GI, Improving Outcomes, Mythbusting

The Better Poop Route.

This is a study comparing PO vs colonoscopy inserted fecal microbiota transplant for cdiff with the primary outcome the proportion of patients without a recurrence 12 weeks after stool transplantation.

 

Survey says- it doesnt matter how you do it, but both have their ups and downs.

 

While PO meds were significantly less costly, it was significantly less pleasant (44% vs 66% rated it “not at all unpleasant”) – understandably so as patients took FORTY capsules- under direct observation no less- which were made from a singular 80-100g donation. Colonoscopy implantation was performed with placement of 360cc of “fecal slurry in the cecum” – and was significantly more expensive ($874 vs $308). Colonoscopy patients had a 12.5% rate of minor adverse events vs 5.4% of the PO group (mostly nausea/vomiting or abdominal discomfort).

Further fun facts, participants most frequently characterized fecal transplants as “innovative treatment” (63% of patients), a “natural remedy” (41%), and “unpleasant, gross, or disgusting” (30%); which is surprisingly realistic to how providers feel about this same treatment.

Its nice to see the lower cost, less invasive treatment work equally well (both clocked in at about 95% rates of non-recurrence at 12 weeks), but geez, 40 tablets of poop seems a bit more like a lost dare than a medical necessity.

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Mythbusting

HEART score predicts adverse events for no risk chest pain patients – for a whole 66 patients.

There has been some buzz about one particular HEART score paper on SoMe recently, and while touting the HEART score is all the rage, the excitement over a whopping 66 patients seems downright silly.

This study screened about 5000 patients and excluded roughly 4700 patients – without obvious good reason – as “inclusion criteria were satisfied if the provider ordered an ECG and troponin for the evaluation of ACS. Consistent with prior studies, patients were excluded for the following reasons: new ST -segment elevation > 1mm, hypotension, life expectancy <1 year, a non -cardiac medical, surgical, or psychiatric illness determined by the provider to require admission, prior enrollment, non -English speaking, and incapacity or unwillingness to consent.” Seems like most would be included then, right? Except that was not the case at all. I just do not see how >90% of patients could be excluded based on these criteria, in a study done in the United States.

So we are led to believe that this tertiary care center, which has >100,000 annual ED visits, somehow could only scrounge 282 patients with chest pain to recruit into this study. They randomized 1:1 into the HEART “pathway” (HEART score plus serial troponins – more on this later), with usual care per ACC/AHA guidelines – admit/obs, serial troponins, and provocative testing in consultation with cardiology. They assessed adverse events (MI, revascularization, cardiac death), objective testing (stress or angiography), and future hospitalizations / ED visits within the year.

While yes, all sixty-six patients with a HEART score of 3 or less and 2 negative troponins (yep, a whole 66 no/low risk patients at a 100k + visit ED), did have zero adverse events at 1 year, the question really is, who cares? This is not enough patients to be excited about, and besides, these are essentially no-risk chest pain patients that shouldnt have a high risk of adverse events anyway. They represent a group whom we should not be doing additional testing on anyway!

As for all the others, there was no change in adverse events between HEART vs usual care- about 10% of patients had adverse events in each arm. As such, I dont read this as the HEART pathway being awesome at reducing long term issues, but rather, more of the futility of advanced testing aimed at reducing adverse events; The HEART score is merely equivocal to our current tools at future risk stratification. While this is good, I doubt it will result in fewer downstream tests in “higher risk” patients, if only because old habits die hard, Americans like to do more, and ACC/AHA recommend doing so. Choose wisely, perhaps?

