Relationship between short-term outcome and occurrence of cerebral artery stenosis in survivors of bacterial meningitis

Abstract

To evaluate the influence of cerebral artery stenosis on the outcome of patients with bacterial meningitis we examined prospectively 47 consecutive patients [33 men, 14 women, mean (SD) age, 53 (17) years, range 18-81] with bacterial meningitis caused by various bacterial pathogens. The patients were examined with the use of the Glasgow Coma Scale (GCS) on days 1, 3, 5, 8, 14 and with the use of the Glasgow Outcome Scale (GOS) on day 21 after admission. In addition, focal cerebral signs were recorded separately. At each clinical examination, the patients underwent transcranial Doppler sonography recordings of the mean blood velocity (MBV) and the pulsatility index in all of the main intracranial arteries and in the submandibular internal carotid artery (ICA). A stenosis of the middle cerebral artery (MCA) was diagnosed by an MBV of > or = 120 cm/s or by an MBV ratio > 3 between the MCA and the ICA. An anterior cerebral artery (ACA) stenosis was indicated by an MBV > or = 100 cm/s, a posterior cerebral artery (PCA) stenosis by an MBV of > or = 85 cm/s, and a basilar artery (BA) stenosis by an MBV of > or = 95 cm/s. Twenty-five patients developed stenosis of the cerebral arteries (apart from 1, all within 8 days), 22 patients remained without stenosis. Of 29 focal cerebral signs, 27 occurred within 8 days. For outcome analysis, outcome was classified into two groups: not handicapped (GOS 5) versus handicapped (GOS 2-4) and dead (GOS 1). Based on the disease course up to day 8, risk factors for a handicapped/dead outcome after day 8 were advancing age (odds ratio per year, 1.06; 95% confidence interval (CI), 1.01-1.11; P = 0.03) and the presence of arterial stenosis (odds ratio, 7.3; 95% CI, 1.1-45) using a multivariate logistic regression analysis model. GCS on day 1, cerebrospinal fluid total protein content and the presence of focal cerebral signs were not significantly related to outcome in this series. The patients with stenosis exhibited significantly more frequently a poorer GCS on days 1-5 (Mann-Whitney U test; P < 0.05). In conclusion, the early occurrence of stenosis of the cerebral arteries in bacterial meningitis predicted a worse clinical course of the disease and a poorer short-term outcome of the survivors.

The Use of Clinical Scales in Depicting Cerebrovascular Complications in Bacterial Meningitis

“…Therapeutic interventions are of particular pertinence in bacterial meningitis in view of the nearly constant mortality rate over the past several decades. 1,4,9,16,30 Our data demonstrate that vessel narrowing correlates with a worse outcome. Vessel narrowing can be reflective of vasospasm, external pressure effects on vessel diameter, or inflammatory arteritis with secondary vessel narrowing.…”

Infarto maligno de la arteria cerebral media en una paciente con meningitis bacteriana

“…El compromiso vascular en la MBA se ha asociado a una evolución tórpida y a un desenlace fatal 16 . El deterioro de la circulación posterior es menos grave y clínicamente mejor tolerado que los cambios hemodinámicos de la circulación anterior 5,12,17 .…”

“…Las complicaciones neurológicas secundarias al proceso inflamatorio meníngeo incluyen: alteración del flujo sanguíneo encefálico por aumento de la presión intracraneana (PIC), edema cerebral, hidrocefalia, abscesos cerebrales, convulsiones fo-cales o generalizadas y enfermedad cerebrovascular venosa y arterial, siendo esta última una causa importante que puede explicar el mal pronóstico de las MBA [3][4][5] .…”

Late-Developing Cerebral Arteropathy After Pyogenic Meningitis

“…The severity of stenosis seems to improve in follow-up angiograms after the acute stage. 8 Regarding the late-developing vascular complications, we identified a published report of delayed cerebral infarction in a child 6 years after H influenzae meningitis. 9 Arteriography showed moderate stenoses of the proximal middle cerebral and anterior cerebral arteries, but the time course of evolution of the vasculopathy was unclear.…”