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

December 8, 2012 by · 3 Comments

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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
November 21, 2012 5:04 am via Camera on iOSReplyRetweetFavorite
@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.

Filed Under: critical appraisal, critical care, FOAM · Tagged: ,

Stop putting IV cannulae in the 2nd ICS for tension PTX

November 15, 2012 by · 19 Comments

Though I suspect this is old news by now, I’ve just read a couple of papers on it and thought I’d share my thoughts. They’re both by the very smart and talented Kenji Inaba.

Question

  • where should we put a cannula if we want to decompress a tension pneumothorax?

Inaba, Kenji, Bernardino C Branco, Marc Eckstein, David V Shatz, Matthew J Martin, Donald J Green, Thomas T Noguchi, and Demetrios Demetriades. “Optimal Positioning for Emergent Needle Thoracostomy: a Cadaver-Based Study.” The Journal of Trauma: Injury, Infection, and Critical Care 71, no. 5: 1099–1103. PMID 22071914

METHODS

  • 20 fresh frozen cadavers
  • 14G 5cm cannulae placed in 2nd ICS and 5th ICS
  • throacotomy to assess pleural puncture (considered a +ve outcome)
  • chest wall thickness measured in each cadaver at each puncture position

RESULTS

  • total of 80 punctures
  • all succeeded in the 5th ICS; 57% succeeded in the 2nd ICS

BOTTOM LINE

—

Inaba, Kenji, Crystal Ives, Kelsey McClure, Bernardino C Branco, Marc Eckstein, David Shatz, Matthew J Martin, Sravanthi Reddy, and Demetrios Demetriades. “Radiologic Evaluation of Alternative Sites for Needle Decompression of Tension Pneumothorax..” Archives of Surgery (Chicago, Ill. : 1960) 147, no. 9: 813–818. PMID 22987168

METHODS

  • chart and image review of all their trauma pts over a year who got a chest CT
  • split them into BMI quintiles
  • measured the chest wall thickness on CT  at the 2nd ICS and 5th ICS

RESULTS

  • 680 pts
  • 46mm in the 2nd ICS; 33mm in the 5th ICS
  • half of the pts had a chest thicker than 50mm at the 2nd ICS

BOTTOM LINE 

  • if a standard 14 G cannula is 50 mm then we’re going to fail to drain a whole bunch in the 2nd ICS

—

MY THOUGHTS

I’ve drained a number of tension PTX in the past – it’s usually fun to get the hiss  - all have been in the ED and quickly followed by a chest drain. I’ve received a number from the pre-hospital environment that probably worked initially but now the cannula has kinked and a second cannula shows a second release of air.

All this is a little bit silly I think – as I’m now convinced that we just need to get on and do the bloody drain (or at least make a cut and stick a finger in). If the patient is crashing in front of you and the quickest option is to place a cannula then great – just don’t get lulled into thinking you’ve fixed the problem.

UPDATE:

Haldun Akoglu left a comment about a paper that he just published (PMID 23116647). It was a review of 150 CT scans of people with PTX, mainly traumatic. They found that a 5cm cannula would also fail a lot of the time but failed to find a thinner chest wall at the 5th ICS when compared with the 2nd. I’m not sure why they they didn’t find a difference when Inaba did but either way 5cm cannulas are not the way to go.

Filed Under: critical care, trauma · Tagged: , , ,

Some notes on mechanical complications of MI

March 9, 2012 by · Leave a Comment

Ng R, Yeghiazarians Y. Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies. J Intensive Care Med. 2011 Jul. 11. Ahead of Print

Found this via R&R in the fast lane. Here’s a few notes and thoughts:

  • the bit on severe LV dysfunction isn’t as interesting because nothing really works here apart from reperfusion
  • the bits on complications of MI resulting in cardiogenic shock is much more interesting
  • Uses the big SHOCK registry for a lot of the data
Some factoids:
  • 75% of cardiogenic shock is LV dysfunction
  • echo really useful (well duh…)
  • Cardiogenic shock has mortality of 60% or so
  • Revascualrisation the most important thing
  • Recommendations for pressors but little evidence

ACUTE MITRAL VALVE RUPTURE

  • Acute MR and rupture in 8% of cardiogenic shock so really well worth looking for it seems; median time to rupture of 13 hrs
  • RCA infarcts with right dominant circulation the biggest risk as the PDA supplies valve. In a left dominant it’s supplied by two vessels
  • suggest SNP as a vasodilator to reduce afterload and keep forwards flow but of course not great when BP is low

