The Crashing Asthmatic

May 23, 2013 by · Leave a Comment

UPDATE:

Since making this, StEmlyns have scuppered my take on Mag by reporting the 3MG trial which gave a big great ‘hmpph’ to mag and suggest very little, if any benefit. Check out their take. 

In my current dept, there’s a monthly joint ICU/ED meeting. I recently presented on some of the evidence base and strategies for managing life-threatening asthma. The 15 people there seemed to enjoy it so now i’m sharing it with the rest of the #FOAMed community.

I’ve included some references below from some of the papers cited in the talk.

Two talks in particular deserve mention.

One on EM:RAP by Mel Herbert himself back in 2007 [subscription needed] and the other from EMCrit.

Lim, Wei Jie, Redhuan Mohammed Akram, Kristin V Carson, Satya Mysore, Nadina A Labiszewski, Jadwiga A Wedzicha, Brian H Rowe, and Brian J Smith. “Non-Invasive Positive Pressure Ventilation for Treatment of Respiratory Failure Due to Severe Acute Exacerbations of Asthma..” Cochrane Database of Systematic Reviews (Online) 12 (2012): CD004360. doi:10.1002/14651858.CD004360.pub4.

Mohammed, S, and S Goodacre. “Intravenous and Nebulised Magnesium Sulphate for Acute Asthma: Systematic Review and Meta-Analysis..” Emergency Medicine Journal 24, no. 12 (December 2007): 823–830. doi:10.1136/emj.2007.052050.

Nair, Parameswaran, Stephen J Milan, and Brian H Rowe. “Addition of Intravenous Aminophylline to Inhaled Beta(2)-Agonists in Adults with Acute Asthma..” Cochrane Database of Systematic Reviews (Online) 12 (2012): CD002742. doi:10.1002/14651858.CD002742.pub2.

Rowe, B H, J A Bretzlaff, C Bourdon, G W Bota, and C A Camargo. “Magnesium Sulfate for Treating Exacerbations of Acute Asthma in the Emergency Department..” Cochrane Database of Systematic Reviews (Online) no. 2 (2000): CD001490. doi:10.1002/14651858.CD001490.

Tobin, A. “Intravenous Salbutamol: Too Much of a Good Thing?.” Critical Care and Resuscitation : Journal of the Australasian Academy of Critical Care Medicine 7, no. 2 (June 2005): 119–127.

“British Guideline on the Management of Asthma” (February 2, 2012): 1–151.

CORSSEN, GUENTER, JUAN GUTIERREZ, JOSEPH G REVES, and FRANCIS C HUBER. “Ketamine in the Anesthetic Management of Asthmatic Patients.” Anesthesia & Analgesia 51, no. 4 (1972): 588–594.

 

Filed Under: critical appraisal, FOAM · Tagged: , ,

Standing Test for Long-QT syndrome

April 28, 2013 by · 8 Comments

This was all brand new to me. I was reviewing a syncope patient left over from the night shift before. The hand over was: recent change in anti-hypertensives, now feeling weak and dizzy about 1 week. Syncopal episode at dinner table last night.

She’d been in the department overnight, got some fluids, bloods and an ECG. The ECG was said to be normal.

I went and chatted to the patient and yes indeed it did sound all very like postural hypotension. I went back and looked at the ECG and did my usual syncope ECG review looking for the following:

  • Brugada
  • HOCM
  • WPW
  • intervals – QT and PR

And there it was – a nice big QTc of 550ms staring at me.

I still suspect that postural hypotension was the main cause of her symptoms but it would be a tad on the risky side to call it that in the context of a long QT. K+ and Mg++ were on the low side (3.5 and 0.6) so she got a bit of both and admitted for ECG monitoring.

The interesting bit came in the discussio with admitting doctor who was (for once) interested, enthusiastic and asked about the standing test for Long QT. This was all news to me but effcetively people with a long QT syndrome (LQTS) have an abnormal response in QTc with standing.

In healthy people on standing the heart rate goes up with corresponing shortening of the QT interval. Due to the fact that heart rate goes up more than the QT comes down, the QTc actually goes up slightly,

In LQTS the QTc often goes up substantially.

This paper addresses this concept and while it’s in now waty perfect (ie it examined it in people known to have LQTS which undermines its use as a diagnostic test in undiagnosed QT problems) it suggests that in healthy people an increase in QTc on standing of about 10-15ms is allowed but in LTQS is likely to be in the range of 90-100 ms.

