questionable practices

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xaelia

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  1. Attending Physician
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One of my mini-peeves in my residency and medicine in general is the extent to which we tend to just practice base on mimicry rather than questioning the evidence upon which we base our actions, and actually understand why we do even the simplest things. So, anyway, I have a lecture to give in residency here in a couple months, and I thinking of running through a variety of common and not-so common topics where I thought maybe we could give a little more thought to our practice.

I had sort of a quick list of topics off the top of my head I might include, and I was curious if anyone else had some suggestions. I few topics I've come up with so far:
Narcotic dosing for acute pain
Antibiotics in otitis/sinusitis/strep pharyngitis
Toradol
TPA in ischemic stroke
Antibiotic choices in UTI; fosfomycin
Ketamine and ICP
Steroids in spinal cord trauma
ACLS
IV H2 vs PPI for gastritis
Steroids/racemic epi in croup
Bronchiolitis
Anticholinergics in pediatric asthma
Oxygen in chest pain/MI
Pharmacologic treatment for cough/sore throat

Anything else anyone might suggest you wish people would think about before they do it?
 
One of my mini-peeves in my residency and medicine in general is the extent to which we tend to just practice base on mimicry rather than questioning the evidence upon which we base our actions, and actually understand why we do even the simplest things. So, anyway, I have a lecture to give in residency here in a couple months, and I thinking of running through a variety of common and not-so common topics where I thought maybe we could give a little more thought to our practice.

I had sort of a quick list of topics off the top of my head I might include, and I was curious if anyone else had some suggestions. I few topics I've come up with so far:
Narcotic dosing for acute pain
Antibiotics in otitis/sinusitis/strep pharyngitis
Toradol
TPA in ischemic stroke
Antibiotic choices in UTI; fosfomycin
Ketamine and ICP
Steroids in spinal cord trauma
ACLS
IV H2 vs PPI for gastritis
Steroids/racemic epi in croup
Bronchiolitis
Anticholinergics in pediatric asthma
Oxygen in chest pain/MI
Pharmacologic treatment for cough/sore throat

Anything else anyone might suggest you wish people would think about before they do it?

actually, most of those at my house are treated either based on the evidence or based on the fact that the service taking the patient doesn't go by the best interpretation of the evidence or by the fact that the evidence is equivocal.
 
One of my mini-peeves in my residency and medicine in general is the extent to which we tend to just practice base on mimicry rather than questioning the evidence upon which we base our actions, and actually understand why we do even the simplest things. So, anyway, I have a lecture to give in residency here in a couple months, and I thinking of running through a variety of common and not-so common topics where I thought maybe we could give a little more thought to our practice.

I had sort of a quick list of topics off the top of my head I might include, and I was curious if anyone else had some suggestions. I few topics I've come up with so far:
Narcotic dosing for acute pain
Antibiotics in otitis/sinusitis/strep pharyngitis
Toradol
TPA in ischemic stroke
Antibiotic choices in UTI; fosfomycin
Ketamine and ICP
Steroids in spinal cord trauma
ACLS
IV H2 vs PPI for gastritis
Steroids/racemic epi in croup
Bronchiolitis
Anticholinergics in pediatric asthma
Oxygen in chest pain/MI
Pharmacologic treatment for cough/sore throat

Anything else anyone might suggest you wish people would think about before they do it?


What's your beef with fosfomycin? I mean, I agree that cephalosporins are cheaper and generally more effective, but in the right setting fosfomycin has a role.

O2 in chest pain is also somewhat of a "gimme". While I agree it is of no proved benefit in MI, it does help in other etiologies of CP and until the source is determined...

- H
 
This may be a tough lecture for you as there are so many possible topics. Anyway here's a few more:

bicarb in codes

trendellenburg

staying flat and motionless after an LP

sterile procedure for lacs
 
I echo the concern that you've already got too many topics to cover well. Perhaps you could pick the 3-4 with the widest gap between practice and evidence. Anyway, here are a few more:

Scanning traumas "for mechanism"
Treatment of intracranial hemorrhage in patients with a normal neuro exam
Beta blockers in acute MI
CT vs US in appendicitis
 
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be careful. those fingers will fall right off.

http://journals.lww.com/annalsplast...nephrine_in_Digital_Blocks__Revisited.10.aspx

Epinephrine in Digital Blocks: Revisited

Wilhelmi, Bradon J. MD; Blackwell, Steven J. MD; Miller, John MD; Mancoll, John S. MD; Phillips, Linda G. MD

Abstract

Digital block anesthesia with epinephrine, ring technique, and digital tourniquet have been implicated in causing finger gangrene. An extensive review of the literature provided no case of finger gangrene attributed solely to the adjunctive use of epinephrine with lidocaine for digital block. By causing vasoconstriction, epinephrine complements the local analgesic by prolonging the duration of action and providing a temporary hemostatic effect. Epinephrine augmentation of digital block anesthesia was used in the treatment of 23 finger injuries without a complication.

http://journals.lww.com/plasreconsu..._Look_at_the_Evidence_for_and_against.36.aspx

A Critical Look at the Evidence for and against Elective Epinephrine Use in the Finger
Thomson, Christopher J. M.D.; Lalonde, Donald H. M.D.; Denkler, Keith A. M.D.; Feicht, Anton J. Ph.D.

