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December 12th, 2015

The 2015 ID Fellowship Match “Historic Bad”: Part 1, Debating the Cause

This year’s ID fellowship match has just taken place, and the results were, ahem, not pretty. Part 1 will cover why we’re in this situation; in Part 2, I’ll offer some reasons for optimism, and even some solutions.

According to data provided by NRMP, 117 of the 335 ID fellowship positions were unfilled. Dan Diekema from U of Iowa, who has written frequently on the issue of the ID match, quickly calculated that over 80%  80 programs had at least one unfilled spot.

[That was an important edit — please see Dan’s comments below.]

When I cited this alarming figure, it generated a spirited email exchange about the ID match with Emory’s Wendy Armstrong, the source of the “historic bad” quote in the title. Wendy is also IDSA Chair of the Task Force for Recruitment to ID, so has thought a lot about this issue.

She acknowledged the trend is worrisome:

programs unfilled nrmp

The bulk of our exchange, however, was about the reasons for this alarming trend.

Her view:  It’s multifactorial: Limited ID teaching in medical school, with declining numbers of dedicated microbiology/ID courses. A significant proportion of preclinical curricula are led by microbiologists alone. ID faculty have less exposure to medical students in the hospital. There are fewer clinical electives for residents. There are fewer ID clinicians acting as attendings on medical services. It’s the money.

My view:  It’s the money. At least, it’s mostly the money.

Yes, the factors listed by Wendy are part of it. But since several apply to other medical subspecialties — how many cardiologists or gastroenterologists attend on general medical services? — I’m not sure they are playing much of a role.

Why is the money issue important, and why is it particularly bad for ID? A few thoughts:

  • Debt. Undergraduate medical education in this country is expensive, and a substantial number of doctors in training have significant medical school debt. They look at the 2-3 years of extra training required to become an ID specialist — followed by a lower salary — and cross ID off their list. Or at the very least, strongly consider other options if they are undecided. Or, as put succinctly here:

twitter after ID match

  • The volume/procedure deficit. So long as clinicians are reimbursed primarily based on volume and procedures, ID specialists will be at a disadvantage. Medical complexity and our drive to get the details just right limit the volume part of the equation — you just can’t rush most ID consults, it would be like trying to write a guide to the Louvre after visiting for 30 minutes — and we are not trained to do procedures.
  • The “lifestyle” issue. The revenue disadvantage from not doing procedures is shared with other cognitive specialists, of course, but few have so much of their work focused on hospitalized patients. Importantly, nephrology is the other major specialty with declining numbers of applicants, and I don’t think it’s a coincidence that nephrology also has plenty of hospital work. Hospital-based specialties require extensive weekend and evening call for urgent cases — cases you have to come in and see, not manage from home. Here’s a comment on my wife’s primary care listserv discussing the 2015 ID match:

    ID doctors are always the ones at the hospital late at night working at our hospital. And not compensated for it they way they should be. Many are of retirement age. Only a few younger guys.

    Could it be that potential applicants see ID doctors staying late in the hospital, coming in during the weekends and holidays, and wonder — why should I do that and get paid so (comparatively) poorly? The contrast with cardiology, gastroenterology, and intensivist doctors from a reimbursement perspective is obvious.

  • Primary care subsidies. Primary care providers are also on the low end of the salary scale, but they rarely do extra years of training after residency. Furthermore, primary care practices may be subsidized, both explicitly through the ACA and as a way of large healthcare systems increasing the number of “covered lives”. Again, from the listserv:

    I worked in HIV clinic in urban city in NJ and couldn’t believe what a new grad starts at…one did his fellowship at our hospital and was offered $85k in a private practice and the other was offered $110 as a assistant director so a lot of administrative, teaching, and research in addition to seeing patients. He had to moonlight in the prison system just to make his student loan payment!

    Certainly here in Boston, and anecdotally elsewhere, PCPs start at a significantly higher salary than ID doctors.

  • The rise in hospitalist positions. The winners in this race to a “real salary” in Internal Medicine? It’s the hospitalists, whose salaries generally exceed those of many ID doctors who have been in practice for years. It’s no wonder that many ID applicants today have spent at least a year after residency as a hospitalist, essentially extending their residency in terms of clinical activity, but now getting paid a whole lot more. How many of these hospitalists once considered ID training, but decided ultimately it wasn’t worth it? Longer hours for less pay, no thanks!
  • Biology. In my highly unscientific poll of friends and colleagues, the period at the end of residency is the most common time for doctors to start thinking seriously about starting a family — or, in some cases, actually having babies. Such a major change certainly brings the debt, salary, and lifestyle issues cited above into stark focus.

