Anatomy for EM 034 | The Hand Part 02 | The Fingertip

Onto the fingertip

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Anatomy for EM: 033 | The Hand Part 01 | The lingo and the soft tissues

We’re back… after a few years hiatus (blame the children…) we have a series of podcasts on the hand. The hand needs some special anatomic attention for EM as we see so many injuries and their misdiagnosis and mismanagement has great potential for long term morbidity.

I’m not sure how many podcasts this series will stretch to but let’s get started.

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Conference: VTE Dublin

This is the second year of this conference which I’m involved with. It covers the whole gamut of VTE care from basic science to DVT to PE with all of the different specialties involved.

From an EM point of view we have Kerstin Hogg from Canada and Dan Horner (from St Emlyns). There’s a host of other prominent VTE names too.

It’s a one day conference but we’re offering an Echo and USS for DVT workshop the day before (included in registration)

Registration is cheap (€75 for bosses and €35 for non bosses) so you can’t get better than that.

Would love to see some of you there and don’t forget we’re on twitter too.

[Direct Download PDF]

Download the PDF file .

 

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Tasty morsels of EM 067 – Monro-Kellie 2.0

This is based on Mark Wilson’s paper in the Journal of Cerebral Blood Flow & Metabolism  [Free full text] which i’m sure you all read avidly every month.

COI – I know Mark and had the honour being in the same speaking track as him when he gave a similar talk at SMACC Gold. He was very kind and didn’t point all the things I was wrong about in my talk.

I learned lots from this paper and it turns out there are lots of subtleties to ICP that the classic Monroe-Kellie doctrine doesn’t account for. Level of evidence is as you might expect somewhat low but this is fascinating stuff none the less.

What is Monro-Kellie?

  • Monro (Scotsman with dodgy wig) suggested that skull was a closed box and as soon as you add something to the box either pressure goes up or something gets squeezed out
  • Kelli (Monro’s student) did some autopsy work suggesting Monro was right.

 

click for source

click for source

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Problems with Monro-Kellie (apart from the dodgy wig...)?

  • blood and CSF given the same weight/importance despite the fact that CSF production and flow is tiny and venous flow is huge (equal to arterial inflow at 14% of the cardiac output)
  • it therefore makes sense that a problem with venous outflow or accumulation is likely much more important than CSF.
  • there has been lots of focus on managing the arterial side of things with certain CPP goals that entirely ignore the fact that fiddling with the arterial side when there’s a problem with outflow might miss the point.

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Tell me about these veins then

  • i did a podcast on it once…
  • most people have asymmetric venous drainage and are quite dependent on their dominant side – if this side gets obstructed (maybe by a depressed skull fracture) then that’s probably important
  • they’re formed by little dural folds with no support of their own (unlike the muscular arterial walls) and are hence very dependent on their surroundings. Eg, next time you’re opening a dural sinus in someone sitting upright it’s worth remembering that the dural sinus pressure is probably negative and will cause a massive air embolism. Likewise when you lie someone flat the venous sinus engorges.

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What causes problems with venous drainage or venous hypertension?

causes of venous hypertension wilson

click for source

Mark provides a lovely little classification in the table above

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Some pearls

  • a depressed skull fracture over a venous sinus (esp a dominant one) may cause venous outflow problems worsening ICP. The venous sinus may even thrombose
  • idiopathic intracranial hypertension (that disease of young obese women with papilloedema) is associated with venous sinus stenosis
  • poor head position (slight flexion and rotation) will significantly impair jugular (and hence intracranial) venous drainage. Not to mention the dreaded collars…
  • outside the head, high ventilation pressures transmit to the venous system and indeed even raised abdominal pressure can cause refractory raised ICP (as beautifully described by Tom Scalea
  • even microgravity causes issues with astronauts reporting a syndrome somewhat similar to idiopathic intracranial hypertension during prolonged time in space

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Tasty Morsels of EM 066 – Pneumothorax

pneumothorax

From this lovely review and update paper in Lancet Resp Med. Found this via Josef Liebman’s EMU. One of the slightly more obscure FOAMed resources but he always seems to pluck out some papers i’d never find on my own.

Primary v Secondary:

  • this classification (that forms the mainstay of classification in the hallowed BTS guidelines) dates back to the early 20th century and was mainly used to distinguish those with PTX from TB (who would go to a sanitarium for a year) vs those with PTX from other causes.
  • In reality, there is much more likely to be a continuum between the truly idiopathic PTX and the secondary PTX from severe COPD. Most of those that we call primary PTX probably aren’t and if you look hard enough you will find a cause
  • they don’t say this to totally undermine the binary separation but it’s worth knowing that things are a little bit more complicated than that.

Causes:

  • in the young tall non smoker telling them that their primary PTX is from a single ruptured bleb is probably not true. There is some evidence that there are areas of the visceral pleura have “pores” that permit air leak into the pleural cavity
  • cannabis smoking causes lots of destructive lung disease and lots of PTX
  • Birt-Hogg-Dube syndrome. Only included for your next dinner party conversation…

Management:

  • not entirely clear how expanding a lung is meant to fix the hole in the visceral pleura as there’s no reason to believe that bringing the visceral and parietal pleura together will cause a spontaneous pleurodesis
  • as a result it’s not clear if we really have to intervene at all and the aussies are now trialling a conservative approach for even large PTX.
  • blood patching – not just for post LP headaches. Some data and theory on putting some autologous blood in the pleural cavity in the hope it helps the visceral hole heal. It seems like hocus pocus but then so does blood patch for LP headache and it seems to work…
  • we should probably use Heimlich (he of the maneuver) flutter valves more for OPD management. I think these are great but you’d need a fairly clear follow up mechanism in place.

Recurrence:

  • some debate over this. Some studies said 20% some more recent better data says 40% for a primary PTX. If it’s that high then  perhaps we should be thinking about interventions to prevent recurrence (which seems to be mainly VATS i think)
  • after a VATS recurrence is low, some debate on the number but the paper quoted numbers from 2-5%

 

 

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