Abstract

Background: Medical texts continue to perpetuate the belief that epinephrine should not be injected in fingers. Little attention has been paid to analyze the evidence that created this belief to see whether it is valid. The significance is that elective epinephrine finger injection has been shown to remove the need for a tourniquet, and therefore delete sedation and general anesthesia for much of hand surgery.

Methods: All of the evidence for the antiadrenaline dogma comes from 21 mostly pre-1950 case reports of finger ischemia associated with procaine and cocaine injection with epinephrine. The authors performed an in-depth analysis of those 21 cases to determine their validity as evidence. They also examined in detail all of the other evidence in the literature surrounding issues of safety with procaine, lidocaine, and epinephrine injection in the finger.

Results: The adrenaline digital infarction cases that created the dogma are invalid evidence because they were also injected with either procaine or cocaine, which were both known to cause digital infarction on their own at that time, and none of the 21 adrenaline infarction cases had an attempt at phentolamine rescue.

Conclusions: The evidence that created the dogma that adrenaline should not be injected into the fingers is clearly not valid. However, there is considerable valid evidence in the literature that supports the tenet that properly used adrenaline in the fingers is safe, and that it removes the need for a tourniquet and therefore removes the need for sedation and general anesthesia for many hand operations.

Among others.

I don't know if you were being sarcastic or not.
 
Apparently, also a myth that non-absorbable sutures are advantageous for simple skin closure.

This might actually be true; I've had absorbable sutures fall apart in my forceps on removal.
 
This might actually be true; I've had absorbable sutures fall apart in my forceps on removal.

Who puts absorbable sutures into wounds where the sutures need to be removed?

I've only done one type on one group of patients - drunks with ear lacs. They get absorbables, because they won't return. However, absorbables should be deep, and you shouldn't need to remove them.
 
Who puts absorbable sutures into wounds where the sutures need to be removed?

I've only done one type on one group of patients - drunks with ear lacs. They get absorbables, because they won't return. However, absorbables should be deep, and you shouldn't need to remove them.

After being begged by one of our hand guys to start doing it, I've started using absorbables on the hands of kids who freak out when anyone medical approaches. I'm told the outcomes are good, and that way the kid doesn't have to be traumatized for suture removal.
 
Cosmetic outcomes of absorbable versus nonabsorbable sutures in pediatric facial lacerations.
PMID: 18347489
No significant difference between cosmesis in 47 patients randomized to nylon or catgut.

Comparison of absorbable with nonabsorbable sutures in closure of facial skin wounds.
PMID: 14623686
No significant difference in cosmesis or outcomes in 41 patients randomized to 4-0 Monocryl, 5-0 Prolene, or 5-0 Vicryl.

A randomized, controlled trial comparing long-term cosmetic outcomes of traumatic pediatric lacerations repaired with absorbable plain gut versus nonabsorbable nylon sutures.
PMID: 15231459
No significant difference in cosmesis, infection, or dehiscence in 65 patients randomized to catgut and nylon.

Absorbable versus nonabsorbable sutures in the management of traumatic lacerations and surgical wounds: a meta-analysis.
PMID: 17505281
Seven, heterogenous, citations with small sample sizes suggest non-absorbable sutures are no better than absorbable, but the evidence is not adequate.
 
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Cosmetic outcomes of absorbable versus nonabsorbable sutures in pediatric facial lacerations.
PMID: 18347489
No significant difference between cosmesis in 47 patients randomized to nylon or catgut.

Comparison of absorbable with nonabsorbable sutures in closure of facial skin wounds.
PMID: 14623686
No significant difference in cosmesis or outcomes in 41 patients randomized to 4-0 Monocryl, 5-0 Prolene, or 5-0 Vicryl.

A randomized, controlled trial comparing long-term cosmetic outcomes of traumatic pediatric lacerations repaired with absorbable plain gut versus nonabsorbable nylon sutures.
PMID: 15231459
No significant difference in cosmesis, infection, or dehiscence in 65 patients randomized to catgut and nylon.

Absorbable versus nonabsorbable sutures in the management of traumatic lacerations and surgical wounds: a meta-analysis.
PMID: 17505281
Seven, heterogenous, citations with small sample sizes suggest non-absorbable sutures are no better than absorbable, but the evidence is not adequate.

Two things: first, are the absorbable superficial closure, or using a subcuticular approach, and, if superficial, are they being removed or left in? Second, who uses 4-0 on a face?? I was taught 5-0 or smaller.
 
Two things: first, are the absorbable superficial closure, or using a subcuticular approach, and, if superficial, are they being removed or left in? Second, who uses 4-0 on a face?? I was taught 5-0 or smaller.