Reading the above, you might think I’m pessimistic about the future of our speciality, but — call me crazy — in fact the opposite is true. Having one dominant cause to the problem is in many ways easier than a highly complex, multifactorial situation. Fix the money problem, and the interest in ID will rebound nicely.

In Part 2, I’ll try to justify my optimism.

Here’s a relevant 80s classic:

[youtube http://www.youtube.com/watch?v=pp4suZ4jNXg&w=420&h=315]

December 6th, 2015

Do Electronic Health Records Make You a Better (or Worse) Clinician?

Earlier this week, JAMA Internal Medicine published a study entitled, “Level of Computer Use in Clinical Encounters Associated with Patient Satisfaction”.

A more descriptive title would have been “More Computer Use in Clinical Encounters Associated with Reduced Patient Satisfaction”, as here’s the take home point:

High computer use by clinicians in safety-net clinics was associated with lower patient satisfaction and observable communication differences … Concurrent computer use may inhibit authentic engagement, and multitasking clinicians may miss openings for deeper connection with their patients.

As I’ve mentioned before (probably more times than you’d like), the computer’s power to grab our eyes away from our patients is one of the things I like least about EHRs. Of course people are less satisfied with their care when their doctor spends tons of time typing away at the keyboard and looking at the glowing screen.doctor at computer2

(Brief aside: Some clinicians mention triangulating the encounter by having both patient and doctor review information from the EHR together. Yes you can do this sometimes, but this tactic really doesn’t work when taking a detailed history. Plus, it’s a capitulation — the computer is now the center of attention, not the patient. Finally, it’s all but impossible to pull this off in many exam rooms, especially those originally designed with no computer in mind. You’d practically have to ask your patient sit on a step-stool or hang from a trapeze over your shoulder to make this work. Not such a brief aside after all, I guess.)

I’m bringing this difficult situation up again not solely because of the published study — similar findings have been reported before. This feeling of being trapped by EHRs is not just an issue for patient satisfaction, but clinician happiness as well. One of my colleagues received a letter from her PCP, informing her that she (an experienced internist) planned to retire. It included this paragraph, which I’m sharing with that doctor’s permission:

letter to pts

So it’s not just the patients who don’t like it — we clinicians aren’t too thrilled either. This internist is hardly the first to complain about becoming a click-slave, though she’s the first I know to use this venue (a letter to patients) to express her opinion.

But the EHR must be good for some things, right?

Of course — a short but not all-inclusive list of the benefits could include trending of lab results, bringing up previous medication histories, displaying radiology images, reviewing other clinicians’ notes, issuing reminders about health maintenance tasks, and receiving warnings about dosing errors, allergies, and drug-drug interactions. Access to records remotely is a huge bonus.

Note I’m deliberately excluding the billing and medicolegal features, as frankly they are usually irrelevant to quality patient care. They are part of EHRs for other reasons. See here for what I think of that “functionality” (a word which always makes me cringe).

All of which makes me wonder — do EHRs make us better at what we do? Or worse?

Help please.

Do electronic health records make you a better clinician?

View Results

And just in case you missed it …

[youtube http://www.youtube.com/watch?v=xB_tSFJsjsw&w=560&h=315]

November 29th, 2015

Flu Vaccine Keeps Taking Hits, Still the Best We’ve Got — Don’t Stop “Belivin'” [sic]

For reasons understood only by the geniuses in Mountain View, CA, for some reason my Google news feed picked up this bit of “scientific” reporting:Ohio_Makes_People_Belive_They_Need_A_Flu_Vaccine

Let me allow the author, an unfortunately named “Clapway” (gonorrhea researcher?), to speak for him/herself:

However, is the flu vaccine really worth it? The author of this article never takes it and has not had the flu in years, knock on wood. There have also been various stories around the web that have stated that people who get the vaccine, immediately get the flu. It then has to be considered that the flu vaccine can be risky to take.

Is this an Onion parody? Or did Google stumble on a Junior High School science/tech blog? If so, a brief word of advice to the author — always double-check spelling (especially the title) before posting.

