Indian J Pediatr
DOI 10.1007/s12098-012-0875-9
ORIGINAL ARTICLE
Role of Dexamethasone in Neonatal Meningitis:
A Randomized Controlled Trial
N. B. Mathur & Amit Garg & T. K. Mishra
Received: 23 December 2011 / Accepted: 9 August 2012
# Dr. K C Chaudhuri Foundation 2012
Abstract
Objectives To evaluate the role of dexamethasone therapy in
neonatal meningitis in a randomized placebo controlled
trial.
Methods The participants were eighty neonates with men-
ingitis randomized to receive dexamethasone or saline pla-
cebo. Dexamethasone was started prior to the first dose of
antibiotics in the dose of 0.15 mg/kg intravenous 6 hourly
for 2 d. Primary outcome measure was mortality. Secondary
outcome measures included progression of systemic inflam-
matory response syndrome (SIRS) up to 48 h, differences in
cerebrospinal fluid (CSF) cytokines between baseline levels
and 24 h after enrolment and brain stem auditory evoked
response (BAER) after 4 to 6 wk of discharge.
Results Baseline variables were comparable in both the
groups. Mortality was significantly decreased in dexameth-
asone group (p00.005) and the absolute risk difference was
27.5 % (95 % CI 9.5–45.8 %). There was a significant
reduction in cells per mm3 (62.5 vs. 100) and proteins
(162 vs. 217.5 mg/dl) after 24 h of treatment in the dexa-
methasone group. IL-1β was significantly reduced after
24 h in dexamethasone group (290 vs 665 pg/ml). TNF- α
was significantly lower (157.5 vs 427.5 pg/ml) and sugar
significantly higher (50 vs 38 mg/dl) in the dexamethasone
group after 24 h. Significant difference was noted between
dexamethasone and saline groups in the progression of
SIRS.
Conclusions Dexamethasone significantly reduced fatality,
progression of SIRS and CSF inflammatory indices.
N. B. Mathur (*) : A. Garg
Referral Neonatal Unit, Department of Pediatrics, Maulana Azad
Medical College,
New Delhi 110002, India
e-mail: drnbmathur@vsnl.com
T. K. Mishra
Department of Biochemistry, Maulana Azad Medical College,
New Delhi 110002, India
Keywords CSF cytokines . Dexamethasone . Mortality .
Neonatal meningitis . SIRS . BAER
Introduction
Neonatal meningitis causes significant mortality and neuro-
logic sequelae despite appropriate treatment with antibiotics.
The mortality rate has been estimated at 10–15 % and
sequelae develop in 17–60 % survivors [1, 2]. The use of
dexamethasone as an adjunctive therapy in patients with
bacterial meningitis is based on the observation that host
inflammatory response, especially following the initiation of
antibiotics, may contribute to an adverse outcome [3] Stud-
ies evaluating the role of dexamethasone in meningitis in
older children have found conflicting results with benefits in
H. influenzae and S. pneumoniae meningitis and animal
models [4–8]. There is a paucity of studies on role of
dexamethasone in neonatal meningitis. The present study
was undertaken with the objective of evaluating the effect of
dexamethasone on mortality, systemic inflammatory re-
sponse syndrome, cerebrospinal fluid (CSF) inflammatory
indices and brain stem auditory evoked response (BAER).
Material and Methods
This randomized placebo controlled trial was conducted in
the referral neonatal unit of a tertiary teaching government
hospital. Eligible neonates consecutively admitted with
meningitis (septic neonates with CSF suggestive of menin-
gitis) during the period February 2008 to January 2009 were
enrolled. Neonates with major congenital malformations
and those who had received antibiotics for 24 h or more
were excluded from the study. A sample size of 40 subjects
in each group was calculated aiming reduction in mortality
from 35 % to 10 % (Power of study 80 %, α error of 0.05).

