Clinical Case 116: FEAST or Flush Fluids

Today’s case is about the Resus of severely dry children – very typical of Broome.  But before we get to the case – here is a bit of a review of some recent learning I have had on the topic.   I have started to rethink the traditional acute fluid resuscitation management of these kids.  The FEAST trial was published 4 years ago now.  IN a nutshell it showed that giving IV fluid boluses to sick kids was harmful – lead to higher mortality.  It was one of those trials that, if nothing else, should make us rethink our practice.  Kids with severe dehydration due to diarrheal illness were NOT included in the study, so we cannot really apply it directly to the following case. However, it certainly does make me wonder…

At SMACC in Chicago recently there was an awesome panel discussion by world leaders in fluids / sepsis management.  Dr Kathryn Maitland [lead author of FEAST] was on the stage and answered some tough questions about the role of fluids in extremely sick kids.  The mechanism by which the kids in the “bolus fluid” arm died was discussed.  The children in the “bolus” group seemed to suffer an acute cardiovascular collapse more often than the “no bolus” cohort.  Why is this?  There were a few ideas postulated.  The one that made the most sense to me is that we just might be pushing the pH over the brink of life when using bolus fluids.  But there were a few other mechanisms invoked by the brains trust also.

So anyone who has ever done the APLS or other Paeds Resus course will tell you that the treatment for severe shock is a 10 – 20 ml/kg bolus of IV (or IO) 0.9% saline.  We expect our Med Students to have this number in the front of their mind – it is the “hammer” for all Paeds Resus “Nails”.  However, if you follow the blog or are a fan of the excellent Emcrit series on acid-base therapy then you will know that “normal” SALINE is in fact a nett acidotic fluid which will raise the chloride level [narrow ones’ SID] and force your body to retain H+ ions.  Now this doesn’t matter so much in kids whom are fasting for a theatre case or otherwise well.  However if you are in a scenario where your little patient is sailing very close to the edge of biochemical disaster then a big slug of unbalanced NaCl may just be the thing that pushes them over the egde.  Do we have any direct evidence for this?  No, none that I know of. IV Therapy helps prevent illness, treat acute or chronic health conditions or bring you back to your vibrant self.

Severe dehydration with hypovolemia and malperfusion certainly needs aggressive treatment – we have to try and restore volume / flow and pull them back from multiorgan dysfunction.  So giving fluids seems like a good idea.  But how much, how fast and which fluid to use is certainly a question that I think remains unanswered. Dr John Myburgh gave a great lecture on the ICN series on the history and current state of resuscitation fluids HERE.   My favourite line from his talk was from Dr Malcolm Wilson: “I don’t care if you use dog’s piss, as long as you use it carefully.”  Very Aussie!  But the principle is important – when dealing with really sick kids and fluid Resus – you have to think it through and reassess frequently, proceed with caution.  Fluids are ‘drugs’ just like antibiotics etc.   We need to prescribe the right stuff for the patient in front of us.

So here is the case:

JJ is a 4 month old boy whom has had a diarrheal illness for 5 days.  He has been lethargic and had a few vomits today.  His parents noticed he has been “breathing fast” all afternoon and now at midnght presents with a low-grade fever, diarrhea and lethargy / somnolence.  He is refusing to feed.

Back ground history: born at 36 weeks with IUGR  LBW = 2100g.

Breastfed and has received 1 round of infant immunisations.  Was doing well and putting on weight.  He was weighed in the clinic last week at 4000 g…   but tonight he is weighing in at 3500 g [not good!]

At triage his Obs :  Temp  = 37.3  HR 200, sluggish central cap refill, RR 55/min. He has no recession / tug.  His feet are cooler than his legs

His belly feels soft with hyperactive bowel sounds.  The chest is clear [to Ultrasound!]  The bladder is empty.

This is all consistent with Gastro.  A 500 gram weight loss in this kid equates to about 12% i.e. severe end of the spectrum.

This kid is very sick – we need to know what is going on with his electrolytes / acid:base and renal function.

Luckily an IVC is able to be placed and bloods drawn.  Here is the VBG:

pH = 7.10,   pCO2 = 17    HCO3-= 6.1   BE =  -23.1   Lactate = 3.3

Na = 156  Cl = 128  K+ = 5.1    Creat = 99      The CRP is as always…. 42!

OK…  lets hit the pause button there.  A few questions.

Q1:  Does JJ require a fluid bolus?

Q2: Which fluid and what volume would you give IV in the first instance?

Q3: Assuming he need ongoing fluid replacement – what are you going to prescribe over the coming hours?


