Does the prognostic power of an elevated lactate level translate into better care and better outcomes for patients or does an elevated lactate level lead to interventions that do not help patients but burden care teams?
Thank you for having and sharing this needed debate. I generally agree with Adam Cifu.
I'm commenting because I think there is some important data not mentioned.
- First, we do have a recent RCT called Andromeda Trial comparing targeting capillary refill time vs lactate on mortality and...guess what? Capillary refill time was not just non inferior but also almost superior with a huge numerical but non statistically significant difference. Check it for yourselves. Why wasn't it mentioned?
- The evidence cited criticizing capillary refill time is a meta-analysis with observational studies on children done until 2014. I would call it low quality evidence and doesn't include ANDROMEDA. Not to mention that the lactate cutoff is a very debatable thing which would suffer from the same or worse problem, but there's no cited evidence on that.
- I'm not an expert on the evidence on the sepsis bundles, but I believe almost all of the bundles first created by the sepsis campaign were later disproven, so not that good for an authority argument. And just pointing a maybe coincidential observation from a single hospital and non-published data from another hopital doesn't prove a causal effect. Even if it had, it wouldn't prove the benefit of an universal screening. But for that read the very good articles on the topic from PulmCrit and EMCrit.
- Even the physiological usefulness of lactate is a very debatable topic, and concepts commonly heard such as hyperlactacidemia or actic lacidosis may not be true. Check what Tox and Hound and also EMCrit/PulmCrit have written.
Resuming, bad evidence / evidence against and poor biological plausibility. Not that good for supporting it, in my opinion.
But anyway, I deeply thank you both for having the time of writing this debate!
As an intensivist I find lactate to be a useful adjunct in assessing the serious of a patient's illness. Like most things in medicine (and especially in critical care) it is useful if it helps you think more about your patient. If it instead puts you on a protocol pathway and makes you think less about your patient (as some have described here) it is dangerous.
I think this is an interesting subject, and appreciate the comment that it really hasn't been studied. It seems to be the idea that Lactate is driven by shock and low blood pressure. In my observations, I see it with cardiogenic shock rather than septic shock. In the ED, I suppose it could be either. As a Perfusionist with a Master's in Cardiovascular Sciences, I would say I see it as more accurate to associate it with pulsatile flow. Even with a mean BP over 70 on bypass, when we have long bypass times, we see lactate rise. If the case involves circulatory arrest, there's another factor of tissue damage with very cold blood flow, prolonged times on the pump, and cross clamping a cold, sick aorta, releasing cytokines etc... Flow to the deep tissues and capillaries is compromised, vs a warm patient with a beating heart, and lactate rises. Even if I find myself chasing base deficits, giving preventative solutions (mannitol, benadryl, steroids), perfusion isn't normal and lactate rises. So when looking at lactate as a screening tool, look past blood pressure and sepsis, into EF, CHF and such. I've seen lactate as high as 15+ (max on the GEM 5000) with patient recovery, but those super high levels are grim. When I check lactate levels, I do pay attention, but there's not much more I can do than everything I already am doing. We need to get them off bypass and let their heart beat. Good, pulsatile flow seems to be everything that's needed to keep lactate normal.
Thank you for publishing this debate. From the Emergency Medicine perspective, the screening lactate has morphed into EPIC pop-up alerts with the ever expanding definitions of "sepsis" including SIRS, Sepsis-lite, Severe Sepsis, Severe-Severe Sepsis, This Is Serious Sepsis- pulling random pieces of data from the chart, like the RR at triage of 22, or HR 101 (because of non-septic issues, like pain or mad about waiting, or input error etc). We spend more time documenting WHY the alerts are wrong. Combine this with the regulatory complex of the hospital, such as the well meaning "Quality Control Teams" who are tasked with tracking down physicians who didn't document the "sepsis phrasing" in just the exact way that CMS requires, like "I did the reperfusion exam after a bolus" or "I didn't give a bolus because...(insert the reapproved wording)." They even interrupt us during our shifts about documentation. No matter that Emergency Medicine is an iterative process in real time with multiple patients simultaneously, not a static picture or EPIC algorithmic alerts or care that fits into the "Time Zero" box. The enforcement apparatus is detached from actual patient care and the patient outcomes. -Dr. Carrie Mendoza, Emergency Medicine
Personally, I think the NEG lactate made a difference. I did have IV Rocephin and some fluids, but I was still weak and near syncopal, washed out, still chilling w/o fever. I was not ICU bound, but the future was not exactly clear. The NEG lactate made me and the doc comfortable in sending me home.
