Introduction: The effect of cerebral vasospasm (CVS) on critical closing pressure (CrCP) following subarachnoid haemorrhage (SAH) has not been fully delineated. Using a new methodology we sought to describe the behaviour of CrCP during CVS. As CrCP is the sum of intracranial pressure (ICP) and vascular wall tension (WT), we also explored its role in reflecting changes occurring in small vessels distal to CVS.
Methods: This retrospective analysis included recordings from 98 aneurysmal SAH patients, 52 of whom were diagnosed with CVS through transcranial Doppler measurements. CrCP was calculated non-invasively using the cerebral impedance methodology. Measurements of ICP were available in 21 patients, and were used to validate non-invasive CrCP.
Results: The onset of CVS caused a significant decrease in CrCP (p=0.025) and induced asymmetry, with CrCP ipsilateral to CVS being significantly lower than contralateral to CVS (p=0.025). ICP did not differ with presence of CVS (p=0.134). CrCP was independently to FV associated with outcome, with unfavourable cases assessed at both discharge and at 6 months post SAH having a significantly lower CrCP after the onset of CVS (p=0.014 and p=0.020 respectively).
Conclusions: CrCP became lower in presence of CVS and was associated with an unfavorable outcome. As ICP remained unchanged during CVS, reduced CrCP probably reflects a lower WT and dilated small vessels distal to CVS.
Patient Care: Potentially the new methodology for assessing Critical Closing Pressure can act as a surrogate marker of the behaviour of the vasomotor tone of small vessels distal to spasm. This could indicate quantitatively whether they dilate, compensating for the reduced local perfusion pressure due to the stenosis or not. Knowledge of this could then give an extra insight for medical treatment in regards to maintaining adequate blood flow in patients following aneurysmal subarachnoid heamorrhage.
Learning Objectives: 1)Introduction of a reliable non-invasive method for estimating Critical Closing Pressure
2)How Critical Closing Pressure changes during cerebral vasospasm and why?
3)Can Critical Closing Pressure reflect changes in cerebral microcirculation distal to spastic segments of a vessel?