Critical Care, Improving Outcomes, Mythbusting

Dissections & digitometers

hello. Hello. HELLO!!!!!

Hi there. Just wanted to let you know that I finally rediscoved a use for the digitometer.

No, seriously.

This was a historical matched case-control study from 2002-2014 of 111 aortic dissection patients at 2 Canadian tertiary are centers and one regional cardiac referral center (and 111 case controls) looking specifically at bilateral blood pressure differential as well as pulse deficits as a marker for acute aortic dissection in the ED.

Not surprisingly, combining the two (blood pressure differential and pulse deficit) increased sensitivity (from 21% to 77%), but greatly decreases specificity (99% to 56%) – which is not quite ideal when dealing with needle in the haystack diagnoses.

Now, I do not know if it was because it was documented retrospectively (“oh no, they have a dissection on imaging, I better check pulses!”), or pulled up as part of a macro as a default (“pulses equal and brisk bilaterally’), and I would not be at all surprised if this were the case, but regardless, 21% of dissections having a pulse deficit vs 0.9% of non-dissections is pretty darn good.

Like +LR of 23.4 good. And in line with other studies reporting 24% sensitivity and 92% specificity.

Dont believe that BP differential is not a specific sign? Talk to your triage nurses to see how many times they recheck a blood pressure on a hypertensive patient in triage on the other arm – verified by prior studies showing over 50% of ED patients have >10 mmHg differential, and 19% have >20 mmHg differentials.

So while pulse deficit may possibly be over-exaggerated because of retrospective / biased ED charting, still, the absence of a pulse should at be nudging providers to consider advanced imaging sooner rather than later.

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Cardiology, Improving Throughput, Mythbusting

Yes, No, and Maybe – Magnesium for Afib RVR

I really, really, wanted this study to work.  Few things are more disheartening on an overnight observation shift than needing to place someone on a diltiazem drip after an inability to rate control. Ergo, I have been known to give a few grams of magnesium to try to decrease the likelihood of that happening. Therefore, on the surface, this study seems promising – it looks at standard of care for Atrial fibrillation with rapid ventricular response (dealer’s choice, metoprolol, diltiazem, or digoxin) given in combination with either one of 3 treatments: placebo, 4.5g of magnesium, or 9g of magnesium; with about 150 patients in each arm. This study took 5 years (!) over 3 academic centers in Tunisia, who’s ED’s service 90,000-110,000 patients per year. Patients needed to have a heart rate over 120 bpm, have a systolic BP >90 mmHg, and without: renal impairment, wide-complex tachycardia, decompensated CHF, acute myocardial infarction, or an impaired level of consciousness. All seems fair.

The results, at face value, seem great if you’re a magnesium believer: rate control at 24h of 83.3% for placebo, 97.9% for 4.5g MgSO4, and 94.1% for 9g of MgSO4. This is a great example of completely reading a paper before you start to fight about giving magnesium.

First, all groups used digoxin around 50% of the time for rate control.  This clearly does not mimic US practice. Nor does giving 4.5-9g of magnesium over 30 minutes.  Then the authors sneak this one in:

In a secondary analysis including only patients receiving beta blockers and calcium channel blockers, the obtained results were not significantly different compared to those found in the overall group.

This is sandwiched between mentions of adverse drug reactions (4% flushing in the 4.5g arm vs 12% in the 9g arm vs <1% in the placebo arm, and otherwise there was no significant difference between the 3 arms), and the discussion of 24h rate control. I am not 100% certain what they meant by this statement – were they referring to ADRs? Were they implying that there was no difference between metoprolol and diltiazem treated patients and placebo at 24 hours?  With only about 50% of patients per arm (~75 patients in total/arm) being treated with these agents, it would be hard to show a meaningful improvement.  Not to mention the fact that the actual data for this secondary analysis is nowhere to be found in this paper.  Nor have the authors responded to my email asking for it.

Then, of course, there are the prior trials with less than 60 patients / arm comparing diltiazem to metoprolol showing >90% efficacy with diltiazem.

And, of course, there is the next question, of are we doing any good?  Since rate control has not always shown to be in the patients best interest – a 6 fold higher rate of adverse events– and none of the ED AFib RVR magnesium studies look further out than 24 hours, perhaps we should cautiously, if at all, recommend magnesium, or even suggest waiting until long term outcomes are further elucidated.  Since this study took 5 years to complete, I do not see the desired study happening anytime soon.

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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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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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Improving Outcomes, Improving Throughput, Radiology

Parting the SEA with the almighty H&P (& rapid MRI).

Necessity is the mother of invention, and sometimes, necessity comes in the form of hospital administration after a bad outcome. The authors of this paper, essentially developed a rapid MRI protocol for suspected spinal epidural abscess after “several cases of SEA associated with delayed diagnoses and poor outcomes prompted the chairs of the departments of emergency medicine, neurosciences, medicine, and radiology, and members of the Division of Healthcare Quality, to develop a multidisciplinary, clinical decision support tool and imaging protocol with the goal of facilitating early recognition of SEA.”

Wow. Talk about moving mountains. If you’re department is anything like mine, it takes hours to agree on where we’re getting take out from; I cant imagine adding in 4 entire departments into the lunch-ordering mix, let alone all agree on a protocol.

They took a relatively simple approach – if you have new or worsening back/neck pain AND a history of spinal abscess or current/recent (6 months) bacteremia, straight to MRI. I think the recent bacteremia often gets lost in the work up, so I appreciate that they put this front and center. If there is no recent spinal infection or recent/current bacteremia, They looked at risk factors- and I’ll make this simple and break it into 2 categories: people putting things where they dont belong (IVDA, vascular catheters, spinal procedures/injections) and the recurrently ill: ED visit or antimicrobial treatment within 30 days or an infectious process elsewhere. If yes, head to MRI.

I’m torn a bit on this- while I want to applaud the authors for not dwelling on a variety of risk factors that only a small portion of the population has – alcoholism, HIV, severe COPD, the undomiciled, HepC, oncology patients, transplant patients, etc; to say that this group is pretty much captured in the recent ED visit category probably misses a fair amount of patients on the first go-round. And here is the problem of trying to find a needle in the haystack – its hard to increase sensitivity and specificity without causing a delay at some other portion of the food chain – every stat MRI for so many additional back pain patients pushes out another patient and potentially extends at least 1 other patients length of stay.

However.

Despite an increase from 56 MRI’s in the 7 months pre-intervention to 147 in the 7 months post-intervention, yield for a positive MRI (defined solely as SEA and not vertebral osteomyelitis or infectious discitis), went from 16.1% to 17.7%.

On first glance, that’s not a lot of improvement in yield, but they screened 3 times as many patients without losing yield! This is rather impressive. However, they tripled their ED MRI rate, and, even though they drastically cut turn around times from 8.6 hours to 4.4 hours from time of MRI order to radiology report, thats still well over 4 hours for patients with back pain in a highly optimized system. And while yes, they missed fewer SEAs, they probably still have a good percentage that they missed on first visit – the various forms of immunocompromised – the severe COPDer on repeated steroid prescriptions, the HepC patient, the elderly – these are likely missed on the first go round.

I think this is a great step towards creating a policy towards SEA workup. It needs some refinement, but is the best I’ve seen yet. It poses some issues for smaller facilities that do not have 24/7 MRI capabilities, as well as for consultants (neurology essentially becoming a house officer for ID and neurosurgery), and poses a big time crunch for the ED (again, neurology took control of these cases once the decision to MRI was performed, which the hospitalists must be thankful for!). In the end, there is no such thing as zero miss, but Baystate, with this study, demonstrates that, at least for one day, the H&P is not dead.

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