[I know the video isn't immediately relevant but it's still awesome...]

From the blogs and podcasts, it seems that everyone in the US with a chest and some pain in it will get a rule out in the ED followed by some provocative testing. Amal Mattu (who I’m stalking, seeing at an advanced ECG course pre-ICEM2012) falls into the category of Very Smart People, and I’ve heard him say that we need provocative testing. It has not been my (limited) experience that EDs in the UK and Ireland do provocative testing on everyone.

This study seeks to show that a protocol of not stress-testing everyone is a good and fine thing to do.

METHODS

• observational data on the protocol used in St.Paul BC, Canada
• got in on the basis of triage criteria
• pts got the usual ECG and assessment (and this “assessment” is probably the most important part and the most difficult to quantify and reproduce.)
• trops at 2 and 6 hrs
• if considered low risk, pt could be discharged
• if considered higher they could get EST (or other appropriate stress) within 48 hrs
• fairly low threshold for referral to cardiology it seems
• telephone follow up and they checked death registry if needed
• primary outcome was AMI or confirmed unstable angina within 30 days (the second part is a bit of a problem as admission and tests formed part fo the diagnosis and it’s always hard to know if everything the cardiologists do is gold)

RESULTS

• 1255 pts of whom they removed 55 from the protocol (remember this is a nurse initiated one so this is pretty damn good)
• 50% discharged with no planned provocative testing
• didn’t miss a single ACS by 30 days (oevrall rule in rate was 10% and most picked up in ED, only a few by provocative testing after the initial assessment)
• 2% lost to FU who didn’t attend ED or die in the region
• of note of the 10% rule ins; 10% of these had a TIMI of 0 (but hopefully you’re all clear by now that the TIMI isn’t a clinical decision instrument that we can use as EPs)

MY THOUGHTS

• this is all about patient selection – if we can work out who goes into this protocol then we can rest safe
• reassures us that low risk patients probably are just that
• fairly compelling that we can keep doing what we’re doing – in my experience in Norn Iron we only did provocative testing on a select bunch of our chest pains. There were some who got rule out trops who we did no further testing on.
• It’s useful to know that a 6 hr trop is a useful rule out. Where I’ve previously worked we’ve based things around a 12 hr troponin as our rule out (though I confess it may have changed since I left a couple of years ago.)

Scheuermeyer, F X, G Innes, E Grafstein, M Kiess, B Boychuk, E Yu, D Kalla, and J Christenson. “Safety and Efficiency of a Chest Pain Diagnostic Algorithm with Selective Outpatient Stress Testing for Emergency Department Patients with Potential Ischemic Chest Pain.” Annals of Emergency Medicine 59, no. 4 (April 1, 2012): 256–264.e3. PMID 10.1016/j.annemergmed.2011.10.016 PMID 22221842

This paper¹from WJEM is a narrative review of the available evidence used in forensic settings to link SDH and retinal bleeds with Non-Accidental Injury (NAI).

I have virtually no experience with this but like most I imagine, I thought that retinal bleeds and SDH in young children were near-pathognomonic of abuse.

The author challenges this and examines the original late 60s study that tested whiplash on monkeys and saw that it produced lots of SDH and neck injuries. His key point is that the forces needed to generate SDH would easily have broken the necks of the infants – something that does not seem to be a part of shaken baby syndrome (SBS). He makes a similar argument regarding retinal bleeds.

He argues for a different pathophysiologic mechanism of Intra-Dural Bleeding (from capillary as opposed to bridging veins) and retinal bleed from raised ICP and metabolic catastrophe.

All very interesting.

Then he describes this study² that examined the incidence of SDH in new borns. In brief:

• they took asymptomatic healthy babies at >37/40 at birth
• each got US and MRI of their brains (none needed sedation apparently)
• images reviewed by radiologists
• those with bleeds got follow up scans (no intervention)
• evaluated at 2 years for developmental delay

they found:

• n = 101
• 80% vaginal deliveries, other c-section
• 50% had SDH confirmed at follow up imaging (vast majority <3mm)
• most of the SDHs were in more than one location (most commonly para-falcine)
• when compared to MR, US missed a whole bunch (while no doubt true, it’s a little bit unfair as MR was the gold standard it seems)
• most were resolved by 4 weeks (not everyone got the follow up imaging as kids were fine and parents declined)
• everyone did great

In case you think these were tiny, invisible little bleeds, here’s some images for you.

