If I can add $0.02. The concept of lactate clearance, particularly when defined by only 2 measurements, greatly oversimplifies the complexity of lactate kinetics and may lead to errors in judgement at the bedside.
Serum lactate will be determined by the interactions of poorly understood processes that are difficult to study, partly because the patients are not in a steady state. These processes include: 1) Production - increased in hypoperfusion with rate determined by source control, quality and consistency of resuscitation, metabolic influences such as catechols etc, and "lactate shuttles" (one tissue bed overproduces, another metabolizes lactate). Overproduction may not result in elevated levels when washout is compromised or clearance is robust. This may explain normal lactates in 50% of those with septic shock. Mortality is still markedly increased in severe sepsis or shock with normal lactate 2) Washout & diffusion - increasing degrees of shock are characterized by an increasing lactate gradient between tissue and serum. An *increase *in serum lactate during resuscitation, which we all see with some frequency, may be good news rather than bad. It may reflect improving perfusion and washout that exceeds clearance capacity, but, in the individual case, one never knows. See below. 3) Clearance - important but seldom if ever reduced enough to be the sole cause of increased serum levels. In the individual case there is almost always something going on that makes it impossible to exclude hypoperfusion - advanced liver and/or kidney failure as examples. 4) Dilution - when we give 6-12L of fluid in 6 hours, *everything* is diluted - Hb, albumin... and lactate. 10% drop between first and second measurements is quite possible due to dilution. 5) Exogenous sources - rarely contribute but must be considered with massive transfusion (lactate 30 mmol/L in RBCs stored for 30 days, our typical unit) or large infusions of Ringers Lactate. We've followed lactates Q6 in many patients. In approximately 1/3 of them levels fluctuate and don't move in a consistent direction. So I would offer the following conclusions: 1) "Lactate clearance" can be regarded as a misnomer. Lactate is not subject to zero or first order kinetics. 2) 2 lactate determinations do not define clearance... or "Mission Accomplished". We suggest continuing resuscitation until: all resuscitation targets are achieved including ScvO2, clinical stability, improvement in organ function and normal serial lactates on 2-3 successive determinations in view of the fluctuation phenomenon. Note a lactate reduced to normal does not necessarily mean overproduction is fully corrected; it simply means that production and washout are now exceeded by clearance. 3) Lactate moves too slowly to be the only guide to resuscitation, even if we could measure it continuously. "Clearance" studies seek a 10% drop 2 hours or more after the first level. This means that transfusion or inotropes are titrated only every 2 or more hours... too slow for many clinicians. ScvO2 also has it's problems, but offers a real time guide to ongoing resuscitation efforts. 4) When central access is available, ScvO2 and lactate targets should be regarded as complimentary. 4) If central access is precluded, normalizing lactate, rather than reducing it by 10%, should be included as a resuscitation target. The goal should be 2-3 successive normals rather than a 10% drop from 1st to 2nd determination. Thanks Ron Elkin MD California Pacific Medical Center San Francisco, CA On Mon, May 6, 2013 at 5:01 PM, Daly, Mary Ann <[email protected]>wrote: > More excellent evidence Kathrina**** > > ** ** > > ** ** > > *Thanks, ***** > > ** ** > > *Mary Ann Daly**, RN BSN CCRN DC* > *Regional Clinical Initiative Lead-Sepsis and ICU Liberation (ABCDE)* > *Gordon and Betty Moore Foundation Grant* > *Sutter Health Sacramento Sierra Region* > E-mail:* **dalym1*@SutterHealth.org <[email protected]> > Blackberry: 916.200.5604 Office: 916.614.6370**** > > You never change things by fighting the existing reality. To change > something, build a new model that makes the existing model obsolete. R. > Buckminster Fuller**** > > ** ** > > ** ** > > *From:* [email protected] [mailto: > [email protected]] *On Behalf Of *Jaehne, Anja > *Sent:* Friday, May 03, 2013 7:03 PM > *To:* Erik Benjamin Kulstad; Townsend, Sean, M.D. > > *Cc:* [email protected] > *Subject:* Re: [Sepsis Groups] Noninvasive EGDT**** > > ** ** > > One of the fundamental problems of using lactate clearance as a sole > resuscitation target is that a normal lactate (< 2mM/L) can be present in > 25-50% of *septic shock* patients. The mortality of these patients is > 20-50% even with aggressive therapy. These observations indicate that using > lactate and ScvO2 are complimentary endpoints and not mutually exclusive. > 1-8 <#13e846f875739ba9__ENREF_1> **** > > **** > > *1.* Levraut J, Ciebiera JP, Chave S, et al. Mild hyperlactatemia > in stable septic patients is due to impaired lactate clearance rather than > overproduction. *Am J Respir Crit Care Med. *Apr 1998;157(4 Pt > 1):1021-1026.**** > > *2.* Wacharasint P, Nakada TA, Boyd JH, Russell JA, Walley KR. > Normal-Range Blood Lactate Concentration in Septic Shock is Prognostic and > Predictive. *Shock. *May 1 2012.**** > > *3.* Dugas AF, Mackenhauer J, Salciccioli JD, Cocchi MN, Gautam > S, Donnino MW. Prevalence and characteristics of nonlactate and lactate > expressors in septic shock. *J Crit Care. *Aug 2012;27(4):344-350.