Laughably, the authors open their paper with this line: “Care patterns for the evaluation of Emergency Department (ED) patients with possible acute coronary syndrome (ACS) in the United States are heterogeneous, inefficient, and costly.” And yet, where did we get this “HEART pathway” from? The HEART score did not have two troponins. To boot, neither did the largest study published looking at the HEART score. So what does a second troponin get you? Well, if you believe this study of over 45,000 patients, in which *all* comers had 2 troponins and 2 ekgs, [patients only excluded if abnormal vital signs were present & defined as hypotension (systolic blood pressure <100 mm Hg), tachycardia (pulse >100 beats/min), tachypnea (respiratory rate >20 breaths/min), or hypoxemia (oxygen saturation level <95%), or if they had electrocardiographic ischemia, a left bundle branch block, or a paced rhythm], they only identified a primary end point event in 4 of 7266 patients, 2 of which were noncardiac and 2 of which were possibly iatrogenic.

So, I again ask, where did the two troponin issue come from? Well, here it is- in one singular study, not doing a second troponin would have missed 5 adverse events out of 899 patients. Because the total event rate was 12, the authors state that their sensitivity went from 58% to 100%. While this sounds nice, it can also be reframed as a 1.33% miss rate vs 0.78% miss rate – an overall improvement of…. 0.55% with a second troponin. And, this has not really been replicated to demonstrate the value of a second troponin. So, either use the HEART score as it was meant, or use two troponins and gestalt- both probably get you into trouble and add waste to the system and you reach the point of minimal gains. You’re testing 200 plus patients to find one more bumped troponin that may or may not get a meaningful intervention.

So I ask hospital administrators and EM & cardiology colleagues: is it worth the extra 4+ hours (3 hours for the second troponin, plus time for the draw to occur and test to get processed & resulted), plus all of the associated resources & space not allotted to other patients due to these 4+ hours that are given to thousands of patients annually… is a decrease of 0.55% worth a second troponin? I imagine if time and bed space was allocated to others, the 0.55% increase of adverse events would be more than made up for across the rest of the patients within the department by earlier recognition and treatment of just about every other disease entity within the department.  Sounds like, at a minimum, a time to introduce shared decision making (“hey, we catch one in two hundred with a second troponin, want to stay another 4 hours? and no, you can not go outside and smoke.  How about a nicotine patch and a tuna sandwich?”).

And lastly, no, you can not say the HEART score results in low risk of 1 year adverse events based on a single center study that failed to enroll more than 66 patients.

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Improving Outcomes, Improving Throughput

POCUS guided Flexor Tenosynovitis

It feels good to be back! Now, fresh off the inaugural AAPA18 iScan ultrasound event, its only right that my next post is on two of my favorite things- POCUS and infectious disease.

This is a review of 73 patients presenting to an emergency hand clinic (!) over the course of 3.25 years with a pyogenic flexor tenosynovitis.  Yep, a whole 22 patients a year… at an emergency hand clinic.

All patients underwent a resident and attending surgeon eval as well as labs including CRP and films. 16 confirmed pyogenic flexor tenosynovitis patients were excluded (these were the slam dunk obvious ones)- while the remaining 57 underwent POCUS while pending labs. POCUS was done by either a resident with 2 years experience in MSK sono, an attending surgeon with sono training, or senior radiologist.  Suffice to say, that this isnt exactly us work-a-day EM providers.

Of the remaining 57 patients, there were 29 were ultrasound negative (non-thickened tendon sheath without hyperemia and no peritendonous effusion); all were given PO antibiotics and discharged with every other day follow up until symptom resolution; only one required OR intervention.

Of the 27 patients with positive ultrasound findings- 17 of these had either a positive OR culture or significant purulence seen at the time of OR washout.  While this results in a decreased PPV of 63%, and a decreased specificity of 74% – I maintain POCUS is actually much better; keep in mind these numbers do not include the 16 slam dunks on clinical exam.  It doesnt take into account the rapid sterilization after a single dose of antibiotics seen in CSF and ascites; nor the 30% negative OR-culture rate seen in other pyogenic flexor tenosynovitis studies.  Nor does it take into account that POCUS approaches MRI for sensitivity and specificity in prior studies.

