If you are a resident looking for a nephrology fellowship take a moment to consider St John. We are a small nephrology fellowship that values hand-crafted nephrology education. Ascension St John hospital is a 714 bed hospital that is literally on the border of Detroit and Grosse Pointe. Yes, that Grosse Pointe.
This provides us a steady stream of patients with diverse backgrounds. St John operates a busy ER with a healthy mix of trauma. We get people from the upper socioeconomic classes and their unique presentations and diseases. Importantly, especially for a community program, St John is big enough to offer all the services:
ECMO
CRRT
Plasma exchange
Red and white cell pheresis
Acute PD
Kidney transplant
We still do our own biopsies. We have our own interventional nephrology suite, where we place tunneled venous catheter, provide fistulagrams, and do access angioplasty for our hemodialysis patients.
But the most important part of our fellowship is that we are not a rough and tough, traditional, malignant program. We take a gentler, kinder approach to medical education. Over the last few years we have decoupled our reliance on fellows to do the work of nephrology. It wasn’t trivial and it required buy in from the entire staff but we realize that treating fellows as worker mules was not good for their education. This uncoupling means fellows will be busy, experience requires being busy, but we don’t let our fellows get overwhelmed by the work. Our program takes fellows by the hand and guide them through a bespoke education track to provide them with a top notch nephrology education. Regardless of how unsteady or unsure you are about your kidney knowledge, we will turn you into a first rate nephrologist. That’s our promise.
So if you have finished your interviews but still haven’t found the program that feels like home, check us out.
Perianayagam, A. et al. (2008) ‘DDAVP is effective in preventing and reversing inadvertent overcorrection of hyponatremia’, Clinical journal of the American Society of Nephrology: CJASN, 3(2), pp. 331–336. https://cjasn.asnjournals.org/content/3/2/331
Gharaibeh, K. A. et al. (2015) ‘Risk factors, complication and measures to prevent or reverse catastrophic sodium overcorrection in chronic hyponatremia’, The American journal of the medical sciences, 349(2), pp. 170–175.
The initial infusion rate (mL/hr) of 3% saline can also be simply calculated as a product of patients’ weight (kg) and desired correction rate (mEq/L/hr)
Sood, L. et al. (2013) ‘Hypertonic saline and desmopressin: a simple strategy for safe correction of severe hyponatremia’, American journal of kidney diseases: the official journal of the National Kidney Foundation, 61(4), pp. 571–578. https://www.ajkd.org/article/S0272-6386(12)01471-0/fulltext
Rafat, C. et al. (2014) ‘Use of desmopressin acetate in severe hyponatremia in the intensive care unit’, Clinical journal of the American Society of Nephrology: CJASN, 9(2), pp. 229–237. https://cjasn.asnjournals.org/content/9/2/229
Mohmand, H. K. et al. (2007) ‘Hypertonic saline for hyponatremia: risk of inadvertent overcorrection’, Clinical journal of the American Society of Nephrology: CJASN, 2(6), pp. 1110–1117. https://cjasn.asnjournals.org/content/2/6/1110
Morris, J. H. et al. (2018) ‘Rapidity of Correction of Hyponatremia Due to Syndrome of Inappropriate Secretion of Antidiuretic Hormone Following Tolvaptan’, American journal of kidney diseases: the official journal of the National Kidney Foundation, 71(6), pp. 772–782. https://www.ajkd.org/article/S0272-6386(18)30004-0/fulltext
One of the most distressing things I am seeing is conspiracy-minded conservatives in the US doubting the mortality numbers from the COVID pandemic. I really get upset as these people try to gas light the nation and convince people that COVID wasn’t that bad. And that people are just inflating the numbers for political gain.
I round at a number of dialysis units. At one unit, I cover the first shift. First shifts are popular. Lots of people want to do their dialysis first thing in the morning and have the rest of their day to themselves. I have 20 odd patients on that shift and every couple of months I’ll get a new patient when a chair opens up. This happens when a patient moves, transfers to another unit, gets transplanted, or unfortunately, passes away. Openings on the first shift are rare and they don’t stay open for long.
