

•Spread of the infection from sinuses to the subdural space via valveless emissary veins in association with thrombophlebitis, or via extension of an osteomyelitis of the skull with accompanying epidural abscess.

•Once infection reaches the subdural space, it can spread without interruption over the convexities of the brain.

•The mastoid and middle ear are the source in 10% to 20% of patients.

•Other predisposing conditions in patients with subdural empyema include skull trauma, neurosurgical procedures, and infection of a preexisting subdural hematoma.

A Tunkel. Principles and Practice of Infectious Diseases


Subdural Empyema-Etiology

•Aerobic streptococci most common

•Staphylococci (10% to 15% of cases)

•Aerobic gram-negative bacilli (3% to 10% of cases),

anaerobic streptococci and other anaerobes

•Polymicrobial infections are common

•Postoperative and post-traumatic infections are more

commonly caused by staphylococci and aerobic gram-

negative bacilli.



Subdural Empyema

Clinical Manifestations

•High Fever

•Increasingly severe headache; signs of increased intracranial pressure or meningeal irritation

•Progressive neurologic deficits depending on the site of infection

•Altered mental status (i.e., drowsiness and disorientation), which can progress to obtundationor coma.

•Focal or generalized seizures



Subdural Empyema Diagnosis

• MRI is imaging modality of choice

• CT scan maybe preferred for patients who are critically ill and require immediate neurosurgical intervention


Subdural Empyema Treatment

•Treatment optimally requires a combined medical and surgical approach

•If S. aureus is a suspected pathogen, vancomycin should be used empirically but changed to nafcillin if the organism is found to be methicillin susceptible and the patient is not allergic to penicillin.

•Metronidazole is recommended if anaerobes are suspected.

•For infection likely caused by aerobic gram-negative bacilli, empirical therapy with cefepime, ceftazidime or meropenem is appropriate, pending microorganism identification and in vitro susceptibility testing.



Subdural Empyema Treatment Duration

•Depending on the clinical response, parenteral antimicrobial therapy should be continued for 3 to 4 weeks after drainage; longer periods of intravenous, and perhaps oral, therapy may be required if the patient has accompanying osteomyelitis.

•Antimicrobial therapy alone may be appropriate in patients with minimal or no impairment of consciousness, no major neurologic deficit, limited extension of the empyema without midline shift, and early improvement with antimicrobial therapy alone. These selected patients need careful clinical and radiographic monitoring, and probably longer courses of antimicrobial therapy.



Subdural Empyema Outcome

•Mortality rates among patients with cranial subdural

empyema range from 7 to 12%

•Permanent neurologic deficits can occur

•Cranial subdural empyemas may also be complicated

by septic venous thrombosis, localized cerebritis, and

cerebral abscesses


Spinal Epidural Abscess-Etiology

•Spinal epidural abscess is less common than cranial epidural abscess in children

•Spinal epidural abscess usually occurs secondary to hematogenous dissemination from foci elsewhere in the body to the epidural space, or by extension from vertebral osteomyelitis or congenital dermoid cyst.

•In otherwise normal children without prior surgery, S. aureus is most common followed by GAS.

• Other isolates include aerobic and anaerobic streptococci and aerobic gram-negative bacilli.

Houston et al. World Neurosurg 2019;126:453-460


Spinal Epidural Abscess

Clinical Manifestations•Fever

•Back pain

•The specific neurologic signs depend on the level of

spinal cord involvement; the most common locations

are the thoracic and lumbar epidural spaces.

•Neurologic manifestations are usually reversible

before complete paralysis occurs, thus emergency

imaging studies and intervention are necessary if the

diagnosis is being considered



Treatment•Prompt surgical decompression and drainage of the abscess based on neurologic signs present and extent of the abscess; non-surgical management possible in selected cases determined by neurosurgery and interventional radiology with close monitoring

•Empirical antimicrobial therapy includes vancomycin and nafcillin plus ceftriaxone or ceftazidime/cefepime if there was preceding neurosurgery.

•Antimicrobial therapy can be modified based on in vitro susceptibility testing.

•Duration of antibiotics usually 4 to 6 weeks



Treatment•Patients with spinal epidural abscess and neurologic dysfunction require laminectomy with decompression and drainage performed as a surgical emergency to minimize the likelihood of permanent neurologic sequelae.

• CT-guided aspiration may be used in place of laminectomy in selected patients.

• In collaboration with neurosurgical colleagues, antimicrobial therapy alone can be considered in patients who have localized pain or radicular symptoms without long-tract findings. However, these patients require frequent neurologic examinations and serial MRI studies to demonstrate resolution of the abscess. Emergency surgical decompression should be performed for any patient with increasing neurologic deficit and/or persistent severe pain.

A. Tunkel. Principles and Practice of Infectious Diseases


Ventriculo-Peritoneal Shunt

Infections

•Majority occur within one month of placement

•Incidence is higher in the first 6 months of life

compared to older children

•Prematurity and IVH important patient risk factors

•VP shunt infections are most commonly associated

with inoculation of the organism during surgery or

bacteria colonization during early wound healing




Infections-Pathogens

•Coagulase negative Staphylococci

(normal skin flora and biofilm production)

•Staphylococcus aureus

•Streptococci and Enterococcus spp.

•Corynebacterium and Cutibacterium

•Gram-negative enterics (bowel perforation)

•Candida spp and Mycobacteria-less common

•Streptococcus pneumoniae-hematogenous




Infections-Management

•Most successful approach includes removing the infected

VP shunt and placing an EVD

•Empiric antibiotics include vancomycin +

ceftazidime/cefepime depending on gram stain of

ventricular fluid and severity of illness

•Duration of antibiotics prior to replacement of VP shunt in

patient with abnormal ventricular fluid parameters and after

repeat ventricular fluid cultures are negative

CONS-7d

S. aureus and Gram negative enterics-10 d


Tunkel et al. Clin Infect Dis 2017;64:e34-e65

bacterial central infections in children

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