The diagnosis of neonatal meningitis was made on the basis
of presence of>32 cells/mm3 in the CSF examination in a
sick neonate [9, 10] along with any of the following: abnor-
mal total leukocyte count (TLC) defined as less than 5,000
or more than 20,000/mm3, raised immature/total neutrophil
count ratio, elevated micro-erythrocyte sedimentation rate
(ESR) and raised C-reactive protein(CRP) [11–13]. CSF
examination was done at admission (baseline) and examined
for cells, differential count, protein, sugar, gram stain, cul-
ture and sensitivity. CSF was also collected (0.5 ml) in
Eppendorf tubes. CSF examination was repeated 24±6 h
later for the same parameters. The Eppendorf tubes were
stored in a refrigerator at −70° Celsius immediately after
collection for analysis of cytokine levels by ELISA.
The CSF sample was subjected to cytological examina-
tion, bacterial culture and antibiotic sensitivity, biochemical
analysis, estimation of TNF-α and IL-1β. Processing of all
the samples for cytokines estimation was done at the same
time. Viral and fungal cultures were not performed. Eligible
neonates were randomized to receive dexamethasone or
saline placebo using website (www.randomization.com)
generated random allocation sequence in blocks of 10
patients each. Randomization sequence was concealed using
sealed opaque envelopes. The study was not blinded. How-
ever, the persons who estimated CSF cytokine levels and
brain stem evoked auditory response were blinded. The
study was approved by the institutional ethical committee.
Informed consent was taken from the parents in a written
format. Dexamethasone was given along with the first dose
of antibiotics in the dose of 0.15 mg/kg per dose in a volume
of 0.15 ml/kg body weight intravenously every 6 h for 48 h.
Neonates in the control group received similar volume of
intravenous saline as placebo. Rest of the treatment was
similar in both the groups.
The initial antibiotic therapy consisted of ceftriaxone and
amikacin. Meropenam was added in the presence of the
following: shock at admission, progression of SIRS, persistent
seizures, pupilary abnormalities, or if antibiotic sensitivity
report showed resistance to the antibiotics administered and
the baby was not responding clinically. Outcome parameters
consisted of fatality, progression of systemic inflammatory
response syndrome up to 48 h, brain stem auditory evoked
response after 4 to 6 wk and CSF cytokine levels (TNF α and
IL-1β) after 24±6 h.
CSF examination was repeated 24±6 h later, on day 7
and subsequently every wk if required. Temperature, respi-
ratory rate, heart rate, blood pressure, capillary filling time,
peripheral pulses, mental status, urine output, oxygen satu-
ration and blood gas analysis were recorded in all cases and
progression of SIRS was classified into various stages as
sepsis, sepsis syndrome, early septic shock, refractory septic
shock and multiorgan dysfunction syndrome [14]. These
stages are progressive in severity in the order mentioned.
Indian J Pediatr
The stage of SIRS was observed during the 48 h following
admission and it was considered to have progressed if the
neonate went into a subsequent stage and to have improved
if the neonate went into an earlier stage.
Blood counts, micro-ESR, CRP and blood culture were
done in all the cases. Blood culture was performed under
aseptic conditions by collecting 1 ml of venous blood in a
bottle containing tryptic soy broth. The sensitivity of the
organisms to the commonly used antibiotics was tested.
TNF-α and IL-1β in the CSF was estimated by ELISA
kits supplied by Immunotech (Marseille Cedex 9 France).
TNF-α was estimated by one immunological step sandwich
type ELISA. IL-1 β was estimated by a two immunological
step sandwich type ELISA.
Brain stem auditory evoked response was performed
using click stimuli delivering monophasic square pulses of
100 ms duration at the rate of 10 Hz through headphones.
Contra lateral ear was masked with continuous white noise.
It was done after 4–6 wk of discharge and repeated further
after 4 wk if initial estimation showed abnormality.
The study was approved by the institutional ethical com-
mittee. Statistical analysis was done using the software
version SPSS 16. The continuous variables were tested by
using student t-test and for categorical variables, Pearson
Chi-square test was applied. For variables with non-
Gaussian distribution Mann–Whitney test was applied. Wil-
coxan signed rank test was used to compare pre and post
intervention variables within the same group. Probability
less than 5 % (p<0.05) was considered significant.
Results
Eligible neonates with meningitis were randomized to re-
ceive dexamethasone (n040) or saline (n040). Both the
groups were comparable with reference to age, weight,
gestational age, gender, onset of sepsis and neurological
signs at admission (Table 1).
Mortality was found to be significantly reduced in dexa-
methasone group (12.5 %) as compared to saline group
(40 %) (p 00.005). The absolute risk difference was
27.5 % (95 % CI09.1 %-45.8 %). The number needed to
treat (NNT) was 4 ( 95 % CI02.2 to 10.9). Hearing loss was
41 % in saline group and 17 % in dexamethasone group
amongst survivors. (p00.07) (Fig. 1).
Table 2 shows the results of sepsis screen in the study
population. CRP and immature to total neutrophil ratio were
raised in 100 % and 87.5 % respectively in dexamethasone
group and in 97.5 % each in saline group. Klebsiella was
isolated in blood culture in 4 patients in dexamethasone and
5 patients in saline group while coagulase negative staphy-
lococcus (CONS) was isolated in 4 patients each in both
dexamethasone and saline groups. CONS was considered
Indian J Pediatr

