NeuroTalk Support Groups - Vascular Issues

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- Reflex Sympathetic Dystrophy (RSD and CRPS) (https://www.neurotalk.org/reflex-sympathetic-dystrophy-rsd-and-crps-/)

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No worries whatsoever. Take your time.

I just wanted to make sure you got it. :)

You have so much knowledge and I am so appreciative just to read your posts.

Here's a happy V-day hug :hug: Thanks for your help

To Vicc... some more questions for you...

Quote:

Originally Posted by Vicc (Post 69492)

Hi IHH,

I try to mention my history in occasional posts because your first question would be mine. So here goes, and this is the short version.

I was first disabled in 1979, when an ortho surgeon botched two laminectomies; first by puncturing the dura (the outer of three layers of the spinal cord cover) then not plugging the leak properly. A week later I began leaking cerebro-spinal fluid into the tissue of my lower back. He went back in, couldn't find the leak and so grafted a patch of muscle to the dura much like one would patch an old inner tube.

Its kinda tight in that area, and his graft has been pressing against the spinal cord and causing moderate to severe pain for 26 years. The diagnosis was scar tissue/recurrent disk at L5 and L5 radiculopathy on the left.

After ten years of trying to restore my strength and endurance, I finally realized that I was never going to build a bridge or drive a truck again; so I went to college and became a social worker. I could only walk about 200 feet using a cane, so voc rehab bought me a power wheelchair for work.

Then my job description changed so that it would no longer require a licensed social worker; I would do much the same work and get the same pay, but I wouldn't be a SW, nor would the state provide continuing ed for my license.

I took a job as SW at a state psych hospital, where five months later a large and violent patient grabbed a smaller patient by the wrist and began running full-tilt toward me.

The big patient dodged around me, pulling the smaller one into me...and kept running while still holding her wrist. The top half of my body twisted a bit more than 90 degrees while my butt stayed firmly planted in the chair.

The net result was diagnoses of bilateral epidural fibrosis (scar tissue) at S1, compressing both S1 nerve roots (severe pain); bilateral S1 radiculopathy; bilateral leg pain, and arachnoiditis (scar tissue on the arachnoid, the middle layer of the spinal cord cover), and finally - months later - RSD of the left foot.

A work comp whore wrote that I had faked the 1979 disability and was faking the 1995 injury. The MRIs, ct-scan and EMG confirmed the diagnoses. After five years of Hell, and no treatment for any of my injuries (except a couple of nerve blocks for the RSD) the law judge ruled I was too disabled to attend hearings. WC settled at 99% disability.

The bottom line is that since my 1995 injuries I have not been able to tolerate the pain that would go along with trying to access HBO (it takes the pain three days to subside to normal after a trip to my doc's office).

Next; I can't be sure which studies you refer to, but I would guess they are what is called case studies: individual reports about a specific patient. Case studies are not research, they can't be replicated by following the protocols of the original doc (because there were none), and are generally considered only somewhat more reliable than anecdotal reports.

One would think, however, that with so many RSD patients undergoing physical therapy, if it were effective we would at least see dozens, if not hundreds of case studies reporting cures.

PT is about the only way for patients to maintain any range of motion (ROM), which is critical if we are to keep our joints functioning. If RSD is an IRI, however, PT involving more than minimal weight bearing can be harmful: muscle cells "break down" during exercise and are restored to an even stronger state during rest, but only if they receive adequate oxygen and nutrients. IRI means, by definition, that they aren't.

I am currently working on a long-delayed reply to a post in which I describe exactly why RSD cannot be the result of a nerve injury. In it, I may or may not point out that CRPS-I is different from CRPS-II precisely because there is no nerve injury in the former. There is no nerve injury leading to the latter, either: just a convenient nearby nerve injury that can be blamed.

100% wrong 100% of the time: When RSD was first discovered, it was attributed to nerve damage caused by high velocity impacts such as shrapnel or gunshots. It was thought that these types of wounds injured nerves some distance from the actual site. We know now that that even the most insignificant trauma can lead to RSD. High velocity impacts are not the cause of what was called causalgia at the time.

