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.
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
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.
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.
What causes problems with venous drainage or venous hypertension?
click for source
Mark provides a lovely little classification in the table above
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
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.
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…
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
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.
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%