I distinctly remember going to round at this unit in late May and almost immediately seeing a new face. So I started my routine, new dialysis patient, spiel, “Hello, my name is Joel Topf and I’m going to be your doctor here…”
And then a few chairs down, I saw another new face, “Hello, my name is Joel Topf and I’m going to be your doctor here…”
And then a bit later, “Hello, my name is Joel Topf and I’m going to be your doctor here…”
And once again, “Hello, my name is Joel Topf and I’m going to be your doctor here…”
I met as many new patients on that one day as I typically get on that shift in a whole year. Each of those new faces represented a patient lost to COVID.
We are not lying about the disease.
We are not exaggerating the dead for political gain.
I lost momentum on the COVID diaries, but today as some people are gas lighting the severity of the COVID-19 pandemic I want to finally publish a couple of posts that I started but never published.
As COVID-19 was raging through Italy one of the storylines that made it back to our shores was the number of docs that were getting sick. The number of doctors who were dying. A scary thought entered my head, in the form of a Twitter poll (it is strange how many of my thoughts are arraigned as tweets)
How many doctors at your hospital will die before you start thinking about heading for the hills?
A. Zero. I’m thinking about bugging out now
B. 4
C. 18
D. Infinity. I ain’t no coward.
I asked the question in a group chat but never on open twitter as it felt too inflammatory. My feeling was that it was less the number and more who got sick. The closer you were to the poor doc on the vent in the ICU the more terrifying it would be. Thankfully Ascension St John didn’t lose any doctors, nurses, or employees. But we did have people get sick. A lot of them.
Early in the epidemic we had an outbreak in the cardiology department. At least 8 of the cardiologists got sick and two of them were hospitalized. I don’t know how the ‘Rona spread through their department, but that gave a sense of how fast the disease could spread without precautions.
The housestaff (residents and interns) were also hit hard. Fully twenty-five percent of the internal medicine residents missed work because of COVID-19.
One in four
Thankfully none of them had to be hospitalized.
Probably another dozen doctors in the department of medicine got sick. A number of them were hospitalized, but no one died. Not because we were good, but because we were lucky.
My father is an oral surgeon and the program director of the oral surgery residency at St John and Beaumont Hospitals. His chief resident got COVID-19 and perished. I was on-call in a hospital full of Covid-19 patients when my dad called to tell me. It was startling and focused the mind. After that I found my self calling old friends just to say “hi.” Kind of getting my personal affairs in order, you know, just in case.
Looking back at the docs that got infected, it is noteworthy that the vast majority of infections were early in the epidemic. They were all in late March and early April. The time when we didn’t know what we were doing. I remember seeing videos on how to take off and safely store your mask between COVID patients.
Those halcion days when we thought we could label patients as COVID and NOT COVID. As soon as that lunacy went away and we just started wearing our mask all the time the infections among the staff melted away. It was a stark before and after experiment, but to my eyes masks worked.
If you have a patient with cerebral edema from acute hyponatremia you need to 3% Saline first and ask questions later.
3/ If patients have hyponatremia and have severe symptoms it is 150 ml of 3% then recheck the sodium and give another 150 ml of 3% (I’m using the European guidelines)
This means if the hyponatremia is causing the vomiting, then you have severe symptoms and it is 3% time. But if the vomiting is causing the hyponatremia, that doesn’t automatically indicate severe symptoms and you will need to dig deeper.
4/ The goal of acute mgmt is to raise the Na by 5 or stop the symptoms, which ever is quicker. If you have raised the Na by 5 and they are still seizing, then it is probably not the low Na causing the seizure and you need to 👀 deeper. Algorithm from
Step one check the serum osmolarity (and get a repeat sodium, just to make sure it wasn’t a lab error)
7/ Since we are looking at a low sodium we expect a low osmolarity (don’t worry about the difference between osmolality and osmolarity, anyone who is a stickler about that is being a dick)
If we don’t find a low osmolality something weird is going on:
7b/ Low sodium with a normal osmolarity: Lab error from too much protein (IVIG, multiple myeloma) or too much fat (High lipids or triglys) in the blood. This throws off some lab machines.
