BC HEALTH
Saved by @CodyyyGardner

“Should I give them more fluid?”

Extremely common question during AKI referrals from junior docs.

⛔️ Fluid management is tricky, often misunderstood, & can cause huge iatrogenic harm ⛔️

We try to convey important principles in THREAD 👇

#tipsfornewdocs #medtwitter #tweetorial

 Currently too often patients with high creatinine are given too much IV fluid, driven by an AKI ➡️ fluid reflex

We’ve seen 7 litres be given in one shift.

Medics & surgeons, juniors & seniors, it seems everyone loves to reach for extra IV fluid (especially if urine output poor)
Why does huge volume IV fluid ‘resuscitation’ consistently occur?

Lots of reasons, including FALSE beliefs:
🛑 IV fluid always “treats AKI”
🛑 Hypotension = hypovolaemia
🛑 Lactate >2 means fluid deficiency
🛑 Septic patients are very hypovolaemic
The rule with IV fluids and AKI is to remember this 5 word phrase:

💥 💥 Aim for euvolaemia, then stop💥 💥

Fluid status is like Goldilocks - hypovolaemia is bad for the kidneys BUT excess volume is also harmful for renal function and will cause other complications too.
It is easy to say “target euvolaemia” - but we agree it is more difficult to do!

Fluid status assessment is certainly made harder by a belief that we must only rely on a snapshot assessment of examination features which are NOT specific / sensitive / reliable to elicit like.…
🔹 Cool peripheries
🔹 Bibasal crackles - highly nonspecific in older patients!
🔹 Dry skin
🔹Tachycardia
🔹 x and y descent of the JVP wave…..

Even postural BP drop, one of the better performing signs for hypovolaemia, still has a wide differential diagnosis.
Serial physical examinations by one clinician improves assessment, but this is challenging given shift patterns.

And unfortunately the blood tests can be misleading too - for example check out our previous post about other causes of raised urea 👇 https://t.co/CSiRRnMi1a
TIP - things get better when the adage of ‘history trumps examination’ is observed:

1️⃣ Has there been volume loss?
2️⃣ Has there been decreased intake?

If the answer is “not really” to both of these, then think carefully about what you think more fluid will accomplish.
So….

When phoned as renal reg on-call on day 2-3 we’re usually not thinking “easy hypovolaemic AKI” but are concerned something is being missed.

Three common things:

1. AKI is part of sepsis / hypotension / MOF badness: patient needs ICU & vasopressors, not more IV fluid
2. AKI is intrinsic or post-renal: patient needs a diagnosis (think urinalysis, ultrasound, discussion), not more IV fluid

3. AKI is an additional signal that palliative care may be appropriate (remember stage 3 AKI has terrible 42% mortality at 30 days in patients >75 years)
Pre-renal AKI purely due to hypovolaemia generally improves fast.

If the patient has a great story for hypovolaemia but their creatinine is rising/stuck, then they often have a degree of acute tubular necrosis (ATN).

Let us show you something (it’s not as boring as it appears!)
On left is ATN with gaping spaces in tubules, & on right is healthy kidney with nice plump tubules.

Appreciate that there is actual histological change - this needs TIME to recover

✳️ Just as injured cells in stroke or MI don’t magically heal with IV saline, neither does ATN ✳️
✅ Sometimes you’ll get a patient with ATN to euvolaemia & they still won’t pee. That’s OK - not an indication for more fluids

✅ Remember low urine output is a warning you have less margin for error before causing hypervolaemia - again, shake off the reflex just to ⬆️fluid rate
“Are there exceptions?”

Not really - there’s different risk:benefit in different scenarios
👉 in tumour lysis, myeloma or rhabdo for example we do try to target higher urine outputs

BUT when patient is well-filled & not peeing much, we’re re-thinking rather than ploughing on.
“But does volume overload even matter?”

YES - and it’s not just the obvious pulmonary oedema badness.

Excess fluid ➡️ high venous pressure ➡️ decreased perfusion pressure for heart, brain, liver (& kidneys!!)

Patients with excess volume have:
🛑 longer AKI
🛑 higher mortality
In hypovolaemic AKI aim to stop fluids before complications develop - you do not need to “swell to get well”.

Avoidable dialysis for ⬆️volume continues because of myth that the hugely complex pathophysiology of AKI is easily remedied by IV salty water (pic from Ostermann et al)
So apologies for the rant. But we hope we have made you think about why:

🛑 “I can’t give fluid for their AKI because they are already overloaded” makes no sense 🛑

And why:

🛑 “I’ll keep giving IV fluids until their oxygen sats drop” is just bonkers 🛑
Take home points:

✅ Prescribe IV fluid with the care you would warfarin
✅ Achieve euvolaemia, then sit on your hands
✅ If urine output or BP stays low think “Is a different approach needed here?” rather than autoreaching for more IV fluid
✅ Break your AKI ➡️ fluid reflex
As ever all comments/disagreements very welcome - it’s a tricky topic to teach & not done really at med school, so we at @BukuRenal (@jamiekwillows this time) appreciate any feedback.

