The Quay

Barnacle encrusted stumps remain.
Thrusting, vertebral fossils
From tidal glar pools and rising silt.

The bar is no longer dredged:
Time gently smudges over noisy, dark,
Dangerous memories:
Hard men stooping -
Their iron shovels grate on coal,
Organic metronomes in coal boat bellies.

I remember dimly the last coal boat
That hove to at the quay, then slipped away,
Leaving coal dust to settle, like age.

I’d leap and dive from great stone steps
Measuring days in the high tide times.
I fished here for pollock with dead-man’s-fingers
Torn cruelly from tortured crabs.

But now, luxury seafront apartments crowd
Like schoolyard bullies on the harbour walls
And the silt rises as the stories die.

Moving house

In the spirit of FOAM (Free Open Access Meducation) I have been collaborating with Mike Cadogan from to migrate this blog to it’s own domain. There is some fine tuning yet to do, but the existing content is all now available on – if you follow the blog, and if you follow the RSS feed please change your settings to

Once I am up and running, there will be a few changes on the site, including guest authors among other things. Watch this space. Or more accurately, the other space!

This is the logo for the new site:


I have scaled the pinnacle – retirement is all there is left

I am of course delighted with my receipt of the accolade of a F.UCEM Diploma from the Utopian College of Emergency for Medicine via although this is tinged with disappointment as their promise to invoke “legend” status was cruelly broken with a devious post-hoc goal-post-shifting manoeuvre akin to that performed by the authors of IST-3.

And if I want to overpunctuate something, damn it, I bloody will, @precordialthump !?!?!?!

Not all ST elevation is STEMI – the follow up

So this ECG has generated a fair bit of interest and quite a few comments both here and on Twitter. I trickled out a bit more information in the second post, but here is the final act:

I figured there were essentially three options for this patient (with a few minor variations possible) given that it was midnight and the “cardiology” registrar was a covering respiratory registrar:

1) Activate cath lab
2) Treat like a non-STEMI and consider a cath in the morning
3) Get an Echo looking for regional wall motion abnormalities and use that to guide decision re. primary cath urgently or not

Frankly, I think these are all reasonable options, with only logistical differences. He is a young man, and with his story is going to score a cath at some point anyway – only the timing of it remains to be decided. I thought he had myopericarditis, but that his more severe pain from two days prior sounded suspicious for ischaemic pain, so I wasn’t prepared to ignore that. I toyed with the idea of a late night Echo-tech call-in, but elected to treat him as a non-STEMI-plus, in that he got aspirin, clopidogrel, heparin and in consultation with the very sleepy on-call interventional cardiologist (who I think liked my plan because he got to stay in bed, rather than beacuse of innate superiority to other approaches), a tirofiban infusion. An Echo was organised for the morning and he went to CCU.

Echo report (paraphrased summary):

  • Mildly impaired LV function with two regional wall motion defects (inferoposterior basal and mid segment hypokinesis) with an EF of 50%.
  • There was a tiny posterior effusion.
  • Valves and other chambers NAD other than mild TR.

He not suprisingly went for a cath that morning too:

  • LAD: 70% stenosis, diffuse disease
  • LCx: 100% stenosis
  • Proximal 1st obtuse marginal: 70% stenosis
  • RCA: 60-70% stenosis
  • Conclusion – triple vessel disease, culprit lesion in LCx, akinetic inferior wall

The serial troponins went from 16 to 9 to 6 over the next 24 hours. The patient was discharged and referred for a CABG. The discharge summary prepared by the cardiology resident didn’t mention myopericarditis, but in discussion with the cardiologist himself, it was clear that his opinion was that the patient indeed had myopericarditis secondary to his infarct, which almost certainly occured 2 days prior and correlated with his more severe and typical sounding episode of pain.

This ECG from just before his cath and Echo is much more consistent with myopericarditis, with widespread saddle-morphology ST elevation, PR depression, and PR elevation in aVR:

So there you have it – a late-presenting MI (perhaps STEMI?) AND myopericarditis. This syndrome of early post-MI pericarditis may be rarer in the post-thrombolysis/PCI era, and is also known as PIP or PAMISP. It’s a bit too early for the autoimmune mediated Dressler’s syndrome (which is definitely rare in the post-interventional era), as suggested by some commenters, which tends to kick in from around 2 weeks post-MI. From emedicine on the topic:

“The incidence of early pericarditis after MI is approximately 10%, and this complication usually develops within 24-96. Pericarditis is caused by inflammation of pericardial tissue overlying infarcted myocardium. The clinical presentation may include severe chest pain, usually pleuritic, and pericardial friction rub.

The key ECG change is diffuse ST-segment elevation in all or nearly all of leads. Echocardiography may reveal a small pericardial effusion. The mainstay of therapy usually includes aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs). Colchicine may be beneficial in patients with recurrent pericarditis.”