Ketamine - disadvantages in trauma pts.

[trauma at emergencyunit.com]

I wondered when that old canard of raised ICP would come up. It didn't take
long! It is based on a Japanese study done in around 1974. They took 6
patients with known brain tumours who already had raised ICP and had been
bolted and used ketamine to induce them. They observed a *further* rise in
ICP on induction - but it was immediately abolished by IPPV. That's the
paper. That's it.

However, what this discussion has actually evolved into is the definition of
the word 'safe'. Let us be clear. There is no such thing as a safe drug.
Nothing. So what we need to do is to understand what we are using, what it
may do and how we get out of the mess we may get into. There are
disadvantages to every induction agent, and we need to balance those risks
with the advantages in our patient population. 

Thiopentone. Great rapid induction agent, horrible negative inotropic
effects particularly in the shocked patient. Effect wears off from
redistribution but barbiturate hangs around for days acting on the heart. 

Propofol. Also a great rapid induction agent but also a bit scary in the
shocked patient.

Etomidate and ketamine. See the discussion we have just been having.

Midazolam and fentanyl. Great for cardiac stability but slow onset and gross
respiratory depression.

It's horses for courses. I had an elective procedure myself a year or two
back and the anaesthetic was great. Went to sleep, woke up feeling well and
painfree. Probably midazolam induction. However, we are talking about an
emergency procedure, sometimes in the field in a trapped patient with poor
airway access. We are talking about a human, not a guinea pig (we'd never
have penicillin if it had been tested on guinea pigs - they have a genetic
anaphylactic reaction and die horribly) or a dog. 

Balancing all those risks, I'm happy to use ketamine in the field because it
is just so flexible, particularly in with the wonderful analgesia sliding
into anaesthesia trick. I probably tend toward propofol in hospital, but I'd
be much less keen to use it outside, although I do carry it.

Blueflightmedic.

-----Original Message-----
From: trauma-list-bounces at trauma.org [mailto:trauma-list-bounces at trauma.org]
On Behalf Of IVAN HRONEK
Sent: 03 August 2007 01:16
To: Trauma & Critical Care mailing list
Subject: Ketamine - disadvantages in trauma pts.


not sure if this is OK, but thought it would be easiest just to go to the
main source - Miller's Anesthesia textbook...
 
Ketamine increases cerebral metabolism, CBF, and ICP. Because of its
excitatory CNS effects, which can be detected by generalized EEG development
of theta-wave activity,[463] as well as by petit mal seizure-like activity
in the hippocampus,[482] ketamine increases CMRO2. Whereas theta-wave
activity signals the analgesic activity of ketamine, alpha waves indicate
its absence. There is an increase in CBF that appears to be higher than the
increase in CMRO2 would mandate. With the increase in CBF as well as the
generalized increase in sympathetic nervous system response, there is an
increase in ICP after ketamine administration.
 
Ketamine in vitro probably has negative inotropic effects. Myocardial
depression has been demonstrated in isolated rabbit hearts,[530] intact
dogs,[531] chronically instrumented dogs,[532] and isolated canine heart
preparations.[533] However, in isolated guinea pig hearts, ketamine was the
least depressant of all the major induction drugs.[534] The finding that
ketamine may exert its myocardial effects by acting on myocardial ionic
currents (which may exert different effects from species to species or in
diverse tissue types) may explain the tissue and animal model variance in
direct myocardial action.[535]. The centrally mediated sympathetic responses
to ketamine usually override the direct depressant effects of ketamine.
Ketamine can produce hemodynamic depression in the setting of deep
anesthesia when sympathetic responses do not accompany its administration.
 
 Ketamine-anesthetized patients have profound analgesia but keep their eyes
open and maintain many reflexes. Corneal, cough, and swallow reflexes may
all be present but should not be assumed to be protective.[457]
 
A potential respiratory problem, especially in children, is the increased
salivation that follows ketamine administration (also see Chapter 60 ). Such
salivation can produce upper airway obstruction, which can be further
complicated by laryngospasm. The increased secretions may also contribute to
or may further complicate laryngospasm. In addition, although the swallow,
cough, sneeze, and gag reflexes are relatively intact after ketamine
administration, there is evidence that silent aspiration can occur during
ketamine anesthesia.[457]. Personally I see it in adults quite often....
 
I understand in Africa Ketamine is used all the time, also because they
don't have intubation devices and ETTs. What is their aspiration rate
though, do we know ? Aspiration is rare by itself, however can be a
devastating or lethal iatrogenic complication.
 
In trauma pts. I would be most concerned with the increased ICP - i know we
get away with a lot in this respect, but the last thing I like to see is a
patient herniating and ending his life just after my intubation....
personally I am crazy about all the little things, including raising the
head of the bed, modified rapid sequence with hyperventilation, giving
Lidocaine, using a drug that vasoconstricts cereberal vasculature rather
than increases CBF (Propofol, Thiopenthal) Thanks for the stimulating
discussion, I love it ! Ivan Hronek MDChief, Critical Care & Trauma
AnesthesiaSFMC Gas, Inc.St. Francis Medical CenterLynwood, CA



> From: trauma at emergencyunit.com> To: trauma-list at trauma.org> Date: Fri, 
> 3 Aug 2007 00:15:05 +0100> Subject: RE: Ketamine vs. Etomidate in trauma
pts.> > Well...> > > Disadvantages of Ketamine:> > 1. tachycardia - many
trauma pts. are tachycardic enough already> > Not necessarily a
disadvantage; the tachycardia is actually as a result of a> direct
sympathomimetic action.> > 2. negative inotropic effect (that gets uncovered
if catecholamines are> depleted and there is an insufficient sympathetic
response to the> stimulation by Ketamine). > > It is my understanding that
catchecholamine release does not mediate this> action so I do not understand
that. K MIMICS the action, not releases it.> > 3. seizures (like Etomidate)
and increase brain tissue O2 consumption> (unlike Etomidate)- problem e.g.
in head traumas etc. > > No clinical effect from these - they are
theoretical. I have used ketamine> extensively in head trauma with no
apparent ill effect. Anyone else seen> trouble?> > 4. increased secretions
everywhere> > Usually only a problem with under 3s and can be dealt with
using> glycopyrrholate or atropine.> > If used as analgesic unclear when
transition to general anesthesia with> aspiration risks ..> > The whole
point about ketamine (found in the earliest studies by Dundee) is> that even
at anaesthetic doses aspiration is really rare. Hence its huge> popularity
in Africa for single operator LSCS.> > If you don't use Midazolam the
seizures are more likely, too...> > <shrug> Ditto with alfentanil. If it
happens deal with it. As it happens I> have never seen it, but I probably
will tomorrow having said that! > > I agree though that it is good in all
these other situations, just it cannot> be used in a number of situations
where Etomidate can.. Ivan Hronek MDChief,> Critical Care & Trauma
AnesthesiaSFMC Gas, Inc.Lynwood, CA> > > > --> trauma-list : TRAUMA.ORG> To
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