In 1916, a French Army surgeon during World War I saw his first RSD patient, and noted that every place the soldier said was painful was also purple. He had seen cyanosis in a patient who suffered from "a rare sympathetic disorder" who reported severe pain in cyanotic tissue.

He began investigating RSD; examining patients, and noted that most, but not all, showed cyanosis in the areas they reported pain. This was before anyone realized that minor injuries could lead to RSD, but it fit the causalgia picture.

Most sensory nerves of the peripheral nervous system (PNS) are close to the skin surface, while those of the sympathetic nervous system (SNS) are found deeper inside the tissue, where they are more protected from injury.

LeRiche argued that causalgia was the result of damaged sympathetic nerves. These nerves control arterial blood flow by dilating and contracting the smooth muscle that surrounds arteries, so damaged symp nerves were abnormally constricting blood flow through the arteries. This not only explained cyanosis, but every other sign and symptom of RSD; except one, symptom migration (or spread).

In the early 1940s. a test was developed that could measure arterial blood flow. This test would prove LeRiche was right; but it didnt.

Researchers found that arterial blood flow in RSD affected limbs was equal to, and sometimes greater than that in contralateral (opposite) unaffected limbs and the limbs of control subjects. Abnormal vasoconstriction caused by damaged sympathetic nerves is not the cause of RSD.

LeRiche publicly abandoned his hypothesis: Few others followed suit. This disorder was renamed reflex sympathetic dystrophy about two years after it was proved that it isn't RSD. For the next 60 years, there has been nearly unanimous agreement that RSD is caused by damaged sympathetic nerves, despite this proof.

In 1995, a consensus of the International Association for the Study of Pain (IASP) agreed that this isn't RSD, and should be renamed CRPS. They devoutly believe CRPS is the result of a nerve injury, they just can't figure out which nervous system is involved. No one at IASP seems to have noticed the contradiction between belief in a nerve injury and their definition of CRPS-I as having no nerve injury.

There is now a campaign to attribute RSD/CRPS to a spinal cord issue called central sensitization. I will discuss that in my delayed post, so there is no point in going over that now.

High velocity impact: Wrong. Sympathetic nervous system: Wrong. Central sensitization: nonsense, as I will show this week. 100% wrong 100% of the time.

RSDSA has long clung to the SNS view of this disease. The quote you make is their attempt to keep the nerve damage idea alive. They obviously know what IRI is, and are just as obviously distorting the facts to prove a false claim.

The nerves are getting chemical pain messages from oxygen and nutrient deprived cells, which they pass on to the brain. They are also sending pain messages to the brain because they aren't getting enough O2 or nutrients. They can only communicate with the brain by sending pain messages.

One could, I suppose, argue that pain messages from pain sensory cells are abnormal, but they are a response to an abnormal condition (oxygen deprivation), so they aren't abnormally firing after all. Just telling the brain: Houston, we have a problem

Where does the immune system fit in? IRI begins with the immune response to trauma; a response that goes out of control instead of ending after no threat is discovered.

The entire IRI process has been documented by dozens of researchers under strict, scientific protocols. This mishmash from RSDSA is not the result of research. It comes purely from the imaginations of the authors.

BTW, absence of proof is not proof of absence. (I'm not sure exactly what that means, but it sounds neat). I'm guessing it means that just because you can't prove something (like nerve damage in RSD), it doesn't mean you have proved there isn't nerve damage.

Experts in RSD are fond of saying things like that because there is no published research linking nerve damage to RSD; nor is there any neurological test that can demonstrate abnormal nerve activity in RSD. No evidence of nerve damage in RSD but almost 100% agreement that it exists. 100% wrong 100% of the time.

I can't prove that GSE prevents symptom migration. I can, and have, offered my experience in previous posts at BT, all of which are gone now.