Click for source

As a sort of aside you can see why SDH happen if you check out this paper of someone giving birth in an MRI scanner and the images and MR Video (I’m not kidding) that goes with it. It helps you understand why you’re allowed a little bit of SDH following birth. It looks a little bit like this:

Click for source

The paper³ with it has a great video you should check out if you have access to the journal. Here’s a YouTube edit of some stills:

The conclusion of the author of the first paper from this data is that SDH before 4 weeks of age might be birth related whereas after 4 weeks you need to think NAI.

Not sure if any of this changes practice but fascinating nonetheless.

Refs:

1. Gabaeff SC. Challenging the Pathophysiologic Connection between Subdural Hematoma, Retinal Hemorrhage and Shaken Baby Syndrome. West J Emerg Med. 2011 May;12(2):144–58. PMC3099599 (Free Full Text)

2. Rooks VJ, Eaton JP, Ruess L, Petermann GW, Keck-Wherley J, Pedersen RC. Prevalence and evolution of intracranial hemorrhage in asymptomatic term infants. AJNR Am J Neuroradiol. 2008 Jun.;29(6):1082–9. PMID 18388219 (Free Full Text)

3. Bamberg C, Rademacher G, Güttler F, Teichgräber U, Cremer M, Bührer C, et al. Human birth observed in real-time open magnetic resonance imaging. Am. J. Obstet. Gynecol. 2012 Jan. 13. PMID 22425409 (subscription required)

OK so IST-3 is out. It’s a big and important trial so make sure and read it. Stroke lytics get a lot of attention from EM folks, if only because we seem the only ones not convinced of its efficacy. Jerry Hoffman is probably the most important contentious voice but he’s by no means alone. Ryan Radecki has also some good stuff online and in print about it. I’ve even got my own compendium on it.

When I heard IST-3 was underway and almost ready to report I was quite excited to see someone finally answering the question in a rigorous way – do lytics in acute stroke improve outcomes? The trial that is still cited is the original NINDS trial. It showed a benefit but it was small (comparatively) and there were baseline differences between the groups that may have biased the trial in favour of tPA. This could have been answered by repeating the trial and replicating the results (a fairly common practice). This has never been done and unfortunately IST-3 is not the one to do it either. Now that’s hardly surprising – it was never the question the authors set out to answer.

If you don’t fancy reading the more detailed analysis below here’s the three major problems my point of view.

1. this is an open label trial – It was blinded at assessment but in hospital following treatment everyone knew who got tPA and who didn’t and they were treated differently. This is a potential source of bias
2. it only randomised people currently outside the licence for tPA so it’s testing an entirely different bunch from NINDS. See here for which patients were randomised.
3. it was a negative trial by its primary outcome. Something the authors don’t acknowledge in the conclusion in the abstract.

There are lots of other problems that I’ve highlighted below. I’d be interested in your thoughts.

METHODS

• multicentre international RCT
• a pilot phase (<10% total) was blinded and then in the main trial it was open label. They don’t explain why the main trial was open label but presumably it’s cheaper and easier to do.
• Randomised on basis of uncertainty principle. Basically if you’re unsure whether or not you should give it based on current guidelines then randomise
• all kinds of follow-up but mainly via GP or phone or mailed questionnaire
• originally planned for 6000 but recruitment insufficient so recalculated their power and changed the statistical plan.
• realised that there were big differences in the sub-groups at baseline (mainly on time and stroke severity) and had to apply logistic regression to adjust for them. Seeing as the only +ve results in the trial were in the sub-groups it makes me further question their significance if they were adjusted to compensate for base-line imbalances.