I use fast absorbing gut for almost all of my facial lacs and most other lacs not under tension. Simple interupted sutures, no need to return for removal.

The OMFS guys where I trained got me turned onto this and they feel that outcomes are equivalent.
 
Narcotic dosing for acute pain
Antibiotics in otitis/sinusitis/strep pharyngitis
Toradol
TPA in ischemic stroke
Antibiotic choices in UTI; fosfomycin
Ketamine and ICP
Steroids in spinal cord trauma
ACLS
IV H2 vs PPI for gastritis
Steroids/racemic epi in croup
Bronchiolitis
Anticholinergics in pediatric asthma
Oxygen in chest pain/MI
Pharmacologic treatment for cough/sore throat

What specifically is bad about mimicking your attending's narcotic dosing? If your attending has dosed hundreds of patients in a similar manner with good outcomes, manifested by them not losing their hospital privileges or being sued out of existence, why not try their method?

Do you think that there is never a time for treating strep throat, sinusitis, or otitis media? In the past month, I've diagnosed pneumonia after 2 different patients presented with normal chest x-rays and had pleuritic chest pain, dyspnea, were afebrile, and had normal WBC's. In the old days, I would have missed those patients and probably not given them antibiotics if it weren't for positive d-dimers that made me scan their chest. In this day of Press-Ganey, litigation, and hyper-vigilant public and local rumor-mills, every missed diagnosis is broadcast far and wide and berated from the patients to the CEO of the hospital. Moral of the story, if it sounds like a good story for pneumonia, it is reasonable to give them antibiotics despite what the chest x-ray shows or whether they have a fever or not. Similarly, there are patients who have very early abscesses, or early bacteremia as a result of pharyngitis, and will benefit from antibiotics.

Do you have another non-narcotic IV pain medication other than toradol? Sure it is hard on the kidneys, and might cause some surgical oozing, but it works. What exactly is the controversy you are referring to?

TPA in stroke is the standard of care according to American Heart Association. Will you refuse to give it if a neurologist tells you to?

OK, steroids in spinal cord trauma is a valid topic, but that is quickly going by the wayside and is just a matter of preference on the part of the doctor who is going to take care of the patient as an in-patient.

Do you not like ACLS? You've got to be more specific...surely you don't disagree with cardioverting unstable rhythms.

Ketamine and head trauma is a topic that just hasn't had definitive research done yet. Might it be OK? Sure, but I wouldn't bet my career on it at this second.

I could go on an on, but I think specific examples muddy the picture somewhat.

Mimicry is a great way to learn to practice. If you wanted to read the original articles on every medication, disease, treatment, and intervention that is relevant to Emergency Medicine, and only practice "evidence-based medicine", you would read for the next hundred years and still not get there.

So many times, after researching a certain topic and plowing through the original literature, you tend to come to various conclusions...

1. The data shows a trend, but it isn't totally clear-cut
2. There is little data, more studies are needed
3. There is little data, we will likely never have enough to make conclusions with (What woman would ever volunteer for a study to take unnecessary medications during pregnancy and see if their kids are screwed up as a result?)
4. Damn the data, my patient is not a statistic. They either have a disease or they don't. A treatment will either help or not. If there is even a remote chance that they have a disease and I know of a treatment that could possibly help...I'm giving it a shot, because...what else do I do?

You've got a patient in front of you, asking you to heal them. I wish I had a Harry Potter wand and could wave it and get an exact answer, but all I've got is a history and physical, some medicines, and a few simple procedures. The patient knows my toolbox and expects me to use it.

Mimicry is a short-cut, a way to stand on the shoulders of someone who has come before, studied for decades, read their guts out, seen tens of thousands of patient, and decided that a certain practice is acceptable. Yes, question with boldness, but unless you've got a peer-reviewed article in hand that shows blatant malpractice on the part of your attending, shut-up and move the meat.
 
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😉
 
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Second, who uses 4-0 on a face?? I was taught 5-0 or smaller.

Sorry, I misread the abstract; the deep layers were 4-0 or 5-0 at their discretion. For the skin closure, the wound was closed with 5-0, half the wound with gut, and half nylon.

The larger study from Pediatric Emergency Care is probably the most useful one for drawing conclusions, and those were all simple interrupted gut sutures vs nylon sutures.

Mimicry is a short-cut, a way to stand on the shoulders of someone who has come before, studied for decades, read their guts out, seen tens of thousands of patient, and decided that a certain practice is acceptable. Yes, question with boldness, but unless you've got a peer-reviewed article in hand that shows blatant malpractice on the part of your attending, shut-up and move the meat.

It's a lecture, it's academics. The point is not to pretend I know more than people who have been doing this for years, only that it is important to understand and ask questions regarding why you're doing these things. I'll never get to every topic in an hour, but enough to fulfill my lecture obligation and maybe inspire someone to look at their peers' practice vs. the evidence for themselves and make their own decisions.

