http://jcn.sagepub.com/Journal of Child Neurology

http://jcn.sagepub.com/content/early/2014/09/12/0883073814549247The online version of this article can be found at:

 DOI: 10.1177/0883073814549247

published online 15 September 2014J Child NeurolOzturk

Selim Doganay, Hakan Gumus, Ekrem Unal, Mehmet Kose, Sureyya Burcu Gorkem, Ali Kurtsoy and Mustafa Kursat Mehmet Canpolat, Ozgur Ceylan, Huseyin Per, Gonca Koc, Abdulfettah Tumturk, Sefer Kumandas, Turkan Patiroglu,

TurkeyBrain Abscesses in Children: Results of 24 Children From a Reference Center in Central Anatolia,

  

Published by:

http://www.sagepublications.com

can be found at:Journal of Child NeurologyAdditional services and information for    

  http://jcn.sagepub.com/cgi/alertsEmail Alerts:

 

http://jcn.sagepub.com/subscriptionsSubscriptions:  

http://www.sagepub.com/journalsReprints.navReprints:  

http://www.sagepub.com/journalsPermissions.navPermissions:  

What is This? 

- Sep 15, 2014OnlineFirst Version of Record >>

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Original Article

Brain Abscesses in Children: Results of24 Children From a Reference Centerin Central Anatolia, Turkey

Mehmet Canpolat, MD1, Ozgur Ceylan, MD2, Huseyin Per, MD1,Gonca Koc, MD3, Abdulfettah Tumturk, MD4, Sefer Kumandas, MD1,Turkan Patiroglu, MD5,6, Selim Doganay, MD3, Hakan Gumus, MD1,Ekrem Unal, MD5, Mehmet Kose, MD7, Sureyya Burcu Gorkem, MD3,Ali Kurtsoy, MD4, and Mustafa Kursat Ozturk, MD2

AbstractChildhood brain abscesses are a rare and potentially life-threatening condition requiring urgent diagnosis and treatment. This retro-spective study analyzed the clinical and radiologic findings of 24 (7 girl, 17 boys) cases with brain abscess. Mean age was 92.98+ 68.04months. The most common presenting symptoms were nausea-vomiting (45.8%) and headache (41.7%). Brain abscess was most com-monly located in the frontal region. Diffusion restriction was determined in 78.4% of lesions. The mean apparent diffusion coefficientvalue in these lesions was 0.511 + 0.23� 10–3 mm2/s. Cultures were sterile in 40% of cases. Antimicrobial therapy was given to only16.7% of cases. Predisposing factors were identified in 91.6% of cases (congenital heart disease in 20.8% and immunosuppression in20.8%). Mortality level was 12.5%. In conclusion, immunocompromised states, and congenital heart disease have become an importantpredisposing factor for brain abscesses. Effective and prompt management should ensure better outcome in childhood.

Keywordsbrain abscess, child, clinical and radiologic features

Received June 10, 2014. Received revised July 02, 2014. Accepted for publication August 02, 2014.

Brain abscesses in childhood are rare but serious infectious dis-

ease.1 It is difficult to assess the incidence of brain abscesses, but

it is probably 2 to 3 cases of every 10 000 hospital admissions.2

Approximately 25% of all brain abscesses are seen in childhood,

most commonly between the ages of 4 and 7.3-5 There is gener-

ally an underlying predisposing condition. The majority of brain

abscesses are associated with congenital heart defects and infec-

tions in the face, head, and brain. There is also a risk of brain

abscess in immunosuppressed children.3-7 Brain abscess may not

produce symptoms for weeks. Clinical findings may be mild and

may be affected by various factors such as age and location of

abscess. A classic triad characterized by headache, fever, and

focal neurologic deficit is seen in 9% to 28% of children.4,5 The

main micro-organisms responsible for brain abscess are

aerobic and anaerobic streptococci and staphylococci. The most

prevalent species in the viridans group are streptococci, espe-

cially Streptococcus milleri. Staphylococcus aureus generally

grows in cultures of abscesses developing after trauma. Other

microorganisms that cause brain abscesses are Bacteroides spe-

cies, Proteus species, Haemophilus influenzae, Escherichia coli,

Citrobacter group, Nocardia, Aspergillus, and Corynebacterium

species and Mycobacterium tuberculosis. No growth is

determined in more than 10% of cases, despite the latest culture

techniques.1-8

Management of brain abscesses is both medical and surgi-

cal, although medical treatment alone may be sufficient in

1 Division of Pediatric Neurology, Department of Pediatrics, Faculty of

Medicine, Erciyes University, Kayseri, Turkey2 Division of Pediatric Infectious diseases, Department of Pediatrics, Faculty of

Medicine, Erciyes University, Kayseri, Turkey3 Department of Pediatric Radiology, Faculty of Medicine, Erciyes University,

Kayseri, Turkey4 Department of Neurosurgery, Erciyes University, Faculty of Medicine,

Kayseri, Turkey5 Division of Hematology and Oncology, Department of Pediatrics, Faculty of

Medicine, Erciyes University, Kayseri, Turkey6 Division of Allergy and Immunology, Department of Pediatrics, Faculty of

Medicine, Erciyes University, Kayseri, Turkey7 Division of Pediatric Pulmonology, Department of Pediatrics, Faculty of

Medicine, Erciyes University, Kayseri, Turkey

Corresponding Author:

Huseyin Per, MD, Division of Pediatric Neurology, Department of Pediatrics,

Faculty of Medicine, Erciyes University, Talas, Kayseri 38039, Turkey.

Email: huseyinper@yahoo.com

Journal of Child Neurology1-10ª The Author(s) 2014Reprints and permission:sagepub.com/journalsPermissions.navDOI: 10.1177/0883073814549247jcn.sagepub.com

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

some selected cases. Surgical drainage and antimicrobial ther-

apy are the preferred options in most cases of brain tumor. Sur-

gical drainage (aspiration) or excision is advised if the lesion

diameter is >2.5 cm or if it causes a mass effect.2-5,9-11

The death rate in brain abscesses used to be around 30% to

60%, although there has been a significant decrease in recent

years, to below 10%. Early diagnosis with neuroradiologic

imaging, rapid neurosurgical intervention, and broad spectrum

antimicrobial therapy including both aerobic and anaerobic

bacteria has led to positive outcomes.3-5

The purpose of this study was to analyze the clinical findings,

radiologic characteristics, risk factors, and prognoses of 24 cases

under observation in our clinic with a diagnosis of brain abscess.