Viskin, Sami, Pieter G Postema, Zahurul A Bhuiyan, Raphael Rosso, Jonathan M Kalman, Jitendra K Vohra, Milton E Guevara-Valdivia, et al. “The Response of the QT Interval to the Brief Tachycardia Provoked by Standing: a Bedside Test for Diagnosing Long QT Syndrome..” Journal of the American College of Cardiology 55, no. 18: 1955–1961. doi:10.1016/j.jacc.2009.12.015. PMID 20116193

 

METHODS

  • the normal response to standing after lying is an increase in HR. This would normally be accompanied by a shortedned QT. In LQTS this apparently isn’t the case
  • The intervention was standing and recording QT changes.
  • they did this on high risk LQTS (lots of features but no diagnosis as yet) and those who actually had it genetically documented. The controls were healthy relatives of those pts or volunteers (the vast majority)
  • took them off Beta blockers for a day then lay them flat 10 mins and stood them up for 5 mins with telemetry.
  • blinded investigator performed the measurement had a set part of the trace. Bazzett’s  formula was the main one used.
  • excluded the obviously normal and obviously prolonged

 

RESULTS

  • 68 LQTS; 82 controls
  • the baseline QTs were 380 v 450 – not diagnositcially different but borderline
  • the QT went down in all the normals but less than the RR interval therefore the QTc goes up slightly.
  • the QT of those with LQTS didn’t change at all. In some it went up. Or put another way the QTc of the control group went up 13ms while the LQTS patients the QTc went up 89ms

Not something I’m going to be doing every day, but it’s a fairly nice, bedside test that we can apply in the ED.

Filed Under: critical appraisal, ECG · Tagged: , , , ,

Full Capacity Protocols

March 23, 2013 by · Leave a Comment

[image via NetDance on Flickr. CC License]

Hospitals are busy places. We have no space, no beds, no staff and inevitably less money to make this all happen. This is the situation we have.

We’re fairly pragmatic folks so we find ways to manage the work more efficiently and try and do more as an out patient or involve things like ADPs (accelerated diagnostic protocols)

But when we get slammed and have more admitted patients than you have trolleys to put them on then the system grinds to a halt and you can’t assess treat and admit/discharge anyone new.

In Stony Brook in New York, the hospital (and that’s the important bit, not just the ED) decided that when the ED was choked that they could put some of the stable patients as extras in the hallways of the wards. You can imagine what the ward staff thought of that.

This is a brief paper reviewing their experience.

Viccellio, Asa, Carolyn Santora, Adam J Singer, Henry C Thode, and Mark C Henry. “The Association Between Transfer of Emergency Department Boarders to Inpatient Hallways and Mortality: a 4-Year Experience..” Annals of Emergency Medicine 54, no. 4 (October 2009): 487–491. doi:10.1016/j.annemergmed.2009.03.005. PMID 19345442

This is a review of patient flow effectively and not a trial in any prospective sense. All they wanted to show was that this was happening and what the effects were.

It is not the highest quality science and does not claim to be.

RESULTS

  • 25% of those assigned to a hallway bed actually got a proper bed immediately
  • another 25% got a proper bed within an hour
  • the rest got a proper bed within 8 hrs.

THOUGHTS

Your hospital probably has more beds than they say they do. Spreading the crowding from one place to the whole hospital spreads the moral and professional responsibility to a hospital wide problem. It’s remarkable how that motivates resources.

Importantly it must be realised that this is no panacea for a poorly run hospital. In fact every time a hospital implements something like this it’s a sign that something is deeply wrong. However it can alleviate a crisis.

The Irish Association has a nice statement on FCPs. And indeed a nice EMJ paper on the same too.

Filed Under: critical appraisal, health care systems · Tagged: , ,

EM docs are more burnt out than most but none of us are great…

March 17, 2013 by · 8 Comments

The night shift insomnia that leaves me with about 4 hrs sleep a day has given me the chance to catch up with a bit of reading so here’s a paper for you.

This got a very amount of Twitter attention when it came out as it was a bit of a headline grabber:

Shanafelt, Tait D, Sonja Boone, Litjen Tan, Lotte N Dyrbye, Wayne Sotile, Daniel Satele, Colin P West, Jeff Sloan, and Michael R Oreskovich. “Burnout and Satisfaction with Work-Life Balance Among US Physicians Relative to the General US Population..” Archives of Internal Medicine (August 19, 2012): 1–9. doi:10.1001/archinternmed.2012.3199. PMID 22911330

First a quick run through of the study and then some thoughts

METHODS

  • this was a massive survey of the AMA register of doctors compared with the general population. It was done effectively by mass emailing
  • the survey used the “gold standard” of burnout: the Maslach Burnout Inventory
    • the only problem here is that it’s a bit of a cumbersome tool so they let the docs fill in the whole survey whereas Joe Bloggs only filled in what the authors state are the predictive bits of the survey. They say that doing this has been studied before and is kosher but there you go…

RESULTS

  • only a 26% (7000/27000) response rate in the docs. A response rate of somewhere closer to 70% is considered important as it’s giving a much more representative of the people you’re surveying. If you think about it could be only the pissed off, grumpy docs answering the survey. Or maybe even the opposite and only the calm and cool docs with lots of free time filled it out
  • bottom line was that a lot of docs feel overworked and burnt out. And this is higher than the general population
  • the people with the highest symptoms of burn out were the EM docs. By a clear country mile it seemed. We were much better than the surgeons in terms of work-life balance but despite this we were still burnt out.