And, when an attending adds on a d-dimer to your labs and you ask him: "Name one risk factor or clinical feature this person has for pulmonary embolism." and his answer is: "Well, maybe he has a risk factor that no one's discovered yet, but he has it." maybe mimicry isn't so cool.
 
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One of my mini-peeves in my residency and medicine in general is the extent to which we tend to just practice base on mimicry rather than questioning the evidence upon which we base our actions, and actually understand why we do even the simplest things. So, anyway, I have a lecture to give in residency here in a couple months, and I thinking of running through a variety of common and not-so common topics where I thought maybe we could give a little more thought to our practice.

I had sort of a quick list of topics off the top of my head I might include, and I was curious if anyone else had some suggestions. I few topics I've come up with so far:
Narcotic dosing for acute pain
Antibiotics in otitis/sinusitis/strep pharyngitis
Toradol
TPA in ischemic stroke
Antibiotic choices in UTI; fosfomycin
Ketamine and ICP
Steroids in spinal cord trauma
ACLS
IV H2 vs PPI for gastritis
Steroids/racemic epi in croup
Bronchiolitis
Anticholinergics in pediatric asthma
Oxygen in chest pain/MI
Pharmacologic treatment for cough/sore throat

Anything else anyone might suggest you wish people would think about before they do it?

I am still not sure of the above what your place's practices could be, that deviate from the evidence. For example, do you not use the CENTOR criteria when deciding who to test and treat for strep? Do you not review the literature on which ischemic strokes should be treated with TPA, and practice this way? Do you not follow ACLS (for which the evidence comes from many places including Rochester, MN where I trained?) Granted there is no evidence that created a control group to not receive in oxygen in MI, but are you worried that it is causing harm to your patients?

Your list of topics, are filled with literature supporting practice; are you sure that your attendings aren't practice in concord with it? Or is it that they dont discuss the evidence with you?

Im very curious, and hope your search and presentation helps bring peace to your peeves.

TL
 
I am still not sure of the above what your place's practices could be, that deviate from the evidence. For example, do you not use the CENTOR criteria when deciding who to test and treat for strep? Do you not review the literature on which ischemic strokes should be treated with TPA, and practice this way? Do you not follow ACLS (for which the evidence comes from many places including Rochester, MN where I trained?) Granted there is no evidence that created a control group to not receive in oxygen in MI, but are you worried that it is causing harm to your patients?

Your list of topics, are filled with literature supporting practice; are you sure that your attendings aren't practice in concord with it? Or is it that they dont discuss the evidence with you?

Im very curious, and hope your search and presentation helps bring peace to your peeves.

TL
No, his point is that there is plenty of EBM against the norms of these, but we do them anyway.
No evidence supports ACLS. None. Plenty supports not doing anything beyond electricity and compressions. Intubation is actually harmful in the studies. And yes, O2 might be harmful, we just don't know.
Antibiotics for strep is worthless, so what difference does the CENTOR criteria mean? Testing for something that treating doesn't do anything for is also a waste. No evidence since the 50s supports antibiotics reducing PSGN or Rheumatic Fever. And on and on.
 
No evidence since the 50s supports antibiotics reducing PSGN or Rheumatic Fever. And on and on.

You need a high prevalence of the rheumatogenic strain of strep to have significant benefit in prevention of rheumatic fever from antibiotics in strep; this is the case in places like India. As for suppurative complications like AOM or peri-tonsillar abscess, the Cochrane Reviews and the best evidence I find shows your base rate for suppurative complications with antibiotics is about 4 in 10,000, while without it, your base rate would be about 7 in 10,000. Alternatively, over the last decade, Sweden went on an antibiotic reducing binge, and they successfully decreased their macrolide-resistant streptococcus and their MRSA spread.

As for ACLS in cardiac arrest, there's definitely no solid evidence that doing anything more than cardiocerebral resuscitation and defib have benefit. Evidence such as:
Ann Emerg Med. 2007 Dec;50(6):635-42. Epub 2007 May 23.
Survival outcomes with the introduction of intravenous epinephrine in the management of out-of-hospital cardiac arrest.
PMID: 17509730

JAMA. 2009 Nov 25;302(20):2222-9.
Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial.
PMID: 19934423

Happy to review other evidence, if you have it.
 
While I agree with the sentiment that one should have sound reasons (and preferably, good evidence) for rejecting the received wisdom of medicine, anyone who has been practicing for more than a couple years should be able to recall multiple "standards of care" that have been discredited. If you can't, then you haven't been paying attention. Even BASIC LIFE SUPPORT has changed since I learned it back in med school. A lot of these topics are overdue for review.

Jaracoba's point that tracing each and every practice back to its primary source would be a Herculean task is well-taken. So one person can never do a comprehensive job. I still applaud the OP for wanting to chip away at our ossified practices.
 
Do you not review the literature on which ischemic strokes should be treated with TPA, and practice this way?

