Julia Champey, Clément Mourey, Gilles Francony, Patricia Pavese, Emmanuel Gay, Laurent Gergele, Romain Manet, Lionel Velly, Nicolas Bruder and Jean-François Payen
Various strategies have been proposed to reduce the incidence of external ventricular drain (EVD)–related infections. The authors retrospectively studied the impact of EVD care management on EVD-related infections at 3 French university hospital intensive care units.
Between 2010 and 2014, 462 consecutive adult patients with no evidence of a preexisting CSF infection received EVDs as part of their care at one of the following sites: Grenoble (221 patients), Saint-Etienne (130 patients), and Marseille (111 patients). Written protocols describing the EVD placement procedure, management, and removal were implemented at the 3 sites. Daily CSF sampling and intraventricular administration of antibiotics prior to EVD removal were performed at the Grenoble site only. EVD-related infection was considered for any confirmed ventriculostomy-related infection (VRI) and ventriculitis. VRI was defined as one or more positive CSF cultures or Gram stain with CSF pleocytosis and biochemical abnormalities. Ventriculitis was defined as CSF pleocytosis and biochemical abnormalities with degradation of neurological status and fever.
A total of 6945 EVD days were observed in the entire population. In the Grenoble cohort, the mean cumulative incidence of EVD-related infections was significantly lower than that in the 2 other cohorts: 1.4% (95% CI 0.0%–2.9%) versus 9.2% (95% CI 4.2%–14.2%) and 7.2% (95% CI 2.4%–12.0%) at Saint-Etienne and Marseille, respectively (p < 0.01). Accounting for the duration of external ventricular drainage at each site, the risk for EVD-related CSF infections was significantly higher at Saint-Etienne and Marseille than at Grenoble, with ORs of 15.9 (95% CI 3.6–71.4, p < 0.001) and 10.0 (95% CI 2.2–45.5, p = 0.003), respectively.
These findings indicate that it is possible to attain a low incidence of EVD-related infections, provided that an EVD care bundle, which can include routine daily CSF sampling, is implemented and strongly adhered to.
E. François Aldrich, Randall Higashida, Abdel Hmissi, Elizabeth J. Le, R. Loch Macdonald, Angelina Marr, Stephan A. Mayer, Sébastien Roux and Nicolas Bruder
Aneurysmal subarachnoid hemorrhage (aSAH) is associated with significant morbidity and mortality. The presence of thick, diffuse subarachnoid blood may portend a worse clinical course and outcome, independently of other known prognostic factors such as age, aneurysm size, and initial clinical grade.
In this post hoc analysis, patients with aSAH undergoing surgical clipping (n = 383) or endovascular coiling (n = 189) were pooled from the placebo arms of the Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS)–2 and CONSCIOUS-3 randomized, double-blind, placebo-controlled phase 3 studies, respectively. Patients without and with thick, diffuse SAH (≥ 4 mm thick and involving ≥ 3 basal cisterns) on admission CT scans were compared. Clot size was centrally adjudicated. All-cause mortality and vasospasm-related morbidity at 6 weeks and Glasgow Outcome Scale–Extended (GOSE) scores at 12 weeks after aSAH were assessed. The effect of the thick and diffuse cisternal aSAH on vasospasm-related morbidity and mortality, and on poor clinical outcome at 12 weeks, was evaluated using logistic regression models.
Overall, 294 patients (51.4%) had thick and diffuse aSAH. Compared to patients with less hemorrhage burden, these patients were older (median age 55 vs 50 years) and more often had World Federation of Neurosurgical Societies (WFNS) grade III–V SAH at admission (24.1% vs 16.5%). At 6 weeks, all-cause mortality and vasospasm-related morbidity occurred in 36.1% (95% CI 30.6%–41.8%) of patients with thick, diffuse SAH and in 14.7% (95% CI 10.8%–19.5%) of those without thick, diffuse SAH. Individual event rates were 7.5% versus 2.5% for all-cause death, 19.4% versus 6.8% for new cerebral infarct, 28.2% versus 9.4% for delayed ischemic neurological deficit, and 24.8% versus 10.8% for rescue therapy due to cerebral vasospasm, respectively. Poor clinical outcome (GOSE score ≥ 4) was observed in 32.7% (95% CI 27.3%–38.3%) and 16.2% (95% CI 12.1%–21.1%) of patients with and without thick, diffuse SAH, respectively.
In a large, centrally adjudicated population of patients with aSAH, WFNS grade at admission and thick, diffuse SAH independently predicted vasospasm-related morbidity and poor 12-week clinical outcome. Patients with thick, diffuse cisternal SAH may be an important cohort to target in future clinical trials of treatment for vasospasm.