Hi, so as a follow up to our earlier discussion, which can be found here, Rory and I discuss a recent case he had, which I think exemplifies well many of the clinical conundrums that are seen in fluid resuscitation, one being the general resistance of many to diurese patients who are still in shock on vasopressors, instead preferring to (hopefully) wait until shock resolution to de-resuscitate. But sometimes, it is exactly what they need, as some of this congestion may be, in fact, a cause of shock…
Here you go:
Love to hear opinions, so feel free to reach out.
For those who may be interested at learning some of these POCUS skills, check out H&R2018 (#Hres2018)!
cheers!
Philippe
thinking critical care 
Great to listen guys, thanks, and very timely. I had just read Tremblay’s paper after coming across a very pulsatile PV in a relatively well elderly patient with bad TR. Two questions – which PV are more likely pulsatile in the first place….Tremblay mentions RVF/TR and very thin folk. What is your experience?
Second Question – what did the GB wall/GB fossa look like after the initial very positive fluid balance? Does everyone blow out their GB wall with fluids, or only some?
Great case, loved it. Thoughtful management, brilliant!
I couldn’t help thinking as I listened, that it is so important to avoid over-resuscitation with fluids in the first place. We all know that the majority of crystalloids given will end up as interstitial edema, so any benefit from the increase in stroke volume is temporary at best (consider carefully what you gain and at what cost). Wet lungs=increased mortality, days on the vent, and ICU stays. Wet kidneys=AKI 2-3 days after initial resuscitation and potential RRT. Congested liver=gut edema and continuation of inflammatory cytokines/sepsis syndrome. Too much fluids–>BNP levels rise, high BNP levels in the presence of LPS=glycocalyx shedding, and more interstitial edema everywhere.
I think there is some decent evidence that an early fluid liberal approach combined with a late fluid restrictive approach can potentially benefit a patient in septic shock, but its clear that an overall positive fluid balance does harm. Perhaps, even the early fluid liberal strategy (in sepsis specifically) should be tempered by a careful consideration of what is really going on.
Sepsis is an entity characterized by venous return being limited by a decrease in mean systemic pressure (MSP) due to an increase in venous capacitance, rather than a decrease in fluids that generates the stressed volume (MSP=fluid filling/venous capacitance). The body compensates with an adrenergic response that maintains (or attempts to maintain) MAP by an increase in a catecholamine driven augmentation in cardiac output/contractility. This adrenergic response likely has more to do with the increase in lactate production observed in sepsis, rather than actual tissue hypo-perfusion and anaerobic metabolism mechanism. Increases in CVP inhibit venous return and congest the kidneys and GI tract (the left atrial pressures are the equivalent problem for the lungs, combined with the fact that pulmonary vascular permeability is increased in sepsis as well). Given this, I think in distributive shock, we should fix the lack of MSP by an earlier vasopressor therapy approach, both to supplement and decrease the crystalloid load to the patient, which is un-natural and contrary to their deranged septic physiology.
Also, could the type of crystalloid given be important? NS gives a considerable sodium load compared to LR, and this likely promotes/sustains fluid retention that is difficult to remove during de-resuscitation. The high chloride levels of NS will promote an increase afferent arteriolar vasoconstriction and thus decrease GFR, making it more difficult to diuresis the patient later on, and contribute to AKI beyond the iatrogenic interstitial kidney edema caused by the crystalloids we gave.
If you are involved in the early phase of resuscitation of a shocked patient, consider the downstream consequences of your fluid strategy that you give your patient that may give you a temporary comfort because they will look better in the short term.
This is not to say that an aggressive and upfront resuscitation is not critical–it surely is. I’m saying resuscitate smarter, not wetter. Look for stop points for crystalloids–E/e’ ratios, consider PVPI, RV dilation/TAPSE, hepatic vein doppler, IVC dynamics, portal vein pulsativity, intra-renal venous Doppler patterns and renal resistive index. Fix the hemodynamics from an approach of the root of their problem, rather than pushing fluids for every hypotensive patient (whether you are taking care of them early, or late in the time frame of their illness). Fluids do have their place, but be careful and cognizant of their real down side. Look at your patient, think it through, and make the best actions for them.
Any chance you could post a video here or share a link to a site with some basic techniques on portal vein pulsatility measurement (probe selection, probe positioning, etc)? I’d love to start applying it.
Last week had a lady with MSSA bacteremia who (probably) initially had real ARDS, and then a few days later had “recurrent ARDS”, looking back she was 2-3 liters positive for several days in a row, and her “ARDS” got better with PEEP and diuretics. The nurses gave me some grief about diuresing her because she was “septic”, would love to have a concrete way of conveying to them the concept of organ congestion.
Really enjoyed the conference last week ! Had the opportunity to meet many of the great clinicians that contribute to this website – nice to be able to associate a face to a name now. Good “short snapper” summaries on a variety of topics that everyone sees if they work in an acute care facility. Speakers were well-chosen and presented well. Workshops were small enough to allow good hands-on practice and the ability to pick the brains of those present. Good job to the “Organizing Committee” ! Just awaiting instructions of where I can find the lecture slides when they are available. Thanks again Philippe!!
Thanks Paul, it was great having you. It is, in fact, the synergy of faculty and participants that make an event really interesting. Hope to see you next year!