Methods

Cases diagnosed with brain abscess between September 2003 and May

2014, and monitored by the Erciyes University Faculty of Medicine

Pediatric Neurology and Pediatric Infectious Diseases, Turkey, were

evaluated retrospectively. The demographic findings, presenting

symptoms, underlying medical conditions, predisposing risk factors,

abscess sites, radiologic findings, micro-organisms isolated, treatment

regimes, prognoses, and outcomes were recorded of 24 patients aged

between 1 month and 17 years diagnosed with brain abscess and for

which records were available.

Brain abscess cranial computed tomography (CT) or magnetic

resonance imaging (MRI) findings were assessed retrospectively.

These consisted of lesion number and site, perilesional edema, post-

contrast ring sign, shift, presence of hypointense rim on T2-

weighted MRI, and presence or not of diffusion restriction on

diffusion-weighted MRIs. Apparent diffusion coefficient (ADC) val-

ues from lesions were analyzed quantitatively.

Aspirate material collected during surgery was processed in the

microbiology laboratory for urgent aerobic and anaerobic culture. In

nonsurgical cases, diagnosis was confirmed with typical clinical

symptoms and response to treatment.

Results

Twenty-four cases, 7 (29.2%) female and 17 (71.8%) male,

were diagnosed with brain abscess in the 10-year study period.

Figure 1. Abscess lesion in the right occipital lobe of an 11-year-old boy (case 21). The lesion was multilobulated on T2-weighted image (A) andhad a hypointense rim. Pronounced perilesional edema and shift to the left in midline structures can be seen. T1-weighted image after use ofcontrast (B) shows ring enhancement around the lesion. Note that the lesion exhibits pronounced diffusion restriction (C). T1-weighted image(D) at magnetic resonance imaging (MRI) obtained approximately 1 month after lesion drainage shows a smaller collection area showing ringenhancement in the operation localization. Because of the absence of a hypointense rim (E) and of diffusion restriction (not shown), this wasinterpreted as an operation cavity.

2 Journal of Child Neurology

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Mean age of patients was 92.98 + 68.04 months (minimum 1

month to maximum 204 months). Four cases were referred to

our clinic from other hospitals. General characteristics of cases

are shown in Table 1.

Clinical Features

The most common presenting symptoms were nausea-vomiting

in 11/24 (45.8%) cases, headache in 10/24 (41.7%), convulsion

in 9/24 (37.5%), fever in 7/24 (29.2%), and altered state of con-

sciousness in 7/24 (29.2%) (Table 1).

The most common findings at neurologic examination

were a normal neurologic appearance in 9/24 (37.5%) cases,

altered state of consciousness in 9/24 (37.5%) (stupor in 3 and

somnolence in 6), focal neurologic deficit in 6/24 (25.0%)

(aphasia in 1 case, facial paralysis in 1 case, hemiparesis in

2 cases, and anisocoria in 2 cases), bilateral positive Babinski

reflex in 3/24 (12.5%), papilledema in 1/24 (4.2%), and pos-

itive meningeal irritation findings in 1/24 (4.2%) (Table 1).

The classic triad of fever, headache, and focal neurologic

deficit was determined in 2/24 (8.4%) cases.

Predisposing Factors

Predisposing factors were identified in 22/24 (91.6%) cases.

The most common were congenital heart disease in 5/24

(20.8%) cases and immunosuppression in 5/24 (20.8%). Addi-

tionally, sinusitis was determined in 2/24 (8.3%) cases, dental

procedure in 2/24 (8.3%), autogenic factors in 2/24 (8.3%),

sepsis in 2/24 (8.3%), and trauma in 2/24 (8.3%), whereas the

condition developed postoperatively in 2/24 (8.3%). Pneumo-

nia was a predisposing factor in 1/24 (4.2%) cases and menin-

gitis in 1/24 (4.2%) cases. No predisposing factor was

determined in 2/24 (8.3%) cases (Table 1).

Dissemination

Postoperative spread was determined in 2/24 (8.3%) cases,

contiguous spread in 5/24 (20.8), and hematogenous spread

in 15/24 (62.5%). The 2 cases (8.3%) in which predisposing

factors were not identified were assessed as hematogenous

spread (Table 1).

Radiologic Findings

All cases underwent CT or MRI. Because preoperative images

for 4 cases referred to our clinic were not available from the

hospital records, these cases were evaluated from the records

in the files, and the other 20 cases were evaluated retrospec-

tively using the available images by 2 pediatric radiologists,

GK and SD. All cases were diagnosed radiologically with

brain abscess before surgery. Radiologic findings are given

in Table 2, and sample case images are given in Figure 1.

Abscesses ranged between 3.4 and 54 mm in size (mean +standard deviation ¼ 32 + 14.7 mm). The most common

abscess locations were supratentorial, in 16/20 (80%) cases.

Abscesses were located infratentorially in 1/20 (5%) cases and

were located in both supra- and infratentorial regions in 3/20

(15%) cases. Abscesses were single in 15/20 (75%) cases and

multiple in 5/20 (25%). Abscesses were frontal in 8/20 (40%)

cases, parietal in 1/20 (5%), occipital in 2/20 (10%), fronto-

parietal in 1/20 (5%), parieto-occipital in 1/20 (5%), tempor-

oparietal in 1/20 (5%), temporooccipital in 1/20 (5%),

cerebellar in 2/20 (10%), in the brain stem in 1/20 (5%), and

in the basal ganglia in 3/20 (15%) cases. Lesions were intra-

parenchymal in 16/20 (80%) cases, subdural in 3/20 (15%), and

epidural in 1/20 (5%).

