Tweetorial attention attenuation–updated

My first Tweetorial has turned into my second most popular tweet, only behind:

A tale of two tweets:

Twitter analytics provide a unique opportunity to look deeper than just who saw the original tweet. By checking the analytics of each subsequent tweet in the stream we can see how many people trudged all the way to the end.So how did the hyponatremia tweet stream do? Here are the analytics from the first to the last tweet.The Y-axis is “Impressions.”This is not impressions like Symplur does (used to do?). This is not the tweets multiplied by the number of followers. Twitter is in the unique position to know how many times any particular tweet is delivered to a device. So your cousin who lost her twitter password in 2014 and the sock puppet account that Eugene Gu abandoned in medical school don’t get counted as impressions. The first Tweet had 47,000 impressions. The second had 5,700. That first step is a doozy.From there things were surprisingly stable. Hey Dr V, let’s see a blog post track who reads to the end of the post.More than 3,000 people read pretty much the entire stream. I am quite satisfied. 3000 people is a lot of grand rounds.

 

Update

Some people have wondered about the second drop in participation that occurs at tweet 31.

I think the answer is here:

When you click on the initial tweet, you can see tweets 1-30, but to get the last 5 you need to click on the “5 more replies” link.

The final bump is due to a surge of people tweeting in celebration of completing the tweet stream:

 

How to search Twitter

And this from NephJC by Nimra Sarfaraz.

And the all important advanced search link: https://twitter.com/search-advanced

My first Tweetorial: When salt tablets work in hyponatremia (and when they do not)

I hope you like my first tweetorial

I recently saw a patient with hyponatremia and cirrhosis. He had been started on salt tablets to try to correct the hyponatremia. In a limited number of diagnosis salt tablets can help hyponatremia. Cirrhosis is not one of them. I created this Tweetorial to teach some basic hyponatremia physiology and clear up when they may work and when they will not.

This is my first shot at a Tweetorial. I wrote out the tweets in Apple Notes. I think I will use a spreadsheet with a character counter next time. Too many of my Tweet-length thoughts ended up being a bit too wordy. Having a counter during creation would help.

I also should have more links and pics.

Additionally, I bought the domain Tweetorial.org. Any ideas what I should use it for?

 

Rise of the Tweetorial

One of the interesting developments in MedTwitter has been the chained tweet to demonstrate a point. I think the master of this is Professor Darrel Francis.

This one is nicely relevant to this week’s NephJC:

Another famous innovator of the Medical Tweetorial is Vinay Prasad. Vinay smartly collects the first tweet to his Tweetorials in a pinned tweet.

https://twitter.com/vinayprasadmd/status/1007337958846783488?s=21

Another master of the Tweetorial is Tony Breu. He, similarly, collected his Tweetorials in one place.

This one has relevance to nephrology. Brilliant explanation.

Speaking of relevance to nephrology, Swapnil has thrown his hat in the Tweetorial ring

Paul Sufka has joined the party focusing with a focus on rheumatology:

Here is Bryan Vartebedian’s take on this development. His problems with the rise of the tweetorial can be summed as:

  • Poor indexing and search means these tweetorials will not be able to be found later.
  • Using 280 character tweets to convey 500-word ideas is a mismatch between the medium and message. These ideas would be better conveyed in a blog post rather than chopped up into beads of text to be strung together.
  • MedTwitter is a just a small sliver of the medical community and doing tweetorials traps the ideas in this small box.

In his conclusion, Vartabedian hedges a bit, but it is clear he believes in the blog:

I firmly believe that all of us should be poking at these applications to discover their most creative uses. But what any of us think is less relevant than what sticks with the public community of physicians. The market will bear this one out.

I love Sufka’s lessons on ANA. Prasay’s thread is a bold call to action that challenges the medical industrial publishing complex. It’s an important reminder that we are the publishers and no longer live in a permission-based system of launching ideas to the world.

We just need to remember that there’s a big medical world and a whole lot of eyeballs beyond our Twitter space. Let’s put our brilliance in the right place.

The new divide

When I was a fellow at University of Chicago, just after the turn of the century, I did literature searches and then divided my PubMed bounty into articles I could download directly and those articles I would need to stalks the stacks to retrieve from hardcover bound versions of the journal. Any article in the latter group needed to be really important for it to be worth the extra-effort.

It was bits versus atoms. Bits were so much easier to gather, manage, and organize that it affected the information I would collect.

This artificial division largely fell away as more and more of the archives were moved to electronic format and the stuff that was trapped in atoms became less relevant as it faded further and further from the current time. Today, effectively all the medical literature exists as bits.

