Indian J Pediatr DOI 10.1007/s12098-015-1689-3


Acute Bacterial Meningitis – Early Diagnosis and Complications Satinder Aneja

Received: 24 December 2014 / Accepted: 1 January 2015 # Dr. K C Chaudhuri Foundation 2015

Acute bacterial meningitis (ABM) remains a common life threatening condition in children. In children between 2 mo to 12 y, bacterial meningitis is primarily due to H. influenzae type b (Hib), Streptococcus pneumoniae (Sp) and Neisseria meningitides (Nm). Hib is the commonest etiological organism identified in children less than 2 y in India [1], while Sp is the commonest organism identified in ABM in overall pediatric age group (1 mo to 12 y) [2]. In countries with routine vaccination against Hib and Streptococcus pneumoniae the median age of ABM has shown an increase with proportionately more cases occurring in adults [3]. With introduction of Hib vaccination in several parts of India and neighbouring countries the epidemiology of ABM in India is likely to change. Diagnosis of ABM is based on documenting inflammatory response in cerebrospinal fluid (CSF) and on diagnostic tests that demonstrate the specific causative bacterial agent in CSF (Gram’s stain, culture, tests for bacterial antigen/ DNA). In an accompanying article, Kumar et al. have reported the usefulness of urine strip test to measure the protein, sugar and leucocyte count in CSF for detecting bacterial meningitis [4]. The authors have correlated the semi-quantitative method of estimation at bedside with quantitative laboratory estimation of CSF protein, sugar and cell counts. The authors have documented that estimation of CSF parameters by urine strip can be done with reasonable reliability. However the results of this study should be interpreted with caution. The CSF parameters used to diagnose bacterial meningitis were taken arbitrarily as CSF protein level of 500 mg/dl and cell count of >100. The S. Aneja (*) Department of Pediatrics, Lady Hardinge Medical College, New Delhi 110001, India e-mail: [email protected]

criteria used in the study do not conform to the standard criteria of diagnosing meningitis. These criteria may exclude early and less severe cases of meningitis. The utility of dipstick at best, may be in remote areas to corroborate the diagnosis of bacterial meningitis where facilities for CSF biochemical evaluation are not available and referral is not possible. This will not help in excluding acute bacterial meningitis nor can it differentiate between acute bacterial, aseptic and TB meningitis. CSF culture provides a confirmatory evidence of ABM and is essential for selecting appropriate antibiotic for the etiological organisms. The rate of bacterial isolation is affected by antibiotic use prior to lumbar puncture; further, rate of isolation is increased if direct plating of CSF is done at bedside. The common pathogens of ABM are fastidious and require ambient temperature and specific culture techniques. The bacterial isolation by culture has been reported to be low across several studies from India. This may be due to use of suboptimal microbiological techniques and also due to widespread use of potent antibiotic injections by health care providers/ physician prior to hospitalization. Amplification of 16 S rRNA genes by PCR of CSF has been developed to diagnose ABM in patients pre-treated with antibiotics. A broad range PCR which can detect common pathogens of ABM simultaneously has been reported to have high sensitivity and specificity [5]. Latex agglutination tests can detect the presence of bacterial antigen of common pathogens. However a negative latex particle agglutination (LPA) test cannot exclude bacterial meningitis since this test is limited to a few specific pathogens. Due to high cost these tests should be reserved for patients who have received antibiotics. Third generation cephalosporins-cefotaxime and ceftrioxone are the preferred initial antibiotics for meningitis beyond neonatal age as they are effective against most bacteria

Indian J Pediatr

causing meningitis. Addition of vancomycin to ceftrioxone has been recommended for empiric therapy of ABM; this is primarily done to cover penicillin resistant strains of Sp. In India since the reported rate of penicillin resistance of Sp is low, the initial empiric therapy with ceftriaxone or cefotaxime alone is adequate [6]. In neonatal meningitis, a combination of cefotaxime and aminoglycoside is recommended. Despite advancement in supportive care and potent antibiotics, ABM remains a devastating disease with high rate of sequelae [7]. This is attributed to inflammatory response mounted by the host against the pathogen. The severity of response may be affected by causative pathogens as well as host factors. ABM caused by Sp has the highest case fatality and neurological disability rates compared to those caused by Nm or Hib. In a recent systematic review, the median in hospital case fatality ratio among African children with ABM was 35 % for Sp, 25 % for Hib, and 4 % for N. meningitidis [8]. The acute neurological complications of meningitis include seizures, ventriculitis, hydrocephalus, subdural effusions and brain abscess. In an accompanying article in this issue Kumar et al. have described the clinical profile and outcome of meningitis related ventriculitis [9]. The data, though retrospective gives important information about the usual presentations and challenges of treatment of this disorder. It is more commonly seen in neonates and infants. Purulent ventriculitis may occur when the infection extends into the ventricles with formation of purulent collections that may obstruct the foramina of the ventricular system with blockage of CSF flow and obstructive hydrocephalus. It may occur during course of disease while the patient is on antibiotics since inflammation may not resolve simultaneously in all parts of the CSF compartments, and infection and inflammation may persist in ventricles despite the presence of almost normal lumbar CSF findings. MRI features of ventricultis include thickening and enhancement of ependymal lining, dilated ventricles and presence of debris with irregular margins in dependent portion of ventricles. Ventriculitis can also result in aqueductal obstruction due to inflammatory exudates and may present as congenital hydrocephalus [10]. The diagnosis of ventriculitis is made by examination of ventricular CSF but since it is an invasive procedure, lumbar CSF is often used as a surrogate marker. The concentrations of total protein, albumin and immunoglobulin are generally higher in the lumbar CSF as compared to the ventricular CSF but there may be a wide variation precluding reliable prediction of ventricular fluid values from lumbar CSF [11, 12]. The treatment of ventricultis is primarly medical by giving appropriate antibiotics which should achieve high antibiotic concentration in ventricular space and eliminate the bacteria. In theory, intraventricular administration of antibiotics would help in achieving higher antibiotic concentration. Techniques used for intraventricular administration can be repeated