The discussion of TPA in stroke likely far exceeds the space available in this thread, and almost certainly my humble lecture. There are enough negative studies for TPA in stroke, and far too many manufacturer-supported studies with misinterpreted conclusions from the data, that I am not sold that the increased likelihood of a better outcome is greater than the increased likelihood of a poorer one.

I cannot practice in this legal environment without giving eligible stroke patients TPA, but, certainly, if at any point I can offload that order onto the neurologist (which is frequently the case at our training institution), I am more than happy.

A pop-quiz on the CENTOR criteria amongst our attendings might generate some furrowed brows, both on the criteria, and how to correctly apply it.
 
No evidence supports ACLS. None.

I am traveling currently and dont have all my journals, but I recall reading something in the Journal of Resuscitation that evaluated prospectively in multiple centers the immediate success of resuscitation, 30 day and more long term survival of patients suffering in hospital arrest when comparing teams that had at least one ACLS trained member vs those that had none, and they found significant improvements in all outcomes. I believe it was like 15-20% increased survival in the immediate resuscitative efforts. This was in the last 3-5 years too....so there is evidence my friend. As with everything, we can hope for better studies (please dont randomize me if I code to the non-ACLS group)....but there is evidence.

I do agree that cardiocerebral resuscitation (more compressions, less focus on ventilation) is becoming more interesting and I heard quiet whispers that it would be in the next ACLS iteration while I was in Rochester. It sounds like you are trying to find your own way through the debate too...

As for antibiotics in streptococcal pharyngitis, the reduction is not in rheumatic fever, but in rheumatic heart disease. This may seem like semantics, but it may help you find the evidence. I had once read it, but I wont pretend to remember when and where anymore. I agree antibiotics have not been shown to reduce the incidence of rheumatic fever or post streptococcal glomerulonephritis, or significantly shorten the duration of the illness...but rheumatic valvulopathies my friend is why amoxicillin is still a worthwhile product. (I am speaking as one who has a particular interest in cardiac valvulopathies).

In any case, I am still not sure what the question here is....

TL
 
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The discussion of TPA in stroke likely far exceeds the space available in this thread, and almost certainly my humble lecture. There are enough negative studies for TPA in stroke, and far too many manufacturer-supported studies with misinterpreted conclusions from the data, that I am not sold that the increased likelihood of a better outcome is greater than the increased likelihood of a poorer one.

I cannot practice in this legal environment without giving eligible stroke patients TPA, but, certainly, if at any point I can offload that order onto the neurologist (which is frequently the case at our training institution), I am more than happy.

A pop-quiz on the CENTOR criteria amongst our attendings might generate some furrowed brows, both on the criteria, and how to correctly apply it.

As far as tPA, I am not sold on it for devastating strokes or strokes with minor deficits based on Hoffman's graphic depictions of the data. But I do know that docs are sued more often for withholding it than giving it. Even if I know that the data shows a non-beneficence for it, I'm not going to bet my livelihood on it just because I know it's correct. What I may do is as you said try to get the neurologist to be the one to request it and put the order in for it.
 
The question for antibiotics in strep, like many questions in medicine, is whether we'd rather do a small amount of harm to a large number of individuals vs allow one person to benefit.

Clin Infect Dis. 2009 Jul 1;49(1):78-84.
Seven-year surveillance of north american pediatric group a streptococcal pharyngitis isolates.
PMID: 19480575

Rheumatic fever and rheumatic heart disease - report of a WHO Expert Consultation
http://www.who.int/entity/cardiovascular_diseases/resources/en/cvd_trs923.pdf

Incidence in 1982 of rheumatic heart disease in the U.S. was 1 in 100,000 - over 25 years ago. In 2009, 14-16% of strep strains in the U.S. were the rheumatogenic subtypes - down from 49% in a 1961-68 survey. Even at the peak of rheumatogenesis, only 3% of adults and 0.3% of children afflicted with streptococcal pharyngitis developed rheumatic disease.

Pediatr Infect Dis J. 2009 Jul;28(7):e259-64.
Meta-analysis of trials of streptococcal throat treatment programs to prevent rheumatic fever.
PMID: 19561421

Based on mostly poor-quality studies in populations with high prevalence of disease, the relative reduction in rheumatic fever is going to be about 60% when antibiotics for primary prevention are implemented. The increasingly relevant question, as the disease incidence decreases, is whether the absolute risk reduction justifies the cost expenditures and adverse individual and community effects of antibiotics.
 
The question for antibiotics in strep, like many questions in medicine, is whether we'd rather do a small amount of harm to a large number of individuals vs allow one person to benefit.

