Seizure threshold & Rebreather diving deaths

Sutty

In the light of recent highly experienced rebreather divers dying I thought I'd post some thoughts which I have been musing on for a while. The opinions of any of the diving medics on the board would be particularly welcome.

In the general population there is an incidence of 1st seizures occuring in previously healthy individuals, these may be due to a number of causes including tumours, intra-cerebral bleeds, cerebral infarcts, etc. Some of these seizures are due to late-onset epilepsy, with no structurally identifiable cause (ie nothing would be found at post-mortem should death occur).

High PO2 is a known cause of seizures with a wide variation in the PO2 and duration of exposure required to cause any individual to have a seizure.
It seems likely that some individuals could convulse when exposed to high PO2 as their seizure threshold lowers, but without yet having developed epilepsy - this could potentially occur in individuals who were previously able to tolerate high PO2.

If this were the case we would expect to have reports of witnessed seizures in rebreather divers who were breathing at normal (for RBs) PO2, and within recommended CNS toxicity limits. I don't know how many of these are out there and whether the incidence is higher than the incidence of 1st seizures on land in a similar population.

The real question if this is a cause of incidents and deaths in rebreather divers is whether susceptible individuals could be identified, and if so should Rebreather divers be screened?

If EEG anomalies eg spike&wave during hyperventilation was found in apparently healthy divers, should they then be advised to avoid high PO2?

Would an EEG in hyperoxic conditions +/- hyperventilation be of any value? I suspect that a hyperbaric chamber would be required making any screening unfeasible, but any difference between EEGs hyperventilating on air or on 100% O2 at 1Atm could be interesting.

Although I'm a doctor (anaesthesia/ICU), I freely admit that neurology/epileptology is not really my field! If there is anyone on the board with any more information or informed opinion I'd be very interested.

Neil

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saturation

02 toxicity manifesting as seizures is not a seizure, there are no EEG abormalities. Its called an 02 convulsion, there is no true post ictal state, although level of orientation to normal is variable, most folks snap back quickly but do not recall the convulsion.

The studies showed that convulsions simply occur approximately at random intervals above a threshold P02, > 3.0 is most toxic. In water at rest, 1.6, and with exertion to 1.3 [USN] or 1.4 [NOAA] on nitrox, and 1.2 on helium mixes [Dick Vann and technical diver recommendations]. There is a strong relationship with c02 buildup and cerebral vasodilatation including those caused by anxiety or stressed states .. the latter as a response to epi and norepi intrinsic release during stress, and even bursts of endogenous steroids.

For details, see Bennett and Elliott on the physiologic of hyperoxia in diving.

As for pre-screening 02 convulsive individuals or bring out latent epileptic states and lowering a true seizure threshold by hyperoxia, there is no guarantee the convulsion will not occur at a later date after passing the pre-screening exam on a past date. Screening used to occur among USN divers, and hence abandoned.

For reflection among rebreather divers, 2 issues increase 02 convulsion risk, a tendency to rise blood c02 due to scrubber issues with use, depth and exertion, and the constant high P02 maintained for dives [ the 'set point' ].

In a prior post I had on Fred's most unfortunate accident, there are graphs of old USN rebreather trials than show a sample C02 response curve to depth and exertion. Add to this consider issues with how scrubbers are packed, its rate of usage, etc.,

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Safe Diving and Best Wishes,

I.G. Saturation, MD

{ Comments are informational only and not meant to be medical advice applicable to a particular case. Consult your physician when considering information posted here }

Sutty

Thanks saturation - I hadn't realised there were no EEG changes, makes you wonder what is really happening in the brain with O2 toxicity then!

Also if most people "snap back quickly" and aren't too disorientated there is a better argument for a full-face mask or strap to keep the mouthpiece in. I had thought that a typical post-ictal state with confusion/agitation etc would probably lead to drowning anyway, with the victim pulling the mouthpiece out, but it sounds like this might not be the case.

Neil

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abowie

I can't comment on any of the above statements, but I would make a couple of observations.

Firstly, seizure disorders, and therefore people experiencing first fits, are relatively uncommon in the general population. In order to argue that a raised seizure threshold is contributing to O2 seizures in technical divers you'd have to argue that there was something about having a preponderance to seizures that made you become a technical diver.

