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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In Praise of the Researchers

I read a lot of papers. Mainly for my own education but also for podcasting and blogging purposes.

I’ve done an almost invisible amount of research. One on ballpoint pens and crics, one letter on why LMAs might kill pigs but not humans in cardiac arrest and one on twitter at conferences (that incidentally happens to be the first use of the term FOAM in the medical literature).

These epoch defining research papers aside, I’ve contributed very little to the cornucopia of research out there.

I have done a lot of this blogging stuff, with this site being around since May 2011, well before most of the FOAMed universe.

But let’s not get carried away here. FOAMed, while great and important, and I genuinely believe, a novel and useful contribution to the medical landscape, is not where the graft, sweat and tears are. It’s in producing the research.

FOAMed is mainly (at least for me) sitting around in the evening with a cold one on a laptop in my casual wear hammering out some thoughts and opinions on what other people with proper jobs and academic funding and much larger brains than mine have spent time, sweat and tears producing.

The phrase “those who can, research and those who can’t, blog about it”, springs to mind.

The amount of work, heartbreak and persistence it takes to do clinical research is somewhat mind boggling. And for those of us (by which i mean me of course) who seem to acquire kudos tearing it apart and critiquing it perhaps should try and direct a little bit more of the kudos towards the researchers (and indeed the poor patients) who created the research.

So to you, dear researcher who has ran the gauntlet of funding applications, ethical approval, endless meetings, consenting, collecting data, analysing, drafting, writing and surviving the endless rejection of peer review – to you I give praise and thanks.

And endless apologies for the casual brevity with which this young punk might tear said research apart and use it like a stick to win arguments with…

Post script. There are some who seem to have straddled both worlds of producing research and nailing the FOAMed thing – Rick Body and Simon Carley jump to mind as stellar researchers and commentators.

Post the post script. I don’t mean to devalue the work FOAMed requires, lots of FOAMed guys do incredible blood sweat and tears work, it’s more to make sure the researchers get the kudos they deserve.

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Tasty Morsels of EM 065 – Hyatid disease

hyatid disease

This can definitely be filed under the rare and obscure portion of EM. But i’ve seen it twice in 12 years, and was baffled both times so there you go…

 

  • known as hyatid disease (definitely easier to spell) or echinococcus (and the bunny men) granulosum
  • It’s a parasite duh
  • Mainly acquired in the developing world from poo of course.  Always the poo… (Update, my former Colleage, Dr Adler, an ID chap pointed out in the comments that’s faecoral from the animals – not the humans. We’re “dead end hosts”)
  • Primary infection always asymptomatic and usually in childhood
  • Clinical presentation is usually later (up to 50 years). You will see this (as I recently did) given increased immigration
  • Symptoms are usually related to mass effect in the affected organ so they can be fairly broad
  • Liver the commonest organ so it’s the type of thing you might see either incidentally or pathologically with your bedside ultrasound

Echinococcus

  • They can rupture and cause all kinds of funky spread
  • Cysts can become calcified and appear clearly on plain films

hyatid

  • Important to stop your radiologist trying to biopsy one as they can precipitate spread or even anaphylaxis
  • Diagnosis is usually a combination of imaging and serology
  • Management depends on whether there are complications from the cyst or not.
    • The more complicated it is the more likely surgery will be needed.
    • If you just want to treat the parasitises then reach for the ever faithful albendazole.
  • as always if you want some cool images click through for what Google has to offer

References:

  • Rosen’s 8th Chapter 133
  • UpToDate

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Tasty Morsels of EM 064 – Normal Pressure Hydrocephalus

normal pressure hydrocephalus

There was an article in the Abstracts recently by Djukic in 2015 that looked at how often you can find a potentially reversible cause of dementia. Billy Mallon wrote a nice essay on it. We reviewed the paper over on the RCEM FOAMed podcast

normal-pressure-hydrocephalus-1
Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org. From the case rID: 7258

That in itself but something that cropped up that i was blissfully unaware of was normal pressure hydrocephalus. The entity itself seems somewhat controversial but here’s the gist of it

  • a communicating hydropcephalus
  • enlarged verntricles but normal pressures, at least on LP
  • the classic triad (you kneww there was going to be a triad didn’t you?)
    • demenita
    • gait disturbance
    • urinary incontinence
  • the pathophysiology is likely obstruction of the arachnoid villi like in SAH causing a chronic build up of fluid.
  • tricky to see on imaging as it’s usually old folk with atrophy who tend to have slightly big ventricles to start with. The key seems to be that the ventricles are our of proportion to the cortical sulcal enlargement
  • Can be seen on CT but MRI much better (what a surprise)
  • therapeutic LP (say 40mls) – if better proceed to a shunt. Gait should improve within an hr… This is what they did in the Djukic paper
  • the shunt is the definitive treatment
  • overall very little definitive evidence and guidelines on this
  • it can of course co exist with dementia like alzheimers so just cause you find it doesn’t mean you can fix the patient.

References:

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