The teaching highlight last week was our Journal Club session, where Glenn facilitated presentations by Paula and Lachlan on two big studies with potential implications for our practice (both articles sent around previously by Glenn, attached again above). The PARAMEDIC2 study looked at whether Adrenaline use in out-of-hospital cardiac arrest cases was associated with any difference in survival and neurologic status. Lots of interesting commentary around this study in the media since it was published, and the group was equally interested in the outcomes. Whilst it is hard to extract meaning for patients arresting in the ED setting (given the mean time to therapy (adrenaline administration or control saline group) was 21 minutes), and the large proportion of patients where arrest was unwitnessed, it is hard to argue that adrenaline confers any meaningful patient-focussed benefit for the patients in this study.
What will this mean for us? Will we see the removal of pre-hospital adrenaline from arrest management algorithms? I doubt it, but I suspect people will have less faith in the role of this drug than perhaps they did previously.
The Fluids in DKA trial also caught the interest of the group. My anecdotal experience was that cerebral oedema, whilst a potentially devastating complication of severe DKA cases, was rarely encountered in our practice, and that kids who came in well stayed well. This trial demonstrated that no matter whether the fluid replacement therapy used was hypotonic or isotonic, or whether it was replaced “fast” (half in the first 12 hours) or “slow” (over 48 hours), the incidence of cerebral oedema was unchanged, and remained low at around 1%. For me, I found the use of a surrogate marker of cerebral oedema (a (transient in almost all cases) decline in GCS of 2 points) a weak primary end-point. Whilst easy to understand from a study design perspective, the components of GCS are (in my opinion) not equivalent, and the decrease in GCS was not persistent, which whilst concerning for the treating team involved, the presence of persisting brain injury and decrease in IQ (secondary outcomes) would have been a much more compelling outcome (persisting brain injury was incredibly rare across the study population). This study didn’t focus on the sickest children, and I suspect this is where the impact of iatrogenesis may be most felt. However, I feel like this paper does tell us that variation between commonly used approaches to replacing fluid deficits in children with mild-mod DKA is not producing meaningful differences in cerebral oedema.
In the era of FEAST and concerns around fluid boluses and causing harm, the group was reminded that we should always be cautious when bolusing fluids in patients with diabetic (and other osmotically challenged) emergencies.