Thread by @VTA_Symposium

Next is Prof Fathima Paruk - 'Sub-phenotyping in ICU' #VTA23

At the bedside, we are increasingly responding to the unique profile of the patient in front of us. ARDS and Sepsis, for example, are both widely recognised syndromes that represent a hugely heterogenous patient population. #VTA23

ARDS is a phenotype, characterised by the Berlin Criteria. A further subcategorisation might be a hyperinflammatory vs hypoinflammatory. How deep do you go though? Endotypes look at the mechanisms that produce the subphenotype. #VTA23

This can lead us to identify treatable traits that produce novel therapies, hence the drive to subphenotype these large population groups.
#VTA23

An example of early subphenotypes has already been mentioned - Hypoinflammatory (P1) vs Hyperinflammatory (P2) ARDS. P1 ARDS is characterised by fewer inflammatory markers, and lower PEEP strategies and liberal fluid strategies produce better outcomes compared to P2. #VTA23

There are also cardiovascular subphenotypes in ARDS - Normal CVS function, Mild RV Dysfunciton, RV Failure and High CO Failure. This can lead to specific therapies to each type of cardiovascular profile. doi.org/10.1097/CCM.00…
#VTA23

In Sepsis, a type of subphenotyping currently being explored is trajectory. This can tell us much about those at higher risk of further hits, and may identify a subgroup in whom there will need to be a more heavy investment of resources. #VTA23

On the other hand, there is a risk of 'over' subphenotyping patients. We need real time rapid detection to be able to implement this - these is no point in subphenotyping if you get a profile 3 days after an intervention might have made a difference. #VTA23