Total number of abscesses determined in the 20 cases was

38. Only CT images were available for 1 patient. T2 hypoin-

tense rim was determined in 21/37 (56.8%) lesions (2 lesions

had 2-layer hypointense rims), capsular enhancement in 22/

37 (59.5%) lesions, perilesional edema in 30/37 (81.1%)

lesions, and shift in 8/20 (40%) cases, and diffusion restriction

was determined qualitatively in 29/37 (78.4%). Mean apparent

diffusion coefficient value in these 29 abscesses was 0.511 +0.23 � 10–3 mm2/s. Mean apparent diffusion coefficient value

in the 8 lesions not exhibiting qualitative diffusion restriction

was 1.274 + 0.12 � 10–3 mm2/s.

Microbiology

No growth occurred in blood cultures of the 4/24 (16.7%)

nonsurgical cases. Bacteriological investigation was positive

in 13/20 (65.0%) of cases receiving surgery and from which

abscess specimens were taken.

Positive results were obtained in 3/20 (15.0%) cases at gram

staining. Gram-negative bacillus was observed in 1 case at

Gram staining, but culture was sterile. Gram-positive chain

coke was observed in 2 cases at Gram staining, and Peptostrep-

tococcus grew in culture.

Growth was determined in abscess culture in 12/20 (60.0%)

cases. Peptostreptococcus grew in abscess culture in 4 cases

and Aspergillus in 2 cases. Proteus, Pseudomonas, Bacter-

oides, Streptococcus pneumoniae, S aureus, and E coli grew

in abscess culture in 1 case each (Table 1).

Treatment

Antimicrobial therapy alone was administered in 4/24 (16.7%)

cases, and both surgical and antimicrobial therapy in 20/24

(83.3%). In surgical treatment, excision with craniotomy was

performed in 4/20 (20.0%) cases and drainage surgery with burr

hole in 16/20 (80.0%). Shunt removal surgery and extraventricu-

lar drainage surgery were performed in the same session in 1

case in which drainage was applied. Medical treatment was

administered as antibiotic therapy for 6 weeks. Empiric antimi-

crobial therapy was given in 4/24 (16.7%) cases in which sur-

gery could not be performed and abscess specimens could not

be obtained, on the basis of predisposing risk factor, assumed

origin of infection, or hospital- or community-acquired infection

status. Empiric antimicrobial therapy initiated in 20/24 (83.3%)

cases undergoing surgery was adjusted on the basis of microbio-

logical investigation (Table 1).

Canpolat et al 3

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Tab

le1.

Pat

ients

’C

linic

alC

har

acte

rist

ics.

Pat

ient

Age

Gen

der

Pre

senting

sym

pto

ms

Pre

dis

posi

ng

conditio

nD

isse

min

atio

nN

euro

logi

cex

amin

atio

nSu

rger

yM

icro

bio

logy

(culture

)A

ntibio

tic

trea

tmen

tO

utc

om

e

117

yM

ale

F,N

V,A

CC

RF

(ren

altr

ansp

lant)

,se

condar

yim

munodef

icie

ncy

,pan

cyto

pen

ia,

hem

ophag

ocy

tosi

s

Hem

atoge

nous

Stupor,

Bab

insk

iþ

/þD

TR

hyp

erac

tive

No

Neg

ativ

eM

eropen

emþ

amik

acinþ

fluco

naz

oleþ

amphote

rici

nB

Die

d

213

yM

ale

H,N

VN

oH

emat

oge

nous

Pap

illed

ema

Dra

inag

eN

egat

ive

Cef

tria

xoneþ

met

ronid

azole

Good

31.5

yM

ale

F,N

V,S

Pneu

monia

Hem

atoge

nous

Som

nole

nce

Dra

inag

eN

egat

ive

Cef

tria

xoneþ

met

ronid

azole

þva

nco

myc

in

Good

44.5

yFe

mal

eF,

SA

LLH

emat

oge

nous

Norm

alD

rain

age

Asp

ergi

llus

nig

erA

mphote

rici

nBþ

vori

conaz

ole

Epile

psy

52.5

mo

Mal

eF,

Ps,

som

nole

nce

Uro

sepsi

sH

emat

oge

nous

Som

nole

nce

and

bulg

ing

fonta

nel

le,e

yes

dev

iate

dto

the

left

,ri

ght

hem

ipar

esis

Dra

inag

ePro

teus

Cef

ota

xim

eþ

amik

acinþ

mer

open

em

Epile

psy

,hem

ipar

esis

67.5

yM

ale

H,N

V,S

Max

illar

yan

dfr

onta

lsi

nusi

tis

Contigu

ous

Norm

alN

oN

egat

ive

Cef

tria

xoneþ

met

ronid

azole

þva

nco

myc

in

Epile

psy

714

yFe

mal

eF,

H,N

V,le

ftce

ntr

alfa

cial

par

alys

is

No

Hem

atoge

nous

Faci

alpar

alys

isD

rain

age

Neg

ativ

eM

eropen

emþ

met

ronid

azole

þri

fam

pin

Good

87

yM

ale

F,H

,so

mnole

nce

TG

Aþ

PS

Hem

atoge

nous

Som

nole

nce

Dra

inag

eG

rS!

Gr

(–)

bac

illus

Neg

ativ

eC

eftr

iaxoneþ

vanco

myc

inþ

met

ronid

azole

Epile

psy

99

yM

ale

HT

raum

a:fr

onta

lbone

frac

ture

Contigu

ous

Norm

alD

rain

age

Neg

ativ

eC

eftr

iaxoneþ

vanco

myc

inþ

met

ronid

azole

Good

10

4y

Mal

eS

Ara

chnoid

cyst

soper

ated

Post

oper

ativ

eN

orm

alExci

sion

Pse

udom

onas

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

Epile

psy

11

16

yM

ale

S,par

esth

esia

inth

ele

ftle

gC

GD

Hem

atoge

nous

Unre

mar

kable

exce

pt

for

ora

lm

onili

asis

and

skin

scar

sat

axill

ary

and

per

ianal

regi

on

Dra

inag

eAsp

ergi

llus

fum

igat

usA

mphote

rici

nBþ

vori

conaz

ole

Good

12

14

yM

ale

Spee

chdis

ord

ers,

SSi

nusi

tis

Contigu

ous

Aphas

ia,so

mnole

nce

Dra

inag

eG

rS!

