It is good that you are ok cram.
Ansell Pt Dive Incident
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cram
Contributor
Alright here's the full story.
On the evening of March 31 my buddy and I went for a dive at Ansell Pt, my first time at the site. I had been warned that the hike up from the water to the parking lot was particularly nasty, but decided to go anyway.
The dive itself was fairly deep with at max depth of 104 ft and average depth at 63 ft. However, despite what the article says the ascent rate was very reasonable, IMHO. We descended to about 100 ft, and spent about 10 minutes there. Then ascended very gradually to the 50-60 ft range and spent most of the rest of the dive there. Ascended, again a reasonable rate to about 20ft for a 3min SS and then final ascent. Total time, 46 minutes. Lowest I saw my NDL time hit was 5 minutes, and only briefly. This was my only dive of the day, with my previous dive being three days earlier.
During the trek back up to the vehicles I felt fine, but almost as soon as we reached the top I felt a slight pain in my chest. It gradually got worse and within maybe 10 minutes it was at the point where I was on the ground with severe chest pain and finding it very difficult to breathe. My buddy called 911 and in an impressively short time EMS services arrived. I was put on oxygen and the pain and breathing issues subsided not long after. By the time they got me into the helicopter(!) my only symptom was paresthesia (tingling, like when your leg "falls asleep"), which I had throughout all four limbs.
I was treated at Vancouver General by the hyperbaric medicine specialist Dr. Dave Harrison. Ironically and somewhat embarrassingly I had attended a lecture that he gave on dive safety just a few days earlier. After a few tests to rule out heart and other non-diving related issues, his initial diagnose was carbon dioxide deprivation, not DCS. My understanding is that this was based on the fact that my only symptom remaining was the paresthesia, that my dive profile had been unremarkable, and because of my admission that I make an effort to breathe very slow and deep while I dive. I was released from the hospital that evening after I informed Dr. Harrison that the tingling was basically gone. However, after I got out of the hospital bed and started moving around I could feel it was definitely still there if not very strong. I made the mistake of ignoring this and went home, hoping it would disappear on its own.
The next morning I woke up and the tingling was significantly worse than it had been the night before. I called Dr. Harrison and he informed me that had it been CO2 deprivation this definitely wouldn't happen so we had not choice but to assume DCS.
I spent eight hours in the chamber on Thursday and sure enough the paresthesia slowly disappeared. In the week since I've felt fine.
I'm now supposed to stay out of the water for six weeks to three months, and I intend to take the full three months. The worst part of all of this though, is that I still don't really understand why this all happened. Obviously the steep climb is a contributing factor, but of course it doesn't seem like a good idea to assume that was the only factor and just go back to my normal diving habits sans the exercise. At the same time I don't want to have to drastically cut back on the type of diving I can do just because of one incident. I do have a follow-up meeting with the doctor to discuss these issues, but I'm interested in other SBers opinions.
On the evening of March 31 my buddy and I went for a dive at Ansell Pt, my first time at the site. I had been warned that the hike up from the water to the parking lot was particularly nasty, but decided to go anyway.
The dive itself was fairly deep with at max depth of 104 ft and average depth at 63 ft. However, despite what the article says the ascent rate was very reasonable, IMHO. We descended to about 100 ft, and spent about 10 minutes there. Then ascended very gradually to the 50-60 ft range and spent most of the rest of the dive there. Ascended, again a reasonable rate to about 20ft for a 3min SS and then final ascent. Total time, 46 minutes. Lowest I saw my NDL time hit was 5 minutes, and only briefly. This was my only dive of the day, with my previous dive being three days earlier.
During the trek back up to the vehicles I felt fine, but almost as soon as we reached the top I felt a slight pain in my chest. It gradually got worse and within maybe 10 minutes it was at the point where I was on the ground with severe chest pain and finding it very difficult to breathe. My buddy called 911 and in an impressively short time EMS services arrived. I was put on oxygen and the pain and breathing issues subsided not long after. By the time they got me into the helicopter(!) my only symptom was paresthesia (tingling, like when your leg "falls asleep"), which I had throughout all four limbs.
