More information about text formats
Convulsive status epilepticus (CSE) with fever is one of the very
common presentations to the emergency room (ER) in infants and children.
The management of this clinical entity involves a major medical issue. At
present many questions have to be answered: when to treat, which
antimicrobial to use, and how to investigate CSE with fever?
Different ERs have different protocols to handle this cli...
Different ERs have different protocols to handle this clinical
problem. Despite advances in diagnostic modalities a few ERs use PCR for
rapid diagnosis of infectious organisms. The empirical treatment is the
use of anti convulsive therapy, followed by antibiotic therapy. Many a
times, this does not control the convulsions. Here is the role of time
Did you forget the Viruses? Yes, use Acyclovir in addition!
Approximately 15,000 cases of viral meningitis are reported every year in
US, so why ER physicians often forget this. This delays the diagnosis and
treatment of the viral meningitis for at least 1-4 days in most cases.
Moreover, it also puts other patients at risk, as these patients are not
isolated in hospital many a times.
Due to delay in diagnosis the viral meningitis may worsen to
Encephlitis and many a times to systemic infection and multi organ
failure. So, when a patient has Convulsive status epilepticus (CSE) with
fever, viral etiology can not be ruled out, unless proved otherwise. So
whenever, CSF sample is sent to laboratory, viruses as potential pathogens
should not be forgotten.
With the benefit of hindsight from this study , which refuted the
perception that convulsive status epilepticus is atypical of acute
bacterial meningitis(ABM), cerebrospinal fluid(CSF) sampling might have
been more readily undertaken, and perhaps more blood cultures done, given
the fact that the latter modality sometimes tests positive even when CSF
gram stains are non-contributory.
The crux of the matter is how the index
of suspicion for meningitis is "packaged", and the bottom line is that,
given the fact that both ABM and tuberculous meningitis(TBM) are eminently
amenable to treatment, and without treatment death is an almost ivariable
outcome for both, common ground must be found in the "packaging" in order
to optimise diagnostic potential. A package which does not acknowledge the
true prevalence of disease manifestations risks relegating those stigmata
to oblivion, the latter being the fate of the blanching maculopapular rash
which, notwithstanding its prevalence of 13% in meningococcaemia ,
nevertheless totally escaped mention in the section on ABM in a leading
text book . With a prevalence of 6.5-9.7% in ABM, the CSF which is
characterised by normal cellularity and biochemistry [4,5] is another
parameter that deserves greater recognition than is usually the case,
especially because this is a feature which may characterise TBM as
well [6,7]. One view is that, in the latter context coexisting HIV/AIDS is
the operative factor for this manifestation of TBM .
What is also
evident from the HIV/AIDS epidemic, is that tuberculous patients who
harbour this virus are more likely to have extrapulmonary tuberculosis
than their counterparts who do not have HIV/AIDS . The paradigm shift
dictated by the HIV/AIDS era is that the index of suspicion for miliary
tuberculosis and, hence, TBM, should be correspondingly higher, and that
parallels between ABM and TBM should be more readily recognised. For
example, like the four patients reported with ABM in the absence of
meningeal signs , the 8 month old HIV/AIDS patient with TBM reported by
Janner et al also presented without any clinical signs of meningitis .
Fundoscopy is crucial to the index of suspicion for miliary tuberculosis
and, hence, TBM, given the fact that the presence of choroidal tubercles
will reveal the miliary component even when routine chest radiography has
failed to do so . Among 113 confirmed cases of miliary tuberculosis,
12.4% were undetected by chest x-ray . Choroidal tubercles were detected
by fundoscopy in 5 out of the 14 x-ray negative cases .
The armamentaria for the heightened index of suspicion for ABM as well as
for TBM include a more overt acknowledgment of the significance of the
blanching maculopapular rash in ABM, rotine fundoscopy to detect choroidal
tubercles, a greater willingness to undertake CSF sampling and blood
cultures in convulsive status epilepticus, and a recognition that a CSF
which is normal for cell count and for biochemistry may be a feature of
either ABM or TBM, and so may the total absence of signs of meningeal
(1). Chin RFM et al.
Meningitis is a common cause of convulsive status epilepticus.
Arch dis Child 2005:90:66-9
(2). Marzouk O et al.
Features and outcomes in meningococcal disease presenting with
(3). Rudd PT.
Acute bacterial meningitis
in Forfar and Arneill's Textbook of Pediatrics 1998, Fifth Edition p 1288-
Editor Campbell AGM and McIntosh N
(4). Rosenthal J et al.
Bacterial meningitis with initial normal cerebrospinal fluid findings.
Israel Journal of the Medical Sciences 1989:25:186-88
(5). Coll M-T et al.
Meningococcal meningitis with normal cerebrospinal fluid.
Journal of Infection 1994:29:289-94
(6). Karstaedt AS et al.
Tuberculous meningitis in South African urban adults.
Quarterly Journal of Medicine 1998:91:743-7
(7). Janner D et al.
Cerebral tuberculosis without neurologic signs and with normal
The Pediatrics Infectious Disease Journal 2000:19:763-4
(8). Thomas P et al.
Tuberculosis in human immunodeficiency virus-infected and human
immunodeficiency virus-exposed children in New york City.
Pediatrics Infectious Diseases Journal 2000:19:700-6
(9). Illingworth RS and Lorber J.
Tubercles of the choroid.
Arch Dis Child 1956:31:467-9