Preferred empiric fluid for septic shock

[europeman]

One of my critical care colleagues just told me she only uses NS for resuscitation of septic shock patients empirically mostly because has a higher tonicity than plasmalyte or LR. Now, I know there is like a 20meq differences 'cuz of the greater concentration of sodium in NS, but, clinically, I consider all these fluids to be iso-tonic and therefore good enough for resuscitation. In addition, I don't like killling patients with too much chloride and giving them iatrogenic hyperchloremic acidosis unncessarily. Yeah yeah, patients with no urine and renal function fine.. a little potassium in plasmalyte I know.

Thoughts?

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[proman]

If I use crystalloid, I alternate between NS and LR. I feel that prevents the hyponatremia seens from LR and the hyperchloremia seen from NS. I don't really use much colloid anymore since the Boldt fiasco. In residency we had access to 2 and 3% hypertonic saline with acetate buffer. 2% for peripheral, 3% for central. I don't know if anyone else uses that fluid, or if it makes a bit of difference. You do have to watch sodium values closely.

 

[jdh71]

One of my critical care colleagues just told me she only uses NS for resuscitation of septic shock patients empirically mostly because has a higher tonicity than plasmalyte or LR. Now, I know there is like a 20meq differences 'cuz of the greater concentration of sodium in NS, but, clinically, I consider all these fluids to be iso-tonic and therefore good enough for resuscitation. In addition, I don't like killling patients with too much chloride and giving them iatrogenic hyperchloremic acidosis unncessarily. Yeah yeah, patients with no urine and renal function fine.. a little potassium in plasmalyte I know.

Thoughts?

Find me evidence that shows that the acidosis you get get with NS makes any difference in the outcomes that mater, ie. LOS, morbidity, mortality, etc., you know, "killing patients with chloride" and you may actually have a point, IMHO.

I don't think it's poison. I use it exclusively for resuscitation (+/- blood, of course, if needed for bleeding or EDGT)

 

[proman]

Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study
Crit Care Med. 2009 Oct;37(10):2733-9.
Objective: To describe the composition of metabolic acidosis in patients with severe sepsis and septic shock at intensive care unit admission and throughout the first 5 days of intensive care unit stay.

Design: Prospective, observational study.

Setting: Twelve-bed intensive care unit.

Patients: Sixty patients with either severe sepsis or septic shock.

Interventions: None.

Measurements and Main Results: Data were collected until 5 days after intensive care unit admission. We studied the contribution of inorganic ion difference, lactate, albumin, phosphate, and strong ion gap to metabolic acidosis. At admission, standard base excess was &#8722;6.69 ± 4.19 mEq/L in survivors vs. &#8722;11.63 ± 4.87 mEq/L in nonsurvivors (p < .05); inorganic ion difference (mainly resulting from hyperchloremia) was responsible for a decrease in standard base excess by 5.64 ± 4.96 mEq/L in survivors vs. 8.94 ± 7.06 mEq/L in nonsurvivors (p < .05); strong ion gap was responsible for a decrease in standard base excess by 4.07 ± 3.57 mEq/L in survivors vs. 4.92 ± 5.55 mEq/L in nonsurvivors with a nonsignificant probability value; and lactate was responsible for a decrease in standard base excess to 1.34 ± 2.07 mEq/L in survivors vs. 1.61 ± 2.25 mEq/L in nonsurvivors with a nonsignificant probability value. Albumin had an important alkalinizing effect in both groups; phosphate had a minimal acid-base effect. Acidosis in survivors was corrected during the study period as a result of a decrease in lactate and strong ion gap levels, whereas nonsurvivors did not correct their metabolic acidosis. In addition to Acute Physiology and Chronic Health Evaluation II score and serum creatinine level, inorganic ion difference acidosis magnitude at intensive care unit admission was independently associated with a worse outcome.

Conclusions: Patients with severe sepsis and septic shock exhibit a complex metabolic acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis, which was more pronounced in nonsurvivors. Acidosis resolution in survivors was attributable to a decrease in strong ion gap and lactate levels.

 

[jdh71]

Metabolic acidosis in patients with severe sepsis and septic shock: A longitudinal quantitative study
Crit Care Med. 2009 Oct;37(10):2733-9.
Objective: To describe the composition of metabolic acidosis in patients with severe sepsis and septic shock at intensive care unit admission and throughout the first 5 days of intensive care unit stay.

Design: Prospective, observational study.

Setting: Twelve-bed intensive care unit.

Patients: Sixty patients with either severe sepsis or septic shock.

Interventions: None.