Basically, after studying the research into IRI, it seemed more likely to me that this is an IRI than a nerve injury. One of the things I learned during my review of the research was that IRI from surgeries could be prevented simply by applying vitamin E (an antioxidant) to the wound site.

My RSD had already migrated to my right foot by the time I learned this and decided to begin taking GSE, a more powerful antioxidant. Since I began taking GSE in early 1998, I have not experienced any symptom migration.

I stopped taking GSE twice: once deliberately, deciding to rely on the topical antioxidant DMSO instead; one I was so (literally) distraught over personal issues that I forgot to take any for several days.

Both times, within days of stopping, I began to experience the mild sunburn pain of inflammation over 100% of both arms and both legs. After resuming GSE, these symptoms completely subsided.

I can't prove that these signs of inflammation would have led to RSD, but I know that the disease begins with the red warm skin of inflammation, then develops into the cold, blue to purplish color of cyanosis. That was enough to convince me, and I hope it will be enough to convince others.

Some members have told me they began taking GSE after reading my posts. None have reported any symptom migration. That may change now that I've mentioned it. We will have to see.

Finally, I not only welcome questions, I have been known to beg for them. I don't get many. In fact, it is often true that my name as the last to reply to a thread is the kiss of death to that thread. No more replies; it simply falls off the page.

I have been discouraged by this more than once; feeling that no one is really interested. I bounce back, though. People may not read what I write, but I continue writing about RSD.

There are times I wish some evidence would arise that would prove me completely wrong. Then I could stop working on an article I have never been able limit to under 2500 words and start watching Days of Our Lives (is that still on?).

This post is probably more than 2500 words, and doubtless there are many who long for the days when I was too weak to write anything close to that number...Vic

Hi, Vicc. I appreciate your reply... I have not forgotten to respond, I have just about no energy, but I do have many comments and questions regarding your post.

First, I am going to try the GSE. Anything is worth a try. Though everyone IS different. That seems to be the case with different RSD treatments, as I am about to say again... I think you have to be careful when saying that it prevents migration of symptoms. That is something you really cannot prove. Yes, you believe it did in your case. But everything is so unsure about RSD. For instance, some people's RSD spreads, and others it doesn't. Some people have sucessful treatment with nerve blocks. Others don't. I think that you never can be sure. RSD plays by no certain set of rules.

Could you please give me the link to the article written by one of the RSD "experts" on IRI? I would really like to read up on that.

The study regarding children/ adolescents with RSD who were treated with physical therapy can be found here:

http://www.rsds.org/2/library/articl...ive/index.html
under: Author: Sherry DD, Wallace CA, Kelley C, Kidder M, and Sapp Lyn.
Title: Short-and Long-term Outcomes of Children with Complex Regional Pain Syndrome Type I Treated with Exercise Therapy.

(check out the other articles they have there, too)

I know that this is children being treated with PT, and not adults, but I still think that it is proof that RSD can indeed be TREATED with physical therapy. In fact, in this specific study of 103 children, they did not use any medications. So, there is proof that physical therapy alone CAN be used for RSD patients. In fact, opposite to what you are saying, weight bearing is the most important thing to do!

If you state that you believe HBOT to be the "only available therapy that offers any hope for ending the ravages of RSD", I do have another question... I have a friend who had RSD 12 years ago. He went to PT for a year, and 9 months into it received nerve blocks. All his symptoms and pain dissapeared through them both (along with medications) and he is symptom and pain free to this day. How do you suppose that people do recover, when they do not receive HBOT? Right here I am suggesting that I think your theory cannot be 100% correct. Because everyone is different. With RSD there is not one thing to do. Different treatments help different people.

Since you don't believe RSD involves the sympathetic nervous system, what causes the sweating, and even blood pressure changes that people with RSD experience? Is that not something that the SNS is doing?

More about the HBOT: it is not always sucessful, huh? Do you think it has better results than any other treatment? It certainly isn't 100%.

