Episode 51: Resuscitating and deresuscitating with hypertonic saline, with Sean Barnett

We explore the controversial area of using hypertonic saline to support hemodynamics, protect the kidneys, and facilitate diuresis in the critically ill patient. Our guest is Dr. Sean Barnett, hypertonic aficionado and nephrologist with a focus in critical care.

Takeaway lessons

  1. The furosemide stress test in the shocked patient is a useful means to assess renal prognosis and determine whether oliguria is due to a prerenal state or ATN. 1mg/kg for the diuretic-naive or 1.5mg/kg for those with previous loop diuretic exposure, then monitor urine for the first 2 hours. If they make 200ml of urine, chances are good that the kidneys are still working to some extent, and the patient is less likely to proceed to needing dialysis.
  2. In the case of prerenal azotemia, massive ongoing fluid overload via crystalloids can be mitigated by instead giving small boluses of hypertonic saline. A 100ml 3% saline bolus has a third of the sodium and a ninth of the volume of a 1000ml normal saline bolus, but because of the concentrated sodium load, still increases flow to the kidneys and effectively shuts off the patient’s RAAS axis that’s been activated by the shock. There are few tools that can suppress renin as potently as a hypertonic saline bolus, even a small one.
  3. Angiotensin II is a key driver of capillary permeability: high RAAS = high capillary leak states. Downregulating this feedback loop with hypertonic helps to escape the shock-fluid cycle.
  4. Combine the 3% bolus with furosemide and you’ve increased renal perfusion at the same time as you’ve stimulated diuresis. It’s a great approach for diuresing the patient who’s still in shock.
  5. Albumin is less effective on its own, although albumin combined with hypertonic saline seems to have excellent synergy, outperforming each alone, allowing the preservation of intravascular volume that many believe they’re getting from albumin alone. Concentrated (e.g. 25%) albumin is not as good, does not reduce capillary permeability, and may be nephrotoxic.
  6. Anything you can do to increase renal perfusion will help protect the kidneys during shock, and this is exactly what concentrated hypertonic saline can do.
  7. With the small hypertonic boluses used here (rarely more than ~300ml in a day), the serum sodium usually does not rise by much. Just monitor it and ensure you’re giving adequate free water, especially if diuresis occurs.
  8. Scheduled 3% boluses of ~100 ml every 8 hours or so, combined with scheduled furosemide boluses, is an effective diuretic strategy in the shocked, overloaded patient with heart failure.
  9. Hypertonic saline stimulates ANP and nitric oxide by both stretching and creating hypertonicity in the right atrium; this helps decrease PVR and supports both sides of the heart.
  10. A 3% saline infusion can work brilliantly to facilitate ultrafiltration during CRRT. Overloaded patients may be intolerant of volume removal because it’s being pulled straight out of the RV, which can be a tough stimulus in an unstable heart; hypotension and arrhythmias can occur. Hypertonic saline can support preload without adding much volume; it pulls volume into the vascular space for CRRT to filter out. Trending ScvO2 from the tip of the dialysis catheter can be a good guide as to whether UF is helping or hurting the heart as well.
  11. The best evidence for hypertonic saline is to support diuresis. The next best evidence base is for cirrhosis with volume overload. As an IV fluid, the best data is in the surgical literature, generally showing it as equal or better to other fluids. Using it during CRRT has weaker evidence, although many nephrologists will use it during regular dialysis.
  12. 3% saline is certainly safe and causes no issues with increases blood viscosity. It is safe through peripheral IVs as well.
  13. The effect can be proven by checking the urine sodium and urine osmolality. The former is generally low and the latter high in the patient whose kidneys are conserving due to shock. Give them 3%, and the urine sodium shoots up while the urine osms decrease, as the RAAS axis and ADH become attenuated.


Improved overall fluid balance / UOP / hemodynamics in diverse settings. 



















6 thoughts on “Episode 51: Resuscitating and deresuscitating with hypertonic saline, with Sean Barnett”

  1. Thank you for the opportunity!!

    Anyone who has questions, please let me know. Yes, this is new. Yes, it is incredibly safe, useful, and versatile. No, you will not find a guideline. Yes, it is well described in literature otherwise.

    I have done a thorough literature review on everything I said.

  2. This is fascinating! Would you recommend D/C EPI, Levophed, Phenylephrine, and Vasopressin for Dobutamine? Cardiac support with some reduction in afterload?

    1. Very good question! I usually try to have a stepwise approach with certain clarifiers. For Shock/Cardio Shock reaching pressor/ionotropic needs (or IABP / Impella / ECMO):
      – If the Sodium is <140, 3% is usually my IVF / bolus, so I may have already used and assessed responsiveness, but if I get consulted later and there is immediate need:
      – I LOVE the puzzle, Levo in Most case, Phenyl in Afib RVR, Vaso in PH or PAH, Epi if brady, Dobumtamine if Epi is not the right choice, ATII in COVID shock (my humble opinion ofc)
      – If able to try 3% + Furosemide alone, I will first
      – If planning to start Pressors/Ionotropes, I will also use some in preparation (no downside here, it will not overload them and 100mL is simple)
      – While on Pressors/Ionotropes and when trying to get off and ANY time I want more diuresis, I use 3%!
      – I try to use Urine / MVO2 or ScvO2 / POCUS / VBGs to guide whether I am choosing the right thing or not, and if the patient is getting worse I have no problem admitting I may have chosen wrong

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