I want to talk about REMAP-CAP and the Oseltamivir data. I disagree with stopping of the trial [on the data that I have], and I think the reporting of this should have been accompanied with a preprint or more information. First, this is clearly an unexpected result

Facts, now proven in a MC-RCT.

ARISE-FLUIDS has arrived and it's awesome 🥳 For over a decade, the Surviving Sepsis Guidelines recommended that septic patients get at least 30 cc/kg fluid. In the United States, these guidelines were weaponized into performance metrics, pressuring clinicians to prescribe arbitrary volumes to every patient. Evidence-based clinicians have LONG known that this guideline lacked evidentiary support. For example, I've attached a picture of a blog I wrote about this back in 2017. Despite the lack of evidentiary support and some evidence of harm, the Surviving Sepsis Guidelines INSISTED on perpetually recommending 30 cc/kg fluid resuscitation. We finally have a prospective RCT demonstrating that mandating early administration of 30 cc/kg fluid (as compared to early vasopressors) doesn't help and may actually cause harm. It's important to note that all of the hard endpoints in this trial were neutral (e.g., mortality, days free of organ support). I still think that 30 cc/kg fluid is a pretty reasonable volume of fluid for *most* patients. But the study does suggest that giving too much fluid may promote edema - so we should be *thoughtful* about this intervention rather than mandating it for every septic patient. Based on the subgroup analysis, the fluid-conservative strategy may have helped the subgroup of pneumonia patients the most. This is statistically nonsignificant but aligns with my expectation. ARDSy patients often don't respond well to fluid. (In contrast, I really doubt that a liter of fluids in either direction matters for most urosepsis patients.) This is a great example of the over-reach of guidelines and protocoled medicine. People get all upset about practice variation, so sometimes they try to stomp it out using guidelines and protocols. But these guidelines are highly fallible, so what may occur is that you standardize care in a way that harms everyone equally. 🤦‍♂️

REMAP-CAP Oseltamavir arm: Let me preface this by saying that I've never been a big oseltamivir fan (seriously, who is?). I'd love to see oseltamivir proven ineffective so I'd never need to argue about it ever again. But I don't think the math here works. Applying a Fisher's exact score to the mortality difference yields a p-value of 0.17 which is nowhere *close* to statistically significant (by any standard). I'm increasingly tired of seeing these studies where the p-value is ginormous but the study claims to be a slam-dunk (98% risk of harm!). Stopping a trial prematurely for harm with a p-value of 0.17 will ultimately lead to a lot of confusion about what this study means (spoiler alert: probably not much). Hopefully the manuscript will clarify this, but the math doesn't seem to be mathing. If you're going to claim 98% certainty of a result, then the results should be consistent regardless of how you run the statistics. Just to be clear, I despise oseltamivir, but I'm worried that we're going down a slippery slope when a Bayesian wonderland somehow converts p=0.17 into 98% certainty.

I love POCUS and ECG. For interest, lets take a look at this case from more of an ECG perspective (with extra analysis of these ECGs by the Queen of Hearts @PMcardioApp): 1st ECG: 1⃣ NSR with RBBB 1⃣To my eye this is nonspecific (could be PE, CTEPH, or ischemia). 1⃣ The queen doesn't see ischemia either. But she does flag this as reduced LVEF (<40%) which is unexpected and should be a red flag that something weird is happening. 2nd ECG: 2⃣ RBBB has resolved and now we can discern ischemic STE with TWI in V1-V4. Resolving chest pain and emerging TWI suggest that he may have experienced a transient occlusion overnight with re-perfusion. 2⃣ Could the right precordial TWI be due to PE? It's possible but less likely. Absence of TWI in the inferior leads argues against PE. Significant STE with mild TWI seems more consistent with MI than PE. 2⃣ The queen flags this as a high-risk NSTEMI with 88% probability and continues to flag a reduced LVEF. 2⃣ At this point it's increasingly clear that we're dealing with LAD-territory ischemia. Transient LAD ischemia explains the transient RBBB seen on the 1st ECG (septal perforators from the LAD perfuse the right bundle). The queen keeps on telling us the EF is low. Cardiac cath needed. In retrospect, I think the RBBB pattern may have camouflaged a subtle Wellens pattern in the first ECG. Overall, the ECG and echo data play out in parallel.