I was treated at Vancouver General by the hyperbaric medicine specialist Dr. Dave Harrison. Ironically and somewhat embarrassingly I had attended a lecture that he gave on dive safety just a few days earlier. After a few tests to rule out heart and other non-diving related issues, his initial diagnose was carbon dioxide deprivation, not DCS. My understanding is that this was based on the fact that my only symptom remaining was the paresthesia, that my dive profile had been unremarkable, and because of my admission that I make an effort to breathe very slow and deep while I dive. I was released from the hospital that evening after I informed Dr. Harrison that the tingling was basically gone. However, after I got out of the hospital bed and started moving around I could feel it was definitely still there if not very strong. I made the mistake of ignoring this and went home, hoping it would disappear on its own.
The next morning I woke up and the tingling was significantly worse than it had been the night before. I called Dr. Harrison and he informed me that had it been CO2 deprivation this definitely wouldn't happen so we had not choice but to assume DCS.
I spent eight hours in the chamber on Thursday and sure enough the paresthesia slowly disappeared. In the week since I've felt fine.
I'm now supposed to stay out of the water for six weeks to three months, and I intend to take the full three months. The worst part of all of this though, is that I still don't really understand why this all happened. Obviously the steep climb is a contributing factor, but of course it doesn't seem like a good idea to assume that was the only factor and just go back to my normal diving habits sans the exercise. At the same time I don't want to have to drastically cut back on the type of diving I can do just because of one incident. I do have a follow-up meeting with the doctor to discuss these issues, but I'm interested in other SBers opinions.
Did you receive only normobaric O2, or HBOT treatment when you first arrived, when you had...
Or was your HBOT treatment only the next day?
What sort of test for your heart? EKG? Did Dr. Harrison mention PFO?
cram
Contributor
The night I arrived at the hospital I received only normobaric oxygen. At that point it was believed that I did not have DCS. The HBOT treatment began the following day when the paresthesia persisted and it became apparent that I did have DCS.
Yes, he did mention that there was a good chance that I had a PFO. I forgot to mention that as another potential contributing factor. I did not have the EKG done but I am aware that it is an option. I will ask about that when I go in for my follow-up appointment.
sydney-diver
Contributor
Glad you're alright mate! What is carbon dioxide deprivation (or rather what does it cause, I'm guessing it interfere's with breathing since from my very basic understaning the breathing reflex is caused mostly by CO2 altering blood PH but I've never actually heard this term)?
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Wow - you present with neurological symptoms, a chamber is down the hallway, and you're not treated, despite research that shows delays in treating DCS-2 can cause permanent deficits.
First - you'll probably be fine. What's happened to you has triggered this VERY long answer. I'll conclude with stuff specific to your circumstance. Briefly, if I were in your shoes (ah, to be 29 again!), and I felt ANY symptoms that might be neurological, I'd DEMAND a follow-up HBOT treatment(s) - but at much shorter duration and less pressure. I'll explain why below.
FIRST - I AM NOT A MEDICAL DOCTOR AND YOU SHOULD CONSULT LICENSED MDs TO DETERMINE WHAT IS THE BEST COURSE OF ACTION IN YOUR CIRCUMSTANCE. But I've read hundreds of HBOT research studies - not just the abstracts - and have become aware of an enormous conflict that's been going on within the HBOT industry for years. Follow the money. The controversy starts in the USA (which has influenced Canadian HBOT policy) where only 13 maladies + DCI are officially accepted for insurance reimbursement vs. many developed nations that commonly use HBOT to treat up to 132 maladies because HBOT can be VERY cheap and effective. Ironically, many of the most advanced protocols were pioneered by "outsider" US MDs, but are used to treat more patients elsewhere.
In the USA, HBOT fees in hospital are often 2X to 5X more expensive per-dive vs. treatments at free-standing HBOT clinics run by MDs. The "outsider" MDs could reduce rates even more dramatically via economies of scale, but that won't happen until industry squabbles cease. In the UK medical professionals volunteer their time at clinics that charge $8 per "dive," which is sufficient to cover the facilities overhead costs:
The UHMS works with their sister lobbying organization, the AAWCM, to negotiate what hospitals get to charge the US government and insurance companies for HBOT treatments. And Diversified Clinical Services (DCS) cites UHMS research and other financial data to encourage hospitals to open highly profitable “wound care centers” (i.e. HBOT) as quick as chambers can be built.
