Some thoughts on concussion

December 2, 2012 by · 4 Comments

Concussion is a strange beast. We know what to do with extra-durals (we think) but what do we do with concussion. We don’t even know what it means or what is going on at a cellular level. Yeah the CT looks normal but that doesn’t mean the brain is normal. Certainly, patients with concussion type symptoms don’t feel or behave normally.

So what do we do with a condition like that? Study it lots and come up with consensus statements like this one.

It’s a good read and it’s freely available. Concussion is something we see A LOT of and we need to think a little beyond “is there blood in the brain or not”

The evidence behind all this isn’t wonderful (in terms of high level RCT) but the paper does provide some useful insight into what to tell patients. I’ve given some highlights with commentary below.

Concussion is defined as a complex pathophysiological process affecting the brain, induced by traumatic biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include:

While wordy, it’s fairy accurate – “we haven’t much of a clue but there’s a lot going on.”

1. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an ‘‘impulsive’’ force transmitted to the head.

2. Concussion typically results in the rapid onset of short-lived impairment of neurologic function that resolves spontaneously.

3. Concussion may result in neuropathological changes but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury.

4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course; however it is important to note that in a small percentage of cases however, postconcussive symptoms may be prolonged.

5. No abnormality on standard structural neuroimaging studies is seen in concussion.

This is what I try to explain to patients – though obviously it needs translated into patient speak. Typically I will spend a good 5 minutes talking to patient and family following evaluation for a bump on the head like this. Time well spent for a disease which we have no other intervention for. Talking to patients – hard bloody work but worth it.

The panel however unanimously retained the concept that the majority (80–90%) of concussions resolve in a short (7–10 day) period

I don’t use the numbers in discussion (though I might now) and I say 10-14 rather than 7-10 days but they get the point that most people are better quickly

brain CT (or where available, MR brain scan) contributes little to concussion evaluation

DO NOT SCAN FOR CONCUSSION. Of course – it’s not always that easy to tell but a scan will not help in the slightest for concussion

It is worth noting that standard orientation questions (eg, time, place, person) have been shown to be unreliable in the sporting situation when compared with memory assessment.

I don’t currently do formal memory assessments – it usually becomes clear in the situation (when the patient asks for the 4th time what happened…) that memory is an issue

The cornerstone of concussion management is physical and cognitive rest until symptoms resolve and then a graded programme of exertion prior to medical clearance and return to play

Generally each step should take 24 hours so that an athlete would take approximately one week to proceed through the full rehabilitation protocol once they are asymptomatic at rest and with provocative exercise.

In my current ED we see a lot of young sports players (mainly rugby) whose first question is when can they get back to play

Epidemiological studies have suggested an association between repeated sports concussions during a career and late life cognitive impairment

This is something that seems to reinforce the significance of concussion for patients.

There is no good clinical evidence that currently available protective equipment will prevent concussion

While it seems there’s evidence for helmets reducing fractures, there seems to be none for reducing concussion.

Well worth the read.

McCrory, P, W Meeuwisse, K Johnston, J Dvorak, M Aubry, M Molloy, and R Cantu. “Consensus Statement on Concussion in Sport: the 3rd International Conference on Concussion in Sport Held in Zurich, November 2008..” 43:i76–90, 2009. PMID 19433429

Filed Under: critical appraisal, FOAM, head injury · Tagged: , ,

Anatomy for Emergency Medicine 009: Brain Herniation

March 13, 2012 by · 6 Comments

This is a quick run through of the 3 main brain herniation syndromes. Enjoy

Here’s a lovely case from radiopaedia.org, of SDH with subfalcine and uncal herniation and even an infarct in the anterior cerebral territory.

Filed Under: Anatomy in EM, head injury ·

Tasty Morsels of EM #27 – Head Injury

March 8, 2012 by · 2 Comments
  • EDH is of course normally mid meningeal artery but also be:
    • diploic veins (traversing the skull)
    • venous sinuses
    • mid meningeal vein (same course as the artery)
  • the classic lucid period presentation of EDH is exception rather than the rule
  • SDHs much more likely to have delayed presentations
  • blood from an SDH can be isodense with brain about 7-14 days post event (see CT below)
  • parenchymal contusion is the most common +ve finding over all 
  • cerebral vasospasm can occur after traumatic SAH but much less common than spontaneous SAH

Delayed SDH with midline shift and all that

Refernces:

Harwood-Nuss Clinical Practice of Emergency Medicine, 5th Ed, LWW 2010

Filed Under: harwood nuss, head injury, tasty morsels ·

Do Children With Blunt Head Trauma and Normal Cranial Computed Tomography Scan Results Require Hospitalization for Neurologic Observation? Ann Emerg Med. 2011 In Press

September 3, 2011 by · Leave a Comment

Holmes JF, Borgialli DA, Nadel FM, Quayle KS, Schambam N, Cooper A, Schunk JE, Miskin ML, Atabaki SM, Hoyle JD, Dayan PS, Kuppermann N, TBI Study Group for the Pediatric Emergency Care Applied Research Network*. Do Children With Blunt Head Trauma and Normal Cranial Computed Tomography Scan Results Require Hospitalization for Neurologic Observation? Ann Emerg Med 2011 Jun. PMID 21683474

This is a reasonable question to be asking and a very tricky one to ever conclusively prove

Methods

  • really an analysis of pts from the PECARN data set
  • non-trivial head injury (whatever that means) and could have poly-trauma
  • scanning was entirely at the docs discretion
  • GCS of 14 or 15 who got a CT that was entirely -ve for trauma
  • all were followed (whether admitted or not) to see whether they had a repeat scan or neurosurgery
  • follow-up for discharged patients was a phone call, followed by a mailed questionnaire followed by a trawl of databases

This is where the real problem is (as it is in most similar studies) – if some of the patients lost to follow up have bad outcomes then your conclusions would be radically differently. we’ll come back to this.

