International Symposium on Intensive Care and Emergency Medicine (ISICEM)
The most famous (other than SMACC) ICU conference in the world is underway.
Li Huey Tan, an intensivist currently working at The Alfred hospital in Melbourne is there at the moment and sending over a mini-blog to give those of us who couldn’t make it a bit of a taster…
Click “Read more” to hear about day 1.
March 19 at ISICEM
What an exciting first day at the ISICEM in brussels. Roll out the ICU red carpet to welcome the heavyweights from all four corners of the world: Angus, Kellum, Macintyre, Gattinoni, Jean Louis and in the Aussie corner, Bellomo, Venkatesh, Hillman, Myburgh. The list goes on. Tis is the place to be ICU star struck.
The first afternoon was all about sleeping, urinating and everything in between. In medical terms, sedation, brain injury, circulation and renal function. The sessions on bio markers, MROs and lung injuries had to be missed as my delorean was out of commission.
I started my amuse bouche with Rinaldo Bellomo’s ” Concept of renal shunting”. The kidneys are greedy organs. They take up 20% of the cardiac output. It’s not surprising that shunting also occurs at the micro circulatory level. It’s homeostatic mechanisms are probably oversimplified in textbooks. Arteriovenous shunting can occur in the setting of increase or decrease renal blood flow. This mechanism enables homeostasis of renal tissue oxygenation. However, increase renal blood flow does not always result in increase oxygen delivery, as its seen in sepsis. The decision as to whether the renal vascular bed vasoconstricts or vasodilates in sepsis is not known. But such phenotype heterogeneity may explain why 50% of septic patients develop AKI. Martin Matejovic revisited “renal haemodynamics in sepsis controversies” with an opening slide eliciting renal vasoconstriction as a cause of AKI in sepsis. (I’m confused…) So it turns out, renal vasoconstriction as well as renal vasodilatation can occur depending on the sepsis stimulus. This has been shown in various mice experiment over the last two decades. He revisits the concept of heterogeneity in predisposition to AKI. A good cardiac output also does not always translate to good renal perfusion. However, a reduction in renal blood flow has been associated with increase renal vascular resistance (Prowle CCM 2012). The change in vascular resistance and its effect depends on whether it occurs in the afferent or efferent arterioles.
John Prowle reiterates in “Blood pressure targets for the kidneys”, the complex haemodynamic relationship the kidneys have when injured and how a MAP of 60mmHg may sometimes work for your kidneys. Such as in younger patients, patients on CRRT etc. More is not necessarily always better as an increase in renal blood flow may further compromise oxygen delivery to the medulla. As well as that, a precipitous fall in blood pressure may be more important that an absolute BP.
Niño Stocchetti takes the same view as Prowle when it comes to BP target for the brain. A bit like Goldilocks and the three bears: not too high, not too low but rather just right. He applies this rule in the setting of TBI and SAH patients.
Daniel De Backer discussed the concept of minimal perfusion pressure required for each organ’s microcirculation is different. The kidney appears to be most susceptible to drops in perfusion, interestingly followed by the gut. As expected, poor microcirculation is associated with worse outcome. Once again, heterogeneity is used to explain why not everyone’s micro circulation behave in the same way to the same stimulus. I guess that’s why we have DNA.
ICP and TBI? There is no conclusion according to Stocchetti. He presented a number of papers which did not show a difference in functional outcome between ICP directed therapy versus standard therapy. Patients who had an ICP monitor tended to stay on the ventilator longer. Whilst he is not willing to conclude that we should get rid of ICP monitors altogether, he did show that a small proportion of patients in the high ICP group >30, who historically did worse, may still benefit having an ICP in. Chestnut’s 2012 paper was mentioned here and may be worth having a look.
Despite being late in the afternoon, the sedation talks were very exciting indeed. Bellomo talked about ” Early Goal Directed Sedation” as part of the SPICE III study. This is a large scale multi centred RCT looking at the implementation of EGDS in 4000 patients. His pilot study concluded that EGDS to a RASS of -2 and +1 was effective and safe in the ICU population. The study uses dexmedetomidine as a first line sedative (chaching for Orion and whatever company that markets dex) and aims to minimize benzo use. This looks set to be a game changer in sedation practice since Kellum in 2002.
I guess the move away from conventional sedatives such as propofol and midaz is timely as our ICU patients survive longer to home discharge. Mirski looked at neurocognition and how a number of things affect ICU survivors. Apart from disease process, sedatives play a large role in cognitive impairment post ICU. There are some preliminary studies showing that dexmedetomidine may have better neurocognitive outcomes. Mauro Oddo advocates its use in the post acute neurocrtical unit to prevent opiate withdrawal. Watch out for the bradycardia and hypotension a though. In his lecture on “Sedation in neurocritical care”, he briefly talked about ketamine potentially being used as an adjunctive agent in the neuro ICU. Whilst we all know ketamine increases cerebral blood flow, it also has the effect of reducing cerebral metabolic rate, preventing hypotension. These effects can overall cause a reduction in ICP. Roll on the ketamine in ICP trial!