Admittedly, the recent news on the flu vaccine hasn’t been great — a rehash of reduced effectiveness from repeated immunizations (data are from a study published last year), how poorly the vaccine protects against H3N2, and a study suggesting that statins reduce vaccine efficacy. Of course people taking statins (cardiovascular risk, older) are exactly the people we want to get the vaccine!

On the good news front, we have yet another FDA-approved flu vaccine, this one with the wonderfully named adjuvant squalene to boost immune response. And boy does this new vaccine have a strange-looking brand name — “Fluad.” Good grief. Add it to the zillions of other flu vaccines available — just choose one!

Other good news:  This year’s vaccine seems to match the  circulating flu virus much better than last year. Cautious optimism.

So warts notwithstanding, until the “universal” flu vaccine is available, the current annual vaccine (in all its various permutations) is the best we’ve got. Even during last year’s dismal performance, there’s some evidence it prevented flu-related illness severe enough to cause hospitalization. 

Wise words here from ID colleague Dr. Larry Madoff, who is Director of Epidemiology and Immunization at the Massachusetts Department of Public Health.

Good enough for me.

[youtube http://www.youtube.com/watch?v=VcjzHMhBtf0&w=420&h=315]

November 26th, 2015

Five (OK, Six) ID/HIV Things to be Grateful for this Holiday Season, 2015 Edition

Some quick ID/HIV gratitude items for 2015, done rapidly as we’re hosting a big meal later today.

I wonder what that might be.

  1. New Ebola virus disease cases and deaths have dramatically declined. I write that sentence with some trepidation, as cases continue to occur sporadically, and this late relapse in a nurse was a chilling reminder of how little we know about this disease. Additionally, since what caused the massive outbreak in Western Africa is still poorly understood, complacency about Ebola would be very ill-advised. Nonetheless, the reason we should be grateful is shown clearly in this figure of Ebola incidence:
    evd cases cumulative
    Last year at this time we were right in the middle of that steep upward slope, with no idea when or how cases would decline. That these curves have plateaued is due to massive local control efforts (thank you!); work on both a vaccine and antiviral therapy also continue briskly.
  2. Antibiotic prescribing declines. Whether it’s the growing awareness of the importance of the microbiome, concerns about resistance, publicity about the dreaded C diff, fear of drug toxicity, or (most likely) some combination of the above, people are receiving fewer prescriptions for antibiotics. The data from this study confirm something that most clinicians increasingly see in their patients — some sort of tipping point has been reached, where now a growing number of people are willing to tough out community-acquired respiratory infections and nagging coughs and ear aches rather than berate their doctors with references to “green phlegm” (code for “Give me a Z-pak”). Now if we can just get the farm animals to have a voice in this too — 80% of antibiotic use in this country is for agricultural purposes.
  3. PrEP works really, really well when given to people who want (and need) it. Confession: I thought pre-exposure prophylaxis (PrEP) for HIV was forever going to remain a very small piece of the HIV prevention effort. But I’ve been wrong (many times) before — hey, I thought putting cameras in phones was a ridiculous idea — and it turns out I was wrong about PrEP, too. In both the PROUD and IPERGAY (soon to be published in a major medical journal) studies, men who have sex with men who were at high risk of contracting HIV reduced that risk by nearly 90% by taking TDF/FTC. Not surprisingly, uptake of PrEP has increased dramatically in the past year, a trend I expect will continue given CDC’s efforts to get the word out.
  4. HCV treatment now works just as well in clinical practice as it does in clinical trials. Remember when combination HIV therapy came out in the mid-1990s, and several papers (notably this one) cited far worse outcomes in “real life” than in the clinical trials? Or when the same exact thing happened with telaprevir and boceprevir-containing regimens for HCV? Guess what — current HCV treatment is so good that “real life” (whatever that means) outcomes are outstanding, with cure rates greatly in excess of 90% for most genotype 1 patients. Although every HCV treater has a few examples of treatment failure, they are just that — a few.
  5. Treatment as prevention is staggeringly effective in preventing HIV — still. Did anyone expect zero HIV transmissions from HPTN 052 participants with virologic suppression? Or from those individuals in the cohort studies of “condomless sex”? I bet somewhere the Swiss are muttering under their breath (in French? German? Italian?), I told you so. Bottom line is that there really is all but zero risk.
  6. The end of the “When to Start” debate.  The much-anticipated START study showed that even the healthiest HIV-infected people — those with CD4 cell counts > 500 and no symptoms — benefit from immediate antiretroviral therapy, with fewer HIV and non-HIV related serious medical problems. When you add these results to the transmission benefits in item #5 above, the clear answer to the question, “When to start?” HIV treatment is pretty straightforward. Now!

