I Hate Prehospital Lactate

Picture this scenario: You respond to a nursing home and discover an 88-year-old male patient with a baseline history of mild Alzheimer’s dementia. The nurse... caregiver… nursing home employee explains that the patient’s physician ordered him transported from the nursing home to St. Elsewhere’s emergency department. (She seems to believe that is an adequate reason handoff report.) After your extensive and repetitive investigation, you drag out that the patient has a temperature of 38.2°C. A urinary tract infection is suspected. The patient is a pleasant elderly male who verbalizes no complaints. He is slightly pale but warm and dry and there is nothing abnormal about his physical exam. He has a blood pressure of 104/68 with a heart rate of 96.

Let me pause here for a moment. Do you transport this patient emergently or routine? Flash-and-noise or just drive? I acknowledge you don’t have nearly enough data to mentally simulate a call, but imagine that everything else is unremarkable or normal. Blood sugar, you ask? Normal. Does he have a history of… No. Everything else is normal. Do you transport this patient emergently or routine?

Whatever your decision, on the way to the hospital you call in a prearrival report: “Coming to you with an… uh… how old are you, dude?… oh, yeah, eighty-eight, that’s eight-eight, male with new-onset somnolence from a nursing home. His physical exam is normal and his vitals are 104/68 with a rate of 90ish and a respiratory rate of twenty. We’ll see you in five or six minutes.”

The person receiving your phone call asks you if you have the ability to take a lactate reading. Do you? Would you have checked this patient’s lactate levels?

Lactate. By Edgar181, via Wikimedia Commons

I hate prehospital lactate. Wait. That is probably too strong a statement. I don’t understand the utility of prehospital lactate measurement. Yeah, that's better. No matter how it is explained, though, I don’t get the point of asking medics to check a lactate level. Why would I want to waste my time measuring lactate levels in the prehospital setting?

There. I’ve said it. Let me see if I can talk you into my point of view.

Lactate results from anaerobic metabolism. Most tissues form it, with muscles producing the most. In normal settings, the liver rapidly clears lactate along with some help from the kidneys. Lactate is an end product of anaerobic glycolysis. I’m not going to get into the Krebs and Cori cycles here. Look it up if you care. In the meantime, think of it this way: When you get done with a hard workout, your muscles are sore. That’s lactate. If you’re a little acidotic, it is lactic acidosis.

Hospitals commonly evaluate lactate in acutely ill patients. Elevated lactate is not completely or unanimously defined but high lactate has been stated as a lactate level greater than 4mmol/L in most articles. Most people think of lactate as related to the evaluation of shock states, but lactate can rise for a bunch of reasons. It isn’t as simple as “hypoperfusion (shock) causes lactate to rise.” Even so, lactate levels are often used to establish the severity of a patient’s illness and to guide therapy in the hospital. But lactate rises because more is being produced, less is being cleared by the liver (and kidneys), or a combination of the two.

Causes can be divided into two classes: Those states in which tissue oxygenation is impaired (Type A) and those in which oxygenation is normal (Type B). Type A lactic acidosis is caused, then, by shock; septic, cardiogenic, hypovolemic, and other shocks along with cardiac arrest, carbon monoxide exposure, and trauma. Type B lactic acidosis causes include diabetes mellitus, leukemia and other cancers, alcoholism, HIV infection, and medications or conditions that cause mitochondrial dysfunction.

Type A, Type B, who cares. The most simple way to think of elevated lactate levels is that the patient is experiencing cellular insult. If you remember one thing, remember that. Elevated lactate equals cellular insult.

Why do we care? This is where my question comes up. All of the studies I have found work out that the measurement of a patient’s lactate level is a powerful prognostic tool to stratify mortality rates in hospitalized patients. For example, Shapiro et al. stratified more than 1,200 infection patients into three lactate groups: less than 2.5 mmol/L, 2.5-3.9 mmol/L, and greater than 4.0 mmol/L. The mortality of the lowest lactate group was 4.9% while the highest lactate group had mortality rate of 28.4%. (1) Even prehospital-specific articles present similar findings. For example, a Dutch study found that prehospital patients with lactate over 4.0 mmol/L had a mortality rate of 26.7% and those with lactates under 4.0 mmol/L had a mortality rate of 1.2%. (2) Lactate measurement, then, is apparently a powerful prognostic tool that can drive care and treatment decisions.

There are a lot of studies like that. If you want to look at the research for yourself, I would suggest you start with this full-text overview article. This one from ACEP is a good summary, as well.

It still leaves the question: Why do I care, as a paramedic on a field ambulance?

Obviously, I am talking about urban or suburban American EMS agencies here. Critical care ambulances, rural or remote caregivers, and other atypical EMS agencies may find lactate monitoring helpful and important.

Sepsis alert programs are becoming more common. At least, they are becoming common enough for me to recognize that they exist. The most common criteria for a sepsis alert patient is (a) adult, (b) suspected or documented infection, (c) fever, pulse over 90, or respiratory rate over 20, and (d) SBP less than 90 or MAP less than 65 or lactate over 4 mmol/L. Take the lactate out of that mix. What changes? If you have an infectious adult patient with a fever, tachycardia, and hypotension you still have a septic patient. You shouldn’t need the lactate level to tell you that.

Occult sepsis, without hypotension, but with documented/suspected infection, exists. Picture that patient: Adult patient with an infectious process, a little elevated heart rate, maybe with a little tachypnea and fever. Would a lactate reading be the sole deciding factor in that transport decision? Because that is the scenario patient we started this blog post with. And I would transport him nonemergency. If you tested his lactate and found it to be elevated, say at 4.5 mmol/L, would that patient become an emergency transport? Isn’t that treating the monitor and not the patient? Would the minutes I save matter to the patient’s outcome?

If we take the scenario in a different direction, to a sicker patient, I still don’t see the efficacy of prehospital lactate testing. If the patient were altered, pale, diaphoretic, and hypotensive, he would represent a challenging prehospital patient. I would have a lot of work to do. I have a potentially septic or shocky patient and those patients are already labor-intensive. Adding lactate complicates things. Simplify!

Point-of-care lactate monitors and the test strips they use are crazy expensive. My agency would have to buy about 40 monitors and the strips. What benefit would they give? A hospital could buy one, keep it in the ED, use it liberally, and get the lactate data minutes after EMS would have provided it.

Would finding an elevated lactate reading cause me to initiate a treatment that I wouldn’t have otherwise given? Would you give a medication for a high lactate patient that you wouldn’t have otherwise given? Nope. Not that I can think of.

I just don’t see how it would affect my care on an ambulance, and I also can't see how it would save a significant amount of time or work for the emergency department. I’m open-minded. Can you explain it to me?

1. Shapiro NI, Howell MD, Talmor D, et al. Serum lactate as a predictor of mortality in emergency department patients with infection. Annals of emergency medicine. 2005 May;45(5):524–528.

2. van Beest P, Mulder P, Oetmo S, et al. Measurement of lactate in a prehospital setting is related to outcome. Eur J Emerg Med. 2009;16(6):318–322.