Ultimately, it would be fantastic (and likely better medicine!) if, stateside, we could adopt an ultrasound first strategy (especially with a 97% NPV and 94% sensitivity!).  If POCUS negative, patients could get expedited follow up and oral antibiotics.  This is pretty much exactly what this group has done.  Presumably with this strategy, a small fraction of these more ugly “slam dunk” tenosynovitis cases may not require the OR (the group did not comment on positive OR-culture rates), and the patients in the middle ground could get expedited follow up or overnight observation and serial sonography.  It should be noted that “delayed” diagnoses which resulted in poor outcomes were >10 days out from the initiation of symptoms (!); so a day or two may not make much of a difference.  This study comes with the usual caveats- there are few MSK ultrasound courses in the USA (I contacted the Jefferson MSK fellowship, no dice for hand sonography!), different equipment than our usual sonosite machines, more training.  But that certainly does not mean we can not have something to aspire to.

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Cardiology, Improving Outcomes

Rising Risk Factors for CVD

This study looks at, a, um, rising star among cardiovascular risk factors:  erectile dysfunction.  ED and cardiovascular disease share many common risk factors (diabetes, smoking, obesity, etc), and prior studies have shown ED patients to have increased subclinical vascular disease such as increased coronary calcium scores, increased carotid plaque scores, etc.

Utilizing the MESA study, the authors followed ~1750 participants for 3.8 years on average, evaluating for cardiovascular disease (AMI, stroke, cardiac arrest, death) and coronary heart disease. Patients self-reported ED via the Massachusetts Male Aging Study.  Obviously this study is plagued by self-assessments which may or may not accurate, a composite endpoint, and is based on prior studies demonstrating the worsening surrogate markers; the authors do not tease out individual AMI, stroke or death risk from the composite endpoints either.

Ultimately, ED patients had more adverse cardiovascular events (6.3% versus 2.6%), resulting in an unadjusted hazard ratio of 2.6 and the risk persisted even after adjustment for traditional CVD risk factors, depression, and beta-blocker use.  Think of ED as an early warning sign of endothelial dysfunction, inflammation, and possibility, atherosclerosis.  ED is already in some UK risk stratification scores, will it make it to the US?

 

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Critical Care, GI, Improving Outcomes, Mythbusting

Less transfusions, the better, platelet style.

Over 4 years, the Mayo clinic reviewed over 40,000 ICU patients, and sought to determine if prophylactic platelets for critically ill thrombocytopenics matter.

Of these 40,000 ICU patients, they excluded anyone who received RBCs within 24 hours prior to the PLT count that triggered transfusion “to minimize the risk of including those with active bleeding” … The primary outcome was essentially to determine if transfusing platelets led to more RBC transfusions, and, secondarily, all-cause mortality, ICU and hospital free days (among others). Seems backwards, but whatever.

So what falls out of this data?

For all comers, in a propensity matched cohort, one transfusion begets another – (46.3 % of those with platelet transfusions also had an RBC transfusion vs 10.4% of those without platelet transfusions who had an RBC transfusion). Interestingly, those transfused platelets had less ICU free days (22.7 vs 20.8), more hospital free days (15.8 vs 13). When you look specifically at the ~5000 patients with <50k platelet counts and compare those who were/were not transfused platelets, there was no change in ICU mortality, 30 day mortality, ICU-free days, or hospital free days. While this was underpowered to determine statistical significance for those with platelet counts <50k, it is not hard to imagine a larger study to suggest similar benefits of not transfusing these patients- particularly since this study saw fewer hospital free days and fewer ICU free stays (10.2 vs 7.8 days and 19.9 vs 18.3 days respectively) – favoring a more restrictive transfusion strategy (but again, not meeting statistical significance, perhaps due to so few patients with <50k PLT).

This is not the first study I have seen suggesting empiric transfusion or outright canceling of procedures based on platelet counts between 50k and 150k is essentially bunk, and that prophylactic platelet therapy is of little benefit, if not outright harmful. There is even a flicker of a signal that prophylactic platelet transfusions >20k may not be beneficial – but this has yet to be definitively shown true -yet.

