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: New ACEP Community-Acquired Pneumonia Clinical Policy

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ACEP has released a new clinical policy statement for the care of community-acquired pneumonia (CAP) in the ED.

Why does this matter?
This policy statement updates the last one, which was in 2009. It answers three critical questions for the ED management of CAP.


  1. “In the adult emergency department patient diagnosed with community-acquired pneumonia, what clinical decision aids can inform the determination of patient disposition?”
    Level B: PSI and CURB-65 are recommended, but PSI is favored and also recommended by the IDSA/ATS 2019 CAP guidelines.
    – Level C: In patients not on the ventilator and not on vasopressors, ≥3 of the 2007 IDSA/ATS minor criteria* may help determine which patients would benefit from a stay in the ICU vs regular hospital bed. You could also use SCAP or SMART-COP.
    – Level C: Biomarkers don’t augment these clinical decision tools. Also, clinical judgment always wins over decision rules.

  2. “In the adult emergency department patient with community-acquired pneumonia, what biomarkers can be used to direct initial antimicrobial therapy?”
    – Level C: Don’t rely on biomarkers like procalcitonin or CRP to determine viral from bacterial pneumonia in ED patients with CAP.

  3. “In the adult emergency department patient diagnosed with community-acquired pneumonia, does a single dose of parenteral antibiotics in the emergency department followed by oral treatment versus oral treatment alone improve outcomes?”
    – Level C: There really is no good evidence. Make decisions based on risk profile and your preference – says the statement.

*2007 IDSA/ATS Criteria for Defining Severe Community-Acquired Pneumonia

Minor Criteria

  • Respiratory rate ≥ 30 breaths/min

  • PaO2/FiO2 ratio ≤ 250

  • Multilobar infiltrates

  • Confusion/disorientation

  • Uremia (blood urea nitrogen level ≥ 20 mg/dl)

  • Leukopenia (not from chemotherapy) (WBC < 4,000 cells/μl)

  • Thrombocytopenia (platelet count < 100,000/μl)

  • Hypothermia (core temperature < 36°C)

  • Hypotension requiring aggressive fluid resuscitation

Major Criteria

  • Septic shock with need for vasopressors

  • Respiratory failure requiring mechanical ventilation

Clinical Policy: Critical Issues in the Management of Adult Patients Presenting to the Emergency Department With Community-Acquired Pneumonia. Ann Emerg Med. 2021 Jan;77(1):e1-e57. doi: 10.1016/j.annemergmed.2020.10.024.

#2: TXA for TBI – Meta-analysis of Nine RCTs

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In patients with acute traumatic brain injury (TBI), tranexamic acid (TXA) did not improve mortality or neurological outcome among survivors.

Why does this matter?
We’ve covered CRASH-3, which found a slight mortality benefit from TXA for TBI. Then we covered a prehospital RCT which showed no benefit from TXA, and the BRAIN-PROTECT group found possible harm from TXA in patients with severe or isolated TBI. What is the consensus report when we compile even more RCTs?

Hold the TXA for TBI
They found 9 RCTs, with 14,747 patients combined. TXA did not reduce mortality, risk ratio 0.95 (95%CI 0.88-1.02). It also didn’t improve neurological outcome when measured with validated disability scales. But it also didn’t seem to cause harm. I can’t advocate for the use of TXA for TBI, especially since the prehospital study by the BRAIN-PROTECT collaborators found harm and was not included in this meta-analysis. That RCT would have added another 1,827 patients to the meta-analysis and would likely have made these outcome results look worse. Tomorrow we will look at TXA for subarachnoid hemorrhage.

Efficacy and safety of tranexamic acid in acute traumatic brain injury: a systematic review and meta-analysis of randomized-controlled trials. Intensive Care Med. 2021 Jan;47(1):14-27. doi: 10.1007/s00134-020-06279-w. Epub 2020 Oct 20.

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When septic patients with persistent tachycardia after initial resuscitation received ultra-short acting β-blockers, 28-day mortality was significantly lower, NNT 5.5.

Why does this matter?
Catecholamine excess can be bad for the heart (i.e. Takotsubo). But is giving a β-blocker to a tachycardic patient with sepsis like putting a piece of black tape over your car’s “Check Engine” light? Or is the hyper-sympathetic state of sepsis something we could moderate to improve patient outcomes?

If it’s fast, slow it?
This was a systematic review of 7 RCTs, 613 patients, with sepsis and persistent tachycardia after initial resuscitation who received either esmolol or landiolol. Initial resuscitation consisted of an undetermined amount of fluid plus vasopressors in most trials. Six trials (572 patients) were meta-analyzed for the outcome of 28-day mortality; mortality risk was reduced by 32% in patients who received a β-blocker vs placebo (risk ratio, 0.68; 95% CI 0.54 to 0.85). Overall mortality rate was 36.7% in the esmolol/landiolol cohort, 54.9% in the placebo group; absolute risk reduction 18.2%, NNT 5.5. Heterogeneity was low (I2 = 31%). Heart rate was significantly lower in all seven trials in patients who received the β-blocker, but MAP was not significantly reduced. Five of the trials were done in China, one in Japan, and one in Italy, which could impact generalizability. Five of six trials used esmolol. Landiolol is not FDA approved in the U.S. and was used in one trial. Landiolol has a similar β1 cardioselective mechanism of action to esmolol and is also ultra-short acting. This looks encouraging. But there was a wide range of mortality across these centers, from 12-62% in the β-blocker group; 20-80% in the placebo group. All of these were small RCTs. It seems like a large RCT is warranted to confirm this.



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