Today, hospitals make big money treating diabetic foot wounds in HBOT chambers. Such treatment protocols are MUCH shorter vs. treating divers on a 7 to 8 hour USN Table-6. It's not silly to imagine that a hospital administrator doesn't want a revenue-generating multi-place chamber tied up that long with a single diver, which may have been why you didn't get HBOT the day you arrived (pure speculation on my part). Oops - I missed that you said you arrived in the early evening and there may have been a challenge with staff scheduling.
Unfortunately, fewer and fewer hyperbaricists, whether in hospitals or at freestanding clinics, deeply understand diving. Just because a hyperbaricist is an outsider doesn't make them a guru (i.e. buyer beware). Fortunately some, in the opinions of many, are visionary, like Gaylan Rockswold, MD and Paul Harch, MD. Harch is largely responsible for preventing ~13,000 diabetic foot amputations each year; his extended protocol (e.g. 1.5 ATA x 80+ treatments) has enabled divers who suffered profound neurological insults to recover ~ 20 I.Q. points despite having been classified as "plateaud" by UHMS treatment standards. The results of HBOT 1.5 ATA has been dramatic for Veterans with Traumatic Brain Injury. The US military forecasts 320,000 Vets are coming home from Afghanistan and Iraq with TBI, and HBOT is the only treatment that offers any significant recovery of neurological deficit. Currently, TBI Vets are prescribed vast quantities of psychotropic drugs that carry black-box warnings. We divers may be in a unique place in history - to use what we know is occurring within the bowels of the dive industry to advocate for better care for TBI Vets. I digress...
What occurred to you may be (speculation on my part) a predictable result of a sea-change that has factually occurred with DAN and the UHMS. Remember, DAN is a for-profit insurance company owned by the non-profit DAN. Since 1998 DAN and UHMS doctors have met to determine how they can restrict access to HBOT for some cases of DCS. Doing so would reduce payout costs. But I can find no research to justify the findings of this work that takes into account long-term harms of brain and bone lesions that are well established by international research to be an inherent risk of diving. In 2004, DAN and UHMS doctors sponsored a 2 1/2 day meeting; in attendance was the dive industry's #1 go-to defense attorney, Rick Lesser, who helped the group conduct a cost-benefit analysis.
Whereas 60+ years of US Navy medical doctrine says, essentially, "treat early and treat often," the outcome of this 2004 meeting was to proclaim that DCS-1 need not be treated with HBOT. DAN and the UHMS says, essentially, “tough it out, you'll be OK.” You can read the transcript of this meeting yourself: Management of Mild or Marginal Decompression Illness in Remote Locations - Workshop Proceedings. Rather than discussing details of in-water recompression or portable hyperbaric stretchers (previously discussed at smaller regional meetings), the 242 page transcript captures the group’s efforts to draft the new “community standards” to justify the denial of chamber treatment(s) for DCS-type 1, even in cases of severe pain, even if a chamber is just down the hallway. This transcript is a MUST READ for any diver who might ever get bent.
However pain of DCS-1 can mask neurological symptoms of DCS-2. And most hyperbaric MDs are NOT neurologists and have VERY frequently misdiagnosed symptoms per prior research (2004; 2006; 1996). This meeting to redefine when HBOT would be invoked for DCS was VERY MUCH about controlling costs by limiting insurance payouts. The doctors and the lawyer spent hours word-smithing the new “community standard of care.” Some excerpts from the 2 1/2 day meeting:
The Chairman of the meeting admitted (page 188):
Dr. DES GORMAN: Well, most doctors wouldn’t know what a dermatomal was if it walked up and bit them. [A dermatome is an area of skin that is directly related with one of 30 spinal nerves, where odd sensations are symptomatic of DCS-2 / a neurological hit, vs. skin-bends or "niggles."]
(page 203)
Dr. DAVID SMART: The abalone industry in Tasmania is going to absolutely love UHMS for coming out with a statement that supports what they’ve done for the last 20 years, which is not treat DCI or not present with symptoms [i.e. “don’t complain if you feel pain, just tough it out”].
(Page 208)
Dr. DAVID SMART: At the risk of saying, "The emperor’s wearing no clothes," we have had the whole paradigm shift here. We were talking about remote area retrievals and modifying our approach to treatment based on the fact that logistic issues were preventing us from taking the patient to recompression. We’ve now gone to a statement which can be construed by most [of the] industry as that regardless of where you are, you can treat DCI without recompression, and we really have no evidence to suggest that that’s an appropriate response. Based on data presented yesterday, we’ve got a 70 percent success rate treating it with recompression. Do we want to go this sort of length?