  1. casey – great case. I think a fluid bonus is clearly needed and few would disagree as this kid as clear documentation of volume loss. I would use lactated ringers (Hartman’s) at 20cc/kg or another balanced solution.
    I’m no expert on on-going replacement but would gauge it based on how he looks after bolus (may need 2nd bolus) and LR would be fine for continued hydration until he can take adequate PO

  2. Cracking case Casey. My thought process would be analogous to that when replacing fluids in DKA I.e do every thing as slow as possible. Agree with swami he needs a bolus. I would go 10 mls/kg of N saline. Acidosis is a problem but I don’t want to drop his sodium too quickly and I don’t want to give him anything with K in until I am convinced his kidneys were working (he would get an IDC). Would repeat bolus if anuric and reassess. ongoing fluids would be maint + (500ml deficit/48 hrs) as a starter (n saline + 5% Dex) (27mls/hr) vbg at 1 hr then adjust depending on rate of Na decline (may need to switch to 1/2NS + 5%). I think key is going as slow as poss with freq reassessment. Looking forward to seeing what others think

    • Interesting! I am not saying he doesn’t need acute volume replacement – he has pre-renal failure and poor perfusion – so volume is key in the first phase of Resus. But I find it hard to understand why every Paediatric Doc I have ever worked with wants to use either N/saline or a sugar / saline combo – all of which have a SID = 0 and will exacerbate his metabolic acidosis. In adult ICU-land this seems frankly bonkers! Hartmann himself was in fact a Paediatrician!
      There is a small amount of evidence that using the dextrose-containing solutions will in fact lead to hyponatremia (mainly from Paeds Anaesthesia literature). So I would be worried about using 5%+ saline if he is starting out hypernatremic?
      CSL or Ringer’s seems like a nice compromise. Although he is hyperkalemic (plasma) he is surely deplete with all that diarrhoea and acidosis – so I’d be keen to give some K, but this can wait till his kidneys start producing.

      To be honest – I would think about using the “Home-made” 5% glucose with 140 mol NaHCO3… you could add K+ once he is perfusing the beans. It is chloride-free salt with water and some sugar to keep him going.
      Any other takers?

      • I thought that the hyponatraemia was associated with hyponatraemic solutions (like 2.5% + 0.45%) rather than with NS + dex.

        I don’t see any problems with the minimal K content of CSL; I would use a bolus of that, followed by home-made CSL+2.5% dex (an ampoule of 50ml/50% in a bag). Little topup bags of K+ once the kidneys are working and the K starts coming down.

        I’m confused by the diagnosis; this child has a HAGMA (AG of 23) which is not adequately explained by the lactate. Hopefully he hasn’t drunk any metho; you haven’t talked about his ketones. If it’s uraemic then it’s very bad!

        • Thanks Hildy
          There may be a few points of uraemia as the kid was in pre-renal failure, as you say the lactate is not enough o fill the gap.
          However if you use the Fencl-Stewart technique…
          The SID is very narrow due to the high chloride which explains most of the gap.
          I’m not bale to do it completely as there is no albumin level to correct the acidosis.
          Otherise – check out previous post on acid-base and there is a nice review of the hyponatremic effects of various fluids in kids on

          • Even if you use Fencl-Stewart, the SID is actually fairly reasonable; using the Storey simplification:

            NaCl effect = -10
            Albumin effect – unknown – but unless you think his albumin is >42, then this is >0
            Unmeasured anions: >13 (albumin assumption above)
            3.3 for lactate; so we need to find 10 points of unmeasured anions from somewhere. Is 5 days enough to develop uraemic acidosis?

  3. Muhammad "Umer" Shehzad says

    Interesting questions.
    I suppose almost all of us are rural generalists talking to each other. We do a bit of everything. The questions that you have posed Casey, however, are quite specialized and deep. Is it possible to get a pediatric critical care consultant to give his/her input ? It would really add to at least my knowledge base.

  4. Great case Casey! I saw many similar cases working at Katherine NT 5 years ago (there was a Rotavirus epidemic). I think it would be hard to argue not to provide bolus fluid. Clearly this child is shocked. Clinically the cause of shock is hypovolaemia (+/- sepsis). Surely correcting that would help. The only question is, how much? If the FEAST trial tells us anything, it is that overdoing it can cause harm (the volumes they protocolised are greater than what I’ve generally done).
    I agree with the essence Dr Wilson’s cracker quote. It’s the volume more than the type of fluid that counts. And being a believer in the KISS principle, I would give 10mL/kg boluses of Normal Saline and reassess after each bolus until the perfusion, shock and tachycardia improves clinically. Then when I’m satisfied the child are no longer critical, I would replace the deficit + maintenance over 24 hours (0.9% Saline add K add Glu). But I think I’m a little old school.
    Would love to know what a up-to-date Paeds intensivist thinks.

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