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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