PCI for stroke trials

OK, so I admit PCI for stroke is something I made up, but I think it’s a reasonable analogy. Given that treatment for STEMI moved from tPA to PCI then it’s hardly surprising to see a similar trend in the stroke world.

The idea is to remove (or sometimes lyse intrarterially) the cerebral arterial occlusion using interventional radiology. Whatever you make it’s certainly pretty cool and ambitious technology. There are a number of trials and devices out there for this type of thing, perhaps the most famous being the MERCI device.

Below is a review of two recent studies that compared new devices against the MERCI device.

Nogueira, Raul G, Helmi L Lutsep, Rishi Gupta, Tudor G Jovin, Gregory W Albers, Gary A Walker, David S Liebeskind, Wade S Smith, TREVO 2 Trialists. “Trevo Versus Merci Retrievers for Thrombectomy Revascularisation of Large Vessel Occlusions in Acute Ischaemic Stroke (TREVO 2): a Randomised Trial..” Lancet 380, no. 9849: 1231–1240. doi:10.1016/S0140-6736(12)61299-9.

METHODS

  • big sponsored trial to prove that the TREVO is better than MERCI device. Stryker makes both interestingly…
  • both are retrieval devices where the coil goes distal and the clot is withdrawn (there are others called micro aspiration)
  • all had to have failed tPA or be ineligible for it. (ALERT – lots of cherry picking can be done here)
  • lots of exclusion criteria (excluded 80% of those screened)
  • end point was revascualrisation NOT clinical outcome; hardly unsurprising though

RESULTS

  • 180 pts
  • The TREVO (the new device) did better in both the reperfusion and the clinical outcomes.
  • more died in the TREVO group at 90 days (24% v 34%) they somehow neglect to mention this…

———

Saver, Jeffrey L, Reza Jahan, Elad I Levy, Tudor G Jovin, Blaise Baxter, Raul G Nogueira, Wayne Clark, Ronald Budzik, Osama O Zaidat, SWIFT Trialists. “Solitaire Flow Restoration Device Versus the Merci Retriever in Patients with Acute Ischaemic Stroke (SWIFT): a Randomised, Parallel-Group, Non-Inferiority Trial..” Lancet 380, no. 9849: 1241–1249. doi:10.1016/S0140-6736(12)61384-1.

METHODS

  • a Dublin made device being trialled in the US against the only currently approved device
  • similar criteria as the previous trial – either failed tPA or contraindications and within 8 hrs
  • primary outcome was recanalisation NOT clinical outcome

RESULTS

  • total 120 pts
  • excluded 80% assessed
  • stopped early for benefit (always a shame…)
  • solitaire device was better on everything (even mortality in this tiny trial)
  • of note mortality was 44% in the MERCI group and 18% in the Solitaire group. Think about that for a second – in the MERCI group almost half died – that seems a bit off to me – most strokes don’t die in numbers like this – at least not by 90 days. They certainly didn’t die in these rates in the lytic trials.

 

Some thoughts

These are all very selected patients – so this is the best possible picture of the results. This is NOT a treatment that will be available to all your stroke patients. Often it will be limited by anatomy but it’s also only gonna be done in the younger patients with a better chance of outcome. The key will be (as with most things) being able to work out who might actually benefit from this sort of thing.

This may over the next 20 years become like PCI for STEMIs. But i doubt it, for the same reasons I’m dubious about lytics in stroke.

  1. diagnostically stroke is a much more difficult disease than STEMI
  2. the brain and its circulation is a lot more complex and tenuous than the heart (we have a circle of willis for a reason  - a built in collateral circuit in case of failure of flow.)

For added value I’ve added a demonstration video for all 3 devices below. See if you can spot the differences.

Which test for rotator cuff tear following shoulder dislocation?

There are of course a number of papers looking at the same thing but I saw this one recently.

Yuen, Chi Kit, Ka Leung Mok, and Pui Gay Kan. “The Validity of 9 Physical Tests for Full-Thickness Rotator Cuff Tears After Primary Anterior Shoulder Dislocation in ED Patients..” The American Journal of Emergency Medicine 30, no. 8: 1522–1529. doi:10.1016/j.ajem.2011.12.022. PMID 22386341

Great study question  – in shoulder dislocation can we pick up full thickness tears at 10 day follow up using clinical exam?

METHODS

  • ultrasound by the trained EPs as gold standard – this could easily be questioned both in terms of training and in terms of modality – is MRI better?
  • the big problem was the EPs doing the ultrasound were the same guys who did the exam – there was no blinding here so you can effectively find what you want to.