Let's put aside for the moment what's going on with HBOT and divers. What's behind the conflict between "insider" and "outsider" HBOT specialists? I like facts. What is a fact is that Duke University receives millions from many Big Pharma companies as either donations or investments in pharmaceutical research that employs Duke faculty and staff. Some of the maladies that HBOT mitigates, per international peer-reviewed research, are the same maladies that patented drugs now treat. Other drugs in the development pipeline at Duke are for maladies which have long been treated, successfully, with HBOT. Such is the versatility of oxygen! While HBOT can increase stem-cells 8X, HBOT is NOT a panacea. In many cases HBOT is best as an adjunct to potentiate some pharmaceuticals (e.g. some antibiotics are far more powerful when "boosted" with HBOT). Notably, HBOT is not patentable, and the "outsider" MDs give away their protocols for the world to use, for free.
A drug can get licensed if it performs just slightly better than a placebo; many patented drugs fail to work for the majority of patients. The hope of pharmacogenomics is gene-specific drugs with a greater efficacy rate. If they can pull that off at Duke, great - they deserve to get rich. But it's hard to imagine how there could possibly be a firewall on campus, which is also the epicenter of HBOT research in the USA, that would prevent conflicts of interest from delaying HBOT's inroads into the same turf as patented drugs. This is an exact analog to billions of dollars in "Pay to Delay" pharmaceutical deals with generic factories that the US FTC and DOJ have been fighting, and failing to stop.
Given this backdrop it raises questions when you hear from so many parents of CP children that HBOT has enabled their child to walk, without enduring dozens of surgeries (the traditional treatment) to cut and stretch their muscles and tendons that spasm for lack of oxygen. But senior UHMS members have impugned claims that HBOT is efficacious for CP, citing a landmark CANADIAN study that found risks of eardrum damage (in a few rare instances when a child had a cold - it's a risk shared by EVERY HBOT patient).
Has Duke created a window of opportunity for Botox, made by their business partner Allergan, to treat CP by impugning HBOT for CP? I have no idea. This much is fact: the patent holder of Botox is Allergan; Allergan and Duke are co-plaintiffs in a patent-infringement case involving an entirely different drug (that grows eyelashes). Meanwhile, Allergan has been promoting Botox "off-label" for kids with CP. The FDA ordered Allergan to cease, because kids have died and there's ZERO peer-reviewed research to support efficacy. Regardless, Allergan has sued the FDA for limiting its free speech. Do you think this relationship is too cozy?
My skepticism towards DAN / UHMS wouldn't be so great if not for their primary actors being the progenitors of the myth often paraphrased by dive pros: "Diving is as safe as bowling." [cited here -- and detailed here just above this image:]
------------------
OK - now as promised - what about any follow-up HBOT treatment for you? Some of the outsider MDs have a very different opinion vs. some UHMS insider MDs RE delayed treatment of neurological insults involving TINY bubbles. Paraphrasing - subclinical nitrogen bubbles occur during many dive profiles and pass through capillary beds in brain tissues. Oxygen metabolizes, but where nitrogen bubbles lodge in place, a hypoxic condition results (i.e. no O2 reaches tiny areas of tissue). This could MAYBE be what happened to you - that is, tiny nitrogen bubbles dissipated in ~24-hours - no more blockage. If so, there's little reason for a Table-6, or even a Table-5, since there are no bubbles left to drive back into solution. Instead, O2 should perfuse as effectively as possible into brain tissue to potentiate the natural re-growth of capillary beds; insults to brain and nerve tissues need to start healing. Counter-intuitively, the brain has a built-in defense mechanism that restricts O2 and glucose at higher ATA pressure. In other words, like every drug, MORE IS NOT MORE!!!!! Maximum cranial O2 perfusion occurs at 1.5 ATA. Likewise the time component cannot be rushed (MORE IS NOT MORE). Brain tissue re-growth is accelerated with HBOT 1.5, but there are limits; two 1-hour treatments at 1.5 ATA is better than a single 2-hour treatment.