RESULTS

• 3000 over 10 years (which is very slow) 300/yr split between 150 centres means 2/yr/centre
• half over 80 years old
• virtually all outside the current european licence (which is the point of the trial)
• mainly treated at 4.2hrs
• pts who got tPA more likely to go to HDU (24%v17%) than those who didn’t. For this you could perhaps make the assumption that pts who got tPA got better nursing care…
• big spike in early deaths (11% v 7%) but then improved by 6 months (16% v 20%). Overall mortality was identical at 6 months
• found a 2% benefit in primary outcome (alive and independent, 35% v 37%) at 6 months. A difference this small of course did not reach statistical significance. You could call this an NNT of 50 if it was real.

Click for source

• significant ICH 7% v 1%
• oddly an increase in fatal swelling (odd because if tPA works then the infarct would be smaller and the swelling would be less) of infarcts in tPA group of 47 pts v 25 pts. This is played down as inconsistent with prior studies in the paper
• they have a whole ream of things in the forest plot of secondary outcomes (these are the adjusted ones) and only one approaches significance – age >80 yrs. Unfortunately as Ryan points out – if it’s better for those greater than 80 then it’s worse for those <80 – which is the precise opposite of prior trials.

Below is a video of the lead author talking about the results if you’re interested

The paper itself lives here

In the same issue the same authors have published an updated systematic review and meta-analysis that now includes these results. One of the concerns that has been pointed out before is perhaps this heterogeneous data set (now up to 12 very differently ran trials) aren’t actually appropriate to meta-analyse.

There’s a glowing editorial about the trial that makes the slightly odd and even reckless statement that:

Every stroke patient should therefore be classed as a candidate for thrombolysis

This seems a little bit of a stretch seeing as the IST-3 trial used these criteria and excluded lots of pts:

Click for source

My suspicion as always, is that tPA does work for some patients with stroke, but certainly not all and until we can pick out the ones who benefit then I suspect that we shouldn’t have adopted this as wholeheartedly as we already have.

UPDATE – if you look at page 4 of the supplementary appendix there’s a list of the drug treatments that varied between the 2 groups. The two groups were treated differently 

The original Scancrit post can be found here

The paper can be found here.

Here’s the rest of my thoughts on it:

This study was found by ScanCrit a while back now and generated a little bit of discussion on the twitter thingy.

Below are my notes on the study.

METHODS

• sedated pigs with lots of monitors in place
• the common carotid monitor was of course proximal to where the LMA would be so i don’t know if this affects reading seeing as we’re interested in distal flow in the ICA and not the common or the ECA
• there’s some lovely stuff on the model they used
• they performed angios on pigs with the EGDs in to see how it affected things but these were on recently dead pigs which is surely a different thing altogether

RESULTS

• flow dramatically decreased when the EGD was placed

SOME THOUGHTS

• they note that one study in anaesthesia showed reduced flow with EGD but it’s likely of little consequence there and very important in cardiac arrest
• of most importance is the fact the airway of a pig is shaped is so remarkably different that this may be entirely wrong.
• if it’s right however then reducing cerebral blood flow during a critically low flow period might be real bad news.

The podcast itself lives here:

[As always don't forget to hit the HD button in the top corner to see it pretty.]

And here’s a GIF of the CT. Sorry if the scroll is a bit slow. HT to radiology signs for the link to the MakeAGif site.

Left Main Cardiac Cath [Click for source]

• prospective data from Paris in a large centralised system
• OHCA attended by the mobile ICUs that include physicians
• brought to a cardiac arrest centre
• they say that OHCA without an obvious other cause “usually” got an immediate angio – This is the key phrase in the whole paper as i have no idea what “usually” means. And I’m also not sure what they mean by obvious cause.
• PCI and ICU care was standard and involved hypothermia but they don’t tell us much else about the details
• primary outcome was detection of a recent coronary occlusion – again I’m not sure what this means; they reference a couple of papers but I don’t know if they’re the standard definitions for the PCI literature. I’m just sharing my ignorance here so let me know if you know better.
• Interestingly this is not what you would expect given the title of the paper. If the purpose is to identify occlusions then fine, but it seems that the purpose is to associate Trop with occlusion in OHCA patients. It’s not clear but it may be that they just applied logistic regression and the trop was the one that popped up.

