Salt water mastery

A BLOG BY DR JUSTIN MANDEVILLE () FOR OXICM

Wet, full, soggy, overloaded, oedematous. Dry, dehydrated, hypovolaemic, a fire hazard. Euvolaemic, replete, just right. The jargon of fluid status is commonly used, and abused on the ICU.

A 70 year old, with a several day prodrome of anorexia, diarrhoea, vomiting (more latterly blood-stained) arrives hypoxic, obtunded, with mottled peripheries, too much lactate and too little BP. We give some oxygen, some antibiotics to cover whichever horrendococcus is suspected, and some fluid. But how much fluid?

Now look at this diagram:

Screen Shot 2014-10-23 at 23.15.28

Is this an oversimplification? Almost certainly but it illustrates a point. With our patient we need to ask: do we want blood volume improved, do we want to rehydrate, or do we want to edge up the Frank-Starling hill?

Resuscitating sepsis

Our super-sick man will be dehydrated, likely hypovolaemic and will almost certainly be fluid responsive.

Recent evidence

ARISE patients received on average 1-3 litres prior to enrolment, 1-3 further litres over the next 6 hours and 1-7 litres over the next 66 hours with a small (and surely clinically insignificant) difference between the groups.

For ProCESS the numbers were very similar. Without the documented output/losses the fluid balance differences can’t be assessed but may turn up in some post-hoc introspection.

So everyone gets a few litres in 6 hours. These studies were both ‘non-positive’ – maybe the end-points for fluid resuscitation in sepsis don’t matter, within traditional doses and timing. Maybe we shouldn’t bolus at all. Maybe we shouldn’t give extra fluid at all. Just get somewhere near euvolaemia, rehydrate and maintain. Paul Marik enjoys showing us the flaws in the formative work on fluid in sepsis, but whether we’re ready to entertain trying out ‘dry resuscitation’ is debatable.

After 6 hours

Beyond the 6 hour package our patient is unlikely to be hypovolaemic. Beyond 6 hours we are very short on evidence-based guidance. Optimizing volume to optimise cardiac output is traditionally the next task. His CVP, PAWP, IVC dimension, LV end-diastolic area, corrected flow time, stroke volume and a number of other measurements all may have some theoretical value, but in actuality are worthless. Predicting fluid responsiveness is not about assessing frank hypovolaemia, for which some of these markers may be of value.

If you want to see how stable a system is, then give it a nudge. Bolus some fluid, or if your keen to avoid an unnecessary bolus then provoke the circulation with a breath (SVV, PPV, VTI variation) or a reversible 2-legs-worth bolus (passive leg raise). An alternative approach, although less applicable to our situation, you could take some fluid away and assess response.

Screen Shot 2014-10-23 at 23.13.17

These dynamic markers predict short term response to fluid. They make no promise about what the cardiac output will be in half an hour, and they make no promise about what the blood pressure will do. They tell you that cardiac output will improve, not that you need it or that it will benefit the patient in the short or long term.

Cut to day 2

Our man by this stage has some sort of ‘LipiccODM rapido™’ device which says his cardiac index is 2.9. TTE shows a capable LV without clear signs of septic cardiomyopathy but mild diastolic impairment. His lactate is 1.0. Noradrenaline is running at 0.2 mcg/kg/min. His urine output might be at or just above the magical 0.5ml/kg/hr but you know he’s taken a bit of a renal hit.

You find yourself mid-way through prescribing a bag of Hartmann’s because you absent-mindedly agreed with a comment “there’s a swing on that A-line, fill him up”.

Why increase his cardiac output. He might be fluid responsive but why does his cardiac output need to be max’d out. It’s at this point you should look ahead to the rest of his stay. Every water molecule and every salt molecule in that bag of fluid you’ve just prescribed needs to be got rid of somehow in the near future. If you enjoy creating a marsh-mallow man and watching him struggle with oedematous lungs, chest wall, abdominal viscera through the rest of their slow wean, then go right ahead.

Admittedly we’re short of a good blood volume monitor but knowing when your markers of fluid responsive are flawed is a good start. A swinging arterial line is normal in a patient breathing patient. And ‘swing’ does not reliably mean a high SVV or PPV.

Screen Shot 2014-10-23 at 23.15.13

Fluid removal

At some point our patient will tolerate fluid removal, or he’ll do it himself once kidney/endocrine/circulatory stars are aligned. No one knows how to manage this phase best but it’s becoming clear that following the theoretical yellow line below will get our man off the unit quicker, potentially in a healthier state, than following the red line.