If readers think there's an alphabet soup of dive training organizations and pointless in-fighting, the dive industry has nothing on the healthcare industry. This 3-page PDF, The Polemics of Hyperbaric Medicine by Drs. Neubauer and Maxfield, recaps how we've arrived at our current inflection point. This 3-page paper is an absolute must-read for every diver who may ever be in need of a chamber.
First - you'll probably be fine. What's happened to you has triggered this VERY long answer. I'll conclude with stuff specific to your circumstance. Briefly, if I were in your shoes (ah, to be 29 again!), and I felt ANY symptoms that might be neurological, I'd DEMAND a follow-up HBOT treatment(s) - but at much shorter duration and less pressure. I'll explain why below.
FIRST - I AM NOT A MEDICAL DOCTOR AND YOU SHOULD CONSULT LICENSED MDs TO DETERMINE WHAT IS THE BEST COURSE OF ACTION IN YOUR CIRCUMSTANCE. But I've read hundreds of HBOT research studies - not just the abstracts - and have become aware of an enormous conflict that's been going on within the HBOT industry for years. Follow the money. The controversy starts in the USA (which has influenced Canadian HBOT policy) where only 13 maladies + DCI are officially accepted for insurance reimbursement vs. many developed nations that commonly use HBOT to treat up to 132 maladies because HBOT can be VERY cheap and effective. Ironically, many of the most advanced protocols were pioneered by "outsider" US MDs, but are used to treat more patients elsewhere.
In the USA, HBOT fees in hospital are often 2X to 5X more expensive per-dive vs. treatments at free-standing HBOT clinics run by MDs. The "outsider" MDs could reduce rates even more dramatically via economies of scale, but that won't happen until industry squabbles cease. In the UK medical professionals volunteer their time at clinics that charge $8 per "dive," which is sufficient to cover the facilities overhead costs:
The UHMS works with their sister lobbying organization, the AAWCM, to negotiate what hospitals get to charge the US government and insurance companies for HBOT treatments. And Diversified Clinical Services (DCS) cites UHMS research and other financial data to encourage hospitals to open highly profitable “wound care centers” (i.e. HBOT) as quick as chambers can be built.
Today, hospitals make big money treating diabetic foot wounds in HBOT chambers. Such treatment protocols are MUCH shorter vs. treating divers on a 7 to 8 hour USN Table-6. It's not silly to imagine that a hospital administrator doesn't want a revenue-generating multi-place chamber tied up that long with a single diver, which may have been why you didn't get HBOT the day you arrived (pure speculation on my part). Oops - I missed that you said you arrived in the early evening and there may have been a challenge with staff scheduling.
Unfortunately, fewer and fewer hyperbaricists, whether in hospitals or at freestanding clinics, deeply understand diving. Just because a hyperbaricist is an outsider doesn't make them a guru (i.e. buyer beware). Fortunately some, in the opinions of many, are visionary, like Gaylan Rockswold, MD and Paul Harch, MD. Harch is largely responsible for preventing ~13,000 diabetic foot amputations each year; his extended protocol (e.g. 1.5 ATA x 80+ treatments) has enabled divers who suffered profound neurological insults to recover ~ 20 I.Q. points despite having been classified as "plateaud" by UHMS treatment standards. The results of HBOT 1.5 ATA has been dramatic for Veterans with Traumatic Brain Injury. The US military forecasts 320,000 Vets are coming home from Afghanistan and Iraq with TBI, and HBOT is the only treatment that offers any significant recovery of neurological deficit. Currently, TBI Vets are prescribed vast quantities of psychotropic drugs that carry black-box warnings. We divers may be in a unique place in history - to use what we know is occurring within the bowels of the dive industry to advocate for better care for TBI Vets. I digress...
What occurred to you may be (speculation on my part) a predictable result of a sea-change that has factually occurred with DAN and the UHMS. Remember, DAN is a for-profit insurance company owned by the non-profit DAN. Since 1998 DAN and UHMS doctors have met to determine how they can restrict access to HBOT for some cases of DCS. Doing so would reduce payout costs. But I can find no research to justify the findings of this work that takes into account long-term harms of brain and bone lesions that are well established by international research to be an inherent risk of diving. In 2004, DAN and UHMS doctors sponsored a 2 1/2 day meeting; in attendance was the dive industry's #1 go-to defense attorney, Rick Lesser, who helped the group conduct a cost-benefit analysis.