As for the video below, I’ve been waiting eagerly since my 8th grade typing class to see it in action — am very grateful finally to see it.

For the record, the dog doesn’t look so lazy to me, just patient.

Happy Thanksgiving!

November 22nd, 2015

Just Wondering: Quick ID Questions to Consider

germsSeveral quick ID queries, some of them answerable on the Google machine — but I’m not going there. Too busy laundering my white coat!

  • What ever happened to amphotericin A?
  • What’s the difference between a “serovar” and a “serotype”?
  • Do dogs feel bad that Pasteurella multocida is more famous than Capnocytophaga canimorsus?
  • Colistin resistance is bad — but how often does colistin actually work anyway?
  • No one asks you to share a room with a stranger in a hotel — why do we ask sick people in hospitals to do this? Even sick people with infections?
  • Why is there group A, B, C, D, F, and G, but no group E beta strep? At least I don’t think there is. Is it like Windows 9?
  • Why do all the abbreviations for “integrase inhibitor” — InI, INSTI, II — sound and look so silly? Just say “integrase.”
  • Why do we say trimethoprim-sulfamethoxazole with the trimethoprim part first, but the pharmacy usually writes it for our patients the opposite way?
  • Don’t you think that if probiotics really prevented or helped some condition, we’d know it by now?
  • Even though the name has changed, is anyone ever going to stop saying Strep bovis?
  • Why are the guidelines for meningococcal immunization so complicated? Have to look them up every time.
  • Why do C diff precautions start the moment we send the diagnostic test, but MRSA precautions await the results of staph susceptibility testing?
  • Why was optochin never developed into an antibiotic? Is it because it doesn’t end in “-mycin” or “-cillin” or “-floxin”?
  • Does anyone really know the best dosing option for strep throat?
  • What proportion of doctors immediately think Aeromonas hydrophila when they hear about medicinal leeches? And what proportion who read this blog?
  • Who decided it should be MRSA — and not ORSA or NRSA?
  • What percentage of hospital-based ID consults recommend additional blood cultures — even when there are numerous negatives already done on that patient?
  • Why did the new endocarditis guidelines advise against using penicillin for penicillin-sensitive Staph aureus? (In Boston, we call it PSSA — say it, you’ll get the joke.) In vitro, it’s the most active drug, after all.
  • MALDI-TOF or MALDI-TOF MS? Seems the former should be sufficient.
  • Endocarditis cases in Britain rise since they stopped using antibiotic prophylaxis for dental work — evidence that this is in fact an important preventive strategy? Or just that the British have, ahem, dental issues?
  • Why do doctors always use the term “germ” in non-medical communications, but never do otherwise? And why does it mean a virus or bacteria or fungus, but never a parasite?
  • When the inactivated zoster vaccine is approved, what happens to all those zoster vaccine curbside consults?
  • Dogma is that you don’t need antibiotics after I and D of uncomplicated skin abscess. So why is 10 days of TMP-SMX better than 3?
  • Why are certain toxic and little-used HIV drugs (ddI, d4T in particular) still on the market? Is there anyone who wouldn’t benefit from switching to something different?
  • When we will stop using antibiotics to treat C diff?
  • Could this white coat poll be any closer? Memories of Bush vs Gore.

Answers, opinions, speculations welcome!

Seems probiotics helped this guy (listen/watch through 1:50).

[youtube http://www.youtube.com/watch?v=3xJWxPE8G2c]

November 18th, 2015

Are There Remaining Challenges in HCV Therapy?

Prompted by (yet more) spectacular HCV study results, I posted the following questions on Twitter:

To which I got this reply from one of our very energetic second-year ID fellows:

OK, OK, I know what you’re wondering — don’t you two have anything better to do than fool around with a financially struggling social media platform?

Sure we do — but after years and years of “not getting” Twitter, I now (thanks to Phil) see some of the benefits, namely the rapid exchange of information and ideas, in a particularly efficient form.

