Invasive Pressure Monitoring Saves from Tuberculous Meningitis with Fulminant Generalized Brain Edema

Tuberculous meningitis (TM) is difficult to diagnose and treat; clinical features are non-specific, conventional bacteriology is widely regarded as insensitive, and assessment of newer diagnostic methods is not complete. Treatment includes four drugs, which were developed more than 30 years ago, and prevents death or disability in less than half of patients. Mycobacterium tuberculosis resistant to these drugs threatens a return to the prechemotherapeutic era in which all patients with TM died. Research findings suggest that adjunctive treatment with corticosteroids improve survival but probably do not prevent severe disability, although how or why is not known. There are many important unanswered questions about the pathophysiology, diagnosis, and treatment of TM. Here we review the available evidence to answer some of these questions, particularly those on the diagnosis and treatment of TM.

Tuberculous meningitis is a severe form of extrapulmonary tuberculosis. The exact incidence and prevalence are not known. In countries with high burden of pulmonary tuberculosis, the incidence is expected to be proportionately high. Children are much more vulnerable. Human immunodeficiency virus-infected patients have a high incidence of tuberculous meningitis. The hallmark pathological processes are meningeal inflammation, basal exudates, vasculitis and hydrocephalus. Headache, vomiting, meningeal signs, focal deficits, vision loss, cranial nerve palsies and raised intracranial pressure are dominant clinical features. Diagnosis is based on the characteristic clinical picture, neuroimaging abnormalities and cerebrospinal fluid changes (increased protein, low glucose and mononuclear cell pleocytosis). Cerebrospinal fluid smear examination, mycobacterial culture or polymerase chain reaction is mandatory for bacteriological confirmation. The mortality and morbidity of tuberculous meningitis are exceptionally high. Prompt diagnosis and early treatment are crucial. Decision to start antituberculous treatment is often empirical. WHO guidelines recommend a 6 months course of antituberculous treatment; however, other guidelines recommend a prolonged treatment extended to 9 or 12 months. Corticosteroids reduce the number of deaths. Resistance to antituberculous drugs is associated with a high mortality. Patients with hydrocephalus may need ventriculo-peritoneal shunting. Bacillus Calmette-Guérin vaccination protects to some degree against tuberculous meningitis in children. (c) 2009 The Authors Journal compilation (c) 2009 Blackwell Munksgaard.

Tuberculous meningitis (TBM) is the most lethal form of tuberculosis; mortality is high and survivors are often left neurologically disabled. Several factors contribute to this poor outcome, including cerebrovascular involvement with ensuing brain ischemia, hydrocephalus and raised intracranial pressure, direct parenchymal injury, hyponatremia, and seizures. However, there is little standardisation of management with respect to these aspects of care across different centers, largely because the evidence base for much of the supportive treatment of patients with TBM is poor, leading to substantial differences in management protocols. This review emphasizes some of the uncertainties and controversies pertinent to the surgical treatment of hydrocephalus in TBM and the medical supportive management of the patient during the acute phase of the illness, with the aims of raising awareness and stimulating debate. The focus is on the management of hyponatremia, cerebral hemodynamics and intracranial pressure, medical and surgical treatment for hydrocephalus, and the intensive care management of patients in the acute severe stage of the illness. Very little data are available to address these issues with good evidence and so institutional preferences are common; this is perhaps most notable for the management of hydrocephalus, and so in this the review highlights our personal practice. The brain needs protection while the source of the illness is addressed. Without attention to these aspects of management there will always be a limit to the effectiveness of antimicrobial therapy in TBM, so there is a strong imperative for the controversies to be resolved and the limitations of our current care to be addressed. Existing protocols should be rigorously examined and novel strategies to protect the brain should be explored. To this end, a prospective, multi-disciplinary and multi-centered approach may yield answers to the questions raised in this review. Copyright © 2010 Elsevier Ltd. All rights reserved.