Screening lactates are one of the worst things that have happened to critical care medicine. For one, I have seen multiple patients killed because a lactate level was drawn. Typically these patients have unrecognized CHF and come in with nonspecific complaints like generalized weakness or fatigue. A lactate is ordered and comes back elevated, so sepsis is suspected, and the patient gets a couple of liters of saline, and the patient develops flash pulmonary edema. I’ve seen it happen numerous times. The second thing is the utter waste of resources. ER docs typically don’t prove that the patient has an infection before getting a lactate. They just see that the patient doesn’t look good. Then once the lactate comes back elevated everyone presumes infection exists, and then it’s up to the ICU provider (me) to disprove infection. Proving a negative is nearly impossible, so these patients automatically get teed up for ICU admission. Put me on the anti-lactate team.
Could you compare the incidence/mortality plot to one from a country which did not institute screening but is similar to the US in healthcare quality. Perhaps Canada?
I’m of the second opinion- a useful test in context but if used as a screening tool I suspect it would lead to aggressive over treatment of patients. I mean, 2 is the cutoff? Really???
On the other hand, I have recurrent sepsis from my prostate. Initially it was an FUO with painful rigors and I required 10 days of workup and ICU care. It has recurred 6 or 7 times in spite of 2 TURPs. The last recurrence about 2 months ago. Onset was chills, weakness, near syncope, but no fever. I immediately went to the ER where the DX was confirmed. A NEGATIVE lactic acid test (<2) reassured everyone I could be discharged for home treatment.
If your obs were fine I would discharge you at that point without a lactate. If your obs were not fine I would disregard a normal lactate and keep you in. Lactate rarely guides plans unless it gives you a very unexpected result.
Thank you for having and sharing this needed debate. I generally agree with Adam Cifu.
I'm commenting because I think there is some important data not mentioned.
- First, we do have a recent RCT called Andromeda Trial comparing targeting capillary refill time vs lactate on mortality and...guess what? Capillary refill time was not just non inferior but also almost superior with a huge numerical but non statistically significant difference. Check it for yourselves. Why wasn't it mentioned?
- The evidence cited criticizing capillary refill time is a meta-analysis with observational studies on children done until 2014. I would call it low quality evidence and doesn't include ANDROMEDA. Not to mention that the lactate cutoff is a very debatable thing which would suffer from the same or worse problem, but there's no cited evidence on that.
- I'm not an expert on the evidence on the sepsis bundles, but I believe almost all of the bundles first created by the sepsis campaign were later disproven, so not that good for an authority argument. And just pointing a maybe coincidential observation from a single hospital and non-published data from another hopital doesn't prove a causal effect. Even if it had, it wouldn't prove the benefit of an universal screening. But for that read the very good articles on the topic from PulmCrit and EMCrit.
- Even the physiological usefulness of lactate is a very debatable topic, and concepts commonly heard such as hyperlactacidemia or actic lacidosis may not be true. Check what Tox and Hound and also EMCrit/PulmCrit have written.
Resuming, bad evidence / evidence against and poor biological plausibility. Not that good for supporting it, in my opinion.
But anyway, I deeply thank you both for having the time of writing this debate!
Bernardo
As an intensivist I find lactate to be a useful adjunct in assessing the serious of a patient's illness. Like most things in medicine (and especially in critical care) it is useful if it helps you think more about your patient. If it instead puts you on a protocol pathway and makes you think less about your patient (as some have described here) it is dangerous.
I think this is an interesting subject, and appreciate the comment that it really hasn't been studied. It seems to be the idea that Lactate is driven by shock and low blood pressure. In my observations, I see it with cardiogenic shock rather than septic shock. In the ED, I suppose it could be either. As a Perfusionist with a Master's in Cardiovascular Sciences, I would say I see it as more accurate to associate it with pulsatile flow. Even with a mean BP over 70 on bypass, when we have long bypass times, we see lactate rise. If the case involves circulatory arrest, there's another factor of tissue damage with very cold blood flow, prolonged times on the pump, and cross clamping a cold, sick aorta, releasing cytokines etc... Flow to the deep tissues and capillaries is compromised, vs a warm patient with a beating heart, and lactate rises. Even if I find myself chasing base deficits, giving preventative solutions (mannitol, benadryl, steroids), perfusion isn't normal and lactate rises. So when looking at lactate as a screening tool, look past blood pressure and sepsis, into EF, CHF and such. I've seen lactate as high as 15+ (max on the GEM 5000) with patient recovery, but those super high levels are grim. When I check lactate levels, I do pay attention, but there's not much more I can do than everything I already am doing. We need to get them off bypass and let their heart beat. Good, pulsatile flow seems to be everything that's needed to keep lactate normal.
