Delayed Cerebral Vasculopathy in Pneumococcal Meningitis: Epidemiology and Clinical Outcome. A Cohort Study

Abstract

Background: To describe the prevalence, clinical characteristics, impact of systemic steroids exposure and outcomes of delayed cerebral vasculopathy (DCV) in a cohort of adult patients with pneumococcal meningitis (PM). Methods: Observational retrospective multicenter study including all episodes of PM from January 2002 to December 2015. DCV was defined as proven/probable/possible based upon clinical criteria and pathological-radiological findings. DCV-patients and non-DCV-patients were compared by univariate analysis. Results: 162 PM episodes were included. Seventeen (10.5%) DCV-patients were identified (15 possible, 2 probable). At admission, DCV-patients had a longer duration of symptoms (>2 days in 58% vs. 25.5% (p 0.04)), more coma (52.9% vs. 21.4% (p 0.03)), lower median CSF WBC-count (243 cells/uL vs. 2673 cells/uL (p 0.001)) and a higher proportion of positive CSF Gram stain (94.1% vs. 71% (p 0.07)). Median length of stay was 49 vs. 15 days (p 0.001), ICU admission was 85.7% vs. 49.5% (p 0.01) and unfavorable outcome was found in 70.6% vs. 23.8% (p 0.001). DCV appeared 1-8 days after having completed adjunctive dexamethasone treatment (median 2,5, IQR = 1.5-5). Conclusions: One tenth of the PM developed DCV. DCV-patients had a longer duration of illness, were more severely ill, had a higher bacterial load at admission and had a more complicated course. Less than one third of cases recovered without disabilities. The role of corticosteroids in DCV remains to be established.

Steroid Rebound Phenomenon as a Cause of Delayed Cerebral Vasospasm in Post-Splenectomy Pneumococcal Meningitis: A Case Report

“…Pneumococcal meningitis sometimes causes neurological complications such as cerebral infarction, vasospasm, and hydrocephalus [ 3 ]. The causes of these neurological complications are complicated and reportedly caused by the excessive immune response against bacterial microstructures, direct pneumococcus invasion, or cerebral vasculitis [ 5 , 6 ]. Dexamethasone can suppress excessive immune responses to bacterial microstructures by suppressing inflammatory cytokines such as IL-1 and TNF-α in spinal fluid [ 8 ].…”

“…For the prevention of neurological complications, dexamethasone (0.15 mg/kg/day) for four days has been recommended [ 4 ]. The steroid rebound phenomenon which occurs as dexamethasone withdrawal has been reported in pneumococcal meningitis [ 5 , 6 , 7 ]. Hydrocephalus could also occur accompanied by the rebound effect [ 7 ].…”

“…Hydrocephalus could also occur accompanied by the rebound effect [ 7 ]. Its mechanism is characterized by vascular complications caused by the reactivation of the primary inflammatory response by bacterial fragments [ 5 , 6 ]. The inflammatory infiltrates surrounding the cerebral vasculature in the inflated subarachnoid space lead to vasospasms and thromboses of arteries and veins, and subsequent focal cerebral ischemia [ 9 ].…”

“…The inflammatory infiltrates surrounding the cerebral vasculature in the inflated subarachnoid space lead to vasospasms and thromboses of arteries and veins, and subsequent focal cerebral ischemia [ 9 ]. To avoid the rebound effect, a gradual dexamethasone withdrawal rather than the abruptly terminated four-day course, or longer treatment with progressive tapering is advocated [ 5 , 6 ].…”

“…In acute pneumococcal meningitis, four days of dexamethasone is widely used to prevent neurological complications [ 4 ]. In the previous reports, delayed neurological complications have been reported after initial treatment, especially after dexamethasone withdrawal, which has been described as “steroid rebound phenomenon” [ 5 - 7 ]. Here we report a case of delayed neurological complications by usual dexamethasone use in pneumococcal meningitis as OPSI.…”