RESULTS

• recorded 435 in 5 years. That strike me as dodgy – if OHCA usually get an angio in this system then these are tiny numbers for 5 years worth of cardiac arrests. it seems much more likely that this is a highly selected sample.
• 30% of these were STEMI on ECG and so would have got cath anyway hopefully
• of those who got cath they only stented/opened <50%
• trop was +ve in 92% of the pts
• they pull the numbers on trops and come up with the optimum cut-off of 4.66ng/ml with (wait for it…) sens and spec of 67%…. Sigh
• much more interestingly STEMI on ECG was 50% sens and 90% spec for occlusion
• survival 40% overall in this cohort
• they conclude that troponin it’s independently contributive but then pull back and acknowledge the problem that it’s no where near good enough to make calls on.
• they also note the previous (tiny) papers showed much more favourable numbers for cut offs for trop in OHCA

Dumas, Florence, Stéphane Manzo-Silberman, Jérôme Fichet, Zohair Mami, Benjamin Zuber, Benoît Vivien, Camille Chenevier-Gobeaux, et al. “Can Early Cardiac Troponin I Measurement Help to Predict Recent Coronary Occlusion in Out-of-Hospital Cardiac Arrest Survivors?.” Critical Care Medicine (April 6, 2012). PMID 22488008

• data from the resus outcomes consortium – one of the big cardiac arrests research networks
• this data was pulled from people not already in a trial
• the defibs and pads were used to calculate the compression depth numbers
• considered 4cm compression for >60% of the time as high quality (this is the 2005 guidelines)
• primary outcome was survival to hosp discharge
• excluded those who had arrest witinessed by EMS and who got an AED shock

RESULTS

• 25000 potential but only 1000 enrolled, largely because of no depth data available.
• the selected patients had a shorter time to CPR so no doubt they survived more because of it
• otherwise a fairly typical population
• CPR was outside of the guideline depth for 60% of the cases
• people were more likely to survive as compression depth increased
• survival to discharge was 4.9% overall so neuro survival probably wasn’t as good.

THOUGHTS/PROBLEMS

• Note the 2010 guidelines say 5cm and the data in this paper did not support that change.
• There are lots of problems with this and you could easily say that body habitus and chest wall compliance determined outcomes here rather than compression depth
• Despite all the flaws, I think we should be using some form of rate and depth feedback at the very least in ALS courses (it’s been 7 years since I’ve been to one…) and it would be fairly easily done in a hospital setting too.

Stiell, Ian G, Siobhan P Brown, James Christenson, Sheldon Cheskes, Graham Nichol, Judy Powell, Blair Bigham, et al. “What Is the Role of Chest Compression Depth During Out-of-Hospital Cardiac Arrest Resuscitation?..” Critical Care Medicine 40, no. 4 (April 2012): 1192–1198. PMID 22202708]

Nothing to do with milk formula.

This is yet another Zebra diagnosis but it’s a great one for illustrating some of the relevant anatomy. Let me know what you think.

Here’s the link to the article mentioned.

Rudinsky, Sherri L, and Michael J Matteucci. “Emergency Department Presentation of Superior Mesenteric Artery Syndrome: Two Cases in Marine Corps Recruits..” JEM 42, no. 2 (February 2012): 155–158. PMID 19111427

Some of the signs. Click for source.

I think I’ve seen it once when I was doing my stint in paeds. I remember the kid getting IVIg and aspirin and I’m pretty sure we had a debate about steroids.

Apparently, there’s been some prior work on this that has been a bit inconclusive so these guys wanted to try and answer it.

