VTE Dublin 2015

VTE Dublin Header

This is a brief heads up about a new conference coming in Dublin, Friday 18th – Saturday 19th September 2015.

My current hospital as a venous thromboembolism working group (which I am nominally a part of) consisting of the whole gamut of specialties involved in the diagnosis and management of VTE. From the ED to the long term haematology follow up we have it all and everything in between.

We have some really smart and passionate people involved, so much so they’re planning the VTE Dublin 2015 conference.

The speakers come from a wide variety of backgrounds including the vascular medicine specialists who seem to “own” the disease in Europe. If you read the literature you’ll recognise a lot of the names on the programme, it’s a bit of a who’s who in VTE. Perhaps the most familiar name to an EM audience is that of Prof Wells, of the Wells score fame.

It’s looking like a great conference so check it out and the programme and book your place. We’re also on twitter so follow for all the updates

 

VTE Dublin Programme

[DOI: I am a tiny part on the planning committee and will receive some remunerating from developing the website (slowly…)]

The post VTE Dublin 2015 appeared first on Emergency Medicine Ireland.

Chronic Pain Part 2: Medication

ercast.org
Chronic Pain Part 2: Medication

This is part two of a two part series on chronic pain. Pearls: Set realistic expectations when treating patients with chronic pain. For the vast majority of patients, antidepressants are the first-line pharmacologic choice for the treatment of chronic pain. Patients who present after the acute phase of a painful condition, whether it’s 1 week or 2 […]

ercast.org - Emergency medicine podcasts, reviews and curbside consults

The New, Improved, ACEP Clinical Policy for tPA in Stroke

Released with minimal fanfare, approved by the ACEP Board of Directors on June 24th, the revised ACEP Clinical Policy regarding the use of TPA for acute ischemic stroke has gone final.

It is, of course, a vast improvement over the 2012 version – but has, unfortunately, changed for the worse since the draft was posted.

The highlights:

  • The Level A suggestion to consider the risk of ICH with tPA administration has been eliminated.  It has been moved, nonsensically into the Level B recommendations for offering tPA – when, frankly, it’s the only consistent finding across all the evidence.
  • The Level B recommendation in which tPA “may be given” within 3 hours has been strengthened to “should be offered and may be given”.  Obviously, a profound difference.
  • The Level B recommendation for 3-4.5 hours remains unchanged, based on only one flawed piece of Class II evidence (ECASS III), and conflicting Class III evidence (ATLANTIS, IST-3, meta-analyses).
  • The Level C recommendation to engage in shared decision-making now states “when feasible”, which is obviously open to interpretation.
  • No further clarification of “carefully selected patients” or “systems … in place to safely administer the medication” is provided.

Some wins, some losses.  Obviously, the shared decision-making supporting any “offer” of tPA can be very different, depending on an individual clinicians’ interpretation of the evidence – and it is nice to see the prior COI-infested husk of rotten guidelines finally, officially, tossed on the compost heap.  Let us hope (irrationally, of course) the efforts underway in the United Kingdom spur further, independent, investigation with which to better understand and individualize the risks and benefits of treatment with tPA.

“Clinical Policy: Use of Intravenous Tissue Plasminogen Activator for the Management of Acute Ischemic Stroke in the Emergency Department”
http://www.acep.org/workarea/DownloadAsset.aspx?id=102373

A Male in his 40’s with Decreasing Chest pain – what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm.
The QTc is 379 ms.
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 





The clinicians used the subtleSTEMI formula (sidebar excel applet).  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm


If we put these values into the formula, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
_________________________________________________________________________________
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6


Only one value is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 3.5 mm.  RAV4 = 11-12 mm.

Formula value is now slightly lower.

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).


Here is another case in which the T-wave subtly diminishes as the LAD spontaneously opens and pain diminishes (the first 4 are prehospital ECGs):



A Male in his 40’s with Decreasing Chest pain – what do you think?

A male in his 40s presented with decreasing chest pain.  Here was his first ECG:
There is sinus rhythm.
The QTc is 379 ms.
There is ST elevation in V2-V4 that does not meet STEMI "criteria" of at least 1 mm in 2 or more leads (except V2 and V3, which require 2.0 mm of more for men over age 40).

So it looks like early repolarization. 





The clinicians used the subtleSTEMI formula (sidebar excel applet).  I am not sure exactly what numbers they used, but they told me the value they arrived at was 21.2.

Let's examine that:
The computerized QTc was 379 ms.
The R-wave amplitude in lead V4 is from 11-14 mm, depending on the complex used.
Here is a magnification of V3 in order to measure ST elevation at 60 ms after the J-point in lead V3:
The black arrow shows the J-point.  The red arrow is at 60 ms (1.5 small boxes) after the J-point.  The lower edge of the upper green line is where one should measure from.  The upper edge of the lower green line is at the PQ junction.  The distance between these two is 4 mm.  Some might say 3.5 mm


If we put these values into the formula, we get 6 different values depending on the measurements:

                                   RAV4 = 11 (min)                     RAV4 = 12.5 (avg)                  RAV4 = 14 (max)
_________________________________________________________________________________
STE = 3.5 mm                   22.96                                       22.5                                             22.0

STE = 4.0 mm                   23.56                                       23.1                                             22.6


Only one value is very specific for LAD occlusion (23.56, greater than 23.4)

All the rest are greater than 22.0, above which one should definitely be worried and get serial ECGs.

So a second ECG was recorded 12 minutes later:
QTc is now 383 ms.  STE 60 V3 = 3.5 mm.  RAV4 = 11-12 mm.

Formula value is now slightly lower.

These two ECGS are significantly different, but it was not noticed the treating physicians.

Look at the ECGs side by side.  And remember the pain is waning.
The first is on the left, the follow up is on the right.
The T-wave amplitude in V3 is 10 mm on the earlier and only 7 mm on the later one.

This makes it almost certain that the ST elevation on the first one is due to ischemia.

Although the clinicians were uncertain and obtained a very low formula value for both, they were worried about the patients symptoms and appropriately activated the cath lab.

The angiogram showed a 99% thrombotic occlusion with TIMI-II flow (enough coronary flow to prevent outright ST elevation).

It is probable that the artery was fully occluded at the time of maximal chest pain.

Learning Points:
1. Hyperacute T-waves diminish in size as the artery reperfuses
2. The formula is more likely to be falsely negative when there is a reperfusing artery.
3. A value less than 23.4 but still greater than 22.0 may still be due to LAD occlusion or near-occlusion.
4.  Serial ECGs are critical but they must be scrutinized for changes, which may be very subtle (see below).


Here is another case in which the T-wave subtly diminishes as the LAD spontaneously opens and pain diminishes (the first 4 are prehospital ECGs):