Background
 
Hyperlactatemia is typically present in patients with severe sepsis or septic shock and may be secondary to anaerobic metabolism due to hypoperfusion.  The prognostic value of raised blood lactate levels has been well established in septic shock patients [1], particularly if the high levels persist. [2,3]  In addition, blood lactate levels have been shown to have greater prognostic value than oxygen-derived variables. [4]  Obtaining a lactate level is essential to identifying tissue hypoperfusion in patients who are not yet hypotensive but who are at risk for septic shock.
 
Limitations

However, the interpretation of blood lactate levels in septic patients is not always straightforward.  A number of studies have suggested that elevated lactate levels may result from cellular metabolic failure in sepsis rather than from global hypoperfusion.  Elevated lactate levels can also result from decreased clearance by the liver.  Although blood lactate concentration may lack precision as a measure of tissue metabolic status, elevated levels in sepsis support aggressive resuscitation.
 
Implications

Given the high risk for septic shock, all patients with elevated lactate >4 mmol/L (36 mg/dL) enter the early goal-directed therapy portion of the Severe Sepsis Resuscitation Bundle, regardless of blood pressure. 
 
This approach is consistent with the trial that established the value of early goal-directed therapies, Rivers et al. [5]
 
Turnaround Time

Serum lactate must be available in your institution with rapid turnaround time (within minutes) to effectively treat severely septic patients.  An arterial blood gas analyzer located in the clinical laboratories usually accomplishes this.  However, any means of rapid turnaround time will be acceptable.  It is essential for hospitals to invest in adequate equipment in order to meet present standards of care for septic patients.
 
The technique of obtaining serum lactate by venipuncture typically carries a 24- to 48-hour turnaround time and will not be suitable to care for septic patients.  This technique also requires special collection conditions, such as without the use of tourniquet, hindering clinical care.

Arterial vs. Venous Lactate

In the course of the Campaign the question has been raised many times as to whether an arterial or venous lactate sample is appropriate.  While there is no consensus of settled literature on this question, an elevated lactate of any variety is typically abnormal, although this may be influenced by other conditions such as a variety of medications, hepatic insufficiency, or hyperlactatemia due to primarily cardiac causes of hypoperfusion. 

Grading the Evidence

The use of lactate as a method to detect severe sepsis and septic shock and as a rationale for further therapies was evaluated as part of the larger recommendation on initial resuscitation in the 2008 Guidelines.  There, the guidelines committee recommended the protocolized resuscitation of a patient with sepsis-induced shock, defined as tissue hypoperfusion (hypotension persisting after initial fluid challenge or blood lactate concentration equal to or greater than 4 mmol/L).   (Grade 1B).  

This is a strong recommendation for care based on a number of qualitative considerations.  “B” level evidence generally derives from randomized control trials with certain limitations or very well-done observational or cohort studies.

Tips

1. If serum lactate is not rapidly available in your institution, invest in equipment to make rapid assessment possible.  This should be presented to hospital and laboratory administration as a present standard of care.

2. Create a standardized protocol to manage severe sepsis that includes measurement of lactate.

3. Include a prompt on arterial blood gas requisitions or physician order entry to prompt users to order lactate for suspected severe sepsis.
 
References

1. Weil MH, Afifi AA. Experimental and clinical studies on lactate and pyruvate as indicators of the severity of acute circulatory failure (shock). Circulation. 1970;41:989–1001.
2. Vincent JL, Dufaye P, Berre J, et al. Serial lactate determinations during circulatory shock. Crit Care Med. 1983;11:449–451.
3. Friedman G, Berlot G, Kahn RJ, et al. Combined measurements of blood lactate concentrations and gastric intramucosal pH in patients with severe sepsis. Crit Care Med. 1995;23:1184–1193.
4. Bakker J, Coffernils M, Leon M, et al. Blood lactate levels are superior to oxygen derived variables in predicting outcome in human septic shock. Chest. 1991;99:956–962.
5. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–1377.
6. Mikkelsen, M, Miltiades, A, Gaieski,D, et al. Serum lactate is associated with mortality in severe sepsis independent of organ failure and shock. Crit Care Med. 2009;37:1-8.
 
Content adapted extensively from:

• Vincent JL, Gerlach H. Fluid resuscitation in severe sepsis and septic shock: An evidence-based review. Crit Care Med. 2004;32(11):(Suppl.)S451-S454.
•  Dellinger, RP, Levy, MM, Carlet, JM, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med. 2008; [published correction appears in Crit Care Med. 2008; 36:1394-1396] 36:296-327

Tools

Evaluation of Severe Sepsis Screening Tool