Thank you for publishing this debate. From the Emergency Medicine perspective, the screening lactate has morphed into EPIC pop-up alerts with the ever expanding definitions of "sepsis" including SIRS, Sepsis-lite, Severe Sepsis, Severe-Severe Sepsis, This Is Serious Sepsis- pulling random pieces of data from the chart, like the RR at triage of 22, or HR 101 (because of non-septic issues, like pain or mad about waiting, or input error etc). We spend more time documenting WHY the alerts are wrong. Combine this with the regulatory complex of the hospital, such as the well meaning "Quality Control Teams" who are tasked with tracking down physicians who didn't document the "sepsis phrasing" in just the exact way that CMS requires, like "I did the reperfusion exam after a bolus" or "I didn't give a bolus because...(insert the reapproved wording)." They even interrupt us during our shifts about documentation. No matter that Emergency Medicine is an iterative process in real time with multiple patients simultaneously, not a static picture or EPIC algorithmic alerts or care that fits into the "Time Zero" box. The enforcement apparatus is detached from actual patient care and the patient outcomes. -Dr. Carrie Mendoza, Emergency Medicine
Amen to all of this
I really enjoyed this debate. As a GP/Family physician this topic has almost no relevance to me but the EBM debate was brilliant.
Could you possibly do point of care CRP testing next? Should this be rolled out into the community to guide admissions and antibiotic prescriptions?
https://open.substack.com/pub/medicurious/p/no-58-the-12-medical-gifts-of-christmas?r=p3tn3&utm_campaign=post&utm_medium=web
I am enjoyed Sensible Medicine so much, I have been recommending it to all of my friends and colleauges, even included it in my christmas last!
Personally, I think the NEG lactate made a difference. I did have IV Rocephin and some fluids, but I was still weak and near syncopal, washed out, still chilling w/o fever. I was not ICU bound, but the future was not exactly clear. The NEG lactate made me and the doc comfortable in sending me home.
Screening lactates are one of the worst things that have happened to critical care medicine. For one, I have seen multiple patients killed because a lactate level was drawn. Typically these patients have unrecognized CHF and come in with nonspecific complaints like generalized weakness or fatigue. A lactate is ordered and comes back elevated, so sepsis is suspected, and the patient gets a couple of liters of saline, and the patient develops flash pulmonary edema. I’ve seen it happen numerous times. The second thing is the utter waste of resources. ER docs typically don’t prove that the patient has an infection before getting a lactate. They just see that the patient doesn’t look good. Then once the lactate comes back elevated everyone presumes infection exists, and then it’s up to the ICU provider (me) to disprove infection. Proving a negative is nearly impossible, so these patients automatically get teed up for ICU admission. Put me on the anti-lactate team.
Could you compare the incidence/mortality plot to one from a country which did not institute screening but is similar to the US in healthcare quality. Perhaps Canada?
I’m of the second opinion- a useful test in context but if used as a screening tool I suspect it would lead to aggressive over treatment of patients. I mean, 2 is the cutoff? Really???
On the other hand, I have recurrent sepsis from my prostate. Initially it was an FUO with painful rigors and I required 10 days of workup and ICU care. It has recurred 6 or 7 times in spite of 2 TURPs. The last recurrence about 2 months ago. Onset was chills, weakness, near syncope, but no fever. I immediately went to the ER where the DX was confirmed. A NEGATIVE lactic acid test (<2) reassured everyone I could be discharged for home treatment.
Huh. Really? I’d have observed you for a few hours. Lactate rise/low perfusion is a relatively late sepsis sign.
I was in ER 7 hours, 10 hours from onset.
If your obs were fine I would discharge you at that point without a lactate. If your obs were not fine I would disregard a normal lactate and keep you in. Lactate rarely guides plans unless it gives you a very unexpected result.
Interesting debate. I’m curious whether either of the authors sees a role for a POC renin test in the management of these patients.