The Royal college of emergency medicine is having its annual conference starting tomorrow. It’s being organised by RIck Body and all the folk better known as st emlyns

The line up looks amazing and the conference is actually sold out. 

As part of the rcemfoamed network I’ll be one of a group creating a daily  podcast and blog summary of the conference. Be sure to get the feed to follow us

Hashtag is #RCEM15

If you’re at the conference please come along and say hi. 

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Getting started with FOAMed

Just a little note to state that I have collated a few resources for those looking to get started with both consuming and creating FOAMed. There’s a little link at the top right of the page.

I also recorded some talks recently for the RCEM FOAMed network on creating podcast type material. Hopefully they’re of some use:

01 – recording a solo podcast

Scott Weingart on getting started in FOAMed

Andy Neill’s Social Media Workshop


02 – recording a skype interview

03 – recording a screencast

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Hypoxia in Pulmonary Embolus

mechanism hypoxia featured

Hypoxia is almost ubiquitous in PE. Yet it is not immediately clear why. You might think you know but certainly when I start to think about it too much it all becomes very muddy. This is mainly due to my poor understanding of respiratory physiology no doubt. I’ve tried to correct that somewhat with this post.

My basic thinking has always been. A PE is a big clot in the lung, this means part of the lung doesn’t work right, ipso facto then there must be hypoxia. That gets you through day to day existence in emergency medicine but it’s hardly a detailed description of the problem.

The terminology doesn’t really help here as V/Q mismatch technically seems to mean that there is an imbalance ventilation to perfusion. In the context of PE people state that the hypoxia is due to V/Q mismatch but don’t clearly state if it’s a high or low V/Q state.

The terms shunt and venous admixture are also used with some frequency which has a tendency to confuse the anatomist in me where the I can tell where the superior oblique is and what direction it runs in purely from the name…

I started with Rosen’s 8th Edition. The PE chapter is written of course by Jeff Kline.

A lodged clot can redistribute blood flow to areas of the lung with already high perfusion relative to ventilation and therefore cause more blue blood to pass through the lung without being fully oxygenated. This venous admixture is probably the primary cause of hypoxemia with PE and the increased alveolar-arterial oxygen difference

This actually is a pretty decent explanation of what seems to be happening. PE causes redistribution and instead of the left lung getting 50% of the cardiac output it suddenly gets 80% and the ventilation isn’t sufficient to oxygenate the blood.

But  figured I’d do a bit of further reading just to see what else is out there.

Paper #1

Huet Y, Lemaire F, Brun-Buisson C. Hypoxemia in acute pulmonary embolism. Chest. 88(6):829-36. 1985. [pubmed]


These guys studied a whopping 7 people,  all 1-9 days post PE, but 2 hrs post their formal angio that was used to diagnose it. Most had greater than 50% pulmonary vascular occlusion and most had some CXR changes too (something we don’t see very commonly). They all had Swan-Ganz catheters placed hence all the lovely data they got to play with.

They were all on heparin and were given urokinase after their “gas exchange test”. This involved infusing a bunch of inert gases dissolved in dextrose and measuring lots of things.

They suggest that the hypoxia had different causes depending on the patient and interestingly could be related to their CXR changes.

  • if they had atelectasis on CXR then there hypoxia was from shunt.
  • if the CXR was normal it was due to perfusion of lung units with low V/Q ratios (ie overperfusing a lung unit with no increase in ventilation)


In PE there is a degree of shifting of ventilation away from and around the underperfused lung, this presumably, is the lung autoregulating itself. This shifting is not particularly well done and after a while atelectasis occurs and as a result of that you now have shunt as an additional cause of hypoxia.

They conclude from their data that initial hypoxia is due to V/Q mismatch (in particular ,perfusion of lung units with low V/Q ratios) and later in the disease course it is likely shunting.

Paper #2

Burton GH, Seed WA, Vernon P. Observations on the mechanism of hypoxaemia in acute minor pulmonary embolism. British medical journal (Clinical research ed.). 289(6440):276-9. 1984. [pubmed]

These were probable PEs, all diagnosed on V/Q scans. All were tachy and breathless with normal CXRs and patients were identified through chart review. Mostly post op. They describe them as minor PE but I suspect they were all quite impressive and may well be termed “submassive” in these days of right heart strain and trops…

Most were a week post symptoms and the ABG was taken just after the diagnostic V/Q scan.

They garnered a huge 11 pts. The V/Q all showed reduced perfusion in areas well ventilated (which seems to be the definition of PE on a V/Q scan) and lots of other distal areas that were overperfused comared to how well ventilated they were. The more severe the V/Q scan changes the more severe the ABG abnormalities.

One of the big issues here is that they assume the cardiac output was normal or raised i their calculations but they don;t actually measure it. The prior study did measure CO in their patients and that it was reduced in all patients.

This doesn’t really help much in working out what’s going on to be honest

Paper #3

D’Alonzo GE, Bower JS, DeHart P, Dantzker DR. The mechanisms of abnormal gas exchange in acute massive pulmonary embolism. The American review of respiratory disease. 128(1):170-2. 1983. [pubmed]

I had to work off the abstract here as I couldn’t get full access. They studied two patients here, both with “massive PE” (they don’t provide a definition in the abstract) using the inert gas method and found that shunt was the main issue, not V/Q mismatch . They state that 20% and 39% of blood flow was through unventilated lung. They conclude that shunt is the main issue.