Do PPIs cause COPD exacerbations? Meh. I doubt it. PPIs are perpetually being *correlated* with poor outcomes, because they tend to be taken by multimorbid patients. But PPIs are rarely proven to *cause* adverse events. Over the years there have been a TON of these associative studies that got LOTS of interest, but subsequently aren't shown to be true (e.g., PPIs have been implicated in causing dementia, renal failure, hip fracture, MI, pneumonia, etc.). Getting back to PPIs and COPD: A meta-analysis of prospective RCT data suggests that PPIs might even *reduce* COPD exacerbations (Yu et al PMID 35252272). Although very limited, this is the only prospective RCT data we have. I don't think a retrospective study correlating PPIs with COPD exacerbations should affect clinical management (especially given the history of such studies rarely sustaining the test of time). Of course, if the patient doesn't have a good indication for PPIs, then PPIs should be stopped! Indeed, unnecessary PPIs serve an index of thoughtless medical care (yet another source of confounding!).

broomedocs.com/2026/06/rant-… Lactate - evolution is smarter than us? #FOAMed

Sepsis AKI bradycardia home beta blocker or CCB = BRASH syndrome. Anand Swaminathan, MD (@emswami) from ResusX:ReUnion: This isn't an OD — their kidneys just stopped clearing the drug. Standard pressors won't work. What's your next move at the bedside? Comment below.👇

True x 1000. This is the disconnect b/w GDMT evangelists and every day HF care. Never forget: trials enroll the best pts. Table 1 tells an important story

VZV pneumonia 😳 Epidemiology: 🧑‍🤝‍🧑 Usually occurs as a primary infection in someone not previously exposed or vaccinated. 🧑‍🤝‍🧑 Tends to be more severe in pregnancy, older age, or immunocompromised states. Key clues: 🔍 "Chicken pox" rash: Usually starts on the trunk and spreads to the face and extremities. 🔍 CT shows a random distribution (miliary pattern) of nodules ~1-10 mm in size. Nodules are often ill-defined, or surrounded by ground-glass halos. Diagnosis: 🧬Send skin fluid from vesicles for PCR. 🧬Honestly I'd probably consult dermatology because rashes are hard for intensivists (inadequate exposure). Treatment: IV acyclovir (start empirically if high index of suspicion; PCR may take 48 hrs to turn around). Prognosis: Mortality in ~15% of hospitalized patients.

SOHO trial in NEJM: 🏙️ Multicenter RCT comparing high-flow nasal cannula vs. low-flow oxygen among patients with acute hypoxemic respiratory failure (mostly pneumonia) 🏙️ Inclusion criteria required a respiratory rate >25 and substantial hypoxemia (P/F <200) 🏙️ No difference in the primary endpoint of mortality (not surprising, the mortality endpoint is nearly always neutral in modern RCTs evaluating the nuances of supportive care). 🏙️ HFNC reduced the rate of intubation and increased the number of ventilator-free days. 🏙️ No significant signals of harm from HFNC. This is similar to the FLORALI trial (by the same group of investigators). However, FLORALI showed *improvement* in mortality, whereas the current study didn't. Why do these studies disagree about mortality? The FLORALI trial found no mortality difference between HFNC versus conventional oxygen among ALL PATIENTS. However, it DID find a mortality difference in the *subgroup* of patients with P/F <200. So this is a classic tale in critical care - a subgroup analysis from one trial subsequently fails to replicate. (At least, in terms of the mortality benefit.) But chasing mortality in these trials is a fool's errand. Overall, the SOHO trial still supports the use of HFNC in acute hypoxemic respiratory failure (in terms of reduced intubation and improved ventilator-free days). Using HFNC for sick pneumonia patients is already standard care, so I don't see this changing practice very much. Keep calm and HFNC on. 🌬️

diffuse subendocardial ischemia from GI bleed make sure to call GI & provide volume/blood resuscitation immediately avoid calling cardiology up-front (this may scare away GI) key: repeat ECG should normalize after resus troponin may go uncomfortably high

apixaban would have been pharmacokinetically superior in renal failure it's curious how this editorial very subtly implies this, while skirting gingerly around the issue it avoids using the word "apixaban" these editorials often seem biased in favor of the trial & sponsor