Clinical Pearls:What’s up with the lactate?
In 2001 a research article was published expounding early goal directed therapy as a treatment strategy for sepsis. Spearheaded by Emmaunel Rivers this ground breaking study involved using resuscitation end points including a reduced lactate level. Key points in the article suggest that physical exam findings are subpar for directing resuscitation and that measures such as lactate, SCVO2, base deficit, and pH are more accurate measures of adequate treatment. There were certainly other factors, and the take home message was to find the source and start antibiotics early, but volume resuscitate until tissue hypoxia improves was the practical application of this research. As a result lactic acidosis has become a bad omen to be feared by all. Several guideline updates have since been published, the most recent in 2021 with weak evidence to suggest using lactate as an end-point measurement. Practically speaking though, the word is out that a high lactate = bad bad badness. I’m not saying it isn’t bad, but there are plenty of reasons why an elevated lactate alone is not the end of the world. In this post we’ll discuss causes for lactate elevation, what should be cause for alarm and what shouldn’t, and how to manage it.
There are several forms of hyperlactatemia. The two(ish) main types are divided up by severity and only one truly represents concern for global tissue ischemia.
1) Pseudo-hyperlactatemia
Not indicative of actual tissue ischemia. Causes as below.
The tourniquet was too tight or on for too long.
Incorrect tube not sent on ice.
Sample obtained from an ischemic limb.
2) Type B
Represents local but not global tissue ischemia so less worrisome.
Look for signs of end organ damage, if none this is a regional issue (type B) which should be addressed but isn’t as emergent as Type A.
Type B does not raise high concern for end-organ damage and therefore does not necessitate aggressive resuscitation.
These are the pt’s who tend to have just a little extra lactate (think 2-6ish range) and it may remain very stubbornly elevated. Unless you take away the offending medication, cure the liver failure/cancer it is likely to remain elevated. You have to put into context whether or not this should induce panic, concern, or just a (meh) shoulder shrug. The “abnormal” number in red is just a number unless clinical context is considered.
Causes as below.
Local tissue hypoperfusion: hypoxia, seizures, hypothermia with shivering, excessive exercise.
Metformin at higher levels (think diabetes + renal failure on Metformin).
DKA.
Cancer.
Alcohol or Methamphetamine ingestion (these are very common so I gave them their own bullet point).
Ingestion of toxins/drugs: Metformin, Depakote, Linezolid, Nipride, Propofol, HAART therapy, Cocaine (many many more drugs, I only list the common ICU meds).
Decreased clearance: liver failure, alcoholism.
Decreased metabolism: thiamine deficiency, alcoholism.
3) Type A
More worrisome 2/2 global tissue hypoperfusion. Causes below.
All forms of shock.
Cardiac arrest.
Prolonged hypotension, diffuse trauma or burns, anemia, carbon monoxide poisoning, cyanide poisoning.
Local complications: limb ischemia, gut (mesenteric) ischemia, local trauma, crush injury, burn, necrotizing fasciitis.
Over exertion which can be local or global: strenuous exercise, seizure, severe rhabdo.
There is a D type elevation which will not be discussed in this article as it is exceedingly rare.
So what do you do about it? Well it starts with gaining a decent understanding of what type you have. There is often a multi-factorial etiology. Take for example the pt in shock on Epi. Is it the shock or is it the medication? The answer is yes. Lol, it’s both. You will have to look at other clinical signs and tests to determine if your shock is persistent or ongoing and needs more attention or if you can attribute the non-clearing lactate to Epi without worsening shock.
What clinical signs should you assess? Signs of end organ failure whether local or global.
Local
Think critical limb ischemia - sensory-motor function intact or not, palpable pulse, cap refill, extremity color and temperature, look for signs of chronic changes like hyperpigmentation, shiny hairless limb.
Think gut ischemia - abd pain, diarrhea esp if bloody, nausea/vomiting, fever, CT with contrast preferred for diagnosis (very subtle to see and can be missed - have a surgeon review it). Late signs lead to a Type A lactic acidosis with shock.
Think local infection/compartment syndrome - severe cellulitis is not common but local pockets of infection like an abscess -> gangrene, nec fasc. Lots of pain out of proportion to exam, rapid expansion of demarcated pigmentation. Fever, leukocytosis, etc.
Global
Think about your post cardiac arrest patients. What organs do you worry will fail? Same here. Go through each one systematically. Multi-system organ failure does = badness.
Cap refill/oliguria/confusion - the triad of badness. The organs least protected in a state of systemic hypo-perfusion are the kidneys, brain, extremities. Start by assessing these organs.
The infinitely wise body starts by shunting blood from the periphery to the more important organs. Look for decreased distal pulses, skin color changes, mottling, decreased cap refill. I find mottling to be highly associated with an elevated lactate.
Use diagnostics such as SCVO2, CO/CI, Flowtrack with SVV (to measure dynamic compliance and determine if a pt is volume responsive), bedside echo (to look at pump, estimate filing pressures, and assess IVC collapsibility), etc.
How To Work This Patient Up
Is there a metabolic acidosis? Check the pH and anion gap.
Is the kidney or liver injured - this will delay clearance. Look up the labs and clinical signs. Note the state of the kidneys in particular - are they making urine, what is the creatinine?
Exam: cap refill, confusion, dizziness, syncope, cold extremities, mottling, decreased pulses, abdominal pain, chest pain, oliguria or anuria, and anything stated above about specific local or global signs.
Labs: ScVo2, CO/CI, increased LFT's, troponin elevation, creatinine/GFR, pH, anion gap, glucose, potassium, toxic alcohol levels, osmolar gap, any relevant medication levels, cbc or other markers of infection, trend the lactate, CPK and other cardiac panel.
Diagnostics: Echo (cardiac function), CT (esp abd looking for ischemia, also any source of infection), EEG (r/o sz if concerned), RUQ US if hepatic function unknown or looking for cholecystitis or other signs of infection,
Figure out the type of lactic acidosis and the etiology. Correct the underlying cause for the elevation and the number itself will come down. If it is shock, do everything in your power to accurately identify the type of shock and narrow your treatment plan. Instead of knee jerk ordering volume resuscitation first determine if this is hypovolemic or distributive (with a need for volume resuscitation or not). The other forms of shock have more targeted approach, ie. hemorrhagic - stop the bleed, transfuse products; cardiogenic - add an inotrope and consider mechanical support, et).
If this lactate level represents a pseudo level or type B without concerns for tissue hypoperfusion - they likely don’t need to come to the ICU or have the crisis alarm bells rung. Talk with the primary team about etiology, red-herrings, things that will delay clearance, meds that will do the same and discuss the appropriateness of stopping them or accepting the lactate, waiting for the meth or alcohol to dissipate and trending the lactate until then. And so forth.
Side note: administering Lactated Ringers will not drive up the serum lactic acid level. This is a common misconception and one you have to correct. There is plenty of evidence out there but if you are in a pinch this one is pretty straight forward: https://www.ncbi.nlm.nih.gov/books/NBK500033/
Other references:
https://acutecaretesting.org/en/articles/increased-blood-lactate-levels-a-marker-of
http://dickyricky.com/Medicine/Papers/2019_08_29%20Ann%20Emerg%20Med%20Demystifying%20Lactate%20in%20the%20Emergency%20Department.pdf
https://www.nejm.org/doi/10.1056/NEJMoa010307
Current Surviving Sepsis Guidelines 2021: https://journals.lww.com/ccmjournal/Fulltext/2021/11000/Surviving_Sepsis_Campaign__International.21.aspx
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