But back to the topic at hand, which is the HCV regimen used in these latest studies published in the New England Journal of Medicine.  All include the pan-genotypic NS5A inhibitor velpatasvir with the already-approved nucleotide sofosbuvir, given as  a single pill once daily.

Results? Outstanding:

The results really make you wonder what more we can do to make HCV treatment better. We are definitely at the flat part of the aymptotic functionresponse curve, and fortunately it has plateaued way up there, with 95% or higher cure rates for all but the sickest HCV patients, along with exceedingly rare adverse effects.

So are there remaining issues? Yes, sort of — but none of them is as pressing as the obligatory elephants in the room, which are cost and access. Let’s start with Phil’s proposed challenges, plus a few others:

  • Co-infected patients. Not really a problem at all — people with HIV respond just as well as those without coinfection. (Several examples of studies cited in this post.) In fact, in many ways they’ve been easier to treat, as the patients are already used to taking medications every day.
  • Drug-drug interactions. Compared to what we’ve dealt with using ritonavir and cobicistat and rifampin, these are a piece of cake — unless you’re actually using ritonavir with the “PrOD” regimen. (That’s what I’ve been calling it. I never liked “3D”.)
  • Cirrhosis. Especially with a history of treatment failure to interferon-based therapies. In most studies, the newer drugs don’t work quite as well in these patients — but we’re generally talking small differences. Response rates are still pretty great.
  • Patients who have failed treatment with an NS5A inhibitor-containing regimen. Indeed, this does limit our options quite a bit, and assessing for resistance is anything but straightforward, especially with non genotype 1. But we’re not completely without options — alternative sofosbuvir-based regimens will work in some patients, as the resistance barrier to this particular drug is sky high. I suspect we’ll get some clarity on this issue over the next several months.
  • Patients who can’t take 12 weeks of therapy. Most studies of treatment for less than 12 weeks have been disappointing. Does a shorter course mean better adherence? Lower cost? Better outcomes? Maybe. Hard to beat the current rate of cure, but still — a regimen that could be given for 2-4 weeks would be welcome for some patients. Think H pylori treatment, if you can stand the analogy, since ID doctors know squat about H pylori therapy.
  • Cost. See elephants in the room, cited above. Maybe the soon-to-be-approved grazoprevir/elbasvir. We’ll see.

So what about the second part of that tweet?

And what will HCV researchers do now?

I don’t know — become experts in implementation research? Study how to cure hepatitis B? Switch to steatohepatitis? Fibrosis reversal? Learn how to juggle clubs?

[youtube http://www.youtube.com/watch?v=Ax0wl8pYk4g&w=560&h=315]

November 15th, 2015

Speechless

Friday, November 13, 2015, late afternoon. This time of year, in Boston, it feels like early evening, but the clock says it’s only a bit after 4pm. I log onto our electronic health record to check for lab results and patient messages, and get this:
message of the day

There it is, the “Message of the Day”, complete with the this-is-important exclamation point, but the message box is empty, saying nothing. Must be some sort of programming glitch, a slip-up buried in the millions lines of code and ones and zeros that are supposed to represent our patients.

I’ve never seen this particular error before. What does it mean — what is the EHR trying to tell us, but can’t find the words? Should I report it? If so, the question is to whom — but does it even matter? The easier path is to just click the OK box and move on.

Shortly after dealing with this minor inconvenience, I hear about the events in Paris — over a hundred dead from carefully coordinated terrorist attacks, grim images coming forward of bloodied bodies and a city now frozen in fear.

Sadly, there is no OK box to click for this tragedy.

Words alone are insufficient to describe our support for the people of France.

[youtube http://www.youtube.com/watch?v=l6vGq_rHAmE&w=560&h=315]

November 8th, 2015

New HIV Treatment “ECF-TAF” is Really All About the “TAF” Part

espressoHIV providers and patients recently got this news from the FDA:

The U.S. Food and Drug Administration today approved Genvoya (a fixed-dose combination tablet containing elvitegravir, cobicistat, emtricitabine, and tenofovir alafenamide) as a complete regimen for the treatment of HIV-1 infection in adults and pediatric patients 12 years of age and older.