Gr

(þ)

chai

nco

kePep

tost

repto

cocc

us

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

Epile

psy

13

12

yFe

mal

eH

,N

VO

titis

med

ia,

mas

toid

itis

,m

enin

gitis

Contigu

ous

Men

inge

alir

rita

tion

sign

sposi

tive

Dra

inag

eN

egat

ive

Cef

tria

xoneþ

mer

open

emþ

met

ronid

azole

Epile

psy

14

12

yM

ale

S,co

ugh

WA

S,m

uco

sitis,

lung

absc

ess

Hem

atoge

nous

Norm

alD

rain

age

Pep

tost

repto

cocc

us

Cef

tria

xoneþ

vanco

myc

inEpile

psy

15

3y

Fem

ale

S,so

mnole

nce

ALL

,fe

bri

leneu

tropen

iaH

emat

oge

nous

Som

nole

nce

anis

oco

ria,

Bab

insk

ire

flexþ

/þD

rain

age

Neg

ativ

eC

eftr

iaxoneþ

vanco

myc

inþ

met

ronid

azole

þam

phote

rici

nB

Good

16

3y

Fem

ale

NV

Fora

men

ova

leH

emat

oge

nous

Norm

alD

rain

age

Bac

tero

ides

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

Good

17

4.5

yM

ale

R,N

VD

enta

lpro

cedure

Hem

atoge

nous

Left

hem

ipar

esis

Exci

sion

Pep

tost

repto

cocc

us

Am

pic

illin

/su

lbac

tamþ

amik

acinþ

met

ronid

azole

Epile

psy

,hem

ipar

esis

(con

tinue

d)

4

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Tab

le1.

(continued

)

Pat

ient

Age

Gen

der

Pre

senting

sym

pto

ms

Pre

dis

posi

ng

conditio

nD

isse

min

atio

nN

euro

logi

cex

amin

atio

nSu

rger

yM

icro

bio

logy

(culture

)A

ntibio

tic

trea

tmen

tO

utc

om

e

18

5m

oM

ale

Swel

ling

beh

ind

the

righ

tea

rT

raum

aþ

mas

toid

itis

Contigu

ous

Norm

alExci

sion

Stre

ptoc

occu

spn

eum

onia

eA

mpic

illin

/su

lbac

tamþ

clin

dam

ycin

Good

19

16

yFe

mal

eF,

NV

,H

,A

CT

GAþ

VSDþ

pulm

onar

yhyp

erte

nsi

on

Hem

atoge

nous

Stupor,

anis

oco

ria,

bila

tera

lBab

insk

ire

flexþ

/þN

oN

egat

ive

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

Die

d

20

3m

oM

ale

R,N

V,S

,AC

,hea

dgr

ow

thH

ydro

cephal

usþ

DW

Aþ

VPS

Post

oper

ativ

eSt

upor

and

bulg

ing

fonta

nel

leD

rain

ageþ

shunt

rem

ovi

ng

and

EV

DSt

aphy

loco

ccus

aure

usC

eftr

iaxoneþ

vanco

myc

inD

ied

21

11

yM

ale

H,N

VT

runcu

sar

teri

osu

sty

pe

4H

emat

oge

nous

Norm

alExci

sion

Neg

ativ

eC

eftr

iaxoneþ

vanco

myc

inþ

met

ronid

azole

Epile

psy

22

5y

Fem

ale

HT

GA

Hem

atoge

nous

Norm

alD

rain

age

GrS!

Gr

(þ)

chai

nco

kePep

tost

repto

cocc

us

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

Good

23

11

yM

ale

HD

enta

lpro

cedure

Hem

atoge

nous

Norm

alN

oN

egat

ive

Cef

tria

xoneþ

vanco

myc

inþ

met

ronid

azole

þri

fam

pin

Good

24

1m

oM

ale

Ps,

som

nole

nce

Sepsi

sH

emat

oge

nous

Som

nole

nce

and

bulg

ing

fonta

nel

leD

rain

age

Eco

liC

efota

xim

eþ

rifa

mpinþ

vanco

myc

in

Good

Abbre

viat

ions:

AC

,alter

edco

nsc

iousn

ess;

ALL

,acu

tely

mphobla

stic

leuke

mia

;CG

D,c

hro

nic

gran

ulo

mat

ous

dis

ease

;CR

F,ch

ronic

renal

failu

re;D

TR

,dee

pte

ndon

refle

xes

;DW

A,D

andy-

Wal

ker

Anom

aly;

EV

D,e

xtr

a-ve

ntr

icula

rdra

inag

e;F,

feve

r;G

r(þ

),gr

am-p

osi

tive

;Gr

(–),

gram

-neg

ativ

e;G

rS,g

ram

stai

nin

g;H

,hea

dac

he;

NV

,nau

sea-

vom

itin

g;Ps,

poor

suck

ing;

PS,

pulm

onar

yst

enosi

s;R

,res

tles

snes

s;S,

seiz

ure

s;T

GA

,tra

nsp

osi

tion

of

the

grea

tar

teri

es;V

PS,

ventr

iculo

per

itonea

lsh

unting;

VSD

,ve

ntr

icula

rse

pta

ldef

ect;

WA

S,W

isko

tt-A

ldri

chsy

ndro

me.

5

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Tab

le2.

Pat

ients

’R

adio

logi

cFi

ndin

gs.

