Stimulated by a post over at Echo Praxis and a corrective tweet from Karim Brohi
I think I have a vague memory of this from several years ago but this was an opportunity to properly look into it.
Most of this comes from a generally poor understanding of aortic diseases. I know I’ve got myself in a muddle before with thoracic aortic aneurysms and thoracic aortic dissections and occasionally confabulating with the dissecting thoracic aneurysm…
Traumatic aortic injury is somewhat similar with most folk (including myself apparently) labelling it simply as an aortic dissection when in fact it probably isn’t.
Where do you see these injuries:
- 90% at the isthmus (the bit of the descending aorta between left subclavian and ligamentum arteriosum). The idea is that aorta is a bit tethered here and it’s a point of force transmission
- 5% in the ascending aorta
When should you consider it?
- Most of it seems to be mechanism driven (deceleration). With the era of pan scan, most severe trauma patients are getting CT which is going to be the test of choice for most.
- The O’Connor paper referenced below is a bit old but it does contain a little bit of literature on examination findings. These findings are likely late like most of these things but worth looking for.
- high BP in the upper limbs with
- low BP in the lower limbs
- big mediastinum on CXR
- Lots of people with an aortic injury have a wide mediastinum but that doesn’t necessarily mean the aorta is ruptured. Most of the blood in the mediastinum is coming from much smaller mediastinal vessels and the wide mediastinum is simply reflective of severe trauma to the area and a reason to look further.
Types of traumatic aortic injury
- the Mokrane paper cited below suggests a grading system I-IV with I and II being conservatively managed and III/IV for intervention, ideally endovascular and occasionally open repairs. Though management is no doubt a topic of controversy that i’ll not delve into
- intimal tear or localised haematoma
- pseudoaneurysm involving <50% of aortic diameter
- pseudoaneurysm involving <50% of aortic diameter
- rupture or complete transection of the aorta
- there are lots of imaging artefacts from beam hardening to cardiac pulsation that can look like aortic injuries but aren’t. I remember seeing this years ago and we all got very excited and I think the patient even got transferred before someone caught on it was all artefact
- in the oldies there’s often lots of plaque on the aorta and these are easily confused for lower grade injuries
Karim, of course, also had some tips distinguishing the aortic dissection (usually a medical disease with surgical treatment) from a traumatic aortic injury (a traumatic injury with an interventional treatment):
- Mokrane FZ, Revel-Mouroz P, Saint Lebes B, Rousseau H. Traumatic injuries of
the thoracic aorta: The role of imaging in diagnosis and treatment. Diagn Interv
Imaging. 2015 Jul-Aug;96(7-8):693-706. doi: 10.1016/j.diii.2015.06.005. Epub 2015
Jun 27. PubMed PMID: 26122129. [PubMed]
- St Emlyns Podcast with Karim Brohi on vascular injuries
- O’Connor. Diagnosing traumatic rupture of the thoracic aorta in the emergency department EMJ – Full Text
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Before you all die of boredom it turns out that sodium is really important. it’s something we also seem to get very confused by.
The wonderful Josh Farkas had a post on low Na (mainly about using Bicarb as treatment) with a quote from the European Guidelines (that I didn’t even know existed at the time)
You’d think a guideline would be a fairly dull read and only concerned with grading evidence recommendations. Well it’s a bit more than that and their background section is full of little pearls that occasionally surprised and educated me.
- pseudohyponatremia is the low Na with high proteins like myeloma. This is a measurement problem and is artifactual. This is different from the low sodium that occurs with high sugars (see next point)
- the low na with DKA or high sugars is a “translocational” hyponatremia and merely due to the high sugar drawing water out of the cells and diltuting the sodium. The sodium really is that low, it’s not artefact.
- measured and effective osmolality are different
- measured is a chemical thing of the concentration of all solutes regardless of whether these can move across a membrane
- effective osmolality can be known as tonicity and refers to the number of osmoles that contribute to water movement
- this is why urea will increase the measured osmolality but not the effective osmolality and this is reflected in the equations (alcohol is an ineffective osmole however mannitol is an effective osmole)
- perhaps the most important take home message for emergency physicians
- low Na with severe symptoms = 150ml 3% stat
Prompt infusion of hypertonic saline may save lives and preparing a 3% hypertonic saline infusion takes time. In addition, errors may occur from having to calculate the required amount of sodium chloride in an emergency.