(Specifically but not point of care iStats or ABG laboratories)
7c/ Low sodium with a high osmolality: this is usually due to hyperglycemia (but can be seen with mannitol, glycine and other edge cases). The hyponatremia is real, but due to another osmotically active particle (glucose in most cases) the are no consequences to the hyponatremia
8/ So that leaves the true hyponatremia. Low sodium and low osmolarity. The branch point here is:
What is the urine osmolarity?
The urine osmolarity tells us if the kidney is causing the hyponatremia or just unable to correct the hyponatremia (despite the best intentions)
9/ The urine osmolarity is less than 100 (maybe up to 150 or 200 if the patient has CKD). This indicates a lack of ADH and a kidney that is doing its best to correct the hyponatremia. The problem is not the character of the urine but the amount. Right urine, not enough.
9b/ The differential for low sodium, low serum and urine osmolarity is short:
9c/ In low Na, low serum and urine osmolarity the urine is getting rid of excess water but the kidney cannot make enough urine because:
• Kidney failure (low GFR)
• T & T / Beer drinkers (lack of solute)
• Psychogen polydipsia (you are drinking faster than you are peeing)
10 Low sodium, low serum osm, high urine osm. This is ADH dependant hyponatremia. The kidney, stimulated by ADH, is causing the hyponatremia by generating free water. Making more urine here, just makes the Na fall further.
10b/ ADH can be 𝗽𝗵𝘆𝘀𝗶𝗼𝗹𝗼𝗴𝗶𝗰 due to low volume or a perceived low volume state:
Low volume states: GI losses like diarrhea or vomiting; renal losses like diuretics
High volume/low perceived volume: heart failure, liver failure, nephrotic syndrome
I remember the first days of nephrology fellowship. It was exhilarating. It was terrifying. All through residency, when you came across a patient that had you stumped you could just call the consultant. Now I was the last line of defense. I was on the receiving end of that phone call and I did not feel up to the task. I remember those months as being among the most stressful of my career. I started carrying around a small bottle of Pesto-Bismol to fight the stress induced gastritis.
I felt like a drunk, walking out of the ICU to take little nips from “my little helper.” It’s a lot of self induced pressure to battle the imposter syndrome inherent in being a new fellow, especially one coming from an outside institution.
One of my first consults was a transplant patient. The patient had acute kidney injury (AKI) and hyponatremia. She had recently received IVIG and I was so excited that I figured out that her hyponatremia was due to pseudohyponatremia from the IVIG. (See
this letter to the NEJM). So it was particularly disheartening when the transplant surgeon was not impressed pseudohyponatremia diagnosis especially since I had not been able to make any heads or tails regarding the AKI. He made his displeasure quit clear. I felt pertty humbled going to my attending, Patrick Cunningham, but he said, “Let’s walk through the case” and quickly, and humanely, pointed out the possibility of osmotic nephrosis from the same IVIG I had already blamed for the hyponatremia.
Fellowship is hard. Be humble. Try hard. Read as much as you can. Ask for help. Every person we graduate is a competent nephrologist. You will be one too. Trust the system. Together we’ll get you there.
When it became apparent that COVID-19 would not just be a medical event that happened over there but was going to affect everything I started jotting some notes. They have remained in Drafts for over a month, but now I am going to start publishing these diary entries mostly just to document the strangest, most unexpected experiences of my medical career.
I have lost a lot of patients. We all have. A lot of them were people I never knew. Consults in the ICU with a patient intubated and sedated in kidney failure. You don’t get to know these patients. The ICU discouraged going into the room to examine the patient unless it was absolutely necessary both to protect us from infection, and to minimize consumption of personal protective equipment. There was no family at the bedside. No visitors in the waiting room. I have never had thinner connections to my patients. We worked hard to save them. Most of them died. I can only remember a few of them.
But there are patients I do remember.