Table 1 Baseline evaluation at

admission in study population Variables Dexamethasone group (n040) Saline group (n040) P value

Age at admission(h)
Median 190 118 0.74
IQR 105–369 72–468
Weight(g)
Median 2310 2250 0.08
IQR 1620–2260 1610–2180
Gestational age (wk) Mean(S.D) 37.1(2.2) 37.6(1.7) 0.19
Male gender n (%) 28(70) 23(57.5) 0.24
Early onset sepsis (<72 h) n(%) 14(35) 16(40) 0.64
Duration of symptoms at presentation(h)
Median 76 84 0.70
IQR 48–96 50–108
Place of birth
Home n (%) 16(40) 16(40) >0.99a
Community hospitals n (%) 23(57.5) 23(57.5)
During transport n (%) 1(2.5) 1(2.5)
Bulging anterior fontanelle n (%) 17(42.5) 16(40) 0.83
Abnormal pupillary size n (%) 16(40) 23(57.5) 0.26
Microcephaly n (%) 8(20) 7(17.5) 0.77
a
Cranial nerve palsy n (%) 7(17.5) 4(10) 0.36a
Fischer’s Exact test

significant in presence of clinical sickness combined with
results of blood counts, CRP and ESR. In CSF culture,
Klebsiella predominated with 5 patients in dexamethasone
group and 4 patients in saline group. Klebsiella was sensi-
tive to ceftriaxone in 16 % cases in dexamethasone group
and 25 % cases in saline group; it was sensitive to Amikacin
in 33 % cases in dexamethasone group and 25 % in saline
group. Sensitivity to Meropenam was seen in 67 % cases in
dexamethasone group and 87.5 % in saline group.
Table 3 shows the isolates from blood/CSF culture. The
initial antibiotic in all cases consisted of Ceftriaxone and
Amikacin. Meropenam was added as per predefined criteria
in 13 cases in saline group and in 8 cases in dexamethasone
group (p00.14).
Table 4 shows progression of SIRS during 48 h following
admission. Only 2 patients (5 %) in dexamethasone group as
compared to 9 (22.5 %) in saline group progressed and
expired. Improvement was remarkable in dexamethasone
group (57.5 %) as compared to saline group (25 %).
Table 5 shows comparison of CSF findings in the two
groups. There was a significant reduction in cells, proteins
and IL-1β after 18–30 h of treatment in the dexamethasone
group but not in saline group. Significant reduction in TNF-
α and increase in sugar was observed in both the groups.
However, TNF- α was significantly lower and sugar
significantly higher in the dexamethasone group as com-
pared to saline group after 18–30 h of treatment.
CSF cytology got normalized on day-7 of antibiotic
therapy in 30 out of 36 neonates in the dexamethasone
group and in 13 out of 26 neonates in saline group after
admission (p00.01). None of the lumbar punctures was
traumatic. None of the neonates administered dexametha-
sone developed gastric bleed.
Discussion
The use of dexamethasone as an adjunctive therapy in
patients with bacterial meningitis is based on the observation
that host inflammatory response, especially following the
initiation of antibiotics, may contribute to an adverse out-
come [3]. In the present study dexamethasone treated neo-
nates had significantly lower mortality, compared to controls
(12.5 % vs. 40 %; p00.005). There are only two studies in
published literature on the effect of steroid in neonatal men-
ingitis. The study by Yu et al. [15] is old, retrospective and
had a very high mortality (75 %) in the control group which
lowered to 41 % in steroid group. Daoud et al. observed 22 %
mortality in dexamethasone group and 28 % in controls and
the difference was not significant [16]. However, the study
lacked power due to small sample size. Overwhelming evi-
dence generated in animal models of meningitis supports the
efficacy of dexamethasone in down regulating meningeal
inflammation [17, 18].
 Indian J Pediatr