Whereas 60+ years of US Navy medical doctrine says, essentially, "treat early and treat often," the outcome of this 2004 meeting was to proclaim that DCS-1 need not be treated with HBOT. DAN and the UHMS says, essentially, “tough it out, you'll be OK.” You can read the transcript of this meeting yourself: Management of Mild or Marginal Decompression Illness in Remote Locations - Workshop Proceedings. Rather than discussing details of in-water recompression or portable hyperbaric stretchers (previously discussed at smaller regional meetings), the 242 page transcript captures the group’s efforts to draft the new “community standards” to justify the denial of chamber treatment(s) for DCS-type 1, even in cases of severe pain, even if a chamber is just down the hallway. This transcript is a MUST READ for any diver who might ever get bent.
However pain of DCS-1 can mask neurological symptoms of DCS-2. And most hyperbaric MDs are NOT neurologists and have VERY frequently misdiagnosed symptoms per prior research (2004; 2006; 1996). This meeting to redefine when HBOT would be invoked for DCS was VERY MUCH about controlling costs by limiting insurance payouts. The doctors and the lawyer spent hours word-smithing the new “community standard of care.” Some excerpts from the 2 1/2 day meeting:
The Chairman of the meeting admitted (page 188):
Dr. DES GORMAN: Well, most doctors wouldn’t know what a dermatomal was if it walked up and bit them. [A dermatome is an area of skin that is directly related with one of 30 spinal nerves, where odd sensations are symptomatic of DCS-2 / a neurological hit, vs. skin-bends or "niggles."]
(page 203)
Dr. DAVID SMART: The abalone industry in Tasmania is going to absolutely love UHMS for coming out with a statement that supports what they’ve done for the last 20 years, which is not treat DCI or not present with symptoms [i.e. “don’t complain if you feel pain, just tough it out”].
(Page 208)
Dr. DAVID SMART: At the risk of saying, "The emperor’s wearing no clothes," we have had the whole paradigm shift here. We were talking about remote area retrievals and modifying our approach to treatment based on the fact that logistic issues were preventing us from taking the patient to recompression. We’ve now gone to a statement which can be construed by most [of the] industry as that regardless of where you are, you can treat DCI without recompression, and we really have no evidence to suggest that that’s an appropriate response. Based on data presented yesterday, we’ve got a 70 percent success rate treating it with recompression. Do we want to go this sort of length?
Let's put aside for the moment what's going on with HBOT and divers. What's behind the conflict between "insider" and "outsider" HBOT specialists? I like facts. What is a fact is that Duke University receives millions from many Big Pharma companies as either donations or investments in pharmaceutical research that employs Duke faculty and staff. Some of the maladies that HBOT mitigates, per international peer-reviewed research, are the same maladies that patented drugs now treat. Other drugs in the development pipeline at Duke are for maladies which have long been treated, successfully, with HBOT. Such is the versatility of oxygen! While HBOT can increase stem-cells 8X, HBOT is NOT a panacea. In many cases HBOT is best as an adjunct to potentiate some pharmaceuticals (e.g. some antibiotics are far more powerful when "boosted" with HBOT). Notably, HBOT is not patentable, and the "outsider" MDs give away their protocols for the world to use, for free.
A drug can get licensed if it performs just slightly better than a placebo; many patented drugs fail to work for the majority of patients. The hope of pharmacogenomics is gene-specific drugs with a greater efficacy rate. If they can pull that off at Duke, great - they deserve to get rich. But it's hard to imagine how there could possibly be a firewall on campus, which is also the epicenter of HBOT research in the USA, that would prevent conflicts of interest from delaying HBOT's inroads into the same turf as patented drugs. This is an exact analog to billions of dollars in "Pay to Delay" pharmaceutical deals with generic factories that the US FTC and DOJ have been fighting, and failing to stop.
Given this backdrop it raises questions when you hear from so many parents of CP children that HBOT has enabled their child to walk, without enduring dozens of surgeries (the traditional treatment) to cut and stretch their muscles and tendons that spasm for lack of oxygen. But senior UHMS members have impugned claims that HBOT is efficacious for CP, citing a landmark CANADIAN study that found risks of eardrum damage (in a few rare instances when a child had a cold - it's a risk shared by EVERY HBOT patient).