The first patient that I Iost was a dialysis patient. She was an older lady that had been taking care of for a few years. I remember the last time I saw her. I was rounding in the dialysis unit and she was sitting in her chair, mask on, and I told her that I was seeing patients with COVID and that it was really bad. I told her not to believe Fox News telling people it was just like the flu. She nodded her head. She was in total agreement. he last thing she told me was to be careful. She lived in a nursing home. Nursing homes are COVID tinder boxes. A week later she was gone. 😥
Another dialysis patient was a young (my current definition for young is anyone born after 1969) man. He was a rabid Michigan fan. Every time I saw him he would be hot about the latest U of M athletics story. Satellite camps, Louisville forfeiting the championship over Michigan, trips to the Vatican, sleep overs in tree houses, Beilein leaving for the NBA, it didn’t matter how minor the issue he would get completely worked about it. I loved his passion. He was one of only a handful of my patients that still worked and he was an essential worker at a grocery store. And then one day…he stopped coming to dialysis. We sent the police to his house and he was gone. 😥
Not all of the hospital patients were so isolated. I remember an older gentleman who came in because he fell. He was tested in the ER because we are testing everybody. He tested positive. He had just a small oxygen requirement but he was otherwise nearly asymptomatic. I saw him the day after admission for some mild acute kidney injury. After my evaluation I asked him he needed anything and he asked if I could get him some grapes. One of the strangest asks I have received. I couldn’t. The next day he was moved to the ICU for intubation and a week later he was gone. 😥
I lost a few patients from my advanced CKD clinic. These are patients that I see every four weeks to fight for every milliliter of clearance as we try to hold off on dialysis. The mantra of that clinic comes from the first season of Game of Thrones, paraphrased.
What do we say to the God of Dialysis? Not today.
One that I lost was a patient I had been working with for years. I helped him lose weight after learning about weight loss medications on The Curbsiders. I think it was the first time I consciously changed my practice based on a podcast.
He used to come to clinic with his wife and sometimes with his school-aged kid. He was kind and gentle. A good guy taken too soon. 😥
Another long time patient was a woman who would come to clinic with her sister. I always saw them together. In my clinic. I the hospital. Always together. She had terrible heart disease and we were forever adjusting her anti-angina medications and diuretics. Sometimes winning, sometimes losing. She had tough disease but she was a fighter.
One of my favorite memories of her was she used to wear an iPod nano as a wrist watch for years before finally getting an Apple Watch. loved that look.
Another one taken too soon. 😥
Another patient was not a clinic patient, or a dialysis patient, but a patient with pretty bad CKD that our group knew from frequent admissions. He would repeatedly come in with decompensated CKD and we would nurse him back to health and not see him for a few months until he came in again. Then he came in with COVID-19. 😥
Then there was the man who was shot in the bely. We see too much of that in Detroit. He required all the resources of St John’s trauma center. He was going to make it. He was recovering , still sick, but recovering. Then COVID was everywhere. And he no longer was recovering. Nothing feels more like a failure than a lethal nosocomial infection. 😥
The transplant patient who came to the ER because they thought they had COVID. They didn’t. Sent home. Patient returns days later convinced they had COVID. They didn’t. Sent home. Returns a third time convinced they had COVID. This time they did. I don’t know where they got infected, but I think the ER waiting room was a possibility. Another lethal nosocomial infection. 😥
I already wrote about patients that we thought were wins but we ended up losing. Those hurt. 😥
Then there was another long-term patient of mine. Another one in the advanced CKD clinic. One we were fighting for every milliliter of clearance. Like Al Pacino in Any Given Sunday fighting for every inch.
That patient was admitted with a viral illness at the end of February. The swab was positive for influenza. We didn’t have much capacity to test for COVID-19 and the protocol said that a positive influenza test meant no test for COVID. But I wonder. I haven’t lost a patient to influenza for years. I know it happens, but I wonder if this patient was actually the first patient I lost to COVID-19. 😥
There have been others. Too many other. The numbers are still piling up. Just last week I lost six patients. Six patients. One week.
As the US death toll spirals past the total from Vietnam, I keep thinking about how my medschool roommate, Tim Lamb, described the Vietnam memorial
You start walking and there are just a few names and as you walk, step by step, the names pile up until you are surrounded by names. Drowning in death.
