Acute tuberculous meningitis with fulminant fatal evolution in a 69-year-old man
- 1Hospices Civils de Lyon, Lyon, France
- 2Université Claude Bernard, Lyon 1, France
- 3Pathogénie Bactérienne et Immunité Innée, INSERM U851, Lyon, France
- Correspondence to Dr Tristan Ferry,
An immunocompetent (HIV-negative) 69-year-old Caucasian man with a history of paramedian pontine acute ischaemic stroke requiring intravenous thrombolysis 1 year earlier (ataxia as sequelae only) was admitted with a 7-day history of fever. The patient was in a confused state at admission, with known ataxia but without other neurological signs. His mental status worsened 4 days after admission with occurrence of a coma and neck stiffness. Mild hydrocephalus was observed on a first MRI (figure 1A), and ventriculoperitoneal shunt was not performed. Central nervous system tuberculosis was finally diagnosed (cerebrospinal fluid (CSF) collected 5 days after admission contained 138 white cells/mm3 with acid-fast bacilli on direct examination; the glucose CSF/blood ratio, CSF lactate and protein were 0.9/10 mmol/l, 13.7 mmol/l and 4.64 g/l, respectively). Despite administration of antituberculous chemotherapy (intravenous rifampin–isoniazid–ethambutol and oral pyrazinamid, introduced 7 days after admission) and intravenous corticosteroids (methylprednisolone, 1 mg/kg/day), the mental status progressively worsened. At day 18, hydrocephalus persisted on MRI with the appearance of (i) contrast-enhanced meningeal thickening; (ii) irregular aspect of middle cerebral arteries; and (iii) large zones of cerebral infarction (reaching basal nuclei, cerebral trunc, pedoncules and temporal lobes) suggestive of vasculitis (figure 1B,C). Traditional cultures confirmed susceptible tuberculosis at day 15. The patient died at day 20.
Hydrocephalus, meningeal thickening and cerebral infarction are known to be possible complications during subacute or chronic tuberculous meningitis.1–3 Hydrocephalus is known to increase intracranial pressure that leads to a reduction of the cerebral perfusion. Basal arachnoiditis, which is often associated, leads to vasculitis, small vessels occlusion and cerebral infarction.1 Here, cerebral infarctions occurred rapidly during the course of the disease. Pre-existing arterial lesions could have facilitated the occurrence of rapid cerebral infarction and might partially explain the fulminant fatal evolution. Indeed, as tuberculous meningitis is mainly associated with leptomeningeal exsudates located in the interpedoncular fossa, vasculitis might precipitate thrombus formation if basal vessels already harbour pre-existing artherosclerosis lesion.1 This case illustrates the poor outcome associated with stroke in tuberculous meningitis,1–3 stressing the need for optimal acute care management and new therapeutic approaches.
Vasculitis might occur early in the clinical course of tuberculous meningitis.
Hydrocephalus, vasculitis and cerebral infarction might facilitate fulminant fatal evolution, despite prompt introduction of antituberculous therapy and corticosteroids.