🩺 THIS WEEK IN EM
Acute Heart Failure: EMPULSE Says the SGLT2 Conversation Should Start Earlier
For a long time, SGLT2 inhibitors lived in the outpatient world. You stabilized the acute heart failure patient, admitted them, and assumed the medication optimization would happen later — after discharge, after follow-up, after somebody else owned the problem.
EMPULSE makes that delay harder to defend.
The trial randomized 530 patients hospitalized with acute heart failure — regardless of ejection fraction or diabetes status — to empagliflozin 10 mg daily or placebo, started after clinical stabilization during the hospitalization. At 90 days, empagliflozin produced a significant benefit on the trial's hierarchical primary endpoint, which combined death, heart failure events, and symptom improvement. The win ratio was 1.36 (95% CI 1.09-1.68). Serious adverse events were actually less common in the empagliflozin group, and there was no major safety penalty in hypotension, renal events, or infection.
The ED implication is not that you personally need to become the inpatient heart failure service. It is that the stabilized acute heart failure patient should no longer be framed as someone whose disease-modifying therapy can wait indefinitely. If they are headed upstairs and not already on an SGLT2 inhibitor, this is now a reasonable therapy to raise early rather than leave for some vague outpatient future.
Bottom line: In stabilized acute heart failure patients, early in-hospital SGLT2 initiation improves meaningful clinical outcomes and is increasingly hard to justify delaying.
Voors AA, Angermann CE, Teerlink JR, et al. The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial. Nat Med. 2022;28:568-574.
Nonpurulent Cellulitis: Moran Reminds Us to Stop Overtreating It
Cellulitis is one of those bread-and-butter ED problems that somehow still attracts aggressive treatment. IV antibiotics “just to be safe.” TMP-SMX added to cephalexin “just in case it’s MRSA.” A short, uncomplicated visit turns into a more complicated prescription than the disease actually needs.
The Moran trial pushed directly against that habit.
In this multicenter randomized trial, patients with uncomplicated nonpurulent cellulitis received either cephalexin plus TMP-SMX or cephalexin alone. Adding TMP-SMX did not improve clinical cure. That matters because it lines up with the microbiology most of us already know but sometimes ignore in practice: uncomplicated nonpurulent cellulitis is usually streptococcal, not an occult MRSA problem waiting to embarrass you.
This does not mean every skin infection is simple. Purulence changes the equation. Abscess changes the equation. Toxic appearance, rapid progression, inability to tolerate PO, deep-space concern, or immunocompromise all change the equation. But the stable patient with a red, warm leg and no drainage does not need a maximalist regimen to prove you care.
Bottom line: For uncomplicated nonpurulent cellulitis, cephalexin alone is usually enough. Adding TMP-SMX does not improve cure and mostly adds pill burden.
Moran GJ, Krishnadasan A, Gorwitz RJ, et al. Effect of Cephalexin Plus Trimethoprim-Sulfamethoxazole vs Cephalexin Alone on Clinical Cure of Uncomplicated Cellulitis: A Randomized Clinical Trial. JAMA. 2017;317(20):2088-2096.
Chest Pain: High-Sensitivity Troponin Works Best When You Respect the Observe Zone
High-sensitivity troponin made one of the biggest operational changes emergency medicine has seen in years. The 0/1-hour algorithm can rapidly move a large portion of chest pain patients toward rule-out without the old serial-enzyme purgatory.
But the algorithm only helps if you respect what it actually says.
In a multicenter evaluation of the 0/1-hour strategy using high-sensitivity troponin T, the pathway sorted patients into rule-out, rule-in, and an intermediate group that still needed more work. That intermediate group is the part people like to skip past. They want the assay to end the visit. It doesn't. It narrows the field quickly, but it does not replace judgment, risk stratification, or your institution's specific assay thresholds.
That is the real takeaway for the ED. High-sensitivity troponin is not just faster troponin. It is a structured pathway, and structured pathways only work if you follow the structure. The patient who clearly rules out is great. The patient who clearly rules in is helpful. The patient in the middle is where clinical medicine still lives.
Bottom line: The 0/1-hour hs-troponin pathway is powerful, but only when you use assay-specific cutoffs and take the observe zone seriously instead of pretending every chest pain patient should fit into a binary answer.
Mueller C, Giannitsis E, Christ M, et al. Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T. Ann Emerg Med. 2016;68(1):76-87.e4.
🔭 Next Week
Aspirin in undifferentiated chest pain: The reflex 325 mg — does the evidence still support it before the cath?
Pediatric fever without source in the post-PCV era: How much has the risk landscape actually changed, and does your workup reflect it?
RSI in traumatic brain injury: Ketamine, fentanyl, and the ICP conversation — what the current data says
The Hallway Consult is built for EM clinicians who want the useful version of the literature. Forward it to a colleague if it helped.
— The Hallway Consult team