Magician and pharmacist. views my own
Joined April 2016
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MagicPharm retweeted
Wait… Penicillin V—how did it get its name? 🤔💊
Well… it’s confidential. 🤫😂
The “V” stands for vertraulich, the German word for “confidential” or “secret.”
Penicillin V was the first oral penicillin, developed in 1951.
The name may have reflected an effort to keep the important new development confidential while this orally active penicillin was being developed. 🤫
📚 Antibiotic names have stories!
Wow—this is an amazing, comprehensive review! 🤩
They explore the origin and history behind the names of virtually every antibacterial and antifungal.
🆕🔥🟢 Review | #OFID
What’s in a Name? Etymology and History of Antibacterials and Antifungals
There are so many tables! 📚
I summarized them into 2 infographics 🦠🍄
Check it out! ✨👇 academic.oup.com/ofid/articl…
MagicPharm retweeted
Interesting study comparing dexmedetomidine vs olanzapine for ICU delirium.
There are a lot of limitations which make this study more hypothesis-generating than definitive:
🤔 Single-center
🤔 Combined patients with hypoactive delirium & hyperactive delirium (common & major problem with these studies)
🤔 Dexmedetomidine dosing is low (0.1-0.7 ug/kg/hr)
The mortality difference favoring olanzapine is statistically dubious. However, it's provocative that haloperidol has similarly been found to associate with improved mortality in some RCTs (see fresh meta-analysis by Cheng PMID 40114217)
What is my take-home message from this study & the Cheng et al. meta-analysis?
🥡 Antipsychotics (haloperidol, olanzapine) appear to be safe and effective for the treatment of hyperactive delirium. Haloperidol arguably has the best track record for safety & efficacy at this point.
🥡 Dexmedetomidine is a sympatholytic agent that can cause hypotension and bradycardia. It's NOT a good choice for patients with heart failure, cardiogenic shock, or baseline bradycardia. (Seriously, STOP throwing dexmedetomidine around in cardiac patients, this drives me bananas.)
🥡 Asking which drug is "better" for delirium is probably the wrong question - you need to *match* the right drug with the right patient at the right dose. 🔑
MagicPharm retweeted
If you have ever heard, read or written the phrase “the patient is edematous but intravascular dry”, you have to check this review (doi.org/10.1186/s13054-023-0…) 👇
Fluid normally exchanges freely between the plasma and interstitial space and is returned to the “central circulation” primarily via the lymphatics. In disease states, such as sepsis, the return flow of fluid from the interstitial space to the plasma seems to be very slow, which promotes the well-known triad of "hypovolemia + hypoalbuminemia + peripheral edema"
The authors discuss studies suggesting that there two key mechanisms contributing to this triad:
(1) acute lowering of the interstitial pressure by inflammatory mediators such as TNFα, IL-1β, and IL-6 and,
(2) nitric oxide-induced inhibition of the intrinsic lymphatic pumping
As you know, fluid is filtered in the (pre-)capillary side and reabsorbed at the post-capillary end, right? Well, not really...
According to the traditional model historically taught in introductory physiology and medical school (I still remember it...), in the precapillary (arteriolar) end, the high capillary hydrostatic pressure exceeds plasma oncotic pressure, causing net filtration of fluid out of the vessel into the interstitial space. In the post-capillary (venular) end, the hydrostatic pressure drops below plasma oncotic pressure, creating a net pressure gradient that causes reabsorption of ~90% of the filtered fluid back into the vessels. The remaining ~10% was thought to be drained by the lymphatic system
According to the modern model (established via the discovery of the endothelial glycocalyx), in most tissues under normal, steady-state conditions, there is no sustained venular reabsorption. The endothelial glycocalyx layer acts as the primary semi-permeable filter. The effective oncotic gradient exists between the plasma and the subglycocalyx space, rather than the main interstitial fluid
Under normal blood pressure, capillary hydrostatic pressure exceeds the effective opposing oncotic pressure across the entire length of continuous capillaries and post-capillary venules. Consequently, virtually all fluid filtered at the capillary level is picked up by the lymphatics, which then route the fluid through lymph nodes and return it to the venous system via the lymphatic ducts.
Some exceptions exist in specialized vascular beds designed for continuous fluid absorption, such as the intestinal mucosa and renal peritubular capillaries. Also direct vascular reabsorption may occur temporarily during acute, severe drops in capillary hydrostatic pressure (e.g., severe hypovolemic shock or hemorrhage) to preserve plasma volume
#foamed #foamcc #physiology
MagicPharm retweeted
Nunca se había aleatorizado el oseltamivir en el paciente crítico con influenza.
REMAP-CAP acaba de hacerlo.