Pat

ient

Loca

tion

Num

ber

of

absc

esse

sM

ean

dia

met

erT

2hyp

oin

tense

rim

Cap

sula

ren

han

cem

ent

Per

ilesi

onal

edem

aSh

iftD

iffusi

on

rest

rict

ion

Mea

nA

DC

valu

e

1Fr

onto

par

ieta

lper

iven

tric

ula

rW

M,pons

813.1

+8.2

mm

(þ),

2ofle

sions

loca

lized

inri

ght

fronta

lan

dle

ftpar

ieta

lW

M

(þ),

2ofle

sions

loca

lized

inri

ght

fronta

lan

dle

ftpar

ieta

lW

M

(þ),

5ofle

sions

(–)

(þ)

386.9+

114.4

2R

ight

fronta

llo

be

150

mm

XX

XX

XX

3Bila

tera

lfr

onta

llo

be

325+

8.7

mm

XX

XX

XX

4Le

ftfr

onta

lWM

,rig

ht

fronta

lpar

asag

itta

l,le

ftce

rebel

lar

WM

37.8

+5.0

mm

(þ),

only

1,lo

caliz

edin

left

fronta

llo

be

(þ),

only

1,lo

caliz

edin

left

fronta

llo

be

(þ),

2ofth

ele

sions,

cere

bel

lar

and

left

fronta

l,

(–)

(þ)

266+

133

5Le

ftce

rebra

lhem

ispher

em

ultip

leX

XX

XX

XX

6Le

ftfr

onta

lsu

bdura

lsp

ace

111

mm

(þ)

(þ)

(þ)

(þ)

(þ)

360

7R

ight

lentifo

rmnucl

eus

137

mm

(þ),

double

laye

red

capsu

le(þ

)(þ

)(þ

)(þ

)269

8R

ight

thal

amus

130

mm

(þ)

(þ)

(þ)

( þ)

(þ)

600

9Le

ftfr

onta

lW

M1

30

mm

(þ)

(þ)

(þ)

(–)

(þ)

215

10

Left

occ

ipital

WM

220+

5.7

mm

(þ),

both

(þ),

both

(þ)

(–)

(þ)

931

11

Rig

ht

fronta

lW

M1

24

mm

(þ)

(þ)

(þ)

(þ)

(þ)

337

12

Left

fronta

lW

M1

37

mm

XX

(þ)

(þ)

XX

13

Left

tem

pora

llo

be

1X

XX

X(þ

)X

X14

Left

fronta

l,th

alam

ian

dri

ght

occ

ipital

WM

,le

ftce

rebel

lar

WM

87.9

+4.8

mm

(þ),

lesi

ons

loca

lized

inle

ftfr

onta

llo

be,

cere

bel

lum

(þ),

lesi

ons

loca

lized

inle

ftfr

onta

llo

be,

cere

bel

lum

(þ)

(–)

(þ),

loca

lized

inle

ftfr

onta

llo

be

and

thal

ami

754+

54

15

Left

par

ieta

lW

M1

14

mm

(þ)

(þ)

(þ)

(–)

(þ)

853

16

Rig

ht

fronta

llo

be

128

mm

(þ),

double

laye

red

(þ)

(þ)

(–)

(þ)

802

17

Rig

ht

tem

poro

par

ieta

lW

M1

59

mm

(þ)

(þ)

(þ)

(þ)

(þ)

348

18

Rig

ht

tem

poro

occ

ipital

epid

ura

lsp

ace

137

mm

(–)

(–)

(–)

(–)

(þ)

590

19

Rig

ht

fronta

llo

be

119

mm

(þ)

(þ)

(þ)

(–)

(þ)

375

20

Ret

roce

rebel

lar

154

mm

(þ)

(þ)

(–)

(–)

(þ)

445

21

Rig

ht

occ

ipital

137

mm

(þ)

(þ)

(þ)

(þ)

(þ)

331

22

Rig

ht

fronta

llo

be

246+

17

(þ)

(þ)

(þ)

(þ)

(þ)

296+

50.9

23

Left

fronta

llo

be

18

mm

(–)

(þ)

(þ)

(–)

(–)

1238

24

Bila

tera

lpar

ieto

occ

ipital

-su

bdura

lsp

ace

137

mm

(þ)

(þ)

(–)

(–)

(þ)

698

Abbre

viat

ions:

AD

C,ap

par

ent

diff

usi

on

coef

ficie

nt;

(–),

neg

ativ

e;(þ

),posi

tive

;W

M,w

hite

mat

ter;

X,not

eval

uat

ed.

6

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Outcomes

Three of the 24 patients (12.5%) died during treatment. No neu-

rologic sequelae were observed in 11/24 (45.8%) cases in the

first year of monitoring. Epilepsy was diagnosed in 8/24

(33.3%) cases and epilepsy and hemiparesis in 2/24 (8.3%) in

the first year of monitoring (Table 1).

