A huge accomplishment for our Transplant Program, performing the first fully robotic liver transplant in Boston and New England.
Both the recipient hepatectomy and implantation of the donor liver were performed entirely using robotic techniques through small incisions.
this is a perfect crystallization about my feelings on Bayesian stats 😍
as clinicians, we interpret everything through a Bayesian lens
but the initial analysis should be a no-nonsense frequentist analysis without any BS
then let ME apply MY priors to reach my conclusion
I am all for retrograde intubation, but this feels like just experimenting on patients. This is not an airway or patient where this is clearly indicated.
Retrograde intubation is an undervalued technique that is easy to learn and perform. In the absence of a VL, we conducted training on retrograde intubation for the EM residents. After the session, they were already able to independently perform the procedure successfully.
Surviving Sepsis 2026 is here & it's even more loony tunes than I was expecting.
They're promoting pre-hospital ABX & preemptive broad-spectrum IV antibiotics for intubated patients.
This insane fever dream is an antimicrobial stewardship nightmare.
Embarrassment for SCCM.
The absolute worst thing about the proliferation of 'AI' is being forced to stop using em dashes. I love them, but I've started editing them out to avoid any doubts as to the provenance of my text.
I had patient in cardiac arrest who was receiving CPR and was mouthing "stop" only to have us stop and find he was asystolic but then wake up when we re-started compressions.
Has anyone else encountered this?
(We gave him sedation)
Pan CT following cardiac arrest has become my routine practice for the past 6 years. Why?
1. Their heart stopped --> we need to figure out why.
CT can identify unexpected or difficult to diagnose causes. e.g. PE, pancreatitis, abdominal catastrophe
2. They were just assaulted for X min with CPR . I've seen flail chest, hemothorax + liver/spleen lacerations. They have thoracoabdominal trauma.
3. CT head identifies catastrophic brain injuries (not early gray-white loss or edema which doesn't mean much if done right post ROSC) but rather massive bleeds or sometimes even strokes.
I operationalize it as a CT head non-contrast, CT chest with PE protocol, and then CT abdomen with whatever phase they can get after everything else.
Of course, I do not delay transfer to cath lab or OR if there is a specific indication (e.g. STEMI vs. bleeding) but will get a CT after the cause has been reversed in those cases.
Analytical interference (i.e., "false-positives") in troponin assays is well described. Usually due to fibrin clots, heterophile antibodies, rheumatoid factor or ALP.
I agree with many points in this post but would push back on the use of the term “false-positive” troponin.
Theres no such thing.
ANY elevated troponin is abnormal.
The question is what is the mechanism (i.e. atherothrmobsis vs injury).
#tropomania#FOAMed#meded
Increasing a pressure gradient does reliably increase flow if everything else is held constant, which is not always true in real life.
By definition:
- Spatial pressure gradients give a net force (−∇p).
- Pressure “pushes” on boundaries (it’s the fluid’s normal stress).
12/
If gradients were causes, then simply increasing a gradient would reliably increase flow.
But in physiology:
• gradients often rise while flow falls
• congestion can coexist with poor perfusion
• pressure can be high when throughput is low
That alone tells you gradients are reports, not drivers.
(2/3) First, critical to recognize that if unaddressed this patient WILL die. Not may. WILL.
They have severe microcirculatory dysfunction and macro-circulatory collapse being compensated with high doses of pressors.
Why despite thrombolysis? Once a patient with a PE is thrombolysed, RV failure may be in its own cascading death spiral. Also, the PA pressures do not decrease immediately (these can take hours or even days) due to residual clot AND pulmonary constrictive mediators.
Thrombolysis is the START of management for massive PE but certainly not the end.
This is my general approach and then I will go through the logistics.
1) Defend MAP (MAP >65 for RV perfusion)
2) If in arrythmia, try to fix (e.g. Afib). If slow, speed up (HR 90-110 ideal)
3) Add inotropes. If hypotensive, I like epinephrine > milrinone/dobutamine given less vasodilation
4) Add a pulmonary vasodilator (e.g. NO/prostacyclins/inhaled milrinone). If not intubated, I use inhaled milrinone (5mg neb Q4-6h)
5) Consider and activate MCS EARLY. There is a >50% chance that the patient described above requires MCS despite everything, don't wait until they are arresting.
For this patient I tried 20mcg of epinephrine as a push and saw an excellent hemodynamic response. Immediately started coming down on norepinephrine and started a epinephrine drip at 10mcg/min.
With this, the cap refill didn't improve much.
Next, while waiting for inhaled NO we nebulized 5mg of inhaled Milrinone through the vent.
Finally, the patient had been going in/out of Afib with dorpping pressure in Afib so gave a bolus of amiodarone and started and infusion.
We had a honeymoon period for 2-3 hours while the patient seemed to recover... cap refill 3-4 seconds... mottling improved... lactate steady however, called over to the bedside for "junctional rhythm".
Heart rate was now 60. Huge takehome is that bradycardia (or normocardia) in acute RV failure is a patient about to arrest.
We quickly called back the cardiac surgeons (they were already aware) and cannulated the patient for VA-ECMO.
The best part about VA-ECMO For massive PE is that it immediately decompresses the RV and in typically is only required for a short period of time (24-48 hours).
We decannulated 36 hours later, extubated the next day, and the patient made a full recovery.
(take homes below 👇)
interesting piece on overuse of gabapentin
my pointers on this:
[1] pts absolutely can withdraw from gabapentin so you can't stop it cold turkey
[2] gabapentin is renally cleared; accumulation due to AKI is a common cause of hypoactive delirium
https://t.co/eI1YaqHxk4
So... I'm actually pretty fine with my tax dollars saving the life of someone who's bleeding out on the emergency room floor. I think that's a good idea.
Sometimes the reason for the upgrade is not purely the underlying pathology, but a mismatch between the current resources (e.g., nursing ratios, patient location) and the patient acuity.
See the patient and give your colleagues the benefit of the doubt.
When you're pushing back on an ICU upgrade, please remember that someone who knows the patient better than you do felt uncomfortable with the patient's current level of care.
If you say no, you need to be incredibly confident that nothing is wrong.
Tip 1: Just go see the patient.
When somebody is calling the intensive care unit in the hospital, they are calling for help. We are the 911 for hospitalized patients.
Even if there may not be a clear ICU indication based on your initial phone call with the referring physician or nurse, just go see the patient.
Often I find that we can still improve patient care for those patients even if they don't need vasopressors, ventilator, or inotropes. Often they are quite sick, and our expertise managing sick patients can be very useful.
In 2025, we need to move away from the restricted notion that the intensive care unit expertise only pertains to ventilators, vasopressors, and inotropes.
We are experts in managing acutely unwell patients even before they require ICU, so we should lend our expertise to help patients anywhere in the hospital.
1/
Most people think the heart drives circulation.
But what if that’s backwards?
Anderson’s model flips the whole idea of cardiac output on its head — and it changes how you think about fluid, flow, and failure.
🧵👇
#physiology#FOAMed#MedTwitter#criticalCare#cardiacOutput