I do have other questions for you, but don't have the time or energy right now. I wish I knew 100% that you had it all correctly, but I see flaws with some of the things you are stating. And, I am seriously questioning your statements. Thanks for your time. :Thanx:

I am glad you want questions... but I hope you don't regret that. :D

Hi again, IHH,

Well, you do have a number of questions; comments too, but that's ok. I would like to answer them in detail, but that would take more words than anyone would want to read at a single sitting.

First, I didn't say that GSE prevents symptom migration; I said I can't prove GSE prevents symptom migration, then offered a brief summary of my experiences. In posts at B/T, I wrote in some detail about research into ischemia-reperfusion injury (IRI) that supports the use of GSE to delay onset of symptom migration, and I may write a post here on the same topic. Meanwhile, I would be remiss if I didn't tell others what works for me.

I don't agree that RSD is so different in each individual as to make it impossible to find an effective therapy that works for most: there will always be variables that prevent any therapy, for any disease, from being 100% successful, but that is no reason to stop trying.

You speak of successful outcomes from blocks, but I know of no research confirming this. The consensus today is that blocks provide temporary relief and in the vast majority of cases eventually have no effect whatsoever.

I couldn't find anything in my previous posts about an RSD expert writing about IRI, but I have mentioned it in the past; as an example of someone who knows about IRI and ignores its connection with RSD. His article on IRI is pretty complex, contains a lot of medspeak and says nothing about RSD. I will send it if you want, but it doesn't have anything you're looking for.

Re: The Sherry Study.

Physical therapy has been a component of RSD treatment since Dr Weir Mitchell told his first patient to "walk off the pain". In the 144 years since, there has been only one published article reporting "successful" treatment of RSD patients through PT: this one.

As I said before, if PT were effective, it would have been announced, confirmed and reconfirmed long ago. I won't speculate about the conclusions you cite here, I'll just wait for someone else to confirm them in another article.

As to weight bearing, I am not the only one to say it is harmful; that is the consensus of nearly everything I have read about RSD and PT. I hope you will stop any weight bearing exercises before the pain makes you stop.

When I say that HBOT is the only available therapy that offers any hope for RSD patients, I speak from the perspective of RSD as an IRI; a physical disease process.

The body reacts to physical damage; tries to repair and heal it. Sometimes it works, but most of the time it doesn't. There will be instances of spontaneous remission from RSD, but the rest of us will need to rely upon medical intervention.

The body's response to IRI is to increase production of vascular endothelial growth factor (VEGF), which is the first step in creating new microvascular systems (MVS). But the body doesn't create enough VEGF to do the job.

HBOT is effective in treating RSD because it stimulates production of much larger amounts of VEGF. Interestingly, this is considered an adverse event during HBOT, and many writers consider it sufficient reason to oppose HBO in any but the most extreme emergencies.

I have read skeptics who refer to HBO as a cure in search of a disease. It is the ultimate irony that the very adverse event they warn against is the mechanism of action against the disease HBO has been searching for.

"Different treatments help different people". Nothing helps anyone. The latest rage is ketamine therapy, but as you probably read in another thread, it falls far short of the mark. We will need to wait to see how long the "successful" remissions last.

I don't say the SNS isn't involved in RSD; like everything else in an affected limb it can function abnormally, but that is the result - not the cause - of RSD.

No, HBOT is not always successful. One reason is that few people even resort to it until it is the last, desperate attempt to do something before ending your life. The RSD is usually far along by then. But that isn't why HBO fails too often.

HBO chambers advertise for RSD patients; if it hasn't helped one of their clients already, they know it has helped people, and most are in the business to help fight disease. The problem is that they don't have any idea how it helps, so they usually use 100% oxygen at 2-1/2 atmospheres (ATA); pretty much the industry standard.

2-1/2 ATA works well for emergency situations such as the "bends" and carbon monoxide poisoning, and for late stage diabetic issues such as unhealed wounds, infections and gangrene, but I think it is way too much for RSD.

One reason for this is that HBO is reported to contain as high as 