Asessed for eligibility

(n=101)

Excluded (n=21)
Not meeting inclusion criteria (n=21)
Declined to participate (n=0)
Other reasons (n=0)

Randomised (n=80)

Allocated to Dexamethasone group (n=40) Allocated to saline group (n=40)

Recieved allocated intervention (n=40) Recieved allocated intervention (n=40)
Did not recieve allocated intervention (n=0) Did not recieve allocated intervention (n=0)

Lost to follow up (n=0) Lost to follow up (n=0)

Discontinued intervention (n=0) Discontinued intervention (n=0)

Analysed (n=40) Analysed (n=40)

Excluded from analysis (n=0) Excluded from analysis (n=0)

Expired: 5 (12.5%) Expired: 16 (40%)

Hearing loss: 6 (17%) Hearing loss: 10 (41%)

Fig. 1 Flowchart showing the outcome in study population

To the best of authors’ knowledge, no study has evaluated dexamethasone treated group [19–22].In the present study,
the effect of dexamethasone on CSF cytology, biochemistry IL-1β levels reduced significantly in dexamethasone treated
and cytokine levels in neonatal meningitis. In the present babies (p<0.001), but not in saline group (p00.125). TNF-
study, CSF cells and proteins were significantly lower af- αlevels were reduced by 71 % after 18–30 h in dexametha-
ter18–30 h in dexamethasone treated babies as compared to sone group, while only 18 % reduction was noted in saline
controls. In childhood (post neonatal) meningitis these inflam- group. Dexamethasone is known to block production of TNF
matory indices were found to be significantly lower in
Table 3 Organisms isolated in blood/CSF cultures
Table 2 Sepsis screen in the study population Culture isolates n (%) Dexamethasone Saline group
group (N014) (%) (N021) (%)
Variables Dexamethasone Saline group
group(n040) (n040)
Klebsiella 6(42.8) 8(38)
CRP >10 mg/l (n) 40(100 %) 39(97.5 %) Coagulase negative staphylococci 4(28.5) 4(19)
CRP mg/l (Mean±SD) 40.6±24.4 43.7±23.9 Pseudomonas 2(14.3) 2(9.5)
Raised μ ESR (n) 25 (62.5 %) 30 (75 %) Staphylococcus aureus 1(7) 3(14.3)
Total Leucocyte Count Escherichia coli 0 1(4.7)
Increased (n) 16(40 %) 20 (50 %) Acinetobacter 0 3(14.3)
Decreased (n) 4(10 %) 2(5 %) Group B Streptococcus 1(7) 0
Raised Immature: Total 35 (87.5 %) 39 (97.5 %) Total 14(35) 21(52.5)
Neutrophils (n)
p value(Chi-Square test) 0.11
Indian J Pediatr

