The form of lactate associated with sepsis is called L-lactate. The other form is called D-lactate, and is more commonly associated with short bowel syndrome[2]. The chemicals are stereoisomers of each other, meaning the molecules of both compounds contain the same atoms, but with the atoms arranged differently.
While the two terms are often used interchangeably, lactate is different from lactic acid. Technically speaking, an acid is a molecule which is capable of donating a hydrogen ion. Lactate is chemically similar to lactic acid, but does not possess the extra hydrogen[3]. Elevated lactate in the presence of sepsis is not necessarily caused by anaerobic activity.
In the past, it was thought that sepsis created a rise in serum lactate due to anaerobic metabolism resulting from widespread hypoperfusion of the tissues alone. It is now known that — in the presence of sepsis — lactate is produced by the body in part as cellular fuel in response to stimulation of the beta-2 adrenergic receptors[4].
This is still poorly understood, however, with current theory suggesting that sepsis leads to elevated lactate from both aerobic and anaerobic sources, as well as decreased lactate clearance[5]. Be careful - lactate can be elevated by unrelated conditions. Even though lactate produced in the presence of sepsis may not necessarily be the result of widespread hypoperfusion, lactate can be an indicator that anaerobic metabolism is taking place.
Therefore, lactate is sensitive to sepsis, but not specific to sepsis. A tourniquet left in place for an extended period of time while collecting a blood sample may potentially cause serum lactate to become elevated by restricting blood flow[1].
It is recommended that tourniquets used to facilitate blood draws be left in place for no longer than two minutes at a time in order to minimize this effect. Septic shock: Septic shock should be defined as a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone.
PCT is typically the primary biomarker to aid in detection or rule-out of early sepsis When measuring lactate in the Emergency Department ED setting the results are complementary to other test results, such as PCT for determination of level of bacterial or fungal infection, and together they serve as an important help in assessing the severity of the illness [3]. Adapted from J-L Vincent, personal communications. Detecting sepsis A simple infection can rapidly develop into sepsis a life-threatening condition which requires on-the-spot diagnosis and treatment while the condition is still in its early stages [1].
What is lactate? The value of measuring lactate in the diagnosis of sepsis Patients with elevated lactate levels are seriously ill and require effective treatment here and now. Find out more about sepsis detection. Sepsis The Importance of Early Detection. PCT as the biomarker of choice to aid detection of sepsis. Lactate as an aid in sepsis diagnosis and management.
CRP as an aid in the diagnosis of sepsis. Find out more about sepsis on Acutecaretesting. Cookies are used on this website Use of cookies. Don't show this message again. Already registered with us? Radiometer is using Microsoft Azure AD to authenticate customer access.
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Some Radiometer Web sites participate in online behavioral advertising this is also sometimes called re-target advertising or interest-based advertising. Instead, lactate generation occurs because the TCA cycle simply isn't able to keep up with a very rapid rate of glycolysis.
Lactate serves as a metabolic fuel for the heart and brain in conditions of stress. In a rat sepsis model, depletion of lactate caused cardiovascular collapse, which could be reversed by infusing sodium lactate Levy This study also found that selective blockade of beta-2 receptors decreased lactate levels and reduced survival duration.
Lactate correlates with illness severity, generally being a sign of badness. This may lead to the misconception that lactate itself is harmful. However, like sinus tachycardia, although elevated lactate is an ominous sign it still may function as a beneficial compensatory mechanism.
This alternative understanding of lactate has some implications for bedside patient management. The autonomic nervous system and endogenous catecholamines are mysterious and confounding. When exposed to the same infection, some patients have a weak endogenous catecholamine response and immediately develop hypotension. Other patients have a robust release of endogenous catecholamines which supports their blood pressure, preventing hypotension these are often younger patients who may look deceptively well.
Lactate is a marker of endogenous catecholamine release 2. This makes lactate useful for detecting patients who have occult shock : patients who are maintaining their blood pressure due to a vigorous endogenous catecholamine response.