Remember think Kawasaki in pre-school child with prolonged fever, funny rash, funny tongue, lymph nodes and conjunctivitis. It’s important cause it causes coronary artery aneurysms 

Here’s the study:

METHODS

• open RCT
• used Japanese score to diagnose it (which i think is different from the one we use) with lots of blood tests.
• everyone got IVIg and aspirin as is standard
• steroid group got IV methylpred for a few days and if effective for a while after with a taper
• everyone got an echo which was reviewed blind
• week 1, 2 and 4 were primary endpoints for aneurysms
• power based on a reduction from 20% to 10% (as is usual they overestimated how sick the pts would be)

RESULTS

• n = 242 (excluded over 70% because they didn’t get high enough scores on the Japenese scale)
• mainly 3 yr and a bit
• most day 4 at enrolment ( i don’t even think of it till day 5…)
• ended early for benefit (which is always a shame as we now don’t have power to know if there are any important adverse events of a long and big course of steroids in this populations)
• abnormalities in coronaries 4/120 v 15/120 favouring the steroid

THOUGHTS/PROBLEMS

• we don’t use their score
• They did it early – as I mentioned, this is in my differential for prolonged (>5 days) fever – they were enrolling them in the study at day 4!
• we have no info on hard outcomes like heart failure and death (cause they’re all very long term). I don’t think we necessarily need those type of outcomes but it’s worth bearing in mind.
• is the long course needed? (median 21 days here)

Coronary artery aneurysm. Click for souce

Of course, this is not likely to be something we need to be able to deal with in the ED, but if the early diagnosis thing really pans out, then we’re under even more pressure to pick out a rare disease from the mass of snotty, viral kids out there. Good luck with that.

Kobayashi, Tohru, Tsutomu Saji, Tetsuya Otani, Kazuo Takeuchi, Tetsuya Nakamura, Hirokazu Arakawa, Taichi Kato, et al. “Efficacy of Immunoglobulin Plus Prednisolone for Prevention of Coronary Artery Abnormalities in Severe Kawasaki Disease (RAISE Study): a Randomised, Open-Label, Blinded-Endpoints Trial..” Lancet (March 7, 2012). PMID 22405251

For all I know this may well be something that’s already being done somewhere in the country but it’s a neat idea. There are, apparently, official guidelines on what type of screen radiology reports should be made of – something with a suitable number of pixels.

This little study from the republic of Cork looked at the original iPad loaded with everyone’s faourite DICOM viewer Osirix and compared how radiologists did on a number of dry head CTs versus reads on an official PACS system.

Bottom line: It did pretty well.

More details of the study below:

METHODS

• from cork
• using the original ipad i think (may 2010)
• loaded with osirix
• compared dry CT heads with a PACS system
• did some fancy calibration stuff too to see if the screens were in any way comparable
• reads were done by different people so we can’t be sure that differences weren’t just differences in subjective findings

RESULTS

• 100 scans
• 5 strokes, 5 bleeds
• no misses on the iPad for these
• there was disagreement over some other stuff, the only one of concern might be a subtle lentiform stroke

MY THOUGHTS

• i wonder if results would be any different with the newer iPads

NB – Apple’s European HQ is in Cork and the authors didn’t get any sponsorship from them. Either Apple are tight and horrible (probably true) or the authors wanted a nice conflict free study.

NB –  I have a personal bias against the iPad seeing it as the epitome of consumerism (virtually everyone know has an iPad AND a laptop and iPhone, not instead of…) gone mad but the idea of tablet computers for work situations (as opposed to just really pretty ways to play angry birds) is important and likely to become more so in coming years.

Mc Laughlin, Patrick, Siobhan O Neill, Noel Fanning, Anne Marie Mc Garrigle, Owen J O Connor, Gerry Wyse, and Michael M Maher. “Emergency CT Brain: Preliminary Interpretation with a Tablet Device: Image Quality and Diagnostic Performance of the Apple iPad.” Emergency Radiology 19, no. 2 (December 16, 2011): 127–133. PMID 22173819

More piss-taking photos here

It’s available here through the EMJ if you have access.

As author, I’m also allowed to share the pdf with up to 100 colleagues/friends. I’m not sure I have even a 100 colleagues/friends but if you want a copy just send me an email (emergencymedicineireland [at] gmail] and I’ll send you one.

I’ve put the original proof version of the manuscript here if you don’t want all the hassle of actually sending me an email.

Cric Manuscript

Finally here’s me chatting to Minh Le Cong about it.

More importantly Minh now has his own site so be sure and check that out.

There shall be lots more activity here and podcasts too, whenever I get these (700 or so) exams marked.