Outcomes

  • if it was done – a +ve  second scan for traumatic findings
  • neurosurgical intervention

Important to note that these are not the same thing. A neurosurgical intervention is a big deal. A small contusion is certainly less so. Unfortunately a small contusion is probably not entirely unimportant prognostically. If minor bumps cause long-term post-concussion cognitive problems then a bump big enough to cause a contusion is likely to be relevant. Never mind the potential for subsequent seizures. This is, at present, speculative.

Results

  • roughly 13000 pts included
  • most (80%) were discharged after their normal scan
  • if you had a GCS of 15 and a -ve scan and were sent home
    • 1 in 2000 had a repeat scan that was +ve
    • none had neurosurgery
  • if you had a GCS of 15 and a -ve scan and were admitted
    • 1 in 200 had a repeat scan that was +ve
    • none had neurosurgery
  • the numbers for GCS 14 were higher but still none had a neurosurgical intervention
  • 20% lost to follow-up (by phone or mail)

As I said this is the key problem with all these kind of studies (including the recent SAH studies by Perry et al). If some (or in fact any) of these kids were dead or had neurosurgery then it would probably matter. These guys did a thing called a sensitivity analysis to try to compensate for this.

Basically this means they assume a similar rate of event in the lost to follow-up group to see if this would change the numbers. That’s all well and good but there’s no reason to believe that the lost to follow-up group are the same as the group who did receive follow-up.

Statistical adjustment is no substitute for complete follow-up

Interpretation

Having said all that I still think that the authors conclusions are valid – that if you have a -ve CT in a kid who has a GCS of 14 or 15 then you don’t need to admit them.

I rarely get CTs of kids heads. This seems to be a big practice difference between Ireland/UK and the US – at least from the very distant perspective of reading the literature.

I rarely use the clinical decision aids to decide when to CT. Or at least I use a couple of them but always tempered by gestalt. Which is the great unknown, unproven difficult to articulate, bias ridden thing that we do every day.

I think we’re still waiting on the definitive word of what to do with anti-coagulated patients with a -ve CT scan as these guys definitely do deteriorate on occasion…

Filed Under: critical appraisal, head injury ·

Decompressive Craniectomy in Diffuse Traumatic Brain Injury N Engl J Med 2011;364:1493-502

May 29, 2011 by · 1 Comment

When I worked in New Zealand I was involved in flying our head injured patients to our neuro centre. A few came back after being entered in this trial with a hole in the head and a bit of the skull in the freezer. It was all new to me at the time. I remember being told this trial was underway so it’s kind if cool to finally see the results

I have fairly limited clinical experience in this, I’ve given the mannitol and the hypertonic saline and (largely avoided!) fiddling with CO2s and see what happens to the ICP.

[If you want someone who really knows what they're doing check out the Neuro-ICU podcast]

It’s fascinating physiology but it all seems kind of a zero sum game. It’s been a while since I looked at it but ICP control seems to be a zero-sum game really.

The classic being lowering the ICP by lowering the CO2 which reduces the ICP but also reduces the blood flow to the brain worsening the ischemic insult you were trying to avoid.

Cracking open the brain and letting it swell seems like a great way of avoiding these problems.

To the trial

Patients

  • 15-59 years
  • diffuse brain injured patients, no evacuatable lesions here
  • note recruitment was fairly slow over 8 years
  • they assessed 3500 for the trial and took only 150 (most excluded to have a lesion evacuated or the ICP settled itself)
  • as expected mainly young males in MVAs
  • overall mortality rate roughly 20% so think about whether that’s sicker or less sick than who you treat with comparable injuries

Interventions

  • everyone got the usual ICP treatment if the ICP passed 20mmHg
  • randomised within 72 hours of admission to either continuation of the same or a craniectomy
  • the protocol allowed the non-craniectomy group to cross-over if they failed the conservative treatment (which is a little naughty trial-wise but unavoidable)

Outcomes

  • started as composite (arrgghh stop saying the word…) of death and bad outcome but changed during the trial (also a tad naughty) to neuro outcome at 6/12

Results

  • 20% crossed from the no surgery to having surgery. 20% is a substantial number and means the results are probably a bit skewed
  • the ICP was much better in the surgery group (wa hey!)
  • poor functional outcome at 6/12 was 70% v 50% in favour of conservative treatment (boo!)
  • mortality was essentially the same (though not powered for that type of thing)

Comment

If ICP is so important then fixing it should make a difference. It doesn’t seem to. Maybe the outcome determining factor is the primary brain injury and the inductive  reasoning (that because hypoxia or low BP or high ICP in head injuries is known to make head injuries worse then not having that will make things better) just doesn’t hold up.

(my friend Vinny will hopefully keep me right if I’ve got that inductive bit wrong!..)

I suppose this is another great example of something that seems like a great idea physiologically but doesn’t quite pan out in practice. The cupboard where we’re keeping all such ideas seems to be getting pretty full. Such is the nature of the advance of medical knowledge.

UPDATE

Intensive Care Network have published a great series of videos by one of the guys involved in the trial (Simon Finfner). There’s 3 parts to it and you need to register with the website (free) to get the last 2. It’s well worth it.

He covers most of the similar points but covers the naughty bit about changing the primary outcome in a bit more detail.

Here’s the first bit:

FURTHER UPDATE

I see Cliff Reid has posted on this too with a link to another ongoing trial (that I was unaware of). Makes the important point (also made in the videos above) that the DECRA study enrolled lowish ICP (20mmHg) and the RESCUE-ICP study is taking patients with higher ICPs.

Filed Under: critical appraisal, critical care, head injury ·