Table 4 Progression of SIRS during 48 h following admission In the present study, the progression of SIRS and develop-
Stage Dexamethasone Saline group ment of shock was significantly lower in dexamethasone
group (n040) (%) (n040) (%) treated babies (p00.009). The predominant bacterial isolates
seen in the present study were Klebsiella species followed
Progressed and expired 2(5) 9(22.5) by CONS. Gram negative pathogens were found to be
Remained in same stage 10(25) 17(42.5) common in earlier studies [16, 27, 28].
Progressed but later improved 5(12.5) 4(10) Brain stem evoked auditory response studies in neonatal
Improved 23(57.5) 10(25) meningitis are scanty [16]. In the present study, the
incidence of sensorineural hearing loss was 17 % in
p value (Fisher’s exact test) 0.009
dexamethasone group and 41.6 % in saline group. The
pathogenesis of sensorineural hearing loss due to bacte-
[23] and IL-1 [24] and reduce brain edema [25]. In the rabbit rial meningitis includes early purulent or inflammatory
model of meningitis, dexamethasone had effective anti in- involvement of the cochlea, labyrinth and arachnoid in
flammatory activity if given before or simultaneously with the region of the internal auditory canal. Cortical necro-
the first dose of antibiotic but not if given 1 h later [26]. sis or hypoxia may damage the central auditory path-
No study has evaluated the role of dexamethasone in ways. Septic emboli or thrombophlebitis may involve
reducing the progression of SIRS in neonatal meningitis. the vessels to inner ear [29].

Table 5 Comparison of CSF

findings in study population Variables Dexamethasone Saline group p value (Mann
group(n040) (n040) whitney U test)

Cells Baseline (per mm3)

Median 155 a 100 b 0.602
IQR 120–190 60–165
Cells-Later*
Median 62.5 c 100 d <0.0001
IQR 50–80 65–157.5
Proteins-Baseline (mg/dl)
Median 211.5 e 206 f 0.88
IQR 194–274.5 195.5–250
Proteins-Later*
Median 162 g 217.5 h <0.0001
IQR 136.5–180 177–255
Sugar-Baseline(mg/dl)
Median 38.5 i 36 j 0.28
IQR 31.5–40 30.5–40
Sugar-Later*
Median 50 k 38 l <0.0001
IQR 44–58 29.5–50
TNF-α Baseline(pg/ml)
Median 545 m 520 n 0.587
IQR 414–875 270–872.5
TNF-α Later*
Median 157.5 o 427.5 p <0.0001
IQR 105–200 191–837.5
*after 24±6 h IL-1β Baseline (pg/ml)
p values (Wilcoxan signed rank Median 700 q 735 r 0.754
test) a vs. c0<0.0001, e vs. IQR 440–1,237 400–1002.5
g0<0.0001, i vs. k0<0.0001, m
vs. o0<0.0001, q vs. s0<0.0001, IL-1β Later*
b vs. d00.493, f vs. h00.371, j Median 290 s 665 t 0.003
vs. l00.021,n vs. p00.030, r vs. IQR 210–605 345–1,175
t00.125

Neonatal meningitis is widely diagnosed on the basis of
presence of >32 cells/mm3 in the CSF of a sick neonate [9].
In a study on meningitis in preterm neonates [30], it was
observed that the median WBC count in the CSF in neonates
with culture proven meningitis was 110 cells/mm3. The
sensitivity of WBC count in CSF of more than 25 cells/
mm3 in predicting meningitis was 71 %. In an administrative
database on 6,374 lumbar punctures, traumatic lumbar punc-
tures with meningitis were seen in only 50 (0.78 %) neonates.
Adjustment of white blood cell counts to account for increased
red cells did not improve diagnostic utility [31].
The strength of this study included similarity of groups in
baseline characteristics. Viral and fungal cultures were not
done. The study was not blinded and this may be considered
a weakness. However, the persons who estimated CSF cy-
tokine levels and brain stem evoked auditory response were
blinded.
To conclude, dexamethasone reduced fatality and progres-
sion of systemic inflammatory response syndrome significant-
ly. Reduction of CSF inflammatory indices (cells, proteins and
cytokines) and increase in sugar after 24 h was also significant
in dexamethasone group. Further multicentric trials may be
conducted to substantiate the findings.
Conflict of Interest None.
Role of Funding Source None.
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