(Disclosure:  I have been involved with the clinical trials; you can read my full disclosures here. That involvement notwithstanding, some sort of comment seems appropriate — this is an HIV/ID blog, after all.)

The availability of elvitegravir, cobicistat, emtricitabine, and tenofovir alafenamide — hereafter abbreviated “ECF-TAF” — brings us the fifth one-pill-a-day treatment for HIV. Of course we already have something very similar, which is ECF-TDF, and hence the only thing new here is the TAF component.

So what does ECF-TAF bring us that we didn’t already have with ECF-TDF?

Based on multiple clinical studies, here are what I think are the proven differences between the two:

  • Less effect on bone density. As initial therapy, TAF induces less bone loss than TDF — the former is comparable to NRTI-sparing strategies. Furthermore, in multiple clinical studies, switching from TDF to TAF improves bone density.
  • Decreased renal toxicity. In several trials involving over 3000 patients, no case of tenofovir-related renal toxicity has occurred in an ECF-TAF-treated patient. TAF’s effect on urinary proteins (a surrogate marker for renal effects) is also significantly less than TDF. One unknown is whether it can be safely given to a patient with a history of tenofovir-related renal toxicity; that question is under study. The regimen is approved for use in patients with estimated GFR down to 30 ml/min.
  • A lower milligram dose. As part of ECF-TAF, the dose of TAF is only 10 mg, vs 300 mg for TDF. (When not given with cobicistat or ritonavir, the dose will be 25 mg.) A lower milligram dose means smaller pills and easier coformulations.
  • A novel way to simplify complex regimens. As noted here, ECF-TAF can be combined with 800 mg of darunavir to make a two-pill treatment for some patients with multi-drug resistant virus. You couldn’t do this with ECF-TDF, at least not with confidence — it hadn’t been studied, and the three-way drug-drug interaction between cobicistat, darunavir, and elvitegravir gave me pause.
  • Less lipid-lowering effect. Tenofovir lowers lipid levels (mechanism still unclear), and since TAF delivers 90% lower blood levels of tenofovir than TDF, there is less of this effect. This lower tenofovir exposure is mostly a good thing (see renal and bone above), but not here. I suspect this won’t be clinically relevant, but of course we don’t have enough follow-up data since the incidence of cardiovascular events in short-term clinical trials is so low.

And here’s what’s not different:

  • Antiviral activity. Though in phase I studies TAF induced greater declines in HIV RNA than TDF, virologic outcomes (meaning failures and incident resistance) in studies comparing ECF-TAF with ECF-TDF have been similar.
  • Drug-drug interactions. The “C” in both ECF-TAF and ECF-TDF stands for cobicistat, the ritonavir-like PK “booster” that is necessary for elivitegravir’s once-daily dosing. A cytochrome p450 inhibitor, cobicistat has numerous drug-drug interactions — watch those medication lists carefully! Note that a combination of TAF/FTC and 9883 — an unboosted integrase inhibitor, no cobicistat required — is in development.
  • Subjective side effects. There’s no significant difference in the incidence of patient-reported side effects. In other words, if your patient didn’t tolerate ECF-TDF, there is little point in trying ECF-TAF. Good news is that both are very well tolerated, with extremely low discontinuation rates for adverse events.
  • The price. Encouragingly, ECF-TAF is priced the same as ECF-TDF, a decision lauded by this group. However, integrase-inhibitor based regimens remain relatively expensive (average wholesale price around $30,000/year) compared to NNRTI-based therapies, though cheaper than those that include a boosted PI.

Overall, ECF-TAF is welcome new option for treatment, and to emphasize again it’s the TAF part that makes the (only) difference. Future TAF formulations will include TAF-FTC-rilpivirine and TAF-FTC (which will need at least one other active drug) — these are expected some time next year. TAF-FTC-9883 is further away.

Meanwhile, we can continue to ponder the mysteries of choosing a brand name for a drug — “Genvoya” sounds to me like a high-end coffee maker.

November 1st, 2015

Should Doctors Still Be Allowed to Wear White Coats? You Decide

roll up sleevesIf you’re not immersed in the ID or the Infection Control world, you might not be aware that there’s currently quite the controversy about whether doctors should wear white coats.

I almost wrote “raging controversy” — but the adjective “raging” doesn’t really fit the sort of people who specialize in Infection Control, who are some of the most measured, data-driven, and methodical individuals in all of medicine. You know the stereotype of the brash, volatile, and cowboy surgeon, the person that everyone tiptoes around?