Measurements and Main Results: Data were collected until 5 days after intensive care unit admission. We studied the contribution of inorganic ion difference, lactate, albumin, phosphate, and strong ion gap to metabolic acidosis. At admission, standard base excess was &#8722;6.69 ± 4.19 mEq/L in survivors vs. &#8722;11.63 ± 4.87 mEq/L in nonsurvivors (p < .05); inorganic ion difference (mainly resulting from hyperchloremia) was responsible for a decrease in standard base excess by 5.64 ± 4.96 mEq/L in survivors vs. 8.94 ± 7.06 mEq/L in nonsurvivors (p < .05); strong ion gap was responsible for a decrease in standard base excess by 4.07 ± 3.57 mEq/L in survivors vs. 4.92 ± 5.55 mEq/L in nonsurvivors with a nonsignificant probability value; and lactate was responsible for a decrease in standard base excess to 1.34 ± 2.07 mEq/L in survivors vs. 1.61 ± 2.25 mEq/L in nonsurvivors with a nonsignificant probability value. Albumin had an important alkalinizing effect in both groups; phosphate had a minimal acid-base effect. Acidosis in survivors was corrected during the study period as a result of a decrease in lactate and strong ion gap levels, whereas nonsurvivors did not correct their metabolic acidosis. In addition to Acute Physiology and Chronic Health Evaluation II score and serum creatinine level, inorganic ion difference acidosis magnitude at intensive care unit admission was independently associated with a worse outcome.

Conclusions: Patients with severe sepsis and septic shock exhibit a complex metabolic acidosis at intensive care unit admission, caused predominantly by hyperchloremic acidosis, which was more pronounced in nonsurvivors. Acidosis resolution in survivors was attributable to a decrease in strong ion gap and lactate levels.

I'll have to look at the paper at work tomorrow, but my money says the nonsurvivors were also sicker patients. Sicker patients got more fluids because they were sicker and died because they were sicker not because you gave them a chloremic acidosis. Look at the survivors, they survived because obvious resuscitation goals were met, demonstrated by a decrease in the strong ion gap and lactate, not because they did or did not get NS.

 

[proman]

The amount of fluid given was not statistically different. The non survivors were sicker as evidenced by higher APACHE II and admission SOFA score. The serum creatinine was higher in non survivors. This type of paper can only indicate association, not causation, but it does provide some evidence that hyperchloremic acidosis is not entirely benign. There's additional experimental evidence of that also, particularly in animal models.

 

[jdh71]

The amount of fluid given was not statistically different. The non survivors were sicker as evidenced by higher APACHE II and admission SOFA score. The serum creatinine was higher in non survivors. This type of paper can only indicate association, not causation, but it does provide some evidence that hyperchloremic acidosis is not entirely benign. There's additional experimental evidence of that also, particularly in animal models.

No. It doesn't do that because it can't do that. This paper shows that sicker patients die. Not surprising or provocative to any of us.

The mere fact the Cr was higher would be EXACTLY what you'd expect. Strong ion hypothesis posits kidney compensation for acidosis by clearing chloride along with NH4+, and if the beans aint working right, of course your chloride will be higher, but that still doesn't implicate the the resuscitation fluid as the culprit here - not even close.

And are you talking about the animal studies where pigs bleed more or something like that with NS?

 

[jdh71]

Here's a nice recent (2010) review on NS induced acidosis

http://onlinelibrary.wiley.com/doi/10.1111/j.1778-428X.2010.01135.x/pdf

 

[proman]

I'll read this tomorrow but did skim it. The article does cite Boldt's work. Some 90 papers of his, strongly in favor of colloids, have been retracted. The work was either misrepresented, or more likely, completely fabricated. Nothing from him can be believed.

 

[jdh71]

I'll read this tomorrow but did skim it. The article does cite Boldt's work. Some 90 papers of his, strongly in favor of colloids, have been retracted. The work was either misrepresented, or more likely, completely fabricated. Nothing from him can be believed.

Have the cited articles been retracted? The review isn't about using colloids, it's about hyperchloremic acidosis.

 

[proman]

Well the article is about plasma expansion (title: Hyperchloremic acidosis during plasma expansion), keywords include crystalloids, colloids, fluid therapy. Fluid therapy is a key component to iatrogenic hyperchloremic acidosis. 7 out of 27 references cited in the review are from Boldt. He's had 88 articles retracted. I don't have the time to verify that all seven included in the retraction list, maybe someone could.

 

[jdh71]

Well the article is about plasma expansion (title: Hyperchloremic acidosis during plasma expansion), keywords include crystalloids, colloids, fluid therapy. Fluid therapy is a key component to iatrogenic hyperchloremic acidosis. 7 out of 27 references cited in the review are from Boldt. He's had 88 articles retracted. I don't have the time to verify that all seven included in the retraction list, maybe someone could.

Looks like 3 of those articles cited are now retracted. But they are largely irrelevant to the topic at hand which is hyperchloremic acidosis, and the bigger point that I made that this hyperchloremic acidosis has never been shown to "kill patients". It's much ado about nothing.