The new barrier is not between bits and atoms but between open access bits and paywalled bits.

See this exchange:

https://twitter.com/akshayakeerti/status/1011754523663261698?s=21

We may be moving to a world where if you want to be read (and to be cited) you will need to publish in open access journals.

Unintended consequences: Oxalate nephropathy and bariatric surgery.

Near the end of Swapnil’s sweeping summaries of the renal denervation articles for this week’s NephJC, he discussed safety. In the trials, the procedure was remarkably safe but Swap brought up possible future consequences. These are adverse events that could never be measured in a real-world trial:

Renal denervation is permanent. Blood pressure medications can be stopped. Why does this matter? Maybe if a patient subsequently develops sepsis or hypovolemia? The sympathetic system exists for a reason….See this case report. In this study of sheep with CKD, bleeding caused a much more severe drop in blood pressure.

This reminds me of bariatric surgery. We had been doing Roux-en-Y for weight loss for decades (See meta-analysis) when, in 2005, Nelson published a case series of calcium oxalate stones, including a couple of cases of ESKD with dialysis dependence due to oxalate nephropathy. Their work was backed-up in this report.

A massive meta-analysis ofover 700(!) studies of weight loss surgery from 1990 through 2002.

Oxalate nephropathy is secondary to increased oxalate absorption following the Roux-en-Y procedure. There are two theories as to why this is:

  1. Fat malabsorption, one of the goals of the therapy leads to saponification of intestinal calcium. Since calcium is unavailable to bind and trap oxalate in the gut more is available for passive and active oxalate absorption in the distal ilium.
  2. Decreased bile acid reabsorption in the gut leads to unconjugated bile salts damaging the luminal membrane and increased passive oxalate absorption.

Additionally the malabsorption leads to diarrhea and metabolic acidosis. This decreases urine pH and lowers urinary citrate both of which promote calcium oxalate stones. There is also a decrease in urine volume of about 0.5 liters, further increasing the stone tendency of these patients. Dr. Park defined a lot of this in a prospective study of 24-urines after Roux-en-Y.

I have seen patients with ESKD from Roux-en-Y. It is horrible. Since the primary pathology has not ceased, these patients are at risk for the same oxalate nephropathy following a transplant, making a transplant a risky procedure.

Though oxalate nephropathy after Roux-en-Y does occur, obesity itself is a risk factor for ESKD and bariatric weight loss appears to protect patients from this.

From Chang et al. Kidney International Reports 2017 2(2): 261-270. (Another good reference on ESKD risk after bariatric surgery)

This good news tempered with the risk of disaster makes the decision to go for bariatric surgery a bit more nuanced than it is often portrayed. Does renal denervation have similar future land mines just waiting to be exploded in the future? We have no idea what unexpected horrors from renal denervation lie undiscovered.

E-mail from my first trip to Kidney Week

My wife and I celebrated out eighteenth anniversary last night. We went to dinner in Windsor. While we were in line waiting to cross back into the US, Cathy found and read some of our e-mails back and forth from the first few years of courtship.
Here is one that I sent from my very first first trip to Kidney Week, which wasn’t even called that back then.
From: Joel Topf
Date: October 25, 1998 at 2:59:00 PM EST
To: Cathy
Subject: I met my hero

Cathy, the conference is awesome. I’m having fun.

I just met Burton Rose. He’s the reason I’m going into nephrology. It was a moving experience.

I’ll call you later
love you
always
j

Hyponatremia fan fiction

I think I may have buried the lead in the last blog post. Perhaps this imaginary conversation will clarify what is so important about the George et al study.

Nephrologist: There are now clinical practice guidelines, based on expert opinion, that tell us to correct sodium no more than 8 mmol/L in the first day of hyponatremia.

Internist: That seems cautious. How well are we meeting those guidelines?

Nephrologist: Well in a recent multi-center, retrospective analysis, of nearly 1500 people with an initial sodium below 120, just over 40% went too fast.

Internist: FORTY PERCENT were too fast. Oh my god! We’re doing horrible!

Nephrologist: Yeah, it’s kind of embarrassing.

Internist: So what happened to the 600+ people where the speed limit was exceeded?

Nephrologist: Well, they found 9 people had osmotic demyelination on MRI. But none of them had any documented permanent neurologic deficits and none of them was diagnosed with central pontine myelinolysis.

Internist: So how many people could we help if we worked on protocols, education and training to get that 40% closer to 5 or 10%?

Nephrologist: Well, since with a 40% miss rate we couldn’t find any harm, I guess we couldn’t expect much improvement with a 5 to 10% miss rate.

Internist: We should probably put our energy elsewhere.