[LS2-1B-1] Acute Meningitis
Meningitis is commonly caused by bacteria or viruses, and infrequently by fungi. Reducing morbidity and mortality is dependent on prompt etiologic diagnosis, initiation of appropriate antibacterial/antiviral therapy, and controlling inflammatory response and raised intracranial pressure. These are challenging goals because of limited diagnostic tools, limitation in obtaining CSF for analysis, and lack of effective antiviral and adjunct therapies. In acute bacterial meningitis (ABM), having an estimated global incidence of 34.0/100000 child-years and case fatality rate of 14.4%(5.3%-26.2%), time to death is so short that only modern intensive care is likely to improve outcome.
CSF leukocytosis >100/µL, blood glucose, CSF:blood glucose ratio, and serum procalcitonin (>5µg/L) are useful in differentiating between bacterial and viral infections as also CSF cytokines/IL-6 levels. Broad-range real-time PCR can give early etiologic diagnosis. Neuroimaging is useful in etiologic diagnosis of tuberculosis and some viral meningo-encephalitides. Caution is warranted in using of existing clinical prediction rules (CPRs) to guide hospitalization and treatment of suspected ABM because of low quality and performance of published CPRs for children.
Optimizing cerebral perfusion by raising the blood pressure to 90th-95th centile using vasoactive agents and reduction of raised ICP using 3% hypertonic saline can save lives. Use of oral glycerol, maintenance fluids over restricted fluids in first 48 hours may reduce severe sequelae (evidence quality low). Current data support dexamethasone-use in high-income countries but not low income countries. In low resource-setting dexamethasone increased mortality in suspected but unproven cases of ABM. Possible new strategies for treating vasogenic brain edema, minimising brain cell injury and thus prevent neurological sequelae include blockade or removal of cytokine and chemokine activity with neutralizing antibodies/antagonists. A search for sensitive rapid diagnostic tools, a high-performing and well validated CPR for clinical decision making and effective adjunct and anti-inflammatory therapies for meningitis continues.
CSF leukocytosis >100/µL, blood glucose, CSF:blood glucose ratio, and serum procalcitonin (>5µg/L) are useful in differentiating between bacterial and viral infections as also CSF cytokines/IL-6 levels. Broad-range real-time PCR can give early etiologic diagnosis. Neuroimaging is useful in etiologic diagnosis of tuberculosis and some viral meningo-encephalitides. Caution is warranted in using of existing clinical prediction rules (CPRs) to guide hospitalization and treatment of suspected ABM because of low quality and performance of published CPRs for children.
Optimizing cerebral perfusion by raising the blood pressure to 90th-95th centile using vasoactive agents and reduction of raised ICP using 3% hypertonic saline can save lives. Use of oral glycerol, maintenance fluids over restricted fluids in first 48 hours may reduce severe sequelae (evidence quality low). Current data support dexamethasone-use in high-income countries but not low income countries. In low resource-setting dexamethasone increased mortality in suspected but unproven cases of ABM. Possible new strategies for treating vasogenic brain edema, minimising brain cell injury and thus prevent neurological sequelae include blockade or removal of cytokine and chemokine activity with neutralizing antibodies/antagonists. A search for sensitive rapid diagnostic tools, a high-performing and well validated CPR for clinical decision making and effective adjunct and anti-inflammatory therapies for meningitis continues.