When it became apparent that COVID-19 would not just be a medical event that happened over there but was going to affect everything I started jotting some notes. They have remained in Drafts for over a month, but now I am going to start publishing these diary entries mostly just to document the strangest, most unexpected experience of my medical career.
After the second week of peak COVID; a week where I had my own COVID scare, worked har, lost patients, and had a Quarantine Zoom Seder; I was relaxing on twitter, feeling pretty good when the NEJM dropped the first data on Remdesivir. It was a report on the compassionate use program. One of our patients at St Johns had been part of the program. The data looked promising and it was being published in the highest journal of the land. I had seen the article after reading about it from one of the top doctors on Twitter, Eric Topol.
And after scanning the abstract, I quickly tapped out my 🔥-take.
It may not be my most populat tweet but it is certainly in the top 10.
It may have been popular but mostly at my expense. I was not ratioed, but it sure felt like it. Comments were about 10:1 opposed to my enthusiasm. Here are a few of the best:
My Tweet was the lead in coverage over the reaction to the study by WebMD. No, they didn’t reach out to me for comment.
So now it seems like I own remdesivir. See Waitzman’s comment when the Executive Deputy Editor of NEJM presented Grand Rounds at Beth Israel.
And this week, the study, and my tweet were part of The Curbsiders
And I was Exhibit A in the ID Journal Club Chat (#IDClub)
I think it was an unfortunate tweet made too quickly in the evening. I was hoodwinked by the authority of the NEJM and Topol. It probably dropped my credibly as a science communicator. But the importance of this moment is quickly approaching zero as placebo controlled remdesivir data (both positive and negative) begins to emerge. Live and learn. Tweet and move on.
When it became apparent that COVID-19 would not just be a medical event that happened over there but was going to affect everything I started jotting some notes. They have remained in Drafts for over a month, but now I am going to start publishing these diary entries mostly just to document the strangest, most unexpected experiences of my medical career.
After my first week in COVID land I was on-call and we adapted to the new crisis. That Saturday while on call I was very tired. This is not so unusual, call is tiring. But that night I went to bed at 9:30, that is unusual. I never go to bed that early. By the next afternoon I had a scratchy throat and I started to wonder if I had the ‘Rona. Monday morning I woke up with a headache, body aches and a sore throat. I definitely was having a viral syndrome. No fever though.
I texted one of my favorite ID docs, Miriam Levine, explained my symptoms and she suggest I take the day off and see how things develop. I should also get tested. I called employee health and they took my information and told me they would set up a test and call me back. No time though, just a vague promise that they would call me back. I decided to take matters into my own and get tested through the Detroit Health Department. They were running a drive through testing program at the State Fair Grounds. All you needed was a doctors order and through the magic of self prescribing I got myself an appointment for Tuesday.
The following day, I remained afebrile, the myalgias and sore throat had resolved. I went through the state fair grounds but when I arrived I realized I hadn’t actually written out the prescription for the test. I scrambled around my car and found a script pad but no pen. I tore off the top page and put the black script on the dashboard and hoped no one looked too carefully. Amazingly it worked and I got the brain biopsy, err nasal swab without a hitch. Later that day St John called me and gave me an appointment for testing the next day. That afternoon I did Telehealth visits for my CKD patients.
I also updated Dr. Levine, and she said that if I remained afebrile tomorrow I could return to work. So Wednesday, I went to the St John testing facility on my way to work. While the Detroit Public Health was a wham bam thank you ma’am test, St John had a much more traditional doctor experience, I came in, filled out forms, had an MA take a full set of vitals. Then a doctor came in and did a full history and physical culminating with an influenza swab as well as the desired COVID swab. Later that afternoon I got this text:
I have never returned a page so fast in my life. I was positive for Influenza A. I had previously been immunized so I had a really mild case without fever. The fatigue and viral syndrome I felt on over the week-end bleeding into Monday were real, but they weren’t the COVID. Fake COVID, FauxVID.
And if you are a doctor reading this, don’t send out texts like that.
PS On thursday my COVID came back negative and a week later the Department of Public Health called and told me I was COVID negative.