These Infection Control folks are the polar opposite.

Still, a white coat controversy does exist, and it goes like this:

  1. You can culture all kinds of scary bacteria from the sleeves of white coats.
  2. Doctors don’t launder their white coats very often.
  3. These bacteria could be transmitted to patients.
  4. Therefore, doctors shouldn’t wear white coats.

Not surprisingly, some have advocated a “bare-below-the-elbows” approach to doctors’ attire, and famously the British National Health Service has made it policy, banishing ties as well  (and predictably not pleasing everyone). There was a tremendously entertaining debate on the topic this year year at IDWeek — such a pitched battle it almost met the “raging” criteria, but not quite (you could tell the combatants really liked each other). Right here in Boston, one of our current ID fellows feels quite passionately about the issue, and writes frequently on the topic.

The missing piece in the controversy, of course, is a definitive study showing that patient infection rates are actually reduced when a bare-below-the-elbows (often abbreviated “BBE”) strategy is adopted. Short of that, we’re all essentially hostage to whomever sets these policies wherever we work. And our hospital’s policies basically follow those of Society for Healthcare Epidemiology of America (SHEA), which “balance professional appearance, comfort, and practicality with the potential role of apparel in the cross-transmission of pathogens.”

In other words, wear white coats if you want, but keep them clean.

This data void, however, gives me permission to ruminate over some of the important and not-so-important questions that inevitably come up when contemplating white coats, and our ambivalent feelings about them.

Specifically:

  • Why do some doctors wear them now, and some don’t? My wife the pediatrician said if she or one of her practice partners showed up in a white coat, the office staff would view it as bizarre as if they showed up dressed as a Roman centurion. She didn’t actually say that, but you get the idea — pediatricians don’t avoid white coats because of infection risk, but because they are considered potentially scary to kids. Meanwhile, the brilliant and fearsome Chief of Medicine during my residency considered us housestaff essentially naked unless we were wearing white coats, and the Chief Medical Residents kept a few extra in their offices on days he took Residents’ Report in case we showed up white coat-less — kind of like the maitre d’ at the formal restaurant keeping a few extra blazers in the coat closet in case someone arrives without a jacket.
  • What do the patients want? Demonstrating that she was a far more compensated medical student than I, one of my classmates during medical school actually published a study evaluating patients’ preferences on doctor attireYes, patients liked white coats back then, jeans not so much. It’s one of many such studies appearing in the medical literature over the years; a systematic review of them is summarized in this paper published in the British Medical Journal. Consensus? Patients still seem to like them, but of course for every opinion about the reassuring message of professionalism conveyed by the white coat, there’s an opposite view that they reinforce outdated hierarchical structures in healthcare.
  • What should doctors wear if they don’t wear a white coat? The obvious first thought is scrubs, but there are a few problems here. First, scrubs are basically utilitarian pajamas, and can get pretty nasty unless washed daily. Second, they don’t offer much in the way of insulation, a huge issue in the winter and in ubiquitous over-air conditioned interiors. Third, scrubs can be very unkind to certain body types, male and female alike. (You know what I mean.) Fourth, they have basically no storage space — cell phone, wallet, that’s it — forget the reflex hammer, ophthalmoscope (though it’s useless to me), or pocket manual, and wearing scrubs makes your stethoscope a permanent half-necklace. Finally, the public has lots of negative feelings about scrubs — especially when they see doctors wearing them outside the hospital, which means to adopt scrubs as standard gear means changing when you get to work, ugh. And if not scrubs? Men probably clean their suits less often than they wash their white coats, and my daughter told me recently that button-up short sleeved shirts on men are a huge fashion faux-pas, to be avoided as much as backpacks with wheels and belt clips for cell phones. Who knew?
  • If white coats go, what happens to the “White Coat Ceremony” during medical school? Apparently, 97% of medical schools now have a White Coat Ceremony, the purpose of which is “to welcome new students into the medical profession and to set clear expectations regarding their primary role as physicians by professing an oath.” Does that oath now include a specified frequency of laundering, including minimum water temperature and the need to use bleach? By the way, you youngsters might be surprised to hear that these solemn and moving rituals are relatively new. Back when I was in medical school, they just left you in a room alone with a cadaver, turned out the lights, and timed how long you could stay there before you screamed for help.
  • How would New Yorker cartoons designate doctors if white coats were abandoned? This is a very important question. Take a look — the overwhelming majority have the MD in a white coat, and those few that don’t typically involve surgeons in the OR. Here’s one of the rare exceptions to the above rule and 1) the guy is wearing long sleeves (not BBE!), and 2) it’s not that funny. I’d give it a 7 out of 10 on the funniness scale — now this one is funny. Note that this brilliant cartoonist often adds the head mirror to the white coat, just so you couldn’t possibly think that the white-coated person in his cartoon might be an insurance salesperson or an airline pilot.