Discussion

Brain abscess in children is rare. Clinical presentation is asso-

ciated with a large number of factors, including site of abscess,

number of abscesses, pathogen, presence or absence of accom-

panying meningitis or ventriculitis, the patient’s immune status

and stage of disease. Although fever, headache and vomiting

are seen in 60% to 70% of adults, clinical findings in children

may be nonspecific, especially as age decreases.2-5,9,12 Fever is

a nonspecific finding that may be generally seen at a level of

30% to 70% in various phases of the disease. Headache is seen

in 42% to 80% of adults, although this level may be lower in

children, at 30% to 50%. Nausea-vomiting is a finding of

increased intracranial pressure and is seen in approximately

25% to 50% of patients. Altered state of consciousness is seen

in approximately 2/3 of cases and may vary in degree from a

mild state of sleep to coma.1-7 Brain abscess in children may

lead to increased head circumference, bulging fontanel, and

separation of cranial sutures.1 Presenting symptoms in our

study were nausea-vomiting in 45.8% of cases, headache in

41.7%, convulsion in 37.5%, fever in 29.2%, and altered con-

sciousness in 29.2%. Our clinical findings were similar to those

of other studies involving the same age group.4,5,9,11-17

Focal neurologic deficit may be seen in 20% to 60% of

cases.4,5,9 Location of the abscess determined focal neurologic

deficits. If the abscess is in the parietal lobe, it leads to hemi-

paresis, to dysphagia if it is in the temporal lobe, and to vision

defects if it is in the occipital lobe.9 Cranial nerve paralysis,

nystagmus, and ataxia may also be seen, depending on the loca-

tion of the abscess.1 Papilledema is seen in 41% to 70% of

adults.9,16,18 However, that level decreases in childhood since

the fontanels are still open. In agreement with the literature,

in this study neurologic appearance was normal in 37.5% of

cases, altered consciousness was present in 37.5%, and focal

neurologic deficit in 25.0%, and bilateral Babinski reflex posi-

tivity was determined in 12.5%. The classic triad characterized

by headache, fever, and focal neurologic deficit was deter-

mined in 8.4% of children.4,5

No underlying predisposing factor is determined in 15% to

30% of brain abscesses.1 In this study, no predisposing factor

was identified in 8.4% of children. Predisposing factors in brain

abscesses are contiguous infections, hematogenous dissemina-

tion, and penetrating head injuries, including surgical interven-

tions.9 Neurosurgical procedures are responsible for some 8%to 10% of cases.16,18 In this study, postoperative spread was

present in 8.3% of cases, contiguous spread in 20.8%, and

hematogenous spread in 62.5%. Shachor-Meyouhas et al5

determined predisposing factors at a level of 81% in their

27-case series; sinusitis-mastoiditis-otitis at a level of 30%,

trauma at 15%, meningitis at 15%, anatomic brain cyst at

7%, pulmonary origin at 4%, congenital heart disease at 7%,

and other causes at 4%, whereas no predisposing factor was

identified in 18% of cases. Goodkin et al14 determined conge-

nital heart disease at a level of 51% and sinusitis-mastoiditis-

otitis at a level of 11% and identified no predisposing factor

in 7% of cases. Auvichayapat et al7 identified congenital heart

disease at a level of 35% and sinusitis-mastoiditis-otitis at a

level of 20%. In a 75-case series from Turkey, Ozsurekci

et al4 determined congenital heart disease at a level of

33.3%, sinusitis at 5.3%, mastoiditis-otitis at 16%, pulmonary

origin at 2.6%, trauma at 2.6%, and immunosuppression at

3.9%. Landriel et al19 determined an immunosuppression level

of 18% in their 59-case series. The most common predisposing

factors in this study were congenital heart disease in 20.8% of

cases, immunosuppression in 20.8%, sinusitis in 8.3%, dental

procedure in 8.3%, autogenic in 8.3%, sepsis in 8.3%, trauma

in 8.3%, neurosurgical procedures in 8.3%, pneumonia in

4.2%, and meningitis in 4.2%. Two cases identified as immu-

nosuppression were associated with acute lymphoblastic leuke-

mia and 1 with chronic renal failure and renal transplantation.

Wiskott-Aldrich syndrome was present in one case, and

chronic granulomatous disease–related immune deficiency in

the other. Brain abscess associated with immunosuppression/

immune deficiency has been increasingly frequently reported

in recent years.4,19-21 This may be related to the development

of diagnostic tests in rare immune deficiencies and the easy

availability of such tests.

Imaging techniques help determine abscess location, edema,

and mass effect.1 Cranial CT used to be widely employed in the

diagnosis of brain abscesses. Significant delays in diagnosis

occurred in the pre–CT scan era, leading to high morbidity and

mortality. Today, MRI may be regarded as the primary imaging

technique for intracranial lesions. Abscess lesions appear

hypointense on T1-weighted images and hyperintense on T2-

weighted images. Vasogenic edema is often determined around

the lesion and occupying a broader space than it. A hypointense

capsule may be observed around the abscess on T2-weighted

images, and an iso-hyperintense capsule on T1-weighted

images. Nathoo et al11 reported that 89.6% of abscesses were

supratentorial, 9.4% infratentorial, and 1% both supra- and

infratentorial. In a study of 75 cases, Ozsurekci et al4 deter-

mined single abscesses in 66.6% of cases and multiple

abscesses in 33.3%. The most frequent abscess locations were

25.3% frontal, 22.6% parietal, 14.6% temporal, 5.3% occipital,

14.6% frontoparietal, 6.6% parieto-occipital, 4% temporopar-

ietal, 4% temporoparieto-occipital, 13.3% cerebellum, and

8% brain stem. Other studies have reported that the most com-

mon abscess locations are parietal and/or frontal lobe.4,5,9 In

our study, and in agreement with the literature, 80% of

abscesses were supratentorial, 5% infratentorial, and 15% in

both supra- and infratentorial regions. Single abscess was pres-

ent in 75% of cases and multiple in 25%. The most common

location for abscesses was the frontal region. Underlying

immune deficiency, congenital heart diseases, sinusitis, and

Canpolat et al 7

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

facial infections such as dental infection in cases of frontally

located brain abscess (Tables 1 and 2) were noteworthy as

being compatible with the literature and the general study pop-

ulation as etiologic risk factors. Abscess usually appears in a

pronounced hyperintense form on diffusion-weighted images

and possesses low ADC values, indicating diffusion restriction.

Presence of diffusion restriction helps differentiate abscess

from other cystic lesions (e.g., cystic brain tumors).1,9,22-24

Fanning et al25 showed significantly low ADC signal values

in abscesses. Several studies have reported that diffusion-

weighted images are reliable in differentiating abscesses from

malign cystic tumors in particular. Generally, ADC values

decrease because of intense viscosity appearing because of

their high necrotic living cells, bacteria, and protein content,

whereas cystic-necrotic brain tumors have higher ADC values

because of their more serous structure than that of abscesses.

ADC values defined for abscesses in the literature range

between 0.28 and 0.7 (10–3 mm2/s).25-28 However, diffusion

restriction may not be determined in pyogenic abscess lesions

as presented in our study and relevant literature. There may

therefore be a need for advanced radiologic imaging tech-

niques in the differential diagnosis of cystic tumors.29,30 Dif-

fusion restriction may not appear in fungal abscesses and

abscess lesions containing sterile pus.

In agreement with the literature, T2 hypointense rim was

determined in 56.8% of lesions in this study, capsular enhance-

ment in 59.5%, perilesional edema in 81.1%, and shift in 40%.

