Lumbar drainage following aneurysmal subarachnoid haemorrhage and the role of cytokine and adhesion molecules in the pathogenesis of delayed ischaemic neurological deficit

Introduction Delayed ischaemic neurological deficit (DIND) following aneurysmal subarachnoid haemorrhage (aSAH) is a significant cause of morbidity and mortality. There is some evidence to suggest that its pathogenesis is related to inflammation and that clearing the subarachnoid space of potential pathogens via a lumbar drain may reduce the prevalence and severity of DIND. Aims The aims of the current study are two-fold: 1. To ascertain whether lumbar drainage of cerebrospinal fluid (CSF) following aSAH can reduce the prevalence and severity of DIND. 2. To investigate levels of inflammatory mediators in plasma and CSF and to look for an association with aSAH, DIND and outcome. Material and methods 1. Prospective randomised controlled trial with randomisation into two arms: arm 1 control, no additional intervention; Arm 2 study, insertion of a lumbar drain in order to clear the visible blood load. 2. Prospective cohort study of patients with aSAH. Plasma and CSF samples were obtained on days 3, 5, 7 and 9 following haemorrhage and analysed for 11 mediators. Results 1. Prevalence of DIND 35% (confidence interval (CI) 26.2-45.2%) in the control versus 21% (CI 13.6-30.0%) in the study group (p=0.021). A significant improvement in early clinical outcome in favour of lumbar drainage was noted (Modified Rankin Score 0-2 37.5% in the control versus 55.2% in the study group, p=0.009). There was no difference in outcome at six months. 2. Raised plasma and CSF levels of most mediators when compared with non-aSAH controls. Significantly higher levels of vascular endothelial growth factor within the CSF of patients with DIND on day 5 post ictus when compared to patients without DIND. Generally higher mediator levels were noted within the CSF when compared to plasma. Conclusion This provides some support for the routine use of lumbar drains following aSAH in good grade patients to reduce the prevalence of DIND and improve early clinical outcome. Both a central nervous system and systemic inflammatory response is initiated following aSAH. The former may be associated with DIND. Causality cannot be determined from this study.