**** > > *4.* Cannon CM, Holthaus CV, Zubrow MT, et al. The GENESIS > Project (GENeralized Early Sepsis Intervention Strategies): A Multicenter > Quality Improvement Collaborative. *J Intensive Care Med. *Aug 17 2012.*** > * > > *5.* Hernandez G, Castro R, Romero C, et al. Persistent > sepsis-induced hypotension without hyperlactatemia: Is it really septic > shock? *J Crit Care. *Dec 1 2010.**** > > *6.* Vallet B, Chopin C, Curtis SE, et al. Prognostic value of > the dobutamine test in patients with sepsis syndrome and normal lactate > values: a prospective, multicenter study. *Crit Care Med. *Dec > 1993;21(12):1868-1875.**** > > *7.* Rhodes A, Lamb FJ, Malagon I, Newman PJ, Grounds RM, Bennett > ED. A prospective study of the use of a dobutamine stress test to identify > outcome in patients with sepsis, severe sepsis, or septic shock. *Crit > Care Med. *Nov 1999;27(11):2361-2366.**** > > *8.* De Backer D, Creteur J, Silva E, Vincent JL. The > hepatosplanchnic area is not a common source of lactate in patients with > severe sepsis. *Crit Care Med. *Feb 2001;29(2):256-261.**** > > **** > > Lactate ≠ScvO2**** > > **** > > Kathrina**** > > **** > > **** > > *From:* [email protected] [ > mailto:[email protected]<[email protected]>] > *On Behalf Of *Erik Benjamin Kulstad > *Sent:* Friday, May 03, 2013 12:59 AM > *To:* Townsend, Sean, M.D. > *Cc:* [email protected] > *Subject:* Re: [Sepsis Groups] Noninvasive EGDT**** > > **** > > I suspect new insights to this question will be answered by the ProCESS > study, which is about to enroll the last patient... **** > > **** > > https://crisma.upmc.com/processtrial/info2.asp**** > > **** > > **** > > On Wed, May 1, 2013 at 1:47 PM, Townsend, Sean, M.D. < > [email protected]> wrote:**** > > Did you happen to know that all patients in that trial received a central > line and that CVP was optimized using it? I think therefore we can’t call > that trial “non-invasive.”**** > > **** > > Also, although that trial enrolled 300 patients, the intervention did not > differ until the level of optimizing ScvO2, i.e. all patients that > benefited from CVP, a fluid bolus, antibiotics etc. and met targets > progressively dropped out of the running to actually compare lactate > clearance to ScvO2. Thus, in the end, 29 patients got a head to head > comparison of lactate clearance to ScvO2 optimization.**** > > **** > > This would suggest that enrollment in the trial should have been 3000 > patients in order to test the actual difference in intervention at the > power requirement of 300.**** > > **** > > One can make the argument reasonably that the assertion of non-inferiority > is underpowered by a factor of 10.**** > > **** > > One must also wonder about extraordinarily high lactates. None were > enrolled in the trial. So, if I have a lactate of 9 and clear it by 10% to > 8.1 should I be comfortable that I have hit my resuscitation targets? > Doesn’t make me so comfortable.**** > > **** > > Sean R. Townsend, M.D. > Vice President of Quality & Safety > California Pacific Medical Center > 2330 Clay Street, #301 > San Francisco, CA 94115 > email [email protected] > office (415) 600-5770 > fax (415) 600-1541**** > > **** > > *From:* [email protected] [mailto: > [email protected]] *On Behalf Of *Ram Parekh > *Sent:* Tuesday, April 30, 2013 1:50 PM > *To:* Vipul Kella > *Cc:* [email protected] > *Subject:* Re: [Sepsis Groups] Noninvasive EGDT**** > > **** > > We have at our hospital and at most of the GNYHA hospitals in the New York > area. **** > > > This protocol is based on the non-inferiority study of lactate clearance > by Jones/Shapiro and was implemented with our current Stop Sepsis > collaborative which has given ED providers the option of utilizing the > 'invasive' or 'non-invasive protocol' as EGDT options. Thus, the protocol > was simultaneously implemented in over 50 hospitals at the same time.**** > > On Mon, Apr 29, 2013 at 9:57 AM, Vipul Kella <[email protected]> > wrote:**** > > Has anyone implemented the noninvasive EGDT protocol at their hospital? > What was your experience? > **** > > **** > > -- **** > > Vipul Kella, MD FACEP > Medical Emergency Professionals (MEP)**** > > > _______________________________________________ > Sepsisgroups mailing list > [email protected] > http://lists.sepsisgroups.org/listinfo.cgi/sepsisgroups-sepsisgroups.org** > ** > > **** > > > _______________________________________________ > Sepsisgroups mailing list > [email protected] > http://lists.sepsisgroups.org/listinfo.cgi/sepsisgroups-sepsisgroups.org** > ** > > > > **** > > **** > > -- **** > > Erik Kulstad, M.D., M.S. > Research Director > Advocate Christ Medical Center > Dept. of Emergency Medicine > 4440 W. 95th St. > Oak Lawn, IL 60453 > Clinical Associate Professor > University of Illinois, Chicago**** > > ** ** > ------------------------------ > > CONFIDENTIALITY NOTICE: This email contains information from the sender > that may be CONFIDENTIAL, LEGALLY PRIVILEGED, PROPRIETARY or otherwise > protected from disclosure. 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If you do not believe that our > policy gives you the privacy and security protection you need, do not send > e-mail or Internet communications to us.**** > > _______________________________________________ > Sepsisgroups mailing list > [email protected] > http://lists.sepsisgroups.org/listinfo.cgi/sepsisgroups-sepsisgroups.org > >
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