 

[proman]

Looks like 3 of those articles cited are now retracted. But they are largely irrelevant to the topic at hand which is hyperchloremic acidosis, and the bigger point that I made that this hyperchloremic acidosis has never been shown to "kill patients". It's much ado about nothing.

I agree but why create something when you don't need to? If you give less NS and more LR in a balanced fashion, end result is the same and you avoid a possible complication. Of course, maybe the NEJM article on fluid resuscitation shows we're doing it all wrong (at least in kids).

 

[pseudoknot]

Of course, maybe the NEJM article on fluid resuscitation shows we're doing it all wrong (at least in kids).

It doesn't seem like that article shows that, at least in our population of kids. One of several issues with that paper was the high prevalence of anemia in their population, which may have increased mortality in the fluid bolus group via hemodilution. (You may have already been aware of this, but I'm pointing it out for others as well.)

 

[proman]

It doesn't seem like that article shows that, at least in our population of kids. One of several issues with that paper was the high prevalence of anemia in their population, which may have increased mortality in the fluid bolus group via hemodilution. (You may have already been aware of this, but I'm pointing it out for others as well.)

Yeah I was surprised by the incidence of severe anemia (not that I know anything about childhood sepsis in Africa). It wasn't different between groups. Also, rates of transfusion were similar. The control group did get transfused a bit earlier.

I did some work during fellowship looking at transfusion and cognitive outcomes after cardiac surgery. The major issue with blood is that it's very hard to separate out the effect of transfusion vs hemodilution vs anemia. Either way I think this study is pretty provocative.

 

[europeman]

Let me clarify my statement,

Obviously a little iatrogenic hyperchloremia won't kill anyone. But, if you have a critically ill person (say septic shock) who is getting large volumes of fluid, then why give them a iatrogenic hypercholeremia which inevitabely will require a higher minute ventilation to normalize the pH until their kidneys (assuming they are working) get rid of the chloride?

I mean it just seems more elegant to tailor your solution to the patients electrolytes. If someone comes in with a history of 2 days of emesis and is clearly hyperchloremic, then most doctors would give NS. makes sense.

But if someone is septic, then why resuscitate them only with NS and give them iatrogenic issues?

nOw will a double blind randomized study really bear out the differences? who knows. whatever.

my question though hasn't been answered. and that is....

DOES ANYONE DURING SEPTIC SHOCK PURPOSELY PREFER NS BECAUSE IT HAS A HIGHER TONICITY THAN LR OR PLASMALYTE? if so, what is your rationale? thanks!

 

[Hernandez]

DOES ANYONE DURING SEPTIC SHOCK PURPOSELY PREFER NS BECAUSE IT HAS A HIGHER TONICITY THAN LR OR PLASMALYTE? if so, what is your rationale? thanks!

no I don't prefer NS for this reason, but I do use NS because in the 20-40mL/kg range you're rarely going to cause a hypercloremic acidosis.

 

[SLUser11]

I agree but why create something when you don't need to? If you give less NS and more LR in a balanced fashion, end result is the same and you avoid a possible complication. Of course, maybe the NEJM article on fluid resuscitation shows we're doing it all wrong (at least in kids).

I've read a few papers in the past addressing hyperchloremic acidosis, especially as a junior resident when I was learning about strong ion theory. I remember coming to the conclusion that patients with hyperchloremic acidosis had the same outcomes as patients who were not acidotic.

Here's an editorial that addresses the issue, and the article it references.

I'm sure if we all poke around, we can find some literature to support our biases. Personally, I use a lot of NS, but mostly because that's how I was trained, and we're ultimately a product of our environment. I have to admit, though, that I used to throw some LR in there when the patient's chloride started to bump, just so the other doctors involved wouldn't freak out too much about it.

Now that I'm done with residency, I'm very unlikely to do much critical care, and I think it's probably a good thing because of how fast the pendulum swings on some of these issues.

 

[proman]

So why not avoid the whole issue and just give less NS and more LR? Then this whole discussion becomes a moot point. It's what I do for the long abdominal/ortho cases. I would do the same thing for the sick septic patient. Cardiac surgery gets less than 1L crystalloid so it's never an issue in the immediate perioperative period.

 

[souljah1]

The only time I consider using either LR or 1/2NS with 1.5 amps Bicarb are in situations when I need to treat either hypovolemic or distributive shock in a person who is on a ventilator and we are exercising permissive hypercapnea because of either ARDS or severe obstructive lung disease. If a non-gap acidosis is present in the setting of permissive hypercapnea, I tend to bolus with LR (kidney permitting) or 1/2NS and 1.5 amps Bicarb in an effort to prevent worsening acidemia.

As far as treating a spontaneously breathing patient in shock with gallons of NS - I don't think it is a big deal.