FW: Carboxyhemoglobin Levels

[Bjorn, Pret]

You don't read many pages on HBO before you bump into the assertion that
it's basically a treatment in search of a disease.  But beyond that
debate, let me observe that its benefits -- anecdotal, academic,
hypothetical or otherwise -- must be measured in the context of what a
pain in the ass it is.  

Finding, accessing, and delivering care in a chamber matching the needs
of a critically ill or injured patient usually generates more risk and
frustration than benefit.  A chamber with real medical functionality is,
for most of the planet, out of reach.  Little wonder that there's no
reliable literature when the proper equipment is far more likely to be
found on a sub base than in a licensed hospital, much less a trauma
center.  

JMO

Pret Bjorn
Bangor, ME USA

-----Original Message-----
From: trauma-list-bounces at trauma.org
[mailto:trauma-list-bounces at trauma.org] On Behalf Of Ian Seppelt
Sent: Tuesday, October 24, 2006 10:54 PM
To: Medic541 at hotmail.com; trauma-list at trauma.org
Subject: Re: FW: Carboxyhemoglobin Levels

COHb is merely a marker of CO exposure and the absolute level does not
help a lot without knowing the history (and mechanism) of intoxication
and duration of oxygen therapy before the blood was taken.

It is unfortuantely a medical student myth that CO causes "hypoxic
hypoxia" by irreversibly binding to Hb. While the irreversible binding
bit  is true, it is irrelevant. A patient with COHb 50% is likely to die
(even though there is still 50% oxyHb) while a patient who has lost half
a blood volume on the road (replaced with Ringers) could well be fine,
depending on what the injuries are.

A dog experiment from the 1970s involved severe CO exposure (to COHb 60
- 70%) and then exchange transfusions. The intoxicated dogs died anyway,
even with perfectly good non CO blood from donors, whereas when the COHb
70% blood was infused into other volunteer dogs they were fine, and just
behaved as if they were a bit anaemic (increased HR and CO).

In fact the problem with CO is what the molecule does at the tissue and
enzymatic level, for example the irreversible lipid peroxidation which
explains all the neurological toxicity from CO.

In terms of therapy there is a large can of worms, polarised by true
believers and non believers. True believers in HBO point to significant
improvements in things like the long term neurological sequelae of CO
intoxication, but the quality of evidence is at the level of case
series. There are serious flaws in most of the controlled trials. The
strongest is Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG,
Clemmer TP, Orme JF, Thomas FO, Morris AH. Hyperbaric oxygen for acute
carbon monoxide poisoning. New England Journal of Medicine
2002;347(14):1057-67. 

It is also likely that outcomes vary depending on aetiology. In
Australia most CO intoxication is either due to attempts at suicide, or
due to enclosed fires (ie house fires, where a lot of other nasties are
inhaled as well). In colder climes much more of the exposures are
industrial or accidental, and it is likely that outcomes are different
in these different groups.

The most recent Cochrane review is attached for your interest.

Cheers, Ian

Ian Seppelt FANZCA FJFICM
Senior Staff Specialist
Dept of Intensive Care Medicine
The Nepean Hospital, PO Box 63 Penrith NSW 2751
Clinical Lecturer, University of Sydney

>>> Medic541 at hotmail.com 24/10/2006 7:42am >>>
To all on this group.  Some advice is needed regarding
carboxyhemoglobin
levels on certain patients.  What levels are permissible to treat only
with
1.0 Fio2?  What levels are treated with a hyperbaric therapy?  Let's
start
from neonates all the way up to the elderly.  If anyone has some advice
or a
website that might point me in the right direction.  That would be
helpful
as well.  I'm trying to find hard numbers, but I cant seem to Google it
for
the life of me.  
  Thanks'
  Anthony M. Caruso
  NREMT-P



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