Y el resultado no solo es "no funciona": es probable que aumente la mortalidad a 90 días.
Hilo sobre un preprint que va a incomodar 🧵
1/15
MagicPharm retweeted
ARISE - A neutral trial is not a neutral message
The ARISE FLUIDS trial compared two approaches to early septic shock: giving less fluid and starting vasopressors earlier, or giving more fluid before moving to vasopressors.
The result was described as neutral. Patients in both groups had the same median number of days alive and out of hospital at 90 days.
It would be easy to conclude that the choice between fluid and vasopressors does not matter.
That would be the wrong lesson.
Read about it here fluids.info/news/arise-a-neu…
MagicPharm retweeted
Hyperfiltration is highly prevalent in critically ill older adults. The Cockcroft–Gault equation substantially underestimated actual kidney function, even without meeting the augmented renal clearance criteria. buff.ly/p3FHilh
MagicPharm retweeted
#CCR26 Read the MARCH trial for yourself here nejm.org/doi/full/10.1056/NE…
Join the discussion here or at criticalcarereviews.com
MagicPharm retweeted
🩻Contrast-induced AKI:
one of the biggest myths still shaping clinical decisions
For decades we were taught:
👉 “Contrast damages the kidneys”
👉 “Avoid CT with contrast in CKD”
👉 “Hydrate, protect, delay imaging if needed”
But what if… most of this is wrong?🤔
->The uncomfortable reality
Modern evidence shows:
👉 Low-osmolar contrast rarely causes true nephrotoxicity
👉 Even in CKD, AKI, and ICU patients
👉 The risk is often overestimated—or nonexistent
So where did the fear come from?
📍 1950s high-osmolar contrast (actually toxic)
📍 Poorly controlled observational studies
📍 “Creatinine rise = contrast injury” assumption
👉 Correlation became causation
👉 And the dogma stayed
⚠️What recent data tells us
✔ No difference in AKI rates with vs without contrast
✔ No benefit from bicarbonate, NAC, or aggressive hydration
✔ Even ICU and AKI patients show no worsening outcomes
->Translation to real life
👉 The patient was going to develop AKI anyway...Not because of contrast!!
->The real problem: “Renalism”
👉 Avoiding necessary imaging
👉 Delaying diagnosis
👉 Choosing inferior tests
And that leads to:
❌ Missed PE
❌ Delayed sepsis source control
❌ Worse outcomes
->Clinical mindset shift
Instead of asking:
👉 “Will contrast harm the kidneys?”
We should ask:
👉 “Will NOT doing the scan harm the patient?”
->Who still deserves caution?
✔ eGFR <30
✔ Severe hemodynamic instability
✔ Multiple nephrotoxins
Even then:
👉 Optimize volume
👉 Minimize dose
👉 Don’t delay critical imaging
🤓Bottom line
✔ Contrast nephrotoxicity exists… but is rare
✔ The fear is bigger than the risk
✔ The harm of NOT imaging is often greater
In critical care
👉 We don’t treat creatinine
👉 We treat patients
And sometimes…
👉 The most dangerous thing is NOT the contrast
👉 It’s hesitation.
📃Reference
Florens N, Demiselle J.
Kidney360 7: 445–449, 2026. doi: doi.org/10.34067/KID.0000001…
ALT
MagicPharm retweeted
As an allergist who manages drug allergy regularly in clinical practice. I am glad we have a real data now discussing further. Traditionally, patients labeled as allergic to penicillin have often been considered allergic to the entire penicillin class. However, when you closely examine the chemical structure of piperacillin–tazobactam, it becomes clear that it has a different R1 side chain, making cross-reactivity less likely from a structural standpoint.
Unfortunately, guidelines still treat penicillin allergy as a contraindication to piperacillin–tazobactam use. In my view, the safest and most reasonable approach is to discuss the case with an allergist and perform an assessment, that includes drug allergy testing and, when appropriate, a supervised challenge. In practice, I have found that when you are working with a strong ICU or internal medicine team, they are often willing to help facilitate this approach effectively.
Is piperacillin-tazobactam safe in patients with penicillin allergy?
🆕🔥🟢Piperacillin–tazobactam tolerability in patients with a labeled penicillin allergy (PIPPEN)
Of the 191 patients included, 98% were found to tolerate one or more doses of piperacillin–tazobactam.
This included 95 patients with “low risk delayed reactions,” 90 patients with “high risk anaphylactic reactions,” and 2 patients with “well-documented delayed reactions,” to penicillins. Only four patients out of 191 had documented intolerance to piperacillin-tazobactam post-exposure
All patients in the “anaphylactic allergy or anaphylactic like reaction” subgroup tolerated one or more doses of piperacillin–tazobactam.
cambridge.org/core/journals/…
MagicPharm retweeted
breaking news from @TheOnion:
due to irreconcilable differences between SCCM & ACEP, SCCM now recommends that *all* sepsis resuscitation be done in the back of an ambulance, followed by direct admit to ICU.