Secondly, seizures are pretty uncommon in the other situation where people are exposed to high PO2, hyperbaric treatment. Sure, there are other factors associated with diving that contribute, but if your argument was that hyperoxia was revealing latent seizure disorders in divers you'd expect to see some sort of similar effect at 2.8 ATA in a chamber.

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Andrew Bowie

Rebreather-friendly Buddy

Sutty

I don't think that you need to postulate that "there was something about having a preponderance to seizures that made you become a technical diver" - just that exposing the general population to a pro-epileptic trigger might produce more "first fits".

I agree that you would expect to see a similar effect in chambers at 2.8bar PO2, but I don't know that these effects aren't being seen - if a chamber tech sees facial twitching and takes a patient off O2 for a while it may skew the incidence. I also don't know if we are seeing an effect of course.

Of course if O2 convulsions aren't really seizures then pro-epileptic factors may be irrelevant and there may be a host of other factors that predispose or otherwise to an O2 convulsion.

If O2 convulsions aren't seizures, then what are they?!

Neil

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saturation

Welcome, Neil. For the bolded items above here are some insights:

To the first:
The exact mechanism is unknown but it has to do with brain signals going fast without coordination so its akin to a 'seizure'. By analogy, the same reason why a concussion, not to the spinal cord, leads to unconsciousness: the jarring results in disorganized effects on CNS transmission.

http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_DocSum

To the second, the answer is yes. However, a FFM should not be a panacea against hyperoxic exposure, there should be a better way to reduce the P02 consistently without risking hypoxia.

On this board, jhaaja report is detailed and complete, and he was conscious:

http://www.rebreatherworld.com/rebre...onvulsion.html

One fellow in New Jersey, USA wrote about his 02 convulsions in praise of a FFM, Mark Danik. He will aptly describe what it feels like to convulse, in his case, he was quite conscious at a P02 of 4.0.

http://www.ocean-edge.com/portale/creating3.pdf

He had an easy to use switch on a valve to move between deco and backgas, a condition which led to his 02 convulsions in the pdf above. That same mistake was later instrumental in his death as using the same set up, he did the same mistake in his last dive off the New Jersey coast, USA. In this case, he did not regain consciousness and ran out of gas at depth.

Alas, the original post I cannot find but it is archived here, you need to join the egroup to see the contents:

http://groups.yahoo.com/group/diving...s/message/2959

http://groups.yahoo.com/group/diving...s/message/2458

__________________
Safe Diving and Best Wishes,

I.G. Saturation, MD

{ Comments are informational only and not meant to be medical advice applicable to a particular case. Consult your physician when considering information posted here }

Drmike

Excellent stuff, thanks for this info.

Just a quick off-tangent comment if I may;

Regarding the above comment highlighted in blue:
IMO those people who are considering having a switch block for their OC bail out supplies need to weigh the benefits (I dont see what they are myself) against the potential result of a mistake.

Sorry for the hijack

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its the delusional obsession with a highly dangerous and often inappropriate piece of equipment

abowie

Seizures.

This statement differs somewhat from Lambertsen's description quoted in Bennett and Elliott on page 376 of the current edition of a "tonic-clonic seizure..usually followed by 5 to 30 minutes of gradual recovery of mental alertness".

On the next page in the section entitled "Changes in Brain Electrical Activity" it is stated that "seizure activity was associated with generalised electrical discharges, gross EEG activity" although EEG activity was not "consistently altered proir to the actual event". This seems to be backed up by other research.

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Andrew Bowie

Rebreather-friendly Buddy

Sutty

Certainly the references I have read imply that there are EEG changes consistent with seizure during oxygen convulsions. Although I haven't read a definitive description of changes during a convulsion, they do state that there are no warning EEG changes before a convulsion.

The fact that consciousness is retained during some O2 convulsions does not necessarily mean that they are not seizures. I have had a couple of patients who have retained consciousness during a seizure, one was unilateral and they could still speak after a fashion - they weren't enjoying the experience!

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Sutty

Just found this on the Gap software pages on the web "Current thoughts on mechanisms of hyperoxic seizures" which may be of interest.

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Never forget that life is a finite resource.