Causes of reduced conscious level in North Dublin

[Apologies to anyone offended by the title, my tongue is firmly in cheek if that helps...]

The hospital I currently work in is in one of the poorer areas of Dublin. There are a few hospitals with populations like ours but not many. It makes for an interesting working environment. As a result you become an expert in inner city emergency medicine which has its own specific problems. Here’s a list of differentials for the unconscious patient in my current context. Feel free to suggest any other important ones that i’ve left out

Common:

  • alcohol
  • heroin
  • alcohol and heroin
  • alcohol and heroin and benzos
  • more alcohol
  • benzos
  • ICH/stroke
  • hyponatremia
  • hypercarbia

The ones I probably miss because I assume everything is in the first category:

  • serotonin syndrome
  • the chronic sub dural
  • carbon monoxide
  • myxodema coma
  • liver failure
  • toxic alcohols
  • NMS

[Image via wikimedia commons]

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Age Adjusted D-dimer Cut Offs

This paper recently published trying to confirm if it’s OK to raise the d-dimer cut off in older people.

“Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: the ADJUST-PE Study.” 311, no. 11 (March 19, 2014): 1117–1124. doi:10.1001/jama.2014.2135. PMID 24643601

Hopefully you’ve heard about this already through ER Cast and over on BoringEM (if you want more discussion on d-dimer, then be sure and check out the LITFL page on it.) Basically if you’re over 50 then your new d-dimer cut off is 10 times your age. These guys tested that approach.

METHODS

  • prospective data on pts with suspected PE from Europe.
  • Stratified to low or high risk
  • D-dimers were sent on the low risk ones and if -ve work up was finished. If +ve they went for CTPA
  • follow up at 3 months by phone
  • 3 blinded ‘experts’ adjudicated if something bad happened to them

RESULTS

  • 3300
    • 2900 were ‘non-high’ probability and went down the d-dimer path
    • 400 were high and went straight to scan
  • 330 fell into the ‘age adjusted’ level and all of these guys (who previously would have got advanced imaging) seemed to do well (for what that’s worth)
  • of note their overall rule in rate for PE was 20%, much higher than many contemporary studies

THOUGHTS

We all want ways to rule out PE and avoid the CT scans. This might be another way to safely rule patients out, though it’s worth bearing in mind that it’s only going to affect a small number of patients.

This is by no means a perfect study. The group of interest did not actually get the reference diagnostic test (the CTPA) so we’re dependent on the veracity of their follow up to know if it’s truly OK to pursue this new strategy of age-adjusted cut off and forgo more advanced testing. This is a common problem in studies like this (see the Perry CT for SAH article as a great example of controversy over this very issue) and it doesn’t mean that it’s all nonsense but as always be sure to use your noodle when thinking about it.

[Image Credit: Wikimedia Commons]

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Tasty Morsels of EM 037 – Heart Transplants

I keep a little, ever-expanding note on my phone where I jot down little morsels of goodness that I pick up while listening to or reading one of the many excellent sites/podcasts in the useful resource section. They’re useful in a kind of “board review” way. I tend to skip the really basic stuff and try and focus on what I didn’t know.

I’ll try and transfer them here for your enlightenment.

  • 5 year survival about 75%
  • most common ED complaints are fever, SOB, GI probs, chest pain
  • baseline tachycardia is normal as no vagus innervation to the transplanted heart
  • patient has no pericardium but due to scarring clinical tamponade can still develop
  • chest pain is rarely related to ischaemia as heart is denervated (most anginal pain is probably sympathetically mediated and the sympathetic plexi around the heart would have been disconnected at transplant)
  • however ischaemia is common as atherosclerosis is accelerated in the graft. Often presents as CHF or arrhythmia.
  • CMV is a risk factor for accelerated atherosclerosis.
  • ECG Often demonstrates two p waves. One is from native sinus node (which is often left in place as it lies in the post RA) and the other is from the donor SA node. The donor p wave is the one that should conduct.
Via Wikipedia

Via Wikipedia

  • rarely a heterotropic transplant is done where the the native heart remains in entirety in the chest. The ECG in this scenario is understandably bizarre.

Reference:

Rosen 7th Edition p2369-70

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The ProCESS Trial

This trial is kind of big news. Big news in the way TTM was. Be sure to get the paper (which is free for now) and the supplement that goes with it.

There has already been some great discussion online so be sure and check it out.

So there’s no shortage of great editorialising already out there.

That being said, I wrote most of this on the plane on the way home from SMACC so figured I may at least get it out there.

BACKGROUND

Sepsis is big and sexy in critical care. It covers a huge range of patients and has turned individual conditions into one clinical syndrome. This in itself is controversial. Why should we treat pneumonia and gall bladder sepsis with the same bundle. While sepsis evangelism has undoubtedly raised awareness and probably improved care are we dumbing it down? Anyhow, that’s a little bit off topic.

For now the big focus in ED sepsis research is on working out which parts of a bundle of care that includes very different interventions actually makes a difference. Do we need central venous oxygen saturations or is it as simple as antibiotics and fluids? (Never mind the question of which and how much fluid…)

One of three trials (ARISE and PROMISE still to come) looking at early sepsis management, this is the US led version.

