De-resuscitation

Given the increasing evidence suggesting that fluid overload in ICU patients is associated with morbidity and mortality, Is it time to consider the concept of de-resuscitation?

De-resuscitation meaning ‘an aggressive and active fluid removal by means of diuretics and renal replacement therapy‘ after the initial resuscitative phase.


A

For the less informed (me) this is useful with some further reading at the end – Malbrain et al’s article is interesting. The LITFL take.

Nothing on fluid resuscitation strategies and physiological endpoints but i guess thats a whole topic in itself. 

B

I think this is something that we are increasingly doing on ward 3 without specifically using the term ‘de-resuscitation’. Many of the trauma patients particularly receive significant volume resuscitation in the early stages of management which renders them in a very positive overall balance. This contributes to making the process of weaning from ventilatory support even more challenging and certainly I have seen the use of diuretics, particularly low dose furosemide infusion, in this situation help the process.

C

The Life in the fast lane article mentioned earlier is very good. The concept as a whole is one we should be taking on board.

The problem comes in distinguishing fluid overload from capillary leak and hypoalbuminaemia. Also with how to manage hypernatraemic but fluid overloaded patients. Cumulative fluid balance unless very positive or negative doesn’t necessarily tell you much. We should be doing at least 3x week weights but it’s one of those tasks that seems to get subsumed by everything else the nursing staff have to do.

D

So this is neither peer-reviewed nor referenced, but I’d love to hear some perspectives on the methods advocated by the late Dr John Hinds and the ICU team at Craigavon Area Hospital in Northern Ireland, who take a very protocolised approach to deresuscitation (at least that’s the way John tells it), including somewhat unorthodox things like IV free water and hydrochloric acid.

You can get the full podcast here, which also contains a text summary – I’ve copied and pasted the relevant bits below though.

If the FADE trial gets off the ground it might change things – the furosemide/albumin combo is quite popular in renal medicine (or it was at one point…?)

-Start with Diuretics

Furosemide

    50 mg IV, they infuse over 30 minutes

    Double dose if it doesn’t work

    500 mg/dose max

    Max dose 2g/day

    Back off if they become hemodynamically unstable, BUN/Cr start to rise, or you are needing to go up on Inopressors

[I think in the podcast he talks about taking off litres a day, but can’t remember if they target a particular hourly urine output or negative balance.]

Complications: Metabolic Alkalosis, Hypokalemia, Hypernatremia. Do not stop for these complications–fix them

Metabolic Alkalosis:

    Sig. Metabolic alkalosis ( BE > 6) is always unphysiological and should not be tolerated.

    Treat underlying cause, but you’ll rarely be able to

    If urine pH < 6.5 – acetazolamide 500 mg IV up to TID

    If urine pH > 6.5 or in ARF there are 2 choices-the best is HCl

    Use this formula: Weight (kg) x 0.5 x BE = mmol of HCl or give 80 ml of 0.1 molar HCl in 500 ml D5W via central line over 6 hours

Hypernatremia:

    When Na hits 147, they give IV free water (not D5W)

Hypokalemia:

    Never less than 3.7

-If that doesn’t work, IV Spironolactone (potassium canrenoate)

-If that doesn’t work, Dialyse to 600 ml/hr.

A

Following on from the use furosemide in the context of a very positive fluid balance and clinical signs of excess interstitial oedema following large volume fluid administration.

If the underlying problem is that of total body sodium excess, as with congestive cardiac, liver or renal failure but largely iatrogenic despite ‘balanced’ fluid administration why do we target just water removal with furosemide?

If there is ongoing endothelial dysfunction, low oncotic pressure and an accumulated total body sodium load then should we target another part of the nephron to encourage excretion of urine similar to the composition of plasma?

Perhaps with a thiazide or spironolactone in addition to furosemide from the outset? Or added in later – if so when?  Or not at all.

Does it encourage the development of ‘dehydration’ and its systemic manifestations which may result in a discontinuation of ‘diuresis’ and administration of water when in fact sodium mobilisation is also needed and the desired body weight reduction or negative balance has not been achieved?

I am sure this is very simple but I would appreciate if someone could answer!

E

I usually add Spiro as a natriuretic when trying to offload these patients. Seems to prevent the hypernatraemia that often limits frusemide seat least.

I stated doing this with cardiac patients as they rarely seem to clear the huge sodium load that appears to be a necessary part of every critical care admission these days, but now give it to most patients except brain injuries.

F –

I suspect one of the issues here is an inperfect understanding of therapeutic and pathological regulation of NKCC2. In the acute phase of critical illness, either exogenous for androgynous vasopressin would be expected to increase the activity of NKCC2, thereby promoting both sodium and water retention (although more water than sodium because of the concurrent retention of potassium in a one-to-one ratio). Similarly, the post-acute administration of loop diuretic’s will specifically inhibit the NKCC2 complex, and result in reduced your in re loss of sodium and potassium in equal measures, and I am osmotic loss of water which would therefore exceed that expected by naturiesis alone. In principle, one would expect these to affect to cancel each other out; in practice, additional fluid administration (and therefore additional sodium load) during the resuscitation inevitably promotes overall hyponatraemia. The total daily sodium load in critical illness Resucitation exceeds 225 mmol, more than twice a typical sodium requirement. Water administration positively correlates with this. Reference: http://www.ncbi.nlm.nih.gov/m/pubmed/22404059/

The use of spironolactone, administration of free water et cetera all make good sense in this context. Whether that theoretical advantage is translated to a practical results remains to be seen. Certainly, pilot studies (which could be criticised because of small numbers) have failed to show an advantage of spironolactone over placebo in this setting. Reference: http://www.ncbi.nlm.nih.gov/m/pubmed/19049481/?i=1&from=spironolactone%20critical%20illness


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