Qualitative diffusion restriction was determined in 29 (78.4%)

lesions. Mean apparent diffusion coefficient value in these 29

abscesses was 0.511 + 0.23 � 10–3 mm2/s.

Sterile pus cultures were found in 40% of cases. The level of

sterile pus cultures in the literature ranges between 10% and

56%.3-9,12 Growth was determined in 60.0% of pus cultures

in this study. Peptostreptococcus grew in 4 abscess cultures

(20%) and Aspergillus in 2 (10%). Proteus, Pseudomonas, Bac-

teroides, S pneumoniae, S aureus, and E coli grew in 1 (5%)

abscess culture each. Aspergillus growth was present in 2 of our

immunosuppressed cases and Peptostreptococcus growth in 1.

This was compatible with the literature.1,14,20,21 Gram-negative

organisms such as Klebsiella, E coli, Proteus, and Citrobacter

have been reported to be capable of causing abscesses in new-

borns.1,14,31,32 E coli was determined in pus cultures as an agent

in a 1-month-old case in our study.

Although treatment of brain abscesses is still a subject of

debate in the literature, contemporary treatment is a combina-

tion of antimicrobial therapy and surgical intervention.9 Ther-

apeutic approach depends on several factors, such as stage of

the abscess, its location and origin, virulence of the pathogen

micro-organism, number of abscesses, patient response, and

degree of edema.9,12 Antimicrobial therapy alone is preferred

in abscesses <2 cm in size, in high-density lesions, in multiple

abscesses, in patients whose condition is too poor for surgery,

and if the abscess is located in a position inaccessible to sur-

gery.9 Auvichayapat et al7 used antimicrobial therapy alone in

14.7% of cases, Goodkin et al14 in 12.5%, and Ozsurekci et al4

in 24%. In our study, again in agreement with the literature,

16.7% of cases received antimicrobial therapy alone. There

are no randomized controlled trials about the effectiveness

of antibiotic regimens for treating children with brain

abscess.33 Empiric antimicrobial therapy is dictated by pre-

sumed source, but often includes nafcillin or vancomycin,

cefotaxime or ceftriaxone, and metronidazole. Therapy is

adjusted when the culture results are available. Patients usu-

ally receive a minimum 6- to 8-week course of intravenous

antibiotics, which may be prolonged depending on the clinical

context, such as in immunocompromised patients.1-3,15 In our

study, in agreement with the literature, the most preferred

drugs for combination treatment were vancomycin, third-

generation cephalosporin, and metronidazole (Table 1). There

is a need for a well-designed randomized controlled trial to

evaluate the effects of different antibiotic regimens on brain

abscess.

Generally, combination therapy is preferred. In this study,

83.3% of cases received both surgery and antimicrobial ther-

apy. The most common surgical approach is drainage.1,34 This

is particularly advised if the abscess is >2.5 cm in size.1 In

agreement with previous studies,4-12,14,15,19 craniotomy and

excision were performed in 20.0% of the cases in this study,

and drainage surgery in 80.0%.

Until the 1980s, brain abscess–related mortality rates in

children were 11% to 53%. Although some studies have

reported that mortality rates have decreased to 3.7% to 10%thanks to the use of CT and MRI, rapid advances in microbio-

logical tests, fast and effective antibiotherapy, and advances in

neurosurgery, the general mortality rate today is still approxi-

mately 15%.1-18 The mortality rate in our series was 12.5%.

Although our mortality rate was compatible with the literature,

it was higher than that in some recently published case

series.4,5,7,11,12 We attribute this to the predisposing factors in

fatal cases 1 and 19 and their general condition being too poor

for surgery.

The main limitation of this study is that preoperative radi-

ologic images for 4 cases were unavailable since the analysis

was retrospective.

In conclusion, despite advances in diagnosis and treatment,

brain abscesses in children are still associated with high

neurologic morbidity and mortality. Clinical findings may

sometimes be highly indistinct and diagnosis requires a high

index of suspicion. Diagnosis is made on the basis of a com-

bination of clinical and radiologic tests. In recent years,

immunocompromised states have become an important pre-

disposing factor for the development of brain abscesses.

Surgical drainage combined with specific antibiotic therapy

is recommended in these patients. Effective and prompt

management should ensure a much better outcome of brain

abscess in childhood.

Acknowledgments

We are most grateful to Prof Dr Ibrahim Suat Oktem, Prof Dr Abdul-

hakim Coskun, Dr Alper Ozcan, and Dr Huseyin Baz for their support

for this study. We also extend our grateful thanks to all the patients in

this study and their long-suffering families.

8 Journal of Child Neurology

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

Author Contributions

MC, HP, MKO, SD, MK, AK, TP, SK, and HG planned the study and

prepared the first draft. MC, HP, OC, and GK collected the patient

data. MC, OC, AT, GK, SBG, and EU prepared the manuscript for

publication and reviewed the literature. All the authors were involved

in and contributed to patient monitoring and treatment.

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to

the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship,

and/or publication of this article.

Ethical Approval

This study was approved by Erciyes University Scientific Research

Committee (2014/354).

References

1. Frazier JL, Ahn ES, Jallo GI. Management of brain abscesses in

children. Neurosurg Focus. 2008;24:E8.

2. Hakan T, Ceran N, Erdem I, et al. Bacterial brain abscesses: an

evaluation of 96 cases. J Infect. 2006;52:359-366.

3. Yogev R, Bar-Meir M. Management of brain abscesses in chil-

dren. Pediatr Infect Dis J. 2004;23:157-159.

4. Ozsurekci Y, Kara A, Cengiz AB, et al. Brain abscess in child-

hood: a 28-year experience. Turk J Pediatr. 2012;54:144-149.

5. Shachor-Meyouhas Y, Bar-Joseph G, Guilburd JN, et al. Brain

abscess in children—epidemiology, predisposing factors and

management in the modern medicine era. Acta Paediatr. 2010;

99:1163-1167.

6. Saez-Llorens X. Brain abscess in children. Semin Pediatr Infect

Dis. 2003;14:108-114.