Joel Topf, twitter’s favourite nephrologist made a nice image summarising the treatment options
Image by Joel Topf. Click for source
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This is a nifty little diagnosis and something that you’ll see with some regularity. In the context of sudden unexplained cardiac arrest with ROSC but no neurological response we often get a CT of the head looking for some intracranial disaster to explain what just happened.
One of the images below is a typical SAH the other is consistent with pseudo SAH, can you tell the difference? (click the radiopaedia case links to find out)
Case courtesy of Dr Chris O’Donnell, Radiopaedia.org. From the case rID: 16446
Case courtesy of Dr Saqba Farooq, Radiopaedia.org. From the case rID: 10489
I’ve seen this a couple of times now in post arrest patients and it can cause a lot of confusion as all of a sudden you’re worried about anticoagulation if you were thinking cath lab or maybe you’re tied into doing angios and what not.
Radiopaedia has a great post on it so all kudos to them but I think it’s something we in the EM world really need to know about hence the post.
In the post arrest patient (where I first encountered it) you get lots of cerebral oedema and engorgement of the superficial venous structures.
Can also occur in:
- severe meningitis
- dural venous sinus thrombosis
- bilateral large SDH
How do you tell the difference:
- ask your radiologist
- usually a lower hounsfield unit comared to true SAH
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There’s been a recent rash of ‘non inferiority’ trials in the medical literature. The new oral anticoagulants are a great example. It’s hard to blame investigators. Proving that Drug B is better than Dug A is a very difficult thing to do, especially now that it all needs to be focused on poo (or Patient Orientated Outcomes – what did you think I meant…)
A superiority trial requires a massive sample size to find this difference reliably. Proving that drug B is ‘non inferior’ to Drug A is a lot easier to do. Though not without its problems.
I was doing some prep for one of our national EM training days for which we typically sit an FRCEM style critical appraisal. One of the questions was:
- What is a non-inferiority trial and when should it be used?
As usual, this is typical type of material that FOAMed has not covered especially well.
First off some reading:
Sedgwick P. What is a non-inferiority trial? BMJ 2013 Nov 15;347(nov15 1):f6853–3. [pdf]
Snapinn SM. Non inferiority trials. Curr Control Trials Cardiovasc Med. 2000. [FOAMed pdf]
Here are some take home headlines:
- These are not equivalence trials, though people have used the terms equivalence and non inferiority interchangeable. Bioequivalence trials of drugs are probably the only true equivalence trials
- You must specify a noninferiority margin – for it to be a positive trial the primary outcome has to be within a certain margin of the existing treatment. Selection of this margin is unavoidably subjective and is open to all kinds of fudging.
- These trials are suitable when you are testing something that you assume will be at best non inferior. For example face to face versus telephone consultation – no one expects telephone to be better but it might be non inferior. So instead of assuming the null hypothesis (that there is no difference between treatments – this is what we normally assume in superiority trials) and trying to disprove it; in a non inferiority trial the null hypothesis is that the new intervention is not as good and you are trying to prove that is non inferior.
- Of note, blinding is much less use in a non inferiority trial as a biased but still blinded end point assessor can just give everyone equivalent outcomes and the new drug being assessed comes out as non inferior.
- ‘intention to treat’ and ‘per protocol’ analyses can both bias the results. Typically ITT is the way to go but in non inferiority trials you typically need both ITT and per protocol analyses to be positive for the intervention to be truly non inferior.
- non inferior trials are typically analysed on a confidence interval but without the p value. This is in the Sedgwick paper but I still struggle to understand why they don’t use the p value.
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A chap with a 6 month old ileal conduit for urinary diversion rocks up to your ED feeling more than a little unwell.
A VBG done at triage is like this:
What’s the deal?
Types of urinary diversion
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