Last month I had the pleasure of attending the 12th Critical Care Symposium in the beautiful setting of Manchester Town Hall. The conference brought together a fantastic range of speakers and topics in a packed 2 days, with a strong social media presence to top it off (#12thCCS if you fancy checking it out on Twitter). Whilst covering plenty of the recent advances in critical care medicine, there was also a lot of looking towards the future at what exciting ideas are around the corner. With the battery-draining twitter-storm now settling, it seemed like a good time to bring together some thoughts on the key topics that came up. You can check out the programme and speaker list at the website below:
The Critical Care Symposium
The Critical Care Symposium
Sepsis
As well it should be, sepsis was perhaps the most talked about topic over the 2 days. Most exciting was the talk from Dr Manu Shankar-Hari giving a little teaser about sepsis 3.0, the latest update on our understanding of this common and devastating condition. The focus is continuing to move towards recognising the importance of the patient response to differentiating sepsis from simple infection; sepsis = infection + badness. There were some teasing comments about the criteria that will highlight what this ‘badness’ is, but there will probably be a move away from the SIRS concept that has been a central part of sepsis definitions up until now. The hope is to reduce any confusion that may be occurring in identifying sepsis early and starting appropriate prompt treatment. We’ll have to wait until Autumn 2015 for the details though.
There’s other stuff on the horizon besides this excitement though. The news of a ‘biospleen’ was a bit out of the blue and intriguing for myself. Though still at the animal model stage, this is trying to be the blood filter for all that nastiness we were talking about in sepsis. Still a sounds a bit too sci-fi for me at the moment but you never know, this might be the dialysis of sepsis in a few years time.
The themes of biomarkers and prognostication were both recurring themes over the two days. As mentioned above, talk is increasingly of the body’s maladaptive response to infection in sepsis and the balance of a hyper-inflammatory immune response vs immunosuppression. With this understanding we are in urgent need of good biomarkers to tell us what is going on (the creatinine of the immune system as it was nicely described) and to help identify pathogens earlier (negative blood cultures 48 hours later anyone?). The talk of the transfer of PCR technology to the bedside did genuinely get me rather excited. Though they once again sound a little way off making their way into clinical practice, the idea of putting a blood sample in a machine and just a few hours later getting the guilty pathogen back (or a list of a few) was a pretty cool idea. I think the days of the faithful blood culture bottle (and its false positive contaminants) are numbered, but again we're still a way off.
The Surviving Sepsis Campaign
The Biospleen - Nature
There’s other stuff on the horizon besides this excitement though. The news of a ‘biospleen’ was a bit out of the blue and intriguing for myself. Though still at the animal model stage, this is trying to be the blood filter for all that nastiness we were talking about in sepsis. Still a sounds a bit too sci-fi for me at the moment but you never know, this might be the dialysis of sepsis in a few years time.
The themes of biomarkers and prognostication were both recurring themes over the two days. As mentioned above, talk is increasingly of the body’s maladaptive response to infection in sepsis and the balance of a hyper-inflammatory immune response vs immunosuppression. With this understanding we are in urgent need of good biomarkers to tell us what is going on (the creatinine of the immune system as it was nicely described) and to help identify pathogens earlier (negative blood cultures 48 hours later anyone?). The talk of the transfer of PCR technology to the bedside did genuinely get me rather excited. Though they once again sound a little way off making their way into clinical practice, the idea of putting a blood sample in a machine and just a few hours later getting the guilty pathogen back (or a list of a few) was a pretty cool idea. I think the days of the faithful blood culture bottle (and its false positive contaminants) are numbered, but again we're still a way off.
The Surviving Sepsis Campaign
The Biospleen - Nature
Sepsis 3.0: Sepsis = infection + badness #12thCCS
— Thomas Heaton (@tomheaton88) April 24, 2015
Exciting prospects for the future of sepsis biomarkers. Hopefully at least some will fulfill this promise #12thCCS pic.twitter.com/q3WlFFuucS
— Thomas Heaton (@tomheaton88) April 23, 2015
ARDS
ARDS was another topic that got a fair bit of time devoted to it. The Berlin definition was revisited as a concept for improving our accuracy with assessing its presence and severity and there were a few good reviews with where we are with improving our management of it. Unfortunately, this isn’t that much further forward than we were before. The drug therapies that held potential (steroids, beta agonists) have either still not been shown to do much or actively kill you (salbutamol in the BALTI -2 trial - number needed to kill of 9!). The talk about mesenchymal stem cell therapy was interesting with some hints of promise, and apparently a phase 2 trial now ongoing which is very exciting. ECMO made a brief cameo for the fans, but again there wasn’t talk of the massively transformational intervention that was hoped for (though now less lethal than it used to be, great news).
