This month’s questions:
When is it appropriate to use CVVHDF solely as a means of maintaining a neutral fluid balance or should we just minimise fluids and give diuretics? How is this best done?
Are there any advantages to 0.9% saline vs balanced crystalloids as our resuscitative fluid of choice on ICU?
This month’s paper is a great review on the timing of decompressive craniectomy in stroke and TBI:
Point of order – its CVVHD in Leeds 😉
Better to not put it in than do invasive things to get it back out. More forethought about fluid admin is needed. Diuretics always reasonable to try, overall lower risk (cf vascath and filter) I think its safe to assume. If you can’t get them dry via these methods then I don’t think its unreasonable to use filter. You can never predefine a set of circumstances where/when this is appropriate though.
Deresuscitation is key to improving outcomes, there are loads of papers showing a worse mortality with excessive positive fluid balance, everything from trauma, through sepsis and on to cardiac and non cardiac surgery.
Saline vs balanced – no. See SMART trial. Personal opinion is only if hyponatraemic.
Advocate for limited rational fluid resuscitation alongside early vasopressor use in the majority of shocked patients, rather than the current default of everyone getting several litres of Hartmann’s (with no idea of the response) before getting referred, then getting another couple of fluid challenges from the ICU first-responder. This is partly just bad application of bad guidelines, and partly the capacity-driven need to “prove” a patient can’t be managed solely with fluids and therefore that they definitely need a critical care bed. I also worry about the flawed paradigm of “stroke volume optimisation” aka supranormalisation in anaesthetic GDFT.
I’ve had some impressive results (and a few failures) using a balanced diuresis approach to deresuscitation, using a combination of diuretics (usually loop + proximal + distal targeting e.g. furosemide, indapamide, amiloride). This is based on physiology rather than bulletproof RCTs but seems to (mostly) avoid the classic problem of furosemide infusions converting oedematous patients into hypernatraemic oedematous patients. It’s mainly limited by the need for enteral administration of some of the drugs.
Addition of indapamide to frusemide increases natriuresis and creatinine clearance, but not diuresis, in fluid overloaded ICU patients.
Mobilising oedema in the oedematous critically ill patient with ARDS: do we seek natriuresis not diuresis?
Agree on the indapamide, I’ve started using it fairly recently and it seems to help.
I’ve also used natriuresis including Furosemide, Spironolactone +/- acetazolamide (if alkalotic) with low dose aminophylline to block macula densa feedback. Seemed to allow for clearing decent volumes of water without the hypernatraemia with furosemide alone. I’d be keen to see how indapamide worked as it would undoubtedly be similar.
I think IV chlorothiazide in another potential option to consider (a PICU favourite)
(especially with GI failure)
Back to the original question – there may be some merit in CVVDF, just for fluid management, for a patient with a component of decompensated heart failure who has got onto a ventilator (in certain circumstances)
Intravenous Chlorothiazide versus enteral Metolazone to augment loop diuretic therapy in ICU
2017 Apr;51(4):286-292. doi: 10.1177/1060028016683971. Epub 2016 Dec 16.