RESULTS

  • 50 pts over 4 years (another problem…)
  • 40% had a tear
  • they conclude that the empty can test was the best – which is nice because that’s what I’ve been doing.
  • even at that sens was 90% and spec 55% for the empty can.

 

Desptite the obvious weaknesses of the paper tears are common and contribute to morbidity so they’re worth looking for

Here’s a video of the empty can test just as a refresher

Ketamine use in TBI – the ICP goes down not up.

click for source

H/T Rob Bryant for tweeting the paper.

Ketamine in known elev. ICP. J Neurosurg. Pediatr. 2009 Jul;4(1):40-6 #FOAMed #Iloveketamine http://t.co/jrn7noEk
@RobJBryant13
Rob Bryant

We all love ketamine, or at least Minh does. But there has always been the bogey man stories, that if you use ketamine in someone with a head injury, there brain will explode and you’ll get covered in lots of brain goo which is never  a good luck. As a result, I rarely see people reach for ketamine as an induction agent for these people.

There is increasing evidence that the ICP rise attributed to ketamine is likely a bit of a myth based on faulty early data and even faultier interpretation (a bit like lignocaine/adrenaline is bad for fingers…)

This study provides a little bit more ammo that ketamine is safe for ICP. It’s not gold standard, bullet proof evidence but the case is building.

Bar-Joseph, Gad, Yoav Guilburd, Ada Tamir, and Joseph N Guilburd. “Effectiveness of Ketamine in Decreasing Intracranial Pressure in Children with Intracranial Hypertension..” Journal of Neurosurgery. Pediatrics 4, no. 1: 40–46. doi:10.3171/2009.1.PEDS08319. PMID 19569909

METHODS

  • single centre in Israel in the PICU with kids with TBI
  • two groups, 
    • one who got ketamine for a procedure
    • the other who got ketamine for the ICP specifically
  • ketamine was 1-1.5mg/kg
  • all were on midaz and morphine as sedation
  • some had propofol as well
  • a bunch got mannitol or hypertonic saline or thiopental and some even had decompressive craniectomy

RESULTS

  • 30 patients, 82 episods of ketamine administration, most for treatment of raised ICP
  • it worked, it lowered the ICP by about 5mmHg in both groups of patients

Their only concern is that some of the prior studies showed ICP rises in those who were probably inadequately anaesthetised. This bunch of kids were doped up to the max and they say maybe that’s why the ketamine is safer.

They were surprised that the ketmaine actually lowered the ICP not just didn’t increase it.

This is, of course, a tiny little study and with all the different interventions going on you could make the argument that we can’t tell if it was the ketamine that lowered the ICP. None the less it’s still encouraging that the bogey man of raised ICP is a little bit mythical.

Some thoughts on concussion

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

Should we anti-coagulating all those patients in plaster casts?

Click for source

Interesting enough question. We know having a big cast on is a risk factor for VTE. I’ve seen one young guy die from a massive PE with a big cast on his leg.

It mightn’t be common, it mightn’t justify risk and expense but it’s definitely a valid question. But do we have an answer as yet?

I figured this paper might help me answer it.

Meek, Robert, and Roger Lien-Kien Tong. “Venous Thromboembolism in Emergency Department Patients with Rigid Immobilization for Lower Leg Injury: Incidence and Risk Factors..” Emergency Medicine Australasia : EMA 24, no. 3: 277–284. PMID 22672168

 

INTRO

  • Australia madated that all lower limb casts get LMWH. The guideline was for in patients (from what I can make out) but are ED patients really different.

METHODS

  • chart review using various search terms to pull out all the patients with lower limb casts
  • tried to ascertain from records if they developed a VTE (obviously this can be a little problematic)
  • they also tried to contact everyone in a 3 month period by post and phone to see if they ‘d had a VTE (also a little problematic)

RESULTS

  • initial search yielded 10000, they narrowed this down to 6800 >18 and reviewing records left 1200 who actually got a splint
  • found 33 VTEs (2.7%)
  • in the small 3 month cohort (180 pts) who they actually contacted the rate was 1.7% (or 3 pts…)
  • when they put together the VTE they found on chart review and those they found on postal survey they come up with a number between 3 and 7% incidence.

So after reading that, i’m not sure I really have my question answered. Is there anywhere else I can turn to?

Serendipitously there has just been a Best Bet published on this very topic. They come to the conclusion that the rate is about 11%.

More importantly the bet itself is in part put together by thegreatnortherno who is our great shining hope and is going to tell us all what should be doing. At least that’s what EMManchester says.

As is only fitting StEmlyns have a whole post on it so go read that.