THOUGHTS

I think this is vitally important stuff.

Emergency Medicine is like a puppy – it’s for life not just for Christmas but it seems increasingly both from my own anecdotal experience and now represented in study form in various settings that we’re going to have real difficulty keeping docs in the specialty.

In the US there are comparatively huge numbers of trained Emergency Physicians compared with the UK/Irish model. These guys work shift patterns often for their entire career. They are well paid and work reasonable hours (I was quoted that 30 hrs a week was an average for an EP in the US – can anyone corroborate this?) Despite their resonable work life balance these guys are really burnt out.

Now the UK/Irish model is a service delivered by trainees and non-board certified EPs, (the “sickest looked after by the thickest” as some have joked) these guys are paid less and work more hours than fully trained EPs, of whom we have vanishingly few. Just imagine how much more burn out might apply to those docs who deliver hands on emergency care day in, day out (or night in, night out)…

As I enter my ninth year since graduation from med school with no clear end in sight to my training (largely my own fault I’ll admit) the importance of work-life balance and the threat of burn out becomes more and more apparent. Workforce planning is one of the biggest problems (along with overcrowding) that EM has to face in this part of the world, but if we are to address it in any way we must address sustainability and burn out.

update:

Graham Walker did a survey for EM News on burnout that’s worth a read

http://mobile.journals.lww.com/em-news/_layouts/oaks.journals.mobile/articleviewer.aspx?year=2013&issue=03000&article=00008

Filed Under: critical appraisal, FOAM, thinking about medicine ·

Is pulmonary embolism really all that bad?… Again…

January 10, 2013 by · 11 Comments

CTPA PE

Pollack, Charles V, Donald Schreiber, Samuel Z Goldhaber, David Slattery, John Fanikos, Brian J O’Neil, James R Thompson, et al. “Clinical Characteristics, Management, and Outcomes of Patients Diagnosed with Acute Pulmonary Embolism in the Emergency Department: Initial Report of EMPEROR (Multicenter Emergency Medicine Pulmonary Embolism in the Real World Registry)..” Journal of the American College of Cardiology 57, no. 6: 700–706. doi:10.1016/j.jacc.2010.05.071. PMID 21292129

METHODS

  • this was a large ED based registry study from multiple US EDs to see how PE patients present and what happened to them
  • it included both people who ended up having a confirmed PE and those empirically treated for PE awaiting tests and ultimately ruled out for PE
  • PE diagnosis could be based on lots of different tests (all appropriate I think)

RESULTS

  • 2400 pts, 1800 who had PE
  • vast majority (90%) diagnosed by CT
  • 3% were hypotensive on presentation
  • SOB, pain, and symptoms suggesting DVT were commonest presenting complaints
  • 5% presented with syncope: it happens but it’s not common
  • of those who got echoes (only a quarter) there was RV dyskinesia in half
  • 85% of those with PE got anti-coagulated in the ED – this is lower than I expected, though presumably because they had contra-indications.
  • mortality rate attributable to PE was 1.1% (though all cause mortality was 5.4% meaning that lots of sick people get PEs and die of something else)

COMMENTARY

I know I’ve ranted on this before but I do find it fascinating.

I grew up with the notion that PE killed roughly 1 in 5 of those with the disease. That’s kind of scary. That’s similar to STEMI mortality. There is no doubt that there was a time when the PEs we diagnosed carried that type of mortality. Big feck-off PEs that is.

As the technology has changed we have created a new disease – let’s call them pulmonary fluff instead of pulmonary emboli. Emboli are terrifying, fluff not so much.

We have presumed that pulmonary fluff is the same disease as the big bad pulmonary emboli.

We are left with, i think, with two possible conclusions

  1. we seem to have discovered a treatment (in heparin) that reduces mortality from 20% to 1%. An absolute risk reduction (ARR) of 19%. Considering that lytics for STEMI probably by you a 2% ARR we should be absolutely stunned.
  2. The alternative is that we are now diagnosing lots of pulmonary fluff and the mortality rate from pulmonary fluff is 1% at a baseline and giving all this people heparin to treat their fluff does nothing; an ARR of 0%.

It may be somewhere in between those 2 answers but we have yet to make up our mind which.

 

Filed Under: critical appraisal, FOAM, VTE · Tagged: , , ,
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