1
39
(
confused, with incoherent speech and impaired orienta-
Laboratory Results
tion), with neck stiffness and a positive Kerning’s and
Brudzinski signs. He also had a normal tone and deep
tendon reflexes. There were no cranial nerve deficits.
Chest was clinically clear to auscultation and he had no
murmurs. Abdominal and other system examinations
were essentially normal.
9
White blood cell count (WBC) was 5.6 x 10 /l, Hg/
9
Hct13.9/dl /41%, Platelets 114×10 /L, Cr 1.6, BUN15m-
mol/l, Na 137mmol/l. Cerebrospinal fluid (CSF): open-
ing pressure ~ 200mmH O, gram stain was negative,
2
sugar 42mg/dl, protein 102mg/dl, WBC 75cells/microL,
red blood cell 0-1, lymphocytosis 73%, neutrophils
17%, blood cultures were negative. CSF white cell count
was 65 with 75% polymorphs.
CSF: Bacterial detection antigen screen was negative,
gram stain showed no organism. Polymerase chain reac-
tion (PCR) showed no detection for cytomegalovirus,
herpes simplex virus I&II, Arbovirus panel and Myco-
bacterium tuberculosis and Ebstein barr virus. Miscella-
neous tests such as galactomannan assay, urine histo-
plasma antigen, Quantiferon Gold Assay, HIV tests
were all negative. Computed tomography scan (CT) and
MRI of the brain showed no acute brain lesions. Ibupro-
fen was discontinued and his symptoms resolved within
72 hours of admission with no neurological deficits.
Laboratory Results
9
White blood cell count (WBC) was 2 x 10 /l, haemoglo-
bin / hematocrit ( Hgb/Hct) values were 9.5g/dl /30%,
9
Platelets 20 ×10 /L, Cr 3.6, blood urea nitrogen (BUN)
1
8mmol/l,sodium (Na) 137mmol/l. Cerebrospinal fluid
CSF): opening pressure 200mm H O, gram stain was
negative, sugar 30mg/dl, protein 115mg/dl, WBC
25cells/microl and lymphocytosis 80%. CSF: bacterial
(
2
1
antigen screen was negative, polymerase chain reaction
showed no detection for Cytomegalovirus, Herpes sim-
plex virus I&II, arbovirus panel and Mycobacterium
tuberculosis and Ebstein barr virus. CSF and blood cul-
tures yielded no growth after 48 hours and five of days
incubation respectively.
Other tests done included: Galactomannan Assay, urine
histoplasma antigen, Quantiferon Gold Assay, HIV test
which were all negative. Computed tomography scan
Discussion
(
brain showed no acute lesions.
CT) and magnetic resonance imaging scan (MRI) of the
The two cases presented here were on drugs namely
Bactrim and Ibuprofen respectively. The interval be-
tween drug intake and the development of meningitis
varies widely. Signs and symptoms usually appear
within 24 to 48 hours after drug ingestion, but symptoms
may not appear in some cases for up to two years post-
The child was empirically started on intravenous Ro-
cephin, Vancomycin and Acyclovir pending further evi-
dence of non-infectious etiology. The bactrim was dis-
continued on admission with serial monitoring of
creatinine which trended down to normal prior to dis-
charge. His mental status and neurologic findings im-
proved within 48 hours.
6
therapy. Our patients had symptoms appearing early.
This p7,a8ttern has also been noted and reported previ-
ously.
Platelet transfusion was given prior to lumbar puncture
to prevent bleeding as quantitative versus qualitative
defects could not be ruled out at presentation. The pa-
tient was discharged from the hospital with a presump-
tive diagnosis of aseptic meningitis caused by Bactrim
hypersensitivity. The patient was advised to avoid taking
bactrim in the future. He has continued to do well on
follow up.
Drug-induced aseptic meningitis (DIAM) has been re-
ported as an uncommon adverse reaction to numerous
drugs. It is a diagnosis of exclusion, and clinical signs
5
and CSF findings vary greatly . The incidence of drug
induced meningitis remains unknown as most cases di-
agnosed are unreported and many remain unrecognized.
The body of evidence regarding DIAM is largely in the
form of anecdotal case reports and must be interpreted
6
carefully bearing this in mind . The major categories of
Case II
causative agents are non-steroidal anti-inflammatory
drugs, antimicrobials, intravenous immunoglobulin,
intrathecal agents including steroids, vaccines and a
number of other less frequently reported agents such as
vitamins. Drug induced aseptic meningitis can mimic
an infectious process as well as meningitis secondary to
systemic di6s,9o,1r0ders for which treatment of these drugs
were used.
This was a 15 year old male with no significant past
medical history who was admitted via the emergency
room for evaluation of altered mental status. For the last
three days prior to presentation, he had been taking sev-
eral pills of Ibuprofen for an intractable headache. This
was not his first exposure to Ibuprofen. On examina-
o
tion, temperature was 39 C, blood pressure of 110/65
altered mental status, he was talking irrationally, disori-
ented in time and place, equivocal neck stiffness, Ker-
nig’s sign was positive, hypertonia of the lower limbs.
The other systems examinations were normal. He was
empirically started on intravenous Rocephin and Vanco-
mycin for presumptive bacterial meningitis which were
discontinued after 72 hours as there was no evidence of
infective etiology.
Drug-induced aseptic meningitis may develop in a pa-
tient who initially was able to tolerate the causative
drug. The patients in our report have had previous expo-
sures. Prior exposure to the drug has been noted in 45%
of patients taking NSAIDs; and 35% and 3% for antibi-
2
otics and IVIGs respectively . These rates of prior expo-
sures are not surprising, considering the inappropriate
and high frequency with which NSAIDs and antibiotics
are prescribed.