Strokes caused by a clot are described as ischaemic. When patients experience ischaemic strokes they may be eligible for “clot busting” therapy (thrombolysis). Currently thrombolysis has been shown to improve patient outcome after a stroke if administered within the first 4.5 hours after stroke onset. Up to 25% of patients wake up with symptoms of a stroke. This means they have an unknown onset time for their stroke (so called ‘wake up strokes’). With no known onset time, they are ineligible for thrombolysis. This study will investigate how we might determine stroke onset time.
Our aim is to use Magnetic Resonance Imaging (MRI) in patients with a known stroke onset time to work out characteristics of particular sequences that would then give us effectively a ‘stroke timer’. Another way to consider this is that with MRI we are trying to work out how much damage has been done to the brain and if any of this damage is still reversible (tissue viability). This has already been done in an animal stroke model. We would then use this data to help estimate the onset time in those patients who had woken up with their symptoms. If we can prove that we can predict time of stroke onset accurately from an MRI scan, we could then consider thrombolysis or other treatments in patients who have woken up with their strokes (this work would form separate research to this study).
ISARIC/WHO Clinical Characterisation Protocol for Severe Emerging Infections in the UK (CCP-UK)
People who develop an Acute Kidney Injury (AKI) often have a poor prognosis and many go on to develop chronic kidney disease (CKD). The recognition that AKI and CKD are linked is recent and the molecular pathways that control the transition from acute injury to chronic disease are not well defined. Currently there are no specific treatments that reduce the risk of progressing to CKD after AKI.
Preliminary investigations (not yet published) suggest that AKI causes sustained activation of the endothelin (ET) system to the long-term detriment of renal and systemic haemodynamic function. These pilot data form the basis of our project that seeks to determine whether the ET system is active in patients with AKI and, thus, represents a potential target for therapeutic intervention.
KRAKIL aims to recruit altogether 100 patients from across the emergency department, acute medical unit and inpatient wards at the Royal Infirmary. 50 of which with AKI’s and 50 matched controls with normal kidney function. We will monitor their bloods and urine for 90 days and compare the data from between the two groups.