I'd argue that you need to trend lactate to check your work because a
normal MAP, CVP and ScvO2 do not exclude worsening sepsis.

Lactate gives an indirect measure of tissue oxygenation and improving
lactate indicates improved perfusion.

CVP is supposed to measure volume status (which I'd argue it does poorly),
but adequate volume does not mean the tissues are receiving adequate
oxygen.
A low MAP should be corrected with fluids and/or pressors, but an adequate
MAP also does not exclude tissue hypoxia.
Patients with elevated lactate with otherwise normal hemodynamic
parameters, so called "cryptic shock" are not that rare, and their
mortality is high:

5.4% of patients in this study had a lactate > 4 with *no hypotension* - *Levy
MM, Dellinger RP, Townsend SR, et al; Surviving Sepsis Campaign: The
Surviving Sepsis Campaign: Results of an international guideline-based
performance improvement program targeting severe sepsis. Crit Care Med2010;
38:367–374*

The mortality of these patients with cryptic shock is the same as patients
with overt shock.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3179778/  (*Puskarich
MA, et al. Outcomes of patients undergoing early sepsis resuscitation for
cryptic shock compared with overt shock. Resuscitation. 2011
Oct;82(10):1289-93.*)

ScvO2 would be more reassuring if it were normal as it reflects the balance
between oxygen delivery (DO2) and consumption (VO2).  Too low (< 65%) means
there is impaired tissue oxygenation, and too high (>80%) is sepsis means
there is likely microvasculatory shunting.  Both extremes have increased
mortality.

The number of patients with preexisting liver failure causing an elevated
lactate is going to be a small minority in the general sepsis population.
(How can you be assured that the liver failure is not from the sepsis
itself?  A good review in Critical Care in 2012:
http://ccforum.com/content/pdf/cc11381.pdf)  And in your example, even if
lactate was 2.05 on initial draw, if it elevates to 6 after 3 hours, it is
significant -- the patient has worsening shock regardless if there is
underlying liver disease.  Additionally, there was a study in Critical Care
Medicine in 2001 that found "Splanchnic lactate release is uncommon in
septic patients, even when hyperlactatemia is severe."

* (De Backer D1, Creteur J, Silva E, Vincent JL. The hepatosplanchnic area
is not a common source of lactate in patients with severe sepsis.Crit Care
Med. 2001 Feb;29(2):256-61.) *
 All that to say, trending abnormal lactates (and even rechecking normal
ones) is an important part of sepsis treatment.  It is a grade 2C
recommendation in the 2012 Surviving Sepsis Campaign guidelines.

Hope that helps with your critical care people.

-Andy


Andy Bourgeois, MD, FAAEM
Allied Emergency Physicians
Simi Valley Hospital





On Thu, Jul 10, 2014 at 1:55 PM, CARIANN M DAHLQUIST <[email protected]>
wrote:

>  Hello,
> Inquiring how other facilities are doing with physicians obtaining the
> second lactic acid within 6 hours if initial was > 2mmol/L?   I am having
> some push back from our Critical Care that feel as though this leads to
> additional labs being drawn that they do not feel are needed as they are
> treating the patient based on MAP, CVP, blood pressure, etc...
> They do have several good points such as a patient that has liver failure
> and has a baseline lactic of 2.05, why continue to drawn more labs?
> Any ideas or processes would be appreciated.
> Thanks.
> CariAnn
>
>  *CariAnn Dahlquist RN*
> Quality Management
> Altru Health System | Grand Forks, ND
> 701.780.5339 phone | 701.780.1942 fax | *cdahlquist*@altru.org
> <[email protected]>
>
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