Clin Infect Dis. 2009 Jul 1;49(1):78-84.
Seven-year surveillance of north american pediatric group a streptococcal pharyngitis isolates.
PMID: 19480575

Rheumatic fever and rheumatic heart disease - report of a WHO Expert Consultation
http://www.who.int/entity/cardiovascular_diseases/resources/en/cvd_trs923.pdf

Incidence in 1982 of rheumatic heart disease in the U.S. was 1 in 100,000 - over 25 years ago. In 2009, 14-16% of strep strains in the U.S. were the rheumatogenic subtypes - down from 49% in a 1961-68 survey. Even at the peak of rheumatogenesis, only 3% of adults and 0.3% of children afflicted with streptococcal pharyngitis developed rheumatic disease.

Pediatr Infect Dis J. 2009 Jul;28(7):e259-64.
Meta-analysis of trials of streptococcal throat treatment programs to prevent rheumatic fever.
PMID: 19561421

Based on mostly poor-quality studies in populations with high prevalence of disease, the relative reduction in rheumatic fever is going to be about 60% when antibiotics for primary prevention are implemented. The increasingly relevant question, as the disease incidence decreases, is whether the absolute risk reduction justifies the cost expenditures and adverse individual and community effects of antibiotics.

Great stuff and great discussion. I wonder (and hope) our practice will change, given the amount of antibiotics handed out. Also remember that kids under 3 don't even get rheumatic heart disease, so there's no reason to even test them for strep.
 
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I thought it was kids under 2 rarely get GAS pharyngitis, therefore very difficult to get rheumatic heart disease.

I actually just finished reading about pharyngitis and had a question. It said that for GAS, antibiotics should be given within 9 days of onset of symptoms to prevent rheumatic heart disease. Does this mean if they present after that 9 days you will be unable to prevent it, but you still treat to help the patient get through the infection?
 
I thought it was kids under 2 rarely get GAS pharyngitis, therefore very difficult to get rheumatic heart disease.

I've heard this as well, but that doesn't mean they don't get rheumatic heart disease which is why I was asking for clarification.
 
i use fast absorbing gut for almost all of my facial lacs and most other lacs not under tension. Simple interupted sutures, no need to return for removal.

+1
 
OP, another topic for your consideration: pre-treatment with lidocaine for TBI intubations? Fentanyl?

Cool lecture idea...I hope it goes well. As others have said, pick 3-4 well chosen "peeves" and address those in some detail. Chip away at the house, don't try to knock it down in one move.

Rendar5, Hoffman's '09 paper with the "graphic dipiction" is horrible, please don't use it to make clinical decisions...One cannot create new epidemiologic/data analytic techniques just to show results that fit your personal bias. Horrible.
 
I've heard this as well, but that doesn't mean they don't get rheumatic heart disease which is why I was asking for clarification.

Strangely, I have heard that their immune systems are unable to generate the response required for rheumatic heart disease at very young ages...I dont know the validity of this. Utah has the youngest children in general with RHD...odd fact I have validated in the past.

TL
 
OP, another topic for your consideration: pre-treatment with lidocaine for TBI intubations? Fentanyl?

Cool lecture idea...I hope it goes well. As others have said, pick 3-4 well chosen "peeves" and address those in some detail. Chip away at the house, don't try to knock it down in one move.

Rendar5, Hoffman's '09 paper with the "graphic dipiction" is horrible, please don't use it to make clinical decisions...One cannot create new epidemiologic/data analytic techniques just to show results that fit your personal bias. Horrible.

I don't quite get what's wrong with those graphical depiction considering that there are also problems with the methods used in the original papers: i.e. taking an entire clinical spectrum of disease and treating it as one entire disease. The graphical depiction is one means to look at the data as a whole over a spectrum of disease.

Yes, I realize that using the Hoffman analysis is tantamount to saying there's definitive evidence that steroids help spinal injuries (another example of a secondary group analysis).

But look at it at face value: strokes with a deficit of numbness in a pinky is a different entity than a stroke that causes hemiparesis versus a stroke involving total vegetation. The NINDS study never even looked at degree of improvement in its tools to study the efficacy of tPA. It just looked at whether there was an improvement of 4 on the NIH stroke scale among a couple other studies. And unfortunatley, no one's even allowed to study it properly anymore because it's an ethics concern to not give tpa. Doesn't mean tPA sucks. It means that the data isn't there to compare small degree of disease to medium degree of disease to large degree of disease.
 
Strangely, I have heard that their immune systems are unable to generate the response required for rheumatic heart disease at very young ages...I dont know the validity of this. Utah has the youngest children in general with RHD...odd fact I have validated in the past.

TL
How young?

This is my understanding, though I'll ask our ID guy for more specifics. But basically kids under 3 (some may say 2 to be more conservative) aren't at risk for getting rheumatic heart disease. They can definitely be colonized by GAS and you will pick these kids up with the rapid swab. Whether that represents disease is somewhat controversial but ultimately irrelevant. Either way, since they don't get the complications, don't check for the bug. If you get a positive rapid strep, you've put yourself in a position where you'll probably treat. Amox doesn't really make anyone get better any faster.

The only time I would check and/or treat a kid under 3 would be if the whole family keeps getting symptomatic strep infections over and over again, and you want to find the carrier.