Has Duke created a window of opportunity for Botox, made by their business partner Allergan, to treat CP by impugning HBOT for CP? I have no idea. This much is fact: the patent holder of Botox is Allergan; Allergan and Duke are co-plaintiffs in a patent-infringement case involving an entirely different drug (that grows eyelashes). Meanwhile, Allergan has been promoting Botox "off-label" for kids with CP. The FDA ordered Allergan to cease, because kids have died and there's ZERO peer-reviewed research to support efficacy. Regardless, Allergan has sued the FDA for limiting its free speech. Do you think this relationship is too cozy?
My skepticism towards DAN / UHMS wouldn't be so great if not for their primary actors being the progenitors of the myth often paraphrased by dive pros: "Diving is as safe as bowling." [cited here -- and detailed here just above this image:]
------------------
OK - now as promised - what about any follow-up HBOT treatment for you? Some of the outsider MDs have a very different opinion vs. some UHMS insider MDs RE delayed treatment of neurological insults involving TINY bubbles. Paraphrasing - subclinical nitrogen bubbles occur during many dive profiles and pass through capillary beds in brain tissues. Oxygen metabolizes, but where nitrogen bubbles lodge in place, a hypoxic condition results (i.e. no O2 reaches tiny areas of tissue). This could MAYBE be what happened to you - that is, tiny nitrogen bubbles dissipated in ~24-hours - no more blockage. If so, there's little reason for a Table-6, or even a Table-5, since there are no bubbles left to drive back into solution. Instead, O2 should perfuse as effectively as possible into brain tissue to potentiate the natural re-growth of capillary beds; insults to brain and nerve tissues need to start healing. Counter-intuitively, the brain has a built-in defense mechanism that restricts O2 and glucose at higher ATA pressure. In other words, like every drug, MORE IS NOT MORE!!!!! Maximum cranial O2 perfusion occurs at 1.5 ATA. Likewise the time component cannot be rushed (MORE IS NOT MORE). Brain tissue re-growth is accelerated with HBOT 1.5, but there are limits; two 1-hour treatments at 1.5 ATA is better than a single 2-hour treatment.
If readers think there's an alphabet soup of dive training organizations and pointless in-fighting, the dive industry has nothing on the healthcare industry. This 3-page PDF, The Polemics of Hyperbaric Medicine by Drs. Neubauer and Maxfield, recaps how we've arrived at our current inflection point. This 3-page paper is an absolute must-read for every diver who may ever be in need of a chamber.
Last edited:
Slamfire
Contributor
Cram,
Thanks for posting the account and even more thanks for being open and active doing incident analysis.
Were you diving air or nitrox? If nitrox what was your % O2? I just went through 78 of my latest single gas air dives (lots of them to deeper than 100') and there is one case were the avg depth went past 60' (61'). The vast majority of these are in the 50' to 55' range. Also a lot of these air dives did have some deco obligation on them -- I went past the NDL. Nitrox dives are another story, usually going well into the 60' range depending on the mix.
I know that avg depth is not perfectly indicative of the profile but it does give an relative indication of how much of the dive was spent at lower depths. I do dive with a computer and stay within its parameters. However, I do not dive the computer. What I mean is that usually follow additional steps not dictated by the computer. A computer will tell you that as long as you are within the NDL it is ok to go from 100' to 15' at an ascent rate of 30'/min. It recommends that you stop at around 15' for 3 mins, but it is not an obligation. Then you can ascend to surface at 30'/sec.
On no deco air dives here's what I do different from what my computer is telling me. I'll ascend up to 70' at 30'/sec. Beyond that I slow my ascent to 10'/sec. As I get above 40' I start slowing the ascent even more. I spend a good portion of the dive above 40'. My computer suggests that I do a 3 min safety stop anywhere between 20' and 11'. I try reach the completion of that safety stop without tapping into the minimum gas reserve that I determined for that dive.
After the safety stop is done it is common for me to stay down a little bit longer breathing down a portion of that reserve. I do manage my gas, but at 15' and after the safety stop I really see no point in bringing back to the surface an intact reserve. If problems arise at that depth it is fairly simply to reach the surface ie. I am no longer as dependent on that reserve. Doing this, I see no problem coming up to the surface with 200 psi. The advantage is that I have a little more peace of mind when it comes to DCS prevention.
