Lactate Language

• Lactate is a common marker of patient outcomes used in healthcare specifically as it relates to sepsis.
• Normal levels are 0.5-1 mmol/L and is measured by sensors in a lab. Levels higher than 4 mmol/L in patients with suspected infection yield a 5-fold increase in the risk of death and mortality approaching 30%. A level above 10.0 mmol/l makes up the highest mortality. 
• Lactate levels are a primary area of concern when managing sepsis. Although the underlying cause should always be identified before establishing a treatment plan. Take a look at a complete breakdown of what it is. 

Medical language can educate or confuse. This is true in nurse-provider and patient-provider communications within healthcare. We often take for granted the medical terms that populate our conversations.  

Spend time in an emergency room or intensive care unit, and you will have crossed paths with the term.  

Today, we explore the complexity surrounding lactate in the simplest of terms. 

For two decades, measuring a lactate on your patients is routine practice in early sepsis management. But what is it? And what is driving its use?  

The rates of lactate measurement increased from 11% in 2003 to 48% in 2013, likely driven by the Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock campaign 2012.  

From a clinical perspective, if you had a singular target to aim for in early sepsis, lactate is your mark. On a rudimentary level, it is a general marker of overall badness and poor outcomes. In human physiology, blood lactate levels represent the balance between production and metabolism.  

In healthcare, we focus on sepsis. Where does sepsis arise in this equation? Infections that drive sepsis originate in the community or in healthcare facilities. Half of global sepsis occurs in children. 

What is Lactate?

Two forms exist in nature. L-lactate and D-lactate. L-lactate is the most abundant and more clinically significant. It is measured by the lactate sensors in a hospital’s clinical laboratory.  

Most lactate metabolism occurs in the human liver. The lungs can produce lactate in cases of acute respiratory distress syndrome (ARDS).  

When an imbalance occurs between oxygen delivery and tissue perfusion, irrespective of the underlying etiology, this results in increased lactate generation. The higher the levels, the greater tissue hypoxia and damage.  

Elevated levels, not a direct measure of tissue perfusion, serves as a surrogate, and denotes poor tissue perfusion and oxygen debt, secondary to anaerobic glycolysis.  

In the liver, the metabolism of L-lactate results in pyruvate secondary to L-lactate dehydrogenase.

D-lactate results from the fermentation in the gastrointestinal tract, by lactobacilli and bifidobacterial occupation in the large intestine. D-lactic acidosis (>3.0 mmol/L) is a metabolic derangement that can occur in patients with short-bowel syndrome. 

Lactic Acid vs. Lactate

Are they the same? Well, they are, but differ by a single hydrogen atom. The added hydrogen ion donated makes lactate an acid. It is lactic acid minus the single proton.  

In the human body and sepsis management, its semantics. But, for science’s sake. The human body produces and uses lactate, not lactic acid. 

When cellular hypoxia occurs, pyruvate, reduced to lactate, cannot enter the mitochondria, which causes arterial lactate concentrations to increase.

In the clinical setting, amongst trauma, sepsis, multiple organ failure and elderly patients, elevated lactate correlates with increased morbidity and mortality.

Defining Limits

Normal blood levels are 0.5-1 mmol/L. A level greater than 2.0 mmol/L defines hyperlactatemia. Concentrations above 4 mmol/L represent lactic acidosis.

Levels higher than 4 mmol/L in patients with suspected infection yield a 5-fold increase in the risk of death and mortality approaching 30%. A level above 10.0 mmol/l makes up the highest mortality. 

The common causes of elevated levels include hypoperfusion, related to blood loss and traumatic injury. Seizures, resulting in transient, yet profound elevation of levels. In cardiac arrest, lactate results from ischemia caused by lack of blood flow, and the inflammation of reperfusion injury. 

We can place lactic acidosis into two buckets. As an overview, Type-A lactic acidosis, secondary to hypoperfusion and hypoxia occurs in shock states (septic, cardiogenic, hypovolemic, obstructive). Type-B lactic acidosis absent of tissue hypoxia or hypoperfusion occurs in disease, malignancy, and medications (metformin, epinephrine). 

Treatment for Lactate

When treating lactate, optimizing oxygen delivery, and identifying the underlying cause is the primary goal.  

With hypoperfusion or hypoxemia, medical treatment is on improving perfusion to the affected tissues.  

In cases of cardiovascular collapse, fluid replacement and vasoactive drugs replenish and restore the cardiac muscle.  

In the ED, the surviving sepsis campaign fosters the “Hour-1 bundle.” Established protocols suggest levels measurements within 1h of admission into the ED for patients with suspected sepsis or septic shock.  

Case Study

Your ER patient is afebrile, tachypneic at 36 per minute with oxygen saturations of 98% on room air. On arrival, the patient was in respiratory distress, receiving nebulized Albuterol. Labs include normal complete blood cell count (CBC) and metabolic panel. Baseline lactic acid level was 2.3 mmol/l, which elevated to 4.8 mmol/l in four hours. No significant findings on chest X-ray.

During the patient’s ED stay, symptoms improved, yet lactate trended up to 5.1 mmol/l. The physician considers hospitalization and observation based on the elevateded levels, and further evaluation despite the patient’s improvement.

After a conversation, the treatment team changed Albuterol to Atrovent, and lactic acid levels returned to normal, and they discharged the patient. Remember, a Beta-2 agonist can lead to increased lactate levels. 

Read More