“this frees us up from following evidence we don't like” said the SCCM
🎙️ New podcast episode! Find out why ACEP declined to endorse a new set of guidelines for treating sepsis in EDs. ACEP Pres. Tony Cirillo, MD, FACEP explains why it’s important that EPs have an accurate standard of care to treat sepsis in the ED. 🔗 ⬇️
bit.ly/41wMNDS
MagicPharm retweeted
"the humility of uncertainty" in guidelines. If you want to make a recommendation creating a standard of care, you damn well better have reproducible high quality evidence behind it. If not, write a review summarizing pros and cons of options & admit none of us know for sure.
MagicPharm retweeted
proposal: IV lacosamide loading in the ICU is safe in patients with asymptomatic 1st degree AV block (PR >200 ms)
I encounter a lot of anxiety surrounding this, but the fear doesn't seem to be evidence-based
Other drugs we use in ICU are much more likely to cause bradycardia
MagicPharm retweeted
🧵 Albumin in Critical Care: 70 Years, 700 Papers… Zero Benefit
1/
Albumin is the most studied fluid in critical care.
Decades of trials. Endless meta-analyses.
And yet – not a single clinically meaningful benefit.
Here’s why the entire theory collapses once you understand Extended Starling. 👇
🤖 Made with AI
MagicPharm retweeted
The math on this project should mass-humble every AI lab on the planet.
1 cubic millimeter. One-millionth of a human brain. Harvard and Google spent 10 years mapping it. The imaging alone took 326 days. They sliced the tissue into 5,000 wafers each 30 nanometers thick, ran them through a $6 million electron microscope, then needed Google’s ML models to stitch the 3D reconstruction because no human team could process the output.
The result: 57,000 cells, 150 million synapses, 230 millimeters of blood vessels, compressed into 1.4 petabytes of raw data. For context, 1.4 petabytes is roughly 1.4 million gigabytes. From a speck smaller than a grain of rice.
Now scale that. The full human brain is one million times larger. Mapping the whole thing at this resolution would produce approximately 1.4 zettabytes of data. That’s roughly equal to all the data generated on Earth in a single year. The storage alone would cost an estimated $50 billion and require a 140-acre data center, which would make it the largest on the planet.
And they found things textbooks don’t contain. One neuron had over 5,000 connection points. Some axons had coiled themselves into tight whorls for completely unknown reasons. Pairs of cell clusters grew in mirror images of each other. Jeff Lichtman, the Harvard lead, said there’s “a chasm between what we already know and what we need to know.”
This is why the next step isn’t a human brain. It’s a mouse hippocampus, 10 cubic millimeters, over the next five years. Because even a mouse brain is 1,000x larger than what they just mapped, and the full mouse connectome is the proof of concept before anyone attempts the human one.
We’re building AI systems that loosely mimic neural networks while still unable to fully read the wiring diagram of a single cubic millimeter of the thing we’re trying to imitate. The original is 1.4 petabytes per millionth of its volume. Every AI model on Earth fits in a fraction of that.
The brain runs on 20 watts and fits in your skull. The data center required to merely describe one-millionth of it would span 140 acres.
MagicPharm retweeted
another patient death due to mythological fears about contrast dye.
modern contrast dye for CT scans doesn’t harm the kidneys.
definitive imaging saves lives.
get a contrast CT, save your patient’s life, don’t get sued.
emcrit.org/ibcc/contrast/
MagicPharm retweeted
For nearly 20 years, women have been warned about using codeine while breastfeeding, largely on account of a single case report. The Lancet has now issued an Expression of Concern about that paper.
MagicPharm retweeted
Coroner raises concerns after a prescribing error in hospital led to the death of a baby, after being wrongly prescribed sodium acid phosphate instead of sodium chloride
#PFD #medicinessafety #prescribingerror
pharmaceutical-journal.com/a…
MagicPharm retweeted
“Is IL-6 inflammatory or anti-inflammatory?”
That question sounds basic.
But if you don’t understand it, tocilizumab side effects will always feel like paradoxes.
Let me tell you the IL-6 story the way biology actually works.
IL-6 was not designed to cause disease.
It evolved as a repair cytokine.
When tissue is injured or infected, IL-6 is released to:
• alert the liver
• organize immunity
• protect epithelial barriers
• help tissue heal
This is why IL-6 rises early -before damage spreads.