How and when you achieve this is almost completely evidence free territory. ADQI again have some suggestions regarding targeted fluid removal:

Fluid balance target:

  • Depends on your impression of tolerance (stable dialysis can have litres taken off over a few hours)
  • A common approach is to try 500ml in 12 hours, then increase.

Clinical endpoints:

  • Better oxygenation
  • Less oedema

Safety endpoints:

  • Perfusion safety endpoints – falling BP, SVV > 25% if ventilated, rising noradrenaline requirement, lactate, or ScvO2.
  • Renal endpoints – creatinine or urea rise 10-20%, sodium rise >4 mmol.

Our man needed some help from vitamin F but tolerated over a litre negative balance per day from the third day with a significant decrease in FiO2 after the first 500ml. Extubation was possible on day 4 and renal function was near baseline by day 8 by which time he was back on the medical ward. 

Summary

So it’s no longer about being a ‘wet’ or ‘dry’ unit but being wet and dry in all the right places. Fluid is a drug that both saves lives and slows recovery. The finer points of administration and removal are yet to be elucidated but signals are already in the literature regarding the shaping of a patient’s dynamic fluid balance

P.S. Echocardiography is uniquely suited to assessing all these stages fluid assessment using quantitative and qualitative evaluation. But that’s another story.

  1. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wiedemann HP, Wheeler AP, Bernard GR, Thompson BT, Hayden D, et al. Comparison of two fluid-management strategies in acute lung injury. N Engl J Med. 2006 Jun 15;354(24):2564–75.
  2. Vincent J-L, Sakr Y, Sprung CL, Ranieri VM, Reinhart K, Gerlach H, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006 Feb;34(2):344–53.
  3. Durairaj L, Schmidt GA. Fluid therapy in resuscitated sepsis: less is more. Chest. 2008 Jan;133(1):252–63.
  4. Payen D, de Pont AC, Sakr Y, Spies C, Reinhart K, Vincent JL, et al. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care. 2008;12(3):R74.
  5. Bouchard J, Soroko SB, Chertow GM, Himmelfarb J, Ikizler TA, Paganini EP, et al. Fluid accumulation, survival and recovery of kidney function in critically ill patients with acute kidney injury. Kidney Int. 2009 Aug;76(4):422–7.
  6. Murphy CV, Schramm GE, Doherty JA, Reichley RM, Gajic O, Afessa B, et al. The importance of fluid management in acute lung injury secondary to septic shock. Chest. 2009 Jul;136(1):102–9.
  7. Bagshaw SM, Gibney RTN, McAlister FA, Bellomo R. The SPARK Study: a phase II randomized blinded controlled trial of the effect of furosemide in critically ill patients with early acute kidney injury. Trials. 2010;11:50.
  8. Boyd JH, Forbes J, Nakada T, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011 Feb;39(2):259–65.
  9. Grams ME, Estrella MM, Coresh J, Brower RG, Liu KD, National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome Network. Fluid balance, diuretic use, and mortality in acute kidney injury. Clin J Am Soc Nephrol. 2011 May;6(5):966–73
  10. Heung M, Wolfgram DF, Kommareddi M, Hu Y, Song PX, Ojo AO. Fluid overload at initiation of renal replacement therapy is associated with lack of renal recovery in patients with acute kidney injury. Nephrol Dial Transplant. 2012 Mar;27(3):956–61.
  11. Teixeira C, Garzotto F, Piccinni P, Brienza N, Iannuzzi M, Gramaticopolo S, et al. Fluid balance and urine volume are independent predictors of mortality in acute kidney injury. Crit Care. 2013;17(1):R14.
  12. Schmidt M, Bailey M, Kelly J, Hodgson C, Cooper DJ, Scheinkestel C, et al. Impact of fluid balance on outcome of adult patients treated with extracorporeal membrane oxygenation. Intensive Care Med. 2014 Sep;40(9):1256–66.
JUSTIN IS AN ANAESTHETIC AND ICU CONSULTANT IN BUCKINGHAMSHIRE HOSPITALS, FICM TUTOR AND ECHO GURU AND HAS CREATED A GREAT FOAMCC SITE WITH A COMBINATION OF CRITICAL CARE GUIDELINES, EVIDENCE AND WISDOM; IE INTENSIVE CARE MEDICINE WORTH KNOWING! www.icmwk.com

 

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