Read on Twitter
A Wednesday tweetorial about everyone’s favorite lab: Lactate. So nice, you checked it twice. A #Medtwitter Thread for #EMDocs and everyone else alike.
Several years ago, CMS enacted a quality measure known as the Early Management Bundle for Severe Sepsis/Septic Shock (SEP-1) mandating exactly how patients with severe #sepsis or septic shock must be treated early in their clinical course
CMS tracks hospitals’ performance in achieving these milestones as a marker for quality of care. Patients can even look online to see how their hospitals compare in meeting these milestones https://www.medicare.gov/hospitalcompare/search.html
But are these milestones really markers of quality care?
Tl;Dr: No.
So here's my long-winded view on why, focusing on lactate. https://www.emra.org/emresident/article/critcare-alert-sep1/
Tl;Dr: No.
So here's my long-winded view on why, focusing on lactate. https://www.emra.org/emresident/article/critcare-alert-sep1/
Per the SEP-1 bundle, along with blood cultures & initiating antibiotics, patients with septic shock must have an initial lactate drawn & (if elevated) need 30cc/kg of crystalloid and a repeat lactate within 6 hours
SEP-1 defines septic shock as severe sepsis + hypotension despite fluid boluses. More specifically, we're talking patients with 1) sBP <90 OR 2) MAP <65, OR 3) sBP drop > 40, OR 4) tissue hypoperfusion as indicated by an initial lactate level ≥4 mmol/L
But consider a patient with acute flash pulmonary edema. RR 25, WBC 13, and lactate 4.2. She meets SIRS criteria (RR 25, WBC 13), and signs of end organ damage (lactate 4.2). But is she hypoperfusing because she needs more IV fluid? Would more fluids be considered quality care?
This woman is my mother. She had undiagnosed CAD, newly dilated cardiomyopathy, went into afib, flashed, and couldn't breathe. She showed up at her local hospital with whacked vitals and labs, and because CMS set the expectation to give 30cc/kg of fluid, they reflexively did
She landed in the ICU on BiPAP after becoming progressively hypoxic and hypotensive from the fluid boluses she received in their reflexive, rule-following ED, guided by CMS's favorite lab: lactate. Fortunately, mom is ok. So let's focus our attention on lactate.
Lactate is produced by anaerobic metabolism triggered by impaired circulation. #MedStudentTwitter: Think mesenteric ischemia and a rising lactate from tissue hypoperfusion and dead bowel. So elevated lactate may be due to a low flow state and hypoperfusion. But not always.
Lactate is also produced aerobically as a result of glycogenolysis. B2 adrenergic stimulation increases glycogenolysis to produce glucose to fuel the body’s stress response. Stress -> glycogenolysis -> glucose. And because we all remember the Kreb’s cycle, glucose -> pyruvate
Kreb can’t handle all the pyruvate being produced, so the extra pyruvate gets converted into lactate. And then it shows up in your labs and you order 30cc/kg of LR. But should we flood every patient with fluids just because the Kreb’s cycle can’t meet the SEP-1 quality metric?
Absolutely not. Administering 30cc/kg to every patient with an elevated lactate will help you meet your metric, but it may be harmful to the patient. And it overlooks the fact that the body is driving a stress response that you may need to address first.
In fact, Morelli et al's 2013 JAMA study showed improved outcomes AND decreased lactates for patients with septic shock given beta blockers. So maybe sometimes it's more about stress and less about fluids? https://jamanetwork.com/journals/jama/fullarticle/1752246
The patient with asthma breathing 30 times a minute, with a WBC of 13, pounding his albuterol is driving up his lactate via pyruvate with each puff of his inhaler. He also doesn't need fluids (any more than antibiotics). In fact, not giving asthmatics abx is a quality metric
And my mom with her elevated lactate from tissue hypoperfusion wasn't hypoperfusing because of hypovolemia. She was literally drowning in fluid and desperately needed diuresis. But the SEP-1 bundle told the hospital to fill her up even more.
What's the moral of the story? Not every patient with an elevated lactate has sepsis. But every patient with sepsis does need close monitoring and prompt initiation of treatment. So while lactate can help guide care, we need to recognize real sepsis and what to do when we see it
THAT is what regulators want to track. They want to know that hospitals recognize physiologic shock, treat it, and then assess the patient’s response to treatment. But using fluid boluses and serial lactate draws alone focuses on only part of the puzzle.
So let's re-up the debate about SEP-1. This one-size-fits all strategy doesn't work for every patient. And holding physicians & APPs to those unreasonable and harmful standards only contributes to burnout, fatigue, premature closure, and clinicians on autopilot
And that's not what patients want from the hospital. They want dedication, personalized attention, and high quality care, which are exactly what our financial and regulatory systems should be structured to support and encourage.
cc: @MiscSusan. We really should've written that review article 2 years ago