These patients may have deceptively reassuring vital signs, masking the fact that they are in a catecholamine-dependent shock state simply using their own catecholamines rather than, for example, a norepinephrine infusion. Elevated lactate identifies these patients as having an increased risk of death or decompensation, thus requiring more aggressive management.
Although most often associated with sepsis, occult shock with elevated lactate may be seen with any cause of shock. In Jones et al. In hindsight, both interventions may be equally unnecessary. Currently it is unknown whether adding lactate to other resuscitation endpoints is beneficial. For example, suppose a patient is doing well clinically e. Will escalating the resuscitation based on the lactate level be beneficial, or harmful due to over-resuscitation e.
There is no clear evidence about how lactate might guide treatment intensity within the context of a modern sepsis resuscitation. Many approaches are reasonable. However, lactate is not an indicator of inadequate oxygen delivery, so an elevated lactate should not be blindly used as a trigger to increase oxygen delivery. The common fear of administering lactate reveals a misunderstanding of LR and the role of lactate in shock states.
First, LR contains sodium lactate not lactic acid , and is therefore not acidotic. Second, lactate probably has a beneficial role as discussed above although it is very rapidly metabolized. Occasional concern has been raised about the effect of LR on trending lactate levels, but this effect is minimal and the utility of precisely trending lactate levels is unclear.
Unfortunately, Plasmalyte and Normosol were designed decades ago specifically to avoid the administration of lactate. Their design was misguided, as discussed in further detail here. For most critically ill patients, LR may be the best crystalloid. Epinephrine has been recommended as a second-line vasopressor by many authors including the Surviving Sepsis guideline.
Although popular abroad, it is rarely used in the US. One common reason for avoiding epinephrine is concern that it may cause elevated lactate levels which could be harmful or confound serial trending of lactate. Improved understanding of lactate may allow us to utilize epinephrine more often. As discussed above, serial trending of lactate is of unknown value and should not dissuade us from using epinephrine if this is the best drug.
In Wutrich examined the prognostic value of changes in lactate following initiation of epinephrine infusion in patients with shock mostly septic shock. Survivors had significantly greater increases in lactate over the first four hours of epinephrine therapy compared to nonsurvivors figure below.
Thus, an epinephrine-induced rise in lactate may be a good prognostic sign, indicating that the epinephrine is working. Such patients often have adequate afterload, but need some additional inotropy. At low doses e. For patients who fail to respond to inotropic doses of epinephrine, higher doses of epinephrine will provide inotropy and vasoconstriction as well. Thus, an epinephrine titration may be a simple approach to rapidly trial inotropic support and then provide additional vasoconstriction if needed.
There is only one RCT comparing epinephrine vs. These authors found that compared to dobutamine, epinephrine led to faster hemodynamic stabilization, greater urine output, higher lactate levels, and no mortality difference. Unfortunately this study is very limited by the use of low doses of norepinephrine 0. One advantage of the norepinephrine-epinephrine combination is that it is difficult to screw up. Epinephrine alone is generally adequate for septic shock Myburgh Therefore, any combination of norepinephrine and epinephrine is probably fine.
Any patient with elevated lactate requires careful consideration for these numerous causes. Liver dysfunction: the liver is the primary organ responsible for lactate clearance; injury or failure results in decreased lactate clearance. Genetic: inborn disorders of metabolism, particularly in the pediatric population, may cause elevated lactate levels. Drugs and Toxins that may cause increased lactate: Metformin biguanide Acetaminophen Nucleoside reverse transcriptase inhibitors NRTI Linezolid Beta-2 agonists Propofol Epinephrine Theophylline Alcohols ethanol, propylene glycol and methanol Cocaine Carbon monoxide Cyanide Treatment of elevated lactate levels should be determined by the underlying cause.
If hypoperfusion or hypoxemia is the culprit, focus on improving perfusion to the affected tissues. In shock, treatments include fluid administration, vasopressors, or inotropes. In regional ischemia, surgery may be needed to restore circulation or remove damaged tissue.
References: 1. Anderson, L. Etiology and therapeutic approach to elevated lactate. Mayo Clinic Proceedings, 88 10 , Lactic acidosis.
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