Journal Feed Weekly Wrap-Up

We always work hard, but we may not have time to read through a bunch of journals. It’s time to learn smarter. 

Originally published at JournalFeed, a site that provides daily or weekly literature updates. 

Follow Dr. Clay Smith at @spoonfedEM, and sign up for email updates here.

#1: Demystifying Lactate in the Emergency Department

Spoon Feed
Lactate is a frequently ordered biomarker in the Emergency Department. This is a large review elucidating the diagnostic and prognostic interpretation of lactate in the ED.

Why does this matter?
It may be hubris to think that we understand the ins and outs of every biomarker ordered in the Emergency Department. As the title of this article suggests, lactate is one of these biomarkers that often generates more questions than answers. This piece by Wardi, et al. dispels myths, addresses the physiology, homeostasis, and metabolism of lactate, and delineates the utility of lactate between various conditions. How should we be using lactate as a prognostic or diagnostic tool in the Emergency Department?

The tale of lactate: From sour milk isolate to the biomarker we love to hate


Lactate is an organic acid that is principally found in its ionized form at physiologic pH. Traditionally, it has been viewed as an end product of anaerobic metabolism, but more contemporary understanding recognizes lactate as a key player in energy use even under aerobic conditions. The liver metabolizes 75%. Kidneys metabolize 25%.

This is a large review article, so here are the high points:


  • Tourniquet Use – application of a venous tourniquet does not significantly alter venous lactate levels.

  • Arterial v. Venous Lactate –  there are mild discrepancies with hyperlactatemia. Arterial and central blood samples represent lactate that is systemically circulated, whereas venous samples reflect the local milieu.

  • Effect of LR Solution on Serum Lactate – There is no published evidence that a bolus of LR significantly increases lactate compared to NS, although transient elevations may be observed.

Lactate &…

  • Lactate & Sepsis –  The specific anatomic site of lactate generation in septic patients remains controversial as does the mechanistic reasoning behind hyperlactatemia in sepsis. It cannot be fully explained by tissue hypoxia and resultant anaerobic metabolism but continues to serve as a marker for risk stratification and predictor of mortality.

  • Lactate & Trauma, Burns, Inhalational Injuries – As with sepsis, lactate serves as a prognostic indicator of resuscitation, as well as infectious complications, organ dysfunction, and mortality.

  • Lactate & Seizures – hyperlactemia is known to be caused by local muscle tissue hypoxia. If caused solely by seizure, it should have rapid clearance within 1-2 hours. There is no correlation between degree of lactate elevation and outcome.

  • Lactate & Toxins/Medications – This is a large chunk of the paper, and there is a table provided which includes mechanisms and recommended therapy. It is worth a look.


The diagnostic utility of lactate in the ED is diverse. Elevated levels may be the result of overproduction, impaired elimination, or both. Regardless, an elevated lactate is associated with a worse prognosis in many conditions. Measurement of lactate can be a useful tool in the ED, and a nuanced understanding of lactate levels can help guide us toward appropriate interventions.

Another Spoonful

Demystifying Lactate in the Emergency Department. Ann Emerg Med. 2019 Aug 29. pii: S0196-0644(19)30537-2. doi: 10.1016/j.annemergmed.2019.06.027.

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#2: Is Empiric Anti-MRSA Pneumonia Therapy Harmful?

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Empiric anti-MRSA antibiotics were not associated with improved mortality in hospitalized patients with pneumonia. In fact, this evidence suggests they might actually do worse.

Why does this matter?
Antibiotics have downside risks, such as kidney injury or secondary infections. In the recent IDSA/ATS community acquired pneumonia guidelines, HCAP was abandoned. Broader spectrum therapy was not found to improve outcomes, per these guidelines. Does empiric anti-MRSA therapy help or hurt?

Anti Anti-MRSA?
This was a retrospective multicenter study over 6 years across the Veteran’s Health Administration hospitals, with 88,605 patients hospitalized for pneumonia included. For the primary outcome, patients who received empiric anti-MRSA antibiotics in addition to standard antibiotic therapy (i.e. beta-lactam + macrolide) were propensity matched with those who did not. They found, after adjustment, that the risk of mortality was greater in those who received anti-MRSA treatment than those who did not; adjusted risk ratio, aRR 1.4 (95%CI, 1.3-1.5). They also found an increase in secondary outcomes of kidney injury and secondary infections, such as C. difficile colitis and vancomycin-resistant Enterococcus. Even in the subgroup of patients with risk factors for MRSA*, empiric anti-MRSA therapy suggested higher mortality compared to standard CAP therapy; aRR 1.2 (95%CI 1.1-1.4). There was also no mortality benefit to anti-MRSA antibiotics in patients sick enough to go to the ICU; aRR 1.3 (95%CI 1.2-1.5). Even if propensity matching may not account for all possible confounding – namely, sicker patients got vancomycin and also had higher mortality – this gives me pause to empirically start anti-MRSA drugs in most pneumonia patients.

*Risk for MRSA was defined as: “history of MRSA infection or colonization in the past year or at least 2 of the following: previous hospitalization, nursing home residence, and previous intravenous antibiotic therapy”

Empirical Anti-MRSA vs Standard Antibiotic Therapy and Risk of 30-Day Mortality in Patients Hospitalized for Pneumonia. JAMA Intern Med. 2020 Feb 17. doi: 10.1001/jamainternmed.2019.7495. [Epub ahead of print]

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Spoon Feed
Ultrasound was not sensitive for detecting IJ or subclavian central venous catheter (CVC) malposition but was comparable to CXR for detecting pneumothorax (PTX).

Why does this matter?
CXR is the study of choice after placing a CVC to check position and look for complications, such as a PTX. Would ultrasound do just as well?

Where is that cath tip…
This was a prospective study of post-op ICU patients which included 758 CVC placements. Malposition was determined by directly visualizing the tip, if possible, and also by using a bubble study looking for, “a laminar flow of microbubbles to appear in the right atrium within 2 seconds.” Sensitivity of ultrasound compared to CXR for malposition was 70% (95%CI 49% to 86%); specificity 99% (95%CI 98% to 100%). Ultrasound detected 5 pneumothoraces; CXR detected 11. Since CXR is a poor gold standard for PTX, they looked at agreement. U/S and CXR agreed on PTX 98.9% of the time, with a kappa of 0.5 (95%CI 0.19 to 0.80). That kappa isn’t great. They made the point that, “One clinically relevant malposition out of 758 placements (0.0013%) was missed by ultrasound. Ultrasound and chest x-ray film detected all clinically relevant pneumothoraces.” For example, although a CVC in the brachiocephalic was malpositioned, by study definition, that is still a safe location. And all PTXs that mattered clinically were found. Also, they did not do U/S before line placement. There was comment that some PTXs may have been present before line placement. My take is this: I don’t agree with the author’s conclusion that, “ultrasound is an accurate diagnostic modality to detect malposition and pneumothorax.” It simply was not. A test with a sensitivity of 70% is not a good screening tool. However, if you’re content with the line tip just outside the SVC (which I am), this approach looks pretty good.

Ultrasound to Detect Central Venous Catheter Placement Associated Complications: A Multicenter Diagnostic Accuracy Study. Anesthesiology. 2020 Jan 21. doi: 10.1097/ALN.0000000000003126. [Epub ahead of print]

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