METHODS

  • multi centre RCT, non blinded (as expected, it’s difficult to blind an Edwards catheter)(though as is good practice, the investigators were blinded when doing the analysis)
  • note that these were big academic centres and a requirement to get your centre into the study was use of lactate to screen for cryptogenic sepsis and adherence to the SSC guidelines. The SSC guidelines are not endorsed by Australasia as far I’m aware so this in itself might be a marked difference in practice. What do you think?
  • to get into the trial you had to be early in your sepsis course and have had a decent bolus of fluids
  • three groups:
    1. a protocol based on rivers EGDT model
    2. a protocol  based on international opinion
    3. usual care which would be whatever the doc would normally do.
  • These protocols are as always in a supplementary appendix which you have to search for separately. This is an real personal bug bear of mine –  everyone is reading this electronically and keeping the appendix separate for space saving reasons seem poor form
  • Lead investigators could enrol and manage patients in both protocol based groups but not in the usual care group. I understand why but being looked after by a leading researcher in sepsis is an intervention in itself. [See EMCrits discussion of this on the podcast]
  • primary outcome was in hospital death.
  • they powered the study on the assumption that they’d have a 30-45% mortality (as was the case in the Rivers trial), as happens in a lot of trials this overestimated how sick their patients would be.

RESULTS

  • 31 centres screening 12000 pts and got 1300.
  • no difference in primary outcome (60 day in hospital mortality) 21% v 18.2% v 18.9% for EGDT, protocol, usual care respectively.
  • they report a significant difference in fluid administration but I don’t think the difference is clinically significant. [EMCrit agrees even though the lead author sees a big difference in the three groups] We’re talking a litre difference between the most and the least with the other group half way between. If one group was 6l and one was 2l then that would seem to me a clinically significant difference. Note that the paper reports the numbers as 2.3, 3.3 and 2.8. These figures don’t include the mandatory fluid bolus that was pawrt of the inclusion criteria. So in reality it was more like 4-5 l in each group (HT EMcrit and WessexICS for pointing this out top me.
  • there was a bump in renal failure in the protocol based group but this may well be just noise
  • the only other big difference that caught my eye was differences in transfusion with 10% in the EGDT group and minimal in the other.
  • there was slightly more use of vasopressors in the two protocol used groups but not much.
  • there was an understandably big difference in central line usage. The EDGT protocol mandated a central line whereas the other two left it up to the doc essentially.

THOUGHTS

  • one big issue here is that it might be difficult to find clear water between the groups. If group 2 was developed following international consensus then it will draw on the principles of group 1 Group 3 will likely be the same as group 2 (a doc doing usual care will hopefully be practising in a manner consistent with international standards) This failure to have a major difference between all 3 groups will make it difficult to find an outcome difference between the three.
  • as a result I didn’t expect a big difference in outcomes as I don’t really think they were treated that differently.
  • maybe if the population had been sicker you might be able to draw out a difference.
  • when i deal with a septic patient I use a number of factors to guide my resus. This includes what happens to the lactate and even an ScvO2 if the line is in. Most docs who manage sepsis have some goal in mind that they’re targeting. Maybe all the goals are roughly equal, or if not equal then at least ‘good enough’ to get these outcomes

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(Yet more) reflections on SMACC Gold

Lots of other folk have put their reflections on SMACC Gold online and I’m here to join the crowd.

I missed the first SMACC as purse strings were a little tight. They’re a little tight this year too but I really wasn’t going to miss two SMACCs…

It was great to have an opportunity to come and speak though I’ll confess I was much more comfortable teaching neuroanatomy than being on the airway panel with Levitan, Weingart, John Hinds and Brent May. But it was all good really.

levitan 1

I was very impressed that they chose to devote a 2 hr main area session on end of life issues that incorporated a live integrated twitter discussion.

SonoWars in particular caught my eye as one of the most creative and slickly ran sessions on education I’ve ever seen. Those guys (ultrasoundpod and the sonocave guys) are the best in the business.

The highlight though, without doubt, was the people. This is why you come to SMACC, to meet and be inspired by people. You can throw this off as soft and fluffy and no relevance to medicine but this was the key thing.

smacc gold audience

Ireland has a small EM community and it’s a tough place to do EM. We have a very small number of trained EPs and our departments are crowded, understaffed and morale is frankly pretty low at times. It’s hardly surprising that so many of our trainees or EPs have moved to Oz or New Zealand.

As a result #FOAMed has been an inspiration and an revelation to me. To know the imaginative possibilities of EM out there is what gets me excited about the job. I get to discuss online with some fascinating, interesting and passionate clinicians from whom I can learn. SMACC gold gave me the chance to meet these people in person. And meeting people in person beats twitter hands down.

People who engage in #FOAMed tend to be a little bit off the spectrum in terms of our enthusiasm. We love the medicine, we love to talk about  medicine and we just can’t get enough of talking about medicine so much so that our spouses, our friends and even our medical colleagues get bored of us. SMACC is a conference for all these enthusiastic, excitable little puppies to get together and bond with all the other freaks and geeks.

All these people, the passion, the enthusiasm and the relationships are an inspiration to be a better doctor and a better team member.

So my thanks for SMACC gold are to the people. In particular the committee for being mad enough to invite me and Rob Rogers for being a great roomie – that man rocks!

Here’s some more reflections on SMACC gold so you can check out the love.

I Teach EM

Manu Et Corde

REBEL EM

Injectable Orange

LITFL

Jess

KI Docs

Doug Lynch (with a fascinating set of interview)

Damian Roland

AmboFOAM

Nomadic GP

Bishan

[Let me know if I missed any]

And here’s the opening ceremony

We’ll be in Chicago next year in May 2015 and I for one plan on being there. Be sure and check out the SMACC podcast to catch up on all the talks.

[Images via Oli Flower]

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PK Talk for SMACC 2014

Here’s my PK talk for SMACC for 2014. The PK talks for those who can’t remember are short, snappy focused presentations on anything – the SMACC ones are of course focused on critical care.

I presented the same material at our  joint ICU/ED meeting a few days ago so I figured I may as well share it as a PK.

Genuinely intersted as to whether people are aiming for the higher MAPs in SCI. Was news to me and no one in our department was that impressed by it. The studies aren’t wonderful after all.

For those interested here’s last years PK too.

See you at SMACC Gold people!

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