VENTRIUCLAR SEPTAL RUPTURE

  • VSR occurs about 15 hrs post MI, not as late as we used to think
  • 5% of cardioggenic shock
  • usually LAD lesions
  • left to right shunt is the physiology
  • vasodilators might reduce shunt
  • IABP often needed
  • 80% mortality at 4 weeks – WOW

VENTRICULAR FREE WALL RUPTURE

 

  • 50% within first 5 days; 90% within 2 weeks
  • 2% of cardiogenic shock
  • 4 week mortality of 55% (given the mechanism I suspect it might be much higher than that!)
  • suggest that first MI and single vessel MI more at risk because of lack of collateral supply
  • lateral and post wall probably more at risk but due to their infrequency anterior (from LAD) is much more commonly seen in reality
  • most die immediately; those who survive have smaller ruptures which have plugged off
  • surgical repair the only option

Here’s a great talk from Stuart Swadron on valvular emergencies at All LA conference

Filed Under: cardiology, critical care ·

Colloids for resus in trauma

February 7, 2012 by · Leave a Comment

James MFM, Michell WL, Joubert IA, Nicol AJ, Navsaria PH, Gillespie RS. Resuscitation with hydroxyethyl starch improves renal function and lactate clearance in penetrating trauma in a randomized controlled study: the FIRST trial (Fluids in Resuscitation of Severe Trauma). Br J Anaesth. 2011 Nov.;107(5):693–702. PMID 21857015

I remember when I worked in ICU, reading a packet of some colloid and finding out that it was made from Swiss cow’s hooves. Slightly off putting. Better than the tPA made from chinese hamster ovary cells. Mmmm… Chinese hamster ovary cells…

Anyhow.

Cliff Reid reviewed this paper briefly a while back so be sure and read his (more cogent) thoughts on this first.

However, this paper is a classic of what has previously been called wandering outcomes. Though in this one there’s no problems with the registration, more in the writing and conclusions drawn.

METHODS

  • Blinded RCT pitting Saline against Hydroxyl Ethyl Starch
  • Sponsored by the makers and all the authors have links to industry
  • trauma patients, both penetrating and blunt and were analysed separately
  • inclusion criteria included a 3L fluid resus, though it’s not clear what they meant by this. They did say that they weren’t allowed more than 2L crystalloid before randomisation
  • Below is a little snapshot of their resus algorithm

I just want to point out that that’s a fairly complex protocol which could be questioned at many different points:

  • Dutton et al and I’m pretty sure EMCrit would agree that the appropriate fluid to replace in trauma is blood
  • the CVP is a poor guide for this
  • and in trauma resus do you really wait for the Hb to come back before transfusion?

You get the point that this isn’t crazy-sick-seat-of-your-pants resus but likely a little bit more of a slow controlled environment and probably not the way that I would practice. Though I’d be interested to hear your thoughts on whether or not this is a dodgy algorithm.

RESULTS

  • 109 patients split over 4 groups (penetrating v blunt; v HES v saline)
    • the SAFE study (the best one on colloids v crystalloids) had 7000 patients
  • HES patients were quite a bit sicker
  • HES patients needed double the amount of blood
  • mortality 16.5% and they say there were no differences statistically but I can’t find the actually mortality figures in the paper. In a study this size 10% v 20% would probably not be statistically significant…
  • But none of that is the best bit. Here are the primary outcomes:

Primary outcome variables were the volumes of FIRST fluid needed in the first 24 h after enrolment and the number of patients achieving normal gastrointestinal function by day 5.

Now there’s 2 of them which is a bit naughty but we can live with that. But here are the conclusions in the paper (not even the abstract)

In conclusion, this randomized, controlled, double-blind study has demonstrated faster lactate clearance in penetrating trauma with the use of HES 130/0.4 compared with 0.9% saline without clinically relevant coagulopathy. The superior resuscitation had an outcome benefit, in that no HES patients demonstrated renal injury compared with an incidence of 16% in the saline group. No advantage could be shown for HES in blunt trauma

Now technically all of their conclusion is true (though you could argue about the “outcome benefit” that they claim) but the key point is that in neither the abstract, nor manuscript conclusions do the authors mention the primary outcome. In other words the title, abstract and conclusions give the impression that this was a +ve trial when in fact it was strikingly -ve.

The primary outcome (on which the whole trial is predicated) becomes a side issue to the surrogate outcomes.

Sigh…

Filed Under: critical appraisal, critical care, trauma ·

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 ·