Ok, so controversy not resolved. Please vote!

Should doctors still be allowed to wear white coats?

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October 29th, 2015

The Most Important HIV Study at IDWeek 2015

After reporting my choice for the most important HIV study at ICAAC, I received this email from a colleague:

If that’s the most important study, I really didn’t miss much …

Now she has notoriously high standards — hard to impress her — but her opinion notwithstanding, I still think the STRIIVING study has some important messages we can apply to clinical practice today. So I stick by my choice.

Now let me see if I can meet her approval with an IDWeek 2015 (which took place earlier this month) selection. It’s another HIV switch study, although this time with a twist. Instead of the usual switch-study population (first regimens, or only those with no history of virologic failure or resistance), it looked at a very different group — patients who were virologically suppressed but highly treatment-experienced, all with 2-class (or more) resistance, and taking multiple pills a day with a darunavir-based regimen.

Subjects were then randomized to continue their current therapy or switch to the two-pill treatment of elvitegravir-cobicistat-FTC-TAF (ECF-TAF) plus darunavir 800 mg, both once daily. (Thanks to Greg Huhn, the presenting author, for sharing the slides.)

ss study design

At baseline, the regimens included a median of 5 pills, and around 60% were taking at least 6 or more pills a day. Most had a history of M184V, and a significant minority had K65R and/or PI resistance.

At week 24, 97% vs 91% of the ECF-TAF + DRV vs continued baseline regimen groups had HIV RNA < 50 cop/mL; at week 48, it was 94% and 76%, a significant advantage of ECF-TAF + DRV.

ss results

No new resistance was observed in those with virologic failure on the 2-pill arm; one subject developed resistance in the baseline regimen group, but not integrase resistance. A PK substudy demonstrated acceptable levels of both EVG and DRV, greatly exceeding IC95 and IC50 respectively.

Some comments on this study:

  • Approval of ECF-TAF is expected soon, and I suspect this particular indication for switch will not be part of the product label. The data are very recent, and the study is relatively small.
  • Even if it’s not in the label, however, these study results certainly suggest that some patients on complex regimens (many of whom are yearning to take something simpler) will be able to shift to just two pills a day — a welcome change.
  • The PK substudy was extremely reassuring, greatly diminishing concerns about the head-spinning three-way interaction between elvitegravir, cobicistat, and darunavir. That interaction, by the way, is the reason why we shouldn’t use darunavir with the currently available ECF-TDF.
  • Take a close look at those eligibility criteria — in particular the resistance ones — because they’re important. It’s why I italicized the words “some patients” in my comment above.
  • Why is this so important? Patients with more than 3 TAMs, the multi-NRTI resistance mutations Q151M or T69S, or darunavir mutations were excluded. We don’t know if switching patients with any of these criteria to ECF-TAF and darunavir will maintain virologic suppression.
  • Virologic rebound for patients with multi-class resistance who are stably suppressed could be disastrous — it would be terrible to take a patient with 3-class resistance and virologic suppression to 4-class resistance (including integrase) and rebound, especially since the HIV drug pipeline has relatively few investigational agents.

The take home message from this study is that when ECF-TAF is approved, a subset of our patients who are taking complex regimens could safely switch to two pills a day — ECF-TAF + darunavir.

Finding the right patients will take meticulous scrutiny of their historical genotypes. But of course that’s why they pay us the big bucks!

Next year’s meeting? October 26-30, New Orleans.

[youtube http://www.youtube.com/watch?v=pXHdqTVC3cA&w=420&h=315]

HIV Information: Author Paul Sax, M.D.

Paul E. Sax, MD

Contributing Editor

NEJM Journal Watch
Infectious Diseases

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