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Jason,
> Firstly, 20% of observable shunting in divers is in no way
>predictive of 20% DCI rate in new divers. It is suggested that shunting
>is contributory, or provocative, not the sole cause of DCI.
Correct. My point is that if a PFO is important in the aetiology of DCI
then one would expect an relationship between DCI and PFO. My veiw is that
in the population of divers, there is no relationship between DCI and PFO.
> Also, if the P<.01 then the numbers *are* for real, I'm sure
>you're aware, Chi2 does take some account of the sample size, and is
>slanted to avoid false H0 rejection.
Ahh statistics. Chi2 is unreliable when the expected count in one or more
cells is less than 5 for this data set. I'd rather see more people in the
study than trust the 'fudge factor' for small group sizes.
> Also, wrt Wilmshursts work (the 4/24 late onset DCI figure); my
>understanding was that shunting was blamed for certain types of DCI with
>certain types of time delay. I wouldn't expect a classic 'bend' to be
>shunting induced, but a neurological late onset I would (just
>exptrapolating from the model). What statistical weight does Wilmshurst
>apply to his figures?
Well, one of the difficulties of this thread is the confusion over what
different terms mean to different people. Rapid onset DCI is likely due to
bubbles actually entering the brain arterial circulation. This could be a
greater risk factor for divers with PFO. The thread started (I think) with
shoulder pain etc as a symptom. These late symptoms may not necessarily be
related to arterial bubbles.
> So I believe from the above that shunting *is* contributory to
>observed DCI. I don't see that the rate is sufficiently increased (like
>90% of DCI = shunting) to be a great problem, although the 61% for
>serious DCI does worry me.
>
> And now, as promised, the questions; the complement is
>relatively new to me (no-one answered a previous question I posted to
>techdiver).
>
> Are you suggesting that natural variation between individuals,
>in their complement balance, is more significant in DCI provocation?
Yes
> Is the variation of comp. bal. within one indiviual over time
>capable of significantly affecting their DCI risk? (natural variation)
Yes
> Can you deplete your complement during bubble loading, such that
>repeated exposure to decompression stress leads to reduced DCI risk?
In experiments, yes.
> Is there an opening for drug treatments to reduce DCI risk
>(profilaxis)?
I expect so. Dutka, Hallenbeck et al and more recently the New Zealand Navy
have mooted a trial of lignocaine as a therapy adjunctive to HBO for DCI. I
expect it will work although not for the same reasons they would like to
undertake the trial.
> I understand to public blindness to molecular biology, and hence
>the difficulties that might be found in spreading such an idea. How new
>is it? How seriously is it taken? Is there a good review of the subject?
Hyperbaric O2 therapy has been used to treat CAGE both because it is
believed bubbles obstruct the circulation (and so must be compressed) and to
provide hypoxic tissue with O2. It has been the obvious choice for the
Navies of the world which have air compressors and hyperbaric pressure
vessels at their ready disposal. Although the symptoms of some patients
resolve without hyperbaric treatment, compression within 5 minutes of onset
of symptoms frequently results in rapid and frequently complete recovery
[Baskin & Wozniak 1975; Catron et al 1984; Gorman 1984; Kinsey 1954; Thiede
& Manley 1976]. However, many patients deteriorate later, often
progressively, and often with different neurological manifestations to those
of the initial presentation [Dutka 1990]. This may occur even after
apparently successful recompression treatment [Greene 1978; Leitch et al
1984c; Nishimoto et al 1978; Pearson & Goad 1982]. A mechanistic
explanation for this deterioration invokes re-embolism due to redistribution
of emboli from elsewhere in the body to the cerebral circulation (viz; from
the pulmonary vascular bed) or expansion of other in situ residual gas
reservoirs on decompression. An alternative explanation is that secondary
deterioration is due to local circulatory obstruction and progressive
impairment of microperfusion due to endothelial damage and accumulation of
formed elements from the circulation [Hallenbeck et al 1979].
Polymorphonuclear leukocytes may further release vasoactive or other
substances such as free radicals which damages the neural tissue. Platelets
and erythrocytes may also aggregate around damaged endothelium and further
exacerbate the gas embolism related coagulopathy.
You also need to read "Pathophysiological basis of cerebral arterial gas
embolism (DCI)" available for A$250 from the University of Adelaide
> A common idea I come across is that after diver education, 'PFO'
>is the next big DCI factor to be 'ironed out' wrt the tables. I
>personally think that there are things happening at higher pressures
>(30m plus) that aren't yet modelled properly, and these are more
>contributary to the incidence of DCI than shunting or complement are
>likely to be; but it's only a gut feeling.
I think you are right in the sense that the mechanistic explanation for DCI
is an oversimplification.
/Rat
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
shelps@ac*.ma*.ad*.ed*.au*|Stephen Helps PhD Ack! ___/|
FAX (08)232-3283 |Anaesthesia & Intensive Care \O.o|
Voice (08)224-5495 |University of Adelaide =(___)=
|ADELAIDE, 5005, South Australia U
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
"I believe OS/2 is destined to be the most important operating system, and
possibly program, of all time" Bill Gates, CEO, Microsoft Corporation
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