Every COVID week feels unique. The pandemic keeps reforming. This week I began to see patterns of admissions. I’m now thinking that they fall into one of a few types. And since I am a nephrologist and we love three letter acronyms married to a few subtypes I give you Covid Typical Admission (CTA) types 1-3
CTA Type 1 COVID Classic
The patient is either admitted with hypoxia or pretty quickly develops hypoxia. These patients have viral pneumonia and develop profound immune dysregulation. This week, here in Detroit, we are still seeing CTA Type 1 but at a much lower rate than what was crushing us a few weeks ago. A patient is admitted, and may even appear stable to go to the floor, but then they become hypoxic, get intubated, develop profound multi-system disease including ARDS, hypercoagulability, and often AKI. We sometimes can get them stable enough to begin a long, slow, recovery from ARDS or they die in an ugly cytokine storm.
CTA Type 1 Is really hard on the staff. I was talking to a resident because she was canceling a consult she had requested earlier because the patient had since been made comfort care. She commented, that’s it was her fifth death in two days. These kids are seeing more death compressed into a couple of months than I saw in my entire Med-Peds residency.
CTA Type 2. Come in. Get sick. Get better. Get sick again.
These patients are breaking my heart. I tweeted about this last week. (Boy, it feels like a month)
It is soul crushing to see a patient on the vent in kidney failure, and then to see them get better, get extubated, transfer out of the ICU, start discharge and disposition planning,and then see them slide back, get sick and die. Placement is difficult. Finding subacute rehab or long-term care is tough when you have COVID-19. Everything takes a few more days and I’m seeing people deteriorate during the delay. In my mind I have already tallied these patients as ones the virus didn’t get. These are patients that are a win, right up until they get snatched away.
It’s a sucker punch. And it hurts.
CTA Type 3. Patients being READMITTED with a previous diagnosis of COVID.
This week I started to see patients admitted who has already been admitted here or elsewhere and diagnosed with COVID-19. Apparently, the index hospitalization was at the beginning of the illness. They had pretty mild disease and were sent home without an oxygen requirement. But now 4, 8, or 10 days later they are being readmitted after they failed to shake the disease. Of course CTA Type 3 walks hand-in-hand with Type 2. These are the patients where there wasn’t a delay in discharge. They were able to make it home or a sub acute rehab facility. But the virus didn’t get better. They got sick again. The First discharge seemed like a win, but we were looking at a premature outcome.
A lot of these rE-admissions seem pretty benign. A fair amount of altered mental status. Some hypoxia that is easy to treat with nasal cannula oxygen. Some falls with mild trauma. I don’t have a good feel for how sick these people will get, but so far, it seems pretty mild. But this disease is teaching me not to turn my back.
Update on Remdesivir
And since I will always be chained to this infamous tweet, I will comment on the two remdesivir trials that dropped today.
It is these CTA type 2 and type 3 people where I hope that remdesivir has potential. People in the ICU, people that are in the middle of the cytokine storm are not going to benefit from an antiviral. We don’t care about the match once the house is on fire. But earlier in the course, the drug might abort future catastrophes. I hope that if we start treating future CTA Type 3 patients during their index admission we will derail them from severe disease.
Today’s Lancet paper
This Lancet publication was leaked last week, but today we get to see the manuscript. It is a negative study but it is not all terrible. There are some glimmers of hope peaking through the darkness.
I think the data teases that early therapy could be where this drug has promise. Giving the drug later could be like trying to give vanco and cefipime in the middle of sepsis:
an effective therapy given too late to be an effective therapy.
The other remdesivir data is more promising, this larger study of 1000 patients was stopped early because the drug was meeting it’s primary endpoint. The data safety monitoring board (DSMB) just met on April 27 (two days before the press release), so to say it is early is a bit of an understatement. The early bird is still hitting the snooze button. The positive finding was a shorted duration of illness: 15 days for placebo, 11 for remdesivir. Mortality did not meet significance, but the trend makes me excited. I also expect these numbers change as we get more follow up. See CTA Type 2 and 3 above.
I back calculated the number of deaths by using the percent mortality times half the N of 1063. 42 deaths with Remdesivir, 61 deaths with placebo.