These are general guidelines I follow somewhat loosely. It does not mean that I fanatically follow these with absolutely no deviation. But I do follow them close enough to have almost all of my single gas air dives end with an avg depth of 55' or less. One more thing: after I've gone above 33', I try not to descend more than 5'. For instance, if I see an interesting feature that's more than 5' below me and I am currently at 28', I will not drop down to see it. This is not what any specific agency recommends. It's just the way I tend to dive and its worked so far for my buddies and I. So take it with a grain of salt.
I hope I have not overstepped through your invitation to hear the opinions of others. I kinda feel this reads a little bit like unsolicited advice.
Thanks for posting the account and even more thanks for being open and active doing incident analysis.
Were you diving air or nitrox? If nitrox what was your % O2? I just went through 78 of my latest single gas air dives (lots of them to deeper than 100') and there is one case were the avg depth went past 60' (61'). The vast majority of these are in the 50' to 55' range. Also a lot of these air dives did have some deco obligation on them -- I went past the NDL. Nitrox dives are another story, usually going well into the 60' range depending on the mix.
I know that avg depth is not perfectly indicative of the profile but it does give an relative indication of how much of the dive was spent at lower depths. I do dive with a computer and stay within its parameters. However, I do not dive the computer. What I mean is that usually follow additional steps not dictated by the computer. A computer will tell you that as long as you are within the NDL it is ok to go from 100' to 15' at an ascent rate of 30'/min. It recommends that you stop at around 15' for 3 mins, but it is not an obligation. Then you can ascend to surface at 30'/sec.
On no deco air dives here's what I do different from what my computer is telling me. I'll ascend up to 70' at 30'/sec. Beyond that I slow my ascent to 10'/sec. As I get above 40' I start slowing the ascent even more. I spend a good portion of the dive above 40'. My computer suggests that I do a 3 min safety stop anywhere between 20' and 11'. I try reach the completion of that safety stop without tapping into the minimum gas reserve that I determined for that dive.
After the safety stop is done it is common for me to stay down a little bit longer breathing down a portion of that reserve. I do manage my gas, but at 15' and after the safety stop I really see no point in bringing back to the surface an intact reserve. If problems arise at that depth it is fairly simply to reach the surface ie. I am no longer as dependent on that reserve. Doing this, I see no problem coming up to the surface with 200 psi. The advantage is that I have a little more peace of mind when it comes to DCS prevention.
These are general guidelines I follow somewhat loosely. It does not mean that I fanatically follow these with absolutely no deviation. But I do follow them close enough to have almost all of my single gas air dives end with an avg depth of 55' or less. One more thing: after I've gone above 33', I try not to descend more than 5'. For instance, if I see an interesting feature that's more than 5' below me and I am currently at 28', I will not drop down to see it. This is not what any specific agency recommends. It's just the way I tend to dive and its worked so far for my buddies and I. So take it with a grain of salt.
I hope I have not overstepped through your invitation to hear the opinions of others. I kinda feel this reads a little bit like unsolicited advice.
StuartT
Contributor
Hi Dustin was wondering if you guys had a rest once you got out of the water or went up the stairs right away?
cram
Contributor
I'm not 100% sure that deprivation was the word that he used, but the basic idea was that my CO2 levels were too low, presumably as a result of hyperventilation. Wikipedia's hyperventilation page describes it pretty well, including a list of symptoms that match fairly well with what I experienced. Too bad this wasn't what I actually had - when this was the diagnosis I was only supposed to stay out of the water for two weeks as a precaution.sydney-diver:
@JonKranhouse: Thanks for the detailed reply. I haven't had time to do more than skim your post, but I'll check it out tonight.
Just air. I'm not nitrox certified but that might change during my extended SI.Slamfire:
Yeah, looking back this is probably my deepest average dive ever. It didn't really "feel" all that deep because my max depth has been deeper several times.Slamfire:
No problem! This is all good feedback.Slamfire:
We took only a very short break before heading up. We also paused for a short breather on each of the landings going up the stairs, but again probably not nearly as long as we should have. I'm now kicking myself for not taking your advice and leaving Ansell for a boat dive.StuartT:
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