intraventricular tap or by use of omaya reservoir. Ventricular taps are invasive and known to be associated with development of porencephalic cysts. Use of intraventricular antibiotics in addition to intravenous antibiotics resulted in 3-fold increased risk for mortality as compared to IVantibiotics alone in neonatal meninigitis, hence intraventricular antibiotics are not recommended for meningitis related ventriculitis [13]. More than 3/4th of the patients required some form of CSF drainage for treatment of acutely raised ICP in this study. Since no uniform protocol was followed for treatment, it is difficult to draw conclusions regarding relative efficacy of different modalities of CSF drainage. However, it is apparent that this serious complication requires individualized management plan in consultation with neurosurgical team. The treatment of shunt or external ventricular drainage related ventriculitis comprises of removal of the infected shunt and/ or some component of external drainage, along with appropriate antimicrobial therapy [14]. The high neuromorbidity following ventriculitis observed by the authors highlights the need for early and adequate treatment of meningitis with appropriate antibiotics. Duration of treatment of meningitis especially in neonates and young infants should be for 2–3 wk depending upon the offending pathogen, clinical response to treatment and CSF findings. Cranial sonography is a non-invasive imaging modality which can provide useful information in the evaluation of critically ill infants with meningitis. Cranial sonography should be done in all infants with meningitis if there is adequate size of the fontanelle. A repeat sonography should be performed if any clinical deterioration occurs, such as increasing head circumference, occurrence of new neurological findings, and lack of response to therapy. Since currently available vaccines cannot prevent neonatal meningitis, early diagnosis and treatment of complications of meningitis is essential for the prevention of neurodevelopmental sequelae. Conflict of Interest None. Source of Funding None.

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Indian J Pediatr 4. Kumar A, Debata PK, Ranjan A, Gaind R. The role and reliability of rapid bedside diagnostic test in early diagnosis and treatment of bacterial meningitis. Indian J Pediatr. 2014. doi:10.1007/s12098-014-1357-z. 5. Wu HM, Cordeiro SM, Harcourt BH, Carvalho M, Azevedo J, Oliveira TQ, et al. Accuracy of real-time PCR, Gram stain and culture for Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenza meningitis diagnosis. BMC Infect Dis. 2013;13:26. 6. Thomas K, Mukkai Kesavan L, Veeraraghavan B, Jasmine S, Jude J, Shubankar M, et al. Invasive pneumococcal disease associated with high case fatality in India. J Clin Epidemiol. 2013;66:36–43. 7. Edmond K, Clark A, Korczak VS, Sanderson C, Griffiths UK, Rudan I, et al. Global and regional risk of disabling sequelae from bacterial meningitis: a systematic review and meta-analysis. Lancet Infect Dis. 2010;10:317–28. 8. Ramakrishnan M, Ulland AJ, Steinhardt LC, Moisi JC, Were F, Levine OS. Sequelae due to bacterial meningitis among African children: a systematic literature review. BMC Med. 2009;7:47.

9. Kumar R, Singhi P, Dekate P, Singh M, Singhi S. Meningitis related ventriculitisis—experience from a tertiary care centre in northern India. Indian J Pediatr. 2014. doi:10.1007/s12098-014-1409-4. 10. Udani V, Udani S, Merani R, Bavdekar M. Unrecognised ventriculitis/meningitis presenting as hydrocephalus in infancy. Indian Pediatr. 2003;40:870–3. 11. Sommer JB, Gaul C, Heckmann J, Neundörfer B, Erbguth FJ. Does lumbar cerebrospinal fluid reflect ventricular cerebrospinal fluid? A prospective study in patients with external ventricular drainage. Eur Neurol. 2002;47:224–32. 12. Gerber J, Tumani H, Kolenda H, Nau R. Lumbar and ventricular CSF protein, leukocytes, and lactate in suspected bacterial CNS infections. Neurology. 1998;51:1710–4. 13. Shah SS, Ohlsson A, Shah VS. Intraventricular antibiotics for bacterial meningitis in neonates. Cochrane Database Syst Rev. 2012;7: CD004496. 14. Agrawal A, Cincu R, Timothy J. Current concepts and approach to ventriculitis. Infect Dis Clin Pract. 2008;16:100–4.

Acute bacterial meningitis--early diagnosis and complications.

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