Would love to hear views on how you approach teaching ward junior docs @NephroGuy @icmteaching

More from Health

Tony Breu
Tony Breu
@tony_breu
1/16
Why do B12 and folate deficiencies lead to HUGE red blood cells?

And, if the issue is DNA synthesis, why are red blood cells (which don't have DNA) the key cell line affected?

For answers, we'll have to go back a few billion years.


2/
RNA came first. Then, ~3-4 billion years ago, DNA emerged.

Among their differences:
🔹RNA contains uracil
🔹DNA contains thymine

But why does DNA contains thymine (T) instead of uracil (U)?

https://t.co/XlxT6cLLXg


3/
🔑Cytosine (C) can undergo spontaneous deamination to uracil (U).

In the RNA world, this meant that U could appear intensionally or unintentionally. This is clearly problematic. How can you repair RNA when you can't tell if something is an error?

https://t.co/bIZGviHBUc


4/
DNA's use of T instead of U means that spontaneous C → U deamination can be corrected without worry that an intentional U is being removed.

DNA requires greater stability than RNA so the transition to a thymine-based structure was beneficial.

https://t.co/bIZGviHBUc


5/
Let's return to megaloblastic anemia secondary to B12 or folate deficiency.

When either is severely deficient deoxythymidine monophosphate (dTMP*) production is hindered. With less dTMP, DNA synthesis is abnormal.

[*Note: thymine is the base in dTMP]

https://t.co/AnDUtKkbZh
HEALTH , PATHOPHYSIO
Ary Serpa Neto
Ary Serpa Neto
@a_serpaneto
The #RELAx trial has been published today in @JAMA. It was coordinated by Anna Algera. This thread is to explain the rationale, what we did, the findings and the meaning.
The rationale of #RELAx is based on the following

First, there is NO adequate evidence on the level of PEEP in non-ARDS patients. Most of the studies are old, conducted in post-surgical patients (short-term ventilation), and were not powered to detect differences in patient-centered

Second, despite the absence of evidence, the levels of PEEP used in non-ARDS patients increased over years, from 5 to 7/8 cmH2O, probably as a reflection of studies and practice in ARDS

Third, one IPDM showed that higher levels of PEEP could benefit more severe ARDS patients. However, opposite trends (higher mortality and longer ventilation) were found in mild ARDS with higher PEEP (despite not powered to be statistically

Fourth, most of the weaning protocols include PEEP ≤ 5 cmH2O as a criterion for readiness to wean. Theoretically, a standardized liberal strategy of higher PEEP could delay weaning in some
HEALTH
Advertisement
Noah Sasson
Noah Sasson
@Noahsasson
Before we get too far into 2021, I thought I’d write a thread recapping some of the research that came out of my lab in 2020. Most of this work was led by my talented team of graduate students, Kerrianne Morrison, @kmdebrabander, and @DesiRJones.

Back in January, a news story was published about Kerrianne’s study showing improved social interaction outcomes for autistic adults when paired with another autistic partner.

A detailed thread about the study and a link to the paper can be found here (feel free to DM me your email address if you’d like a copy of the full paper for this study or any of our studies):


Another paper published early in 2020 (it appeared a few months earlier online) showed that traditional standalone tasks of social cognition are less predictive of functional and social skills among autistic adults than commonly assumed in autism research.


Next, @kmdebrabander led and published an innovative study about how well autistic and non-autistic adults can predict their own cognitive and social cognitive performance.
HEALTH
AutisticSciencePerson
AutisticSciencePerson
@AutSciPerson
Okay, let's start this hypersomnia thread!

[note - I am not looking for unsolicited advice.]

Idiopathic hypersomnia or narcolepsy (not the same, but similar) is very hard to describe to people.

When I say "I slept 10 hours last night and I'm still tired" I'm not bragging. 1/16

For me, the accommodations I need are about time. My body doesn't care what I want to do - when I want to wake up or be asleep. My body wants to wake up at 10-11am, and go to sleep at 3am, always.

Just a one hour shift in my sleep schedule can screw me up for days. 2/16

When I tell people that I'd really "prefer it" if we could meet at 10am or later, it's because getting up before that has consequences for me. Big consequences. Most people won't see them. Sometimes I still give in and say it's fine. It ruins 2-3 of my days, sometimes more. 3/16

Let me explain. When I am required to wake up at 9am, esp. in covid times working from home, my body pays me back for it later.

I'm going to show you ways this happens. I can usually withstand 1 day of waking up early, with some consequences, but 2 days in a row kills me. 4/16

Let's say this graph represents Day 1, the first time I am required to get up early. The y-axis is my level of Sleepiness. Any symptom listed higher up includes that symptom + every other symptom below it. Getting up that early means I can't listen or concentrate all day. 5/16
HEALTH
Leandro Steinberg
Leandro Steinberg
@lean_stein
🧵 on Importance of correct indication of colonoscopic surveillance studies (English 🇺🇸🇬🇧)
@KM_Pawlak @KMonkemuller @drkeithsiau @JacquelineChuMD @PerelmansPearls @stevenbollipo @SWexner @DrBloodandGuts @ebtapper @DCharabaty @RashidLui @AdvaniRashmiMD @AtoosaRabiee @DrMohdZein

@GI_Guy @RodriguezParra_ @DrHarryThomas @TennysonMD @AustinChiangMD @KralJan @thomaskroner @alinkmd #GITwitter

1/ The implementation of screening and surveillance programs can reduce the incidence and mortality of

2 / But for these to be effective and to guarantee protection against CCR, they must meet a series of conditions. One of them is the correct indication for endoscopic studies for both screening and surveillance.

