AKI Consult: 👵 ➡️ ED with severe DKA. CT Abdomen and Chest to look for infectious trigger: negative. Tx with IV insulin and balanced crystalloid + 6 L with obvious improvement. Cr was 2.7

Remained oliguric, now in sudden shock with increasing NE dose (0.5 ucg/kg/min) 🚨 1/12
#POCUS Very hyper-dynamic🫀 with increased contractility and no RV dysfunction.

🔎 Look carefully at color of flow exiting the LV:

Aliasing (green color): This means ultrasound system is trying to image an event that is occurring faster than the sample rate

This means flow is fast. But how fast? Choose the CW doppler setting and find out!

In this case acceleration was almost 6 m/s!

Flow acceleration occurs in the setting of obstruction (similar to putting your finger on the hose exit)

So what is causing the obstruction? 3/12
Aortic stenosis is one possibility, if you look at #POCUS 👆 aortic valve looks normal.

In the setting of a hyper-dynamic LV, Dynamic Obstruction of the Left Ventricular Outflow Tract (DOLVOT) should be the first thing that comes to mind!


DOLVOT can occur suddenly whenever there is
🚨Decreased LV filling volume🚨

Predisposing mechanisms:

Asymmetric septal hypertrophy
Sigmoid septum
Motion wall abnormalities (including 🐙)
Systolic anterior motion of the mitral valve (SAM)


Decreased LV filling is always secondary to any of this three variables:

⬇️ Preload: Hypovolemia, Obstruction (RV failure w interdependence)

⬆️ Contractility and Heart Rate: Beta agonist, Norepinephrine

⬇️ Afterload: Sepsis

As such, treatment should focus on:

⬆️ Preload: Fluids.

*sometimes this is enough if the cause is hypovolemia (attached case)

⬆️ Afterload: Alfa agonists with no inotropism

⬇️ Contractility and heart rate: Beta Blockers


In this case, even though cause was not clear, I started fluid bolus and stopped NE.

Then...the patient had abundant GI bleeding 🩸🩸🩸

We aggressively resuscitated with fluid and blood products. Patient improved immediately 8/12
However, one hour later we were back at square one:

Patient was in shock again!

Did patient need more fluid? I performed #LUS: Clear B-lines. Even thought patient is still fluid responsive. She is no longer fluid tolerant!!!

I was not keen on continuing fluids... 9/12
I ordered AngioCT to rule out active recurrent bleeding.

No bleeding.

However diverticulitis with abscess formation was diagnosed!!

Not previously seen because of lack of IV contrast 🤦‍♂️
We started antibiotics and vasopressin (⬆️ afterload with no inotropism). *IV beta-blocker was not available at the moment (public hospital shortage).

Fortunately, vasopressin did the trick and patient improved and oliguria resolved! Repeat #POCUS showed DLVOTO resolution 11/12
💎DLVOTO is easy to diagnose (CW Doppler)
💎Norepinephrine should be avoided at all costs
💎Although these patients improve rapidly with fluid,
💎Treat with Phenylephrine + IV BB

Bonus: Always use IV contrast even in AKI! @PulmCrit

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More from @ArgaizR

16 Feb
Pt w advanced liver cirrhosis. 🏥 Comes w worsening ascites. No fever🤒, no bleeding🩸. 🧠 ok, no asterixis. BP 91/50. Labs📈: AKI (Cr 3.0 mg/dl), UNa 7 mEq/L, bland sediment. #POCUS 👉small cirrhotic liver with significant ascites. Paracentesis ruled out PBE. 📊Poll below👇 1/11
What would your initial treatment be? 2/11
Don't treat reflexively. A thorough physical exam ♥️🩺revealed a systolic murmur at left lower sternal border. Neck exam 👇

Sitting Down (90º) /// Supine (45º) 3/11
Read 11 tweets
10 Feb
📞 Nurse: Patient has a blood pressure of 226/118 mmHg!
📞 Resident: Nifedipine 30 mg STAT!
📞 Me: About that last call, please hold Nifedipine until we assess the patient

A 🧵of some cases of Inpatient Hypertension 👇 1/15
🔎🖥️..This was a pt w ARDS on IMV. Other vitals 🆗. Previous BP= normal, no recent change in sedation, vent 🆗, no asynchronies. UOP = 0 for 2 hrs 🤔. Exam: Distended bladder!

After foley catheter change, BP normalised 😎

Why do we have this reflex to treat acute high BP? 2/15
A big component is the perceived expectation that we must do something! (In our minds, Are we trying to prevent organ injury?)

A great example can be seen here 👇 3/15

Read 15 tweets
16 Oct 20
Elderly ♂️, PMH of T2DM and CKD.

Suspected COVID-19 because of shortness of breath. Sent to the COVID-19 ED service.

No fever, no cough. No chest pain. Physical exam with patient sitting up (almost 90°):

¿Is this neck pulse arterial or venous? 1/8
Pulse is diffuse and the most striking feature is inward movement. I borrowed this table from @AndreMansoor's must-see lecture on Jugular Venous Pulse **Curiously, notice that there is a single peak instead of the expected double peak 🤔 2/8
I had to get my probe! #POCUS showed severely reduced EF with anterior wall motion abnormality and normal RV function.

EKG showed anterior ST segment changes. This was ACS! Cath lab was activated

Read 8 tweets
6 Oct 20
A case for hepatic vein Doppler lovers:

ECG tracing not abvailable on the ultrasound machine (I tried, I swear)

Can we still interpret this HV waveform without ECG?

I speculate we can!

I'll try to do it step by step: 1/7
What can we tell?

For one, there are 2 retrograde waves and 1 antegrade wave.

Given the patient was in sinus rhythm, then one of the retrograde waves MUST be an A wave! 2/7
Given HV waveform sequence should always be A-S-D, AND A wave is always retrograde:

Then this leaves only 2 possibilities: There could either be S wave reversal or D wave reversal 3/7
Read 8 tweets
5 Oct 20
Back on COVID-19 service this month

Went to see this patient with "increased respiratory drive despite high dose sedation and NMB". This is the vent: 1/4
Looking at the patient's monitor, the respiratory curve seems oddly coincident with heart rate: 2/4
Inspiratory pause reveals NO respiratory drive and several cardiogenic oscillations! 3/4
Read 4 tweets
14 May 20
🧵 AKI and #COVID19

68 yo ♂️ PMH obesity, HTN, CAD w stent, OSA, T2DM
➡️ ED w SOB + fever 39.9°C. Poor oral intake

RR 40, Sat 94% Room Air, BP 157/74 HR 124. Alert. Bibasilar crackles

Labs: Cr 1.3 (baseline 0.8), WBC 10, K 5.4, HCO3 17, CK 184. UA and CXR👇 (case from @NEJM)
How would you manage this AKI initially? What is the likely cause of AKI in patients with #COVID19? (this last question discussed in thread 🧵)
No easy answer except to say that FENa is very unlikely to be useful. It is not unreasonable to try fluids for AKI in the setting of perceived hypovolemia. However, this gets complicated when the potential for worsening ARDS exists. I'll try to tackle the answers one by one 💪
Read 17 tweets

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