Of course, you can always diagnose acute otitis media. 😛

There's also data that we are over treating kids with antibiotics (duh), and that this treatment is making it harder to treat real disease. A recent study out showed UTIs were much more likely to be resistant if the kid had been treated with amox for some reason or another in the past month or so.
 
Okay, here's what our peds ID director said (I'll post the email). He uses age 4 for the cut off interestingly (I'll still swab a 4 year old personally).

My feeling is that the reason most people suggest not testing young kids for strep is because they don’t get it much. We just don't see rheumatic heart disease in this age group either. Whether that's because they aren't susceptible or because the disease is rare is hard to say and would be very difficult to study one way or another.

Surveys of causes of tonsillopharyngitis done many years ago consistently demonstrated that strep pharyngitis is a disease of school-age kids, and that it was pretty uncommon in toddlers and preschoolers.

Now, many things have changed since then, including the fact that when those studies were done, most kids never went to “school” until kindergarten, and most of them were not in daycare centers or other situations where they were around a lot of other children. I don't know that anyone has restudied this in the past 10 years.

I still believe (until proven otherwise) that the majority of kids under age 4 do not need to be tested for strep and that you'll just find carriers by checking.
 
Pediatrics. 2003 Nov;112(5):1065-8.
Rheumatic fever in children younger than 5 years: is the presentation different?
PMID: 14595047

Of 541 cases of rheumatic fever between 1985-2000, 5% were under age 5, median 4, as young as 23 months. Half had carditis, and 13/14 of those had valvular disease at 5+ year follow-up.

I can see support for the common teaching that GAS pharyngitis isn't a significant clinical entity under age two, but, if you still believe strep needs to be treated to prevent RHD, then I would swab and treat folks over 2.
 
Pediatrics. 2003 Nov;112(5):1065-8.
Rheumatic fever in children younger than 5 years: is the presentation different?
PMID: 14595047

Of 541 cases of rheumatic fever between 1985-2000, 5% were under age 5, median 4, as young as 23 months. Half had carditis, and 13/14 of those had valvular disease at 5+ year follow-up.

I can see support for the common teaching that GAS pharyngitis isn't a significant clinical entity under age two, but, if you still believe strep needs to be treated to prevent RHD, then I would swab and treat folks over 2.


Out of curiosity, how do you think the risk of anaphylaxis or Stevens-Johnson's Syndrome from antibiotic usage compares to the overall risk of RHD? I'd bet a real analysis would come out AGAINST the use of abx in strep. Just saying, I've seen two cases of SJS in kids in my career and I've lost track of anaphylaxis. I've never seen RHD. Of course, that is an N=1 provider...
 
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Rendar5, Hoffman's '09 paper with the "graphic dipiction" is horrible, please don't use it to make clinical decisions...One cannot create new epidemiologic/data analytic techniques just to show results that fit your personal bias. Horrible.

As opposed to the manufacturer's sponsored studies that "clearly" demarcated the morbidity and mortality of the adverse effects, but treated any positive gain as a complete recovery? I mean come on the original studies are FAR more biased than Hoffman...

tPA unfortunately doesn't work well and for populations as a whole is a bad choice. There are individual patients where it may be a good choice (the 40 year old with the sudden, devastating stroke and no co-morbid conditions), but overall the data are VERY weak, especially when applied to the septo-, octo- and nono-generians that frequent our departments.
 
Out of curiosity, how do you think the risk of anaphylaxis or Stevens-Johnson's Syndrome from antibiotic usage compares to the overall risk of RHD? I'd bet a real analysis would come out AGAINST the use of abx in strep. Just saying, I've seen two cases of SJS in kids in my career and I've lost track of anaphylaxis. I've never seen RHD. Of course, that is an N=1 provider...

The flip side is I've seen two kids with RHD and none with SJS....
 
I mean come on the original studies are FAR more biased than Hoffman...

I am also not impressed by the graphic reanalysis of NINDS. There must be a more straightforward way to make the point they always try to make - which is that differences in baseline disease severity between the placebo group and the treatment group explain all their differences in outcomes.

More usefully, Mallon and Hoffman on the June EMA highlight data from:
Lancet Neurol. 2009 Dec;8(12):1095-102. Epub 2009 Oct 21.
Stroke treatment with alteplase given 3.0-4.5 h after onset of acute ischaemic stroke (ECASS III): additional outcomes and subgroup analysis of a randomised controlled trial.
PMID: 19850525

Specifically, Figure 5 in which you can note the alteplase group only enrolled 37/418 (8.8%) patients with NIHSS >20, while the placebo group enrolled 52/403 (12.9%) - which is basically 4% additional placebo group patients who are never going to reach your favorable mRS at 30- or 90-days.

Entertainingly enough, for someone who is unamused by TPA as much as myself, my first patient in independent practice out in single-coverage moonlighting was a acute CVA with 1.25 hours since symptom onset. All her results were back by 2 hours after onset, and I could have pushed TPA within 2.25.