So after all this talk of exciting stuff, the reality seemed to be that we are still in a situation where we need to get the basics right. I think it was Prof Gattinoni who delivered a great overview of the postulated mechanisms ARDS development and for avoiding injurious ventilation by minimising energy transfer to the lung. The vicious circle of collapsed lung units and increasing ventilation pressures leads to increased energy transmission to no collapsed units and more damage. As such, it’s about doing the basic things right (protective ventilation, fluid restriction) and escalating as needed (prone, higher PEEP, paralysing agents) and hope this is enough to let the whole process calm down. Until we get some magic drugs it looks like this will be our best bet.
The Berlin Definition
The BALTI-2 Trial
Mesenchymal Stem Cell Therapy
So after all this talk of exciting stuff, the reality seemed to be that we are still in a situation where we need to get the basics right. I think it was Prof Gattinoni who delivered a great overview of the postulated mechanisms ARDS development and for avoiding injurious ventilation by minimising energy transfer to the lung. The vicious circle of collapsed lung units and increasing ventilation pressures leads to increased energy transmission to no collapsed units and more damage. As such, it’s about doing the basic things right (protective ventilation, fluid restriction) and escalating as needed (prone, higher PEEP, paralysing agents) and hope this is enough to let the whole process calm down. Until we get some magic drugs it looks like this will be our best bet.
The Berlin Definition
The BALTI-2 Trial
Mesenchymal Stem Cell Therapy
Lung protection = less energy + more homogenous lung pic.twitter.com/K1yB5aBRK9
— Thomas Heaton (@tomheaton88) April 24, 2015
Summary: energy transfer to lung causes badness, collapsed lung puts strain on surrounding lung, recruitment and PEEP protective #12thCCS
— Thomas Heaton (@tomheaton88) April 24, 2015
And The Rest...
There were plenty of other really interesting topics too. Perhaps the highlight of the whole conference was the pro-con debate between Professors Jean Louis Vincent and Mervyn Singer on catecholamines; both very engaging speakers. Does the use of catecholamines trigger undesirable physiological responses that increase mortality or is sympathetic nervous system a vital part of the body’s response to stress? The answer probably lies between the two extremes with them being a necessity to maintain blood pressure and vital organ perfusion in some cases whilst also having a wide range of adverse effects. Basically, obtain the minimal organ perfusion and stop. And I’m not sure about beta blockers in sepsis yet, it just feels a bit weird.
There were some interesting talks on the neurological challenges we face with Bill Coplin giving a great talk on some of the recent updates. The MR CLEAN trial sounded very interesting, suggesting an improvement if we treat ischaemic stroke with aggressive intra-arterial reperfusion strategies rather than systemic thrombolysis, perhaps a bit more like with myocardial infarctions. The REVASCAT trial was also promising, suggesting that the unopposed destruction that ischaemic stroke has wrought may be being increasingly challenged. For a pathology that has such crippling consequences this really is great news. He also talked a bit about the dogma that a GCS of 8 or lower mandates intubation. Where did this all come from? He argues it’s primarily from the massive increase in mortality with even a single episode of hypoxia, and thus a need to keep a patent and protected airway to avoid this. It’s unlikely that GCS 8 is the clear line where this transition of airway control occurs, but thinking about where these concepts come from is as important as knowing what to do.
MR CLEAN Trial
REVASCAT Trial
There were some interesting talks on the neurological challenges we face with Bill Coplin giving a great talk on some of the recent updates. The MR CLEAN trial sounded very interesting, suggesting an improvement if we treat ischaemic stroke with aggressive intra-arterial reperfusion strategies rather than systemic thrombolysis, perhaps a bit more like with myocardial infarctions. The REVASCAT trial was also promising, suggesting that the unopposed destruction that ischaemic stroke has wrought may be being increasingly challenged. For a pathology that has such crippling consequences this really is great news. He also talked a bit about the dogma that a GCS of 8 or lower mandates intubation. Where did this all come from? He argues it’s primarily from the massive increase in mortality with even a single episode of hypoxia, and thus a need to keep a patent and protected airway to avoid this. It’s unlikely that GCS 8 is the clear line where this transition of airway control occurs, but thinking about where these concepts come from is as important as knowing what to do.
MR CLEAN Trial
REVASCAT Trial
Revascat trial: 1.7 reduction in disability from ischaemic stroke. Clot retrieval in stroke the future? #12thCCS
— Thomas Heaton (@tomheaton88) April 24, 2015
Until Next Year
Well that is a very brief overview of a conference that covered a massive range of really interesting topics. There were a number of other great talks on renal developments, the role of protocols in critical care and antibiotic usage. However, it has taken me long enough to put all of this together without talking about all these other great topics so I think I shall leave it there. I would very much recommend checking out the CCS website and the#12thCCS hashtag on Twitter to find a wealth of other information and views, and I hope the links to papers I've included in this blog are useful. Thank you for reading and, as always, please share any of your thoughts, comments and links with us, even if you didn't manage to get down yourself. I’m already looking forward to next year.
Tom Heaton
Tom Heaton
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