3 / According to a recent meta-analysis, the minority of patients who undergo colonoscopies have a correct indication, with less than 50% adherence to the surveillance intervals proposed by scientific
HEALTH

You May Also Like

Dr. Jane Clare Jones
Dr. Jane Clare Jones
@janeclarejones
So, on the subject of bonkers hyperbolic pretzeling over the Bell judgement, Grace 'destroy books I don't like & make inappropriate jokes about sterilising teenage girls' Lavery has some thoughts.

Tell me why my feminism is wrong Grace.

Oh

Well, if anyone thought the Bell judgment was going to make TRAs reconsider making massively overblown claims with no evidence backed up with nothing but a thick wadge of emotional blackmail.... HAHAHA, no one thought that.


A high court in the UK made a delimited judgment about teenager's ability to consent to puberty blockers. This puts all trans people everywhere in the world at risk.

Because if any human anywhere has any thoughts that deviate in any way from the rote line dictated by

the trans rights movement, this puts all trans people everywhere in mortal danger.

Let's be honest Grace. It doesn't put trans people at risk. It puts trans ideology at risk. Because trans ideology depends on the idea of innate gender identity, and the trans child is the

necessary material evidence of the ontology of gender identity.

That is, children are being medicalised to provide evidence to underwrite adults identities.

Nothing to see here.
LAW
Noah Smith
Noah Smith
@Noahpinion
Remember: Just because an idea is old doesn't mean it's good.

Knowing whether old ideas are more likely to be good requires understanding whether conditions have changed in important ways.

Horse archery was an amazing method of warfare for over a thousand years...then people invented guns, and suddenly this great idea that had stood the test of time became obsolete.

Then again, when underlying conditions don't change much, tried-and-true approaches are probably better.

"Learning the lessons of history" usually just means assuming ergodicity and stationarity in an informal time-series model...

(end)
SOCIETY
Advertisement
Elon Musk\u2019s Meme \U0001f171\ufe0fot
Elon Musk’s Meme 🅱️ot...
@theMemesBot
Thats a gg, Satan
FUN
Paul M Domenick\U0001f43a
Paul M Domenick🐺...
@PaulMDomenick
10 Signs of Social Intelligence 🧠

1-Smile
2-Good posture
3-Strong eye contact
4-Fluid hand gestures
5-Let’s others talk more
6-Listens & relates
7-Comfortable Touching people
8-Walk with a swagger
9-Speaks at slower pace
10-Keeps calm under criticism

[ QUICK THREAD ]


1-Smile

How do you feel when you see someone that looks angry?

It’s a downer

No one will want to interact with you if you look pissed all of the time, it’s just negative energy

Plus, smiling is a sign of confidence and boosts others moods


2-Good posture

Don’t walk Into any social setting looking like the hunchback

It’s weak and makes you look low energy

Plus, you’re displaying low status with weak posture

Stand up straight with your chin up & chest out like a god

Walk like you’re proud of yourself


3- Strong eye contact

Ever shake someone’s hand & their eyes are either looking down or darting?

It’s weak & you probably won’t trust them

Or in conversation?

Eye contact while talking means you’re listening and paying *Attention*

Strong eye contact displays confidence


4-Fluid hand gestures

Use your hands to talk & express your points

Don’t stand there like a robot

Using the hands can make what you’re talking about exciting

It can also be used to emphasize

Exciting = positive emotion

Remember, making people FEEL is what’s important
LIFE
sriram
sriram
@SriramKannan77
Swami Ramanujar:
Important personalities in Sri Ramanujas Life :
🌸ASURI KESHAVA SOMAYAJI-Father of Sri Ramanujar .Asuri keshava somayaji was a learned brahmana living in sriperumbudur.


🌸KANTHIMATHI-Mother of Sri Ramanuja. Kanthimathi was the sister of sri periya thirumalai nambi .
🌸SRI YAMUNACHARYA-Acharya of Sri Ramanuja.Also known as Alavandar.
🌸THIRUKOKOSHTIYUR NAMBI-Also known as Ghosti Purna.He instructed the Rahasya Traya to Sri Ramanujar.

He lived in thirukoshtiyur.
🌸THIRUKKACHI NAMBI-Kanchi purna was born in puvirunthavalli near kanchipuram and met the young ramanuja at an important time.He did the service of Lord Varadha.

🌸THIRUVARANGA PERUMAL ARAIYAR-Important acharya lived in srirangam and rendered the service of playing music for lord Sriranganatha.

🌸PERIYA THIRUMALAI NAMBI-He was the maternal uncle of Sri Ramanuja.He taught sri ramanuja about the epic of sri ramayana and other ithihaas and puranas.Served sri venkateswara at tirumala.
ALL