But IL-6 does not act alone.
How it signals matters more than how much is present.
IL-6 has three signaling pathways, and each creates a different clinical reality.
First: Classic signaling
IL-6 binds its membrane receptor, then signals through gp130.
Only a few cells can do this:👇
hepatocytes, macrophages, neutrophils, gut epithelium.
What happens clinically?
CRP rises.
Infection is contained.
Mucosal barriers heal.
Micro-injuries seal.
This IL-6 is protective and regenerative.
Second: Trans-signaling
When inflammation persists, the IL-6 receptor is shed into the circulation.
Now IL-6 can signal on almost any cell - endothelium, fibroblasts, astrocytes.
This changes everything.
Blood vessels leak.
Th17 cells expand.
Inflammation spreads beyond its original site.
Same IL-6.
Different door.
Now pathogenic.
This is the IL-6 you see in RA, GCA, vasculitis, chronic synovitis.
Third: Trans-presentation
This one is subtle and dangerous.
Dendritic cells present IL-6 directly to naïve T cells.
They don’t just activate immunity — they program it.
T cells become Th17.
Tregs are suppressed.
Autoimmunity becomes self-sustaining.
This is why diseases like NMOSD or autoimmune encephalitis keep relapsing.
So IL-6 is not good or bad.
IL-6 heals through classic signaling,
inflames through trans-signaling,
and sustains autoimmunity through trans-presentation.
Now the drugs make sense.
Tocilizumab blocks the IL-6 receptor.
That means it blocks all three pathways.
This is why it works so well:
• arthritis improves
• vasculitis quiets
• NMOSD relapses fall
But it also explains every major side effect.
Take the gut.
The intestine is constantly injured — food, bacteria, pressure.
It survives because it repairs itself continuously.
One of the key repair signals?
👉 IL-6 via classic signaling
When you block that:
micro-injuries don’t heal,
ulcers deepen,
the wall weakens.
Inflammation is silent because CRP is suppressed.
That’s why intestinal perforation on tocilizumab is late, quiet, and catastrophic.
Not excess inflammation.
Loss of repair.
The same logic explains:
• low CRP during sepsis
• muted fever
• delayed infection diagnosis
• lipid rise without CV risk explosion
These are not off-target effects.
They are on-target IL-6 biology.
Now compare the drugs.
Siltuximab binds IL-6 itself.
But IL-6–antibody complexes accumulate.
Clearance is impaired.
Efficacy in autoimmunity is limited.
Tocilizumab blocks everything , powerful, but non-selective.
Olamkicept blocks only IL-6 trans-signaling.
It preserves repair and acute-phase defense.
Once you understand IL-6 pathways,
you stop memorizing side effects
and start anticipating them.
#TheIL6Paradox #Immunology #Rheumatology #MedTwitter @DrAkhilX @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1 @nileshnolkha
MagicPharm retweeted
#TBL 483: RSI: Ketamine or Etomidate for Tracheal Intubation of Critically Ill Adults
thebottomline.org.uk/summari…
Article by @JonathanCaseyMD
Review by @precordialthump
#FOAMed #CCRDownUnder
MagicPharm retweeted
🆕⚡💊 A SNAP Moment — Flucloxacillin Variability Raises a Wake-Up Call to Shift Toward Safer MSSA Options(FLUTE study) |JAC 2025
🚀 What they did
🔬 Retrospective study of 203 hospitalized patients receiving flucloxacillin.
🧪 Measured unbound flucloxacillin ≥48h after starting therapy and compared levels with PK/PD targets (4–10× MIC).
🩺 Assessed links between high unbound levels and nephrotoxicity 🧨 & neurotoxicity ⚡.
👀 Identified patient groups who may benefit most from TDM.
🔥 Key findings
🎯 Only 33% reached target levels.
🟦 35% were too low → underdosing.
🟥 32% were too high → toxicity risk.
⚠️ Toxicity thresholds:
🚨 Nephrotoxicity ≥10 mg/L (66.7% affected).
⚡ Neurotoxicity ≥21 mg/L (46.2% affected).
🧓💧 Most high-level patients had eGFR <50 mL/min, showing classic accumulation.
⚠️ Limitations
🏥 Single center.
📚 Retrospective design.
🔍 Timing of level collection not fully standardized.
💡 Takeaway
Renal impairment + high daily flucloxacillin doses = strong candidates for TDM to prevent AKI and neurotoxicity. With only one-third of patients achieving target levels, this SNAP moment highlights growing evidence pushing us toward safer MSSA options (cefazolin, cephalexin, cefadroxil) where appropriate.
#IDXposts #IEWiki
academic.oup.com/jac/article…