I can not agree more with the last words to the authors, “Finally, it must be acknowledged that while clinical trajectories did not improve for the cohort as a whole after platelet transfusion, it is possible that certain subpopulations may indeed benefit from the intervention, though these subgroups have yet to be identified.”

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Mythbusting

Delayed endocarditis diagnosis? The patient can have as many diseases as they please.

This is exploratory look at patients diagnosed with endocarditis at admission versus those with a delayed diagnosis. Granted, this is not a US study, and over a 9 year period at a single center, but does provide an interesting look at how we manage these patients….

They looked at those with an admitting diagnosis of endocarditis that eventually went on to have this as a final diagnosis as well (54 patients), and compared them to patients with a non-endocarditis initial diagnosis to those who eventually had a final diagnosis of endocarditis (64 patients).

Even in the two slam-dunk groups- the IVDA & those with valve replacements, the diagnosis was delayed in the 38% of the time for those with a history of IVDA. For those with a valve replacement there were also significant delays with native valves delayed 63% of time, vs prosthetics delayed 24% of time…. Are we really bad at diagnosing this? Let’s peel back this onion.

Cases were placed into 3 categories: (1) complications of endocarditis, but not immediately recognized as endocarditis – 70% of cases (2) infectious disease unrelated to endocarditis (14% of cases) – ie, hepatitis (3) inconsistent non-infectious disease (16% of cases).

Of those in the “complications” category, only 10% were unlikely to be dosed with antibiotics – they were admitted for “stroke” or CHF/ pulmonary edema. This is clearly understandable. Do we need STAT echos for the pulmonary edema patient? Or for the stroke? STAT echo’s right away for all of these patients – or perhaps routinely ordering them on all CHF / stroke patients may prove more costly and harmful than its worth.

The author’s make the argument that there is significant mortality involved with an initial missed diagnosis in their cohort- 75% vs 25% (!!!). I’m not certain these represent a complete whiff on the part of the treating clinicians. Rather, I would argue that these patients had their complications recognized and treated appropriately (ie, the pneumonia and UTI’s got antibiotics initially), and that these patients were likely sicker to begin with and that is why they had all the additional complications and higher mortality.

While perhaps a heightened awareness of valve replacement patients, and/or awareness of the disease process may help, but sadly, when you are looking for a needle in the haystack, having a 100% sensitive and specific diagnostic algorithm is unreasonable. When can certainly do better, but how much better without causing harms to the rest of the department remains debatable.

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Mythbusting, Radiology

POCUS gel – hot or not?

“Wow thats cold!”

It’s a common statement after applying the probe to a patient, and wouldn’t you love to know the answer to the age old question, “Does gel temperature matter for patient satisfaction?”… While we have some data suggesting improved patient satisfaction scores with POCUS, but could those scores be better if the gel was warmed? Or perhaps would all the improvement in satisfaction scores be lost with cool gel?

This group performed bedside ultrasound using heated gel (102F) or room-temperature gel (82.3F – quite the warm department!).  The investigators even went so far as to trying to blind those performing the study with a heat-resistant glove (!) – and even validated gel temperature through weekly quality assurance measurements throughout the study period.  The investigators informed all patients that the study entailed investigation into various measures to improve patient satisfaction with POCUS, but did not inform them of their specific focus on gel temperature.  After POCUS was performed, patients completed the following survey: “How satisfied are you with the experience of having a bedside ultrasound today?” (on a 100-mm visual analogue scale (VAS) for satisfaction), as well as, “Are you satisfied with the care you received today in the emergency department (yes or no), as well as “How professional was the provider who performed your bedside ultrasound?” (A Likert scale spanning 1-5)

All in all, 59 patients underwent randomization to POCUS with room-temperature gel and 61 underwent randomization to heated gel.

In the end, heated gel made no difference for any of the three questions posed to patients. While I think those of us utilizing warm gel were probably making space in the blanket warmer, it’s nice to know that this intervention, while nice, does not make much of a difference, and a “special” warmer specific for gel in your department is probably unnecessary.

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