Am J Emerg Med. 2010 Mar;28(3):359-63.
Intravenous tissue plasminogen activator and stroke in the elderly.
PMID: 20223397
Limited n data set showing that functional outcomes are not conclusively improved, and their LR for ICH is greater than their younger comparison.

Eur J Neurol. 2010 Jun 1;17(6):866-70. Epub 2010 Mar 1.
tPA treatment for acute ischaemic stroke in patients with leukoaraiosis.
PMID: 20236179
LR 2.85 for sICH in patients with leukoariosis in single-center consecutive TPA patient cohort.

My patient was 89 years old, leukoariosis, no history of ICH - but had aneurysmal clipping 20 years ago. I felt like her likelihood of outcome improvement vs sICH and death was unfavorable. Discussed it with her, her family, her PMD, did not treat, and documented like crazy. No question I will never forget my first ever patient.

My real problem with TPA? No one ever mentions ECASS or ECASS II or the other negative trials out there. And, the cited studies that are purportedly positive are frequently pharmaceutical company sponsored - and I don't trust the integrity of those protocols at all.

Contemp Clin Trials. 2008 Mar;29(2):109-13. Epub 2007 Aug 16.
Pharmaceutical company funding and its consequences: a qualitative systematic review.
PMID: 17919992
The corruption of medical literature by sponsorship and ghost management of clinical trials.

Am J Psychiatry. 2006 Feb;163(2):185-94.
Why olanzapine beats risperidone, risperidone beats quetiapine, and quetiapine beats olanzapine: an exploratory analysis of head-to-head comparison studies of second-generation antipsychotics.
PMID: 16449469
Sample discussion regarding study bias in second-generation atypical antipsychotics in which 90% of the trials favored the sponsored drug.

Hard to trust anything you read these days.
 
The flip side is I've seen two kids with RHD and none with SJS....

I've seen plenty. And there's also a fair amount of litigation directed towards SJS. Google SJS and the first few hits you come to are lawyers. 😡

That said, I've never seen it after taking amoxicillin. Most has been bactrim, polytrim or dilantin. One time it was ibuprofen.

I'm not sure it would be a reason not to treat though. It does make you think, however; all actions may have unintended consequences.

Thanks for the article xaelia! I will amend my previous statement: I still think kids 3 and under GENERALLY do not need to be tested for GAS in the throat. Exceptions would be:
1) older sibling with culture- or rapid strep-confirmed strep living in the same home
2) classic scarlatiniform rash
3) classic symptoms, living in home with older child who has undiagnosed strep

My feeling is also that GAS doesn't cause cough, hoarseness, or runny/stuffy nose. Therefore, children with those symptoms (of ANY age) probably don't need to be tested for strep.
 
That said, I've never seen it after taking amoxicillin. Most has been bactrim, polytrim or dilantin. One time it was ibuprofen.

Huh, I wonder if you were inpatient or in the unit when I rotated through on ID. We consulted on a kiddo for r/o Kawasaki and thought it was SJS. Derm agreed IIRC. Related to Ibuprofen use.


We've had a small run of rheumatic heart disease where I am. A good portion of them had had abx for strep pharyngitis in the recent past.
 
I've seen 3 acute Steven's Johnson patients, all from bactrim. I've seen one RHD, and they had it as a child and were now in their 50s. They were also from the Phillipines.
 
Huh, I wonder if you were inpatient or in the unit when I rotated through on ID. We consulted on a kiddo for r/o Kawasaki and thought it was SJS. Derm agreed IIRC. Related to Ibuprofen use.

I was on the floor team when that came through. We must have crossed paths!

We've had a small run of rheumatic heart disease where I am. A good portion of them had had abx for strep pharyngitis in the recent past.

What age ranges have you been seeing?
 
We've had a small run of rheumatic heart disease where I am. A good portion of them had had abx for strep pharyngitis in the recent past.

Is your "small run" newly diagnosed RHD or previously diagnosed RHD in immigrants?

Are you practicing in the US or internationally? If you are practicing in a developed country, do you work with a particularly impoverished population (ie. native americans on reservations, indigenous populations of Austarailia, etc.)?

"A small run"😱 of RHD is fairly remarkable, otherwise.

HH
 
First, I have to apologize for a brain-keyboard disconnect. I should have said "a small run of rheumatic fever". I was not involved in all cases so I don't remember contemporaneous carditis/valvular involvement. But since this is interesting, I'll look into it (it just may take a bit; our EMR isn't incredibly helpful in searching for diagnoses, or I don't know how to do that data mining with it). The most recent case was one diagnosis based on the presence of Sydenham's chorea (Dx'd by Child Neuro). Echo was normal IIRC at this time.

I practice in a midwestern state. Again, I was not involved in all cases, so I don't have all details. The above case I was involved in was a native MW family. I've dealt with some phone calls from the parent of a crazy teen who I know has RHD with valvular disease; I believe both parent & teen emigrated from Mexico within last 10 years.
 
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