7. Auvichayapat N, Auvichayapat P, Aungwarawong S. Brain

abscess in infants and children: a retrospective study of 107

patients in Northeast Thailand. J Med Assoc Thai. 2007;90:

1601-1607.

8. Tsou TP, Lee PI, Lu CY, et al. Microbiology and epidemiology of

brain abscess and subdural empyema in a medical center: a 10-

year experience. J Microbiol Immunol Infect. 2009;42:405-412.

9. Gelabert-Gonzalez M, Serramito-Garcıa R, Garcıa-Allut A,

Cutrın-Prieto J. Management of brain abscess in children. J Pae-

diatr Child Health. 2008;44:731-735.

10. Sarmast AH, Showkat HI, Bhat AR, et al. Analysis and manage-

ment of brain abscess; a ten year hospital based study. Turk Neu-

rosurg. 2012;22:682-689.

11. Nathoo N, Nadvi SS, Narotam PK, van Dellen JR. Brain abscess:

management and outcome analysis of a computed tomography era

experience with 973 patients. World Neurosurg. 2011;75:

716-726.

12. Kao KL, Wu KG, Chen CJ, et al. Brain abscesses in children:

analysis of 20 cases presenting at a medical center. J Microbiol

Immunol Infect. 2008;41:403-407.

13. Krajewski R, Stelmasiak Z. Brain abscess in infants. Childs Nerv

Syst. 1992;8:279-280.

14. Goodkin HP, Harper MB, Pomeroy SL. Intracerebral abscess in

children: historical trends at Children’s Hospital Boston. Pedia-

trics. 2004;113:1765-1770.

15. Felsenstein S, Williams B, Shingadia D, et al. Clinical and micro-

biologic features guiding treatment recommendations for brain

abscesses in children. Pediatr Infect Dis J. 2013;32:129-135.

16. Wong TT, Lee LS, Wang HS, et al. Brain abscesses in children—

a cooperative study of 83 cases. Childs Nerv Syst. 1989;5:19-24.

17. Tekkok IH, Erbengi A. Management of brain abscess in children:

report of 130 cases over a period of 21 years. Childs Nerv Syst.

1992;8:411-416.

18. Hirsch JF, Roux FX, Sainte-Rose C, et al. Brain abscess in child-

hood. A study of 34 cases treated by puncture and antibiotics.

Childs Brain. 1983;10:251-65.

19. Landriel F, Ajler P, Hem S, et al. Supratentorial and infratentorial

brain abscesses: surgical treatment, complications and out-

comes—a 10-year single-center study. Acta Neurochir (Wien).

2012;154:903-911.

20. Patiroglu T, Unal E, Karakukcu M, et al. Multiple fungal brain

abscesses in a child with acute lymphoblastic leukemia. Myco-

pathologia. 2012;174:505-509.

21. Patiroglu T, Unal E, Yikilmaz A, et al. Atypical presentation of

chronic granulomatous disease in an adolescent boy with frontal

lobe located Aspergillus abscess mimicking intracranial tumor.

Childs Nerv Syst. 2010;26:149-154.

22. Erdogan C, Hakyemez B, Yildirim N, Parlak M. Brain abscess

and cystic brain tumor: discrimination with dynamic susceptibil-

ity contrast perfusion-weighted MRI. J Comput Assist Tomogr.

2005;29:663-667.

23. Chang SC, Lai PH, Chen WL, et al. Diffusion-weighted MRI fea-

tures of brain abscess and cystic or necrotic brain tumors: compar-

ison with conventional MRI. Clin Imaging. 2002;26:227-236.

24. Lai PH, Hsu SS, Ding SW, et al. Proton magnetic resonance spec-

troscopy and diffusion-weighted imaging in intracranial cystic

mass lesions. Surg Neurol. 2007;68:25-36.

25. Fanning NF, Laffan EE, Shroff MM. Serial diffusion-weighted

MRI correlates with clinical course and treatment response in

children with intracranial pus collections. Pediatr Radiol. 2006;

36:26-37.

26. Ebisu T, Tanaka C, Umeda M, et al. Discrimination of brain

abscess from necrotic or cystic tumors by diffusion-weighted

echo planar imaging. Magn Reson Imaging. 1996;14:1113-1116.

27. Desprechins B, Stadnik T, Koerts G, et al. Use of diffusion-

weighted MR imaging in differential diagnosis between intra-

cerebral necrotic tumors and cerebral abscess. AJNR Am J

Neuroradiol. 1999;20:1252-1257.

28. Noguchi K, Watanabe N, Nagayoshi T, et al. Role of diffusion-

weighted echo-planar MRI in distinguishing between abscess and

tumor: a preliminary report. Neuroradiology. 1999;41:171-174.

29. Sundaram V, Agrawal S, Chacham S, et al. Klebsiella pneumo-

niae brain abscess in neonates: a report of 2 cases. J Child Neurol.

2010;25:379-382.

30. Krabbe K, Gideon U, Wagn P, et al. MR diffusion imaging of

intracranial tumors. Neuroradiology. 1997;39:483-489.

31. Mishra AM, Gupta RK, Jaggi RS, et al. Role of diffusion

weighted imaging and in vivo proton magnetic resonance

Canpolat et al 9

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from

spectroscopy in the differential diagnosis of ring enhancing intra-

cranial cystic mass lesions. J Comput Assit Tomogr. 2004;28:

540-547.

32. Phan H, Lehman D. Cerebral abscess complicating Proteus mir-

abilis meningitis in a newborn infant. J Child Neurol. 2012;27:

405-407.

33. Lumbiganon P, Chaikitpinyo A. Antibiotics for brain abscesses in

people with cyanotic congenital heart disease. Cochrane Data-

base Syst Rev. 2013;3:CD004469.

34. Ciurea AV, Stoica F, Vasilescu G, Nuteanu L. Neurosurgical

management of brain abscesses in children. Childs Nerv Syst.

1999;15:309-317.

10 Journal of Child Neurology

at Erciyes Universitesi on September 15, 2014jcn.sagepub.comDownloaded from