Paper #4

D’Angelo E. Lung mechanics and gas exchange in pulmonary embolism. Haematologica. 82(3):371-4. 1997. [pubmed]

This a review article written by one of the authots above. It’s the best I’ve found and is open access too. Bottom line: shunt and V/Q mismatch are the main causes of hypoxia. (are there any other options???)

It does try and explain why V/Q mismatch causes low O2 – apparently due to the sigmoidal shape of the O2 curve increases in ventilation cannot keep pace with either increased or decreased perfusion. Note this does not apply to CO2 as its curve is linear. This did ring a bell from my ICU reading years ago…

It highlights that some reports have noted bronchoconstriction and airway narrowing is part of PE – though perhaps this is clinically silent for most patients as I can’t say I’ve heard a great deal of wheezing in there.

The atelectasis that occurs (with resulting shunt) could be down to pneumoconstriction from low CO2 or it could be down to humoral mediators from the platelets in the clot surrounding it.



Both shunt (perfusing a totally unventialted lung segment) and V/Q mismatch (poor matching of ventilation to perfusion) are important causes of hypoxia in PE. The shunt is probably the important take away point as we commonly see patients with pleuritic pain for a week with what looks like consolidation/atelectasis on a CXR and we don’t entertain the diagnosis of PE as most of us were brought up believing that we should think of PE in patients with SOB and a clear CXR.

In my search I did find some great videos on basic mechanisms of hypoxia in all conditions which I’ve embedded below.

Any questions, comments, corrections are always welcome.

Image source: https://commons.wikimedia.org/wiki/File:Saddle_thromboembolus.jpg

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Tasty Morsels of EM 057 – Ketamine induced uropathy

As always, this is from the ever expanding google doc on bits and bobs I read and learn from and transfer here for all our learning pleasure.

Wei YB, Yang JR, Yin Z, Guo Q, Liang BL, Zhou KQ. Genitourinary toxicity of ketamine. Hong Kong Med J. 2013;19:(4)341-8. [pubmed] Free PDF

I suspect most of us are aware that chronic ketamine abuse can cause this but I also suspect that we miss this fairly commonly by simply not asking and diagnosing young men with UTI or urethritis and sending them off into the night (and inevitably their cultures are negative)

I’ve seen/suspected this twice in the last few years and no doubt missed it in lots of others.

The paper is a nice summary of theories and potential treatments. There is a lovely free case report in WestJEM of bilateral hydro associated with this (presumably related to ureteric obstruction from bladder thickening) so yet one more excuse to channel your inner sono. 

  • young people
  • chronic ketamine use is a huge issue in south east asia
  • typically chronic abusers (they suggest more than 3 times in a week)
  • mechanisms:
    • unclear (what a surprise)
    • possible toxic effects of metabolites
    • possible damage to microvasculature
    • change in neuromuscular control due to the ketamine
  • typical manifestations are lower urinary tract symptoms including severe dysuria, painful haematuria, urinary urgency, urge incontinence and frequency
  • on imaging you might see an irregular thick walled bladder with small volumes. Hydro is quite common (up to 50%)
  • stopping the ketamine is the most important thing however there are significant numbers for whom this won’t work. the paper suggests resolution in only a third.
  • various treatments suggested
    • oral anti cholinergics
    • intra vesical hyaluronic acid or even botulinum
    • surgery is an option with all kinds of complicated procedures I don’t understand
  • there is genuine bad outcomes here – renal function decline from chronic hydro and irreversible LUTS and quality of life issues. This isn’t a STEMI by any means but it’s important we think of this and refere

Take home message – that young lad with “UTI” for no apparent reason probably doesn’t have a UTI…

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Tasty Morsels of EM 056 – Dystonic reactions

As always, this is from the ever expanding google doc on bits and bobs I read and learn from and transfer here for all our learning pleasure.

[Video via Larry Mellick’s excellent youtube channel]

Anyone working in any ED for any length of timee will have seen this – either from someone using an illicit substance and appearing at triage or in a poor young woman, 30 mins after your treatment for her migraine.

  • common with anti-emetics (metoclopramide/prochlorperazine) and anti-psychotics though the full list of potentials is huge.
  • pathophysiolgy is to do with dopamine in the basal ganglia (blockade of central dopaminergic receptors and some other mechanisms I struggle to follow)
  • Harwood-Nuss has a nice table of associated agents
    • drugs that might be used illicitly: cocaine/ketamine/bupropion/dextromethorphan
    • bizzarely both diphenhydramine and diazepam, (agents that are often used to treat dystonia) are on the list. Even propofol gets a mention
  • Tardive dyskinesia is more severe and usually with long term use of anti psychotics
  • drug or alcohol abuse is thought to be a predisposing factor
  • Look at the mandible the neck and the eyes – these are the commonest areas affected. Can affect the whole body
  • reactions can be delayed up to 5 days if starting a new drug
  • give an antimuscarinic to fix it
    • where I’ve worked this has always been procyclidine
    • elsewhere diphenhydramine and benztropine are commonly suggested agents
  • IV route seems to be significantly quicker in action than IM.
  • Harwood-Nuss suggests oral meds for a few days to prevent recurrence


Harwood-Nuss 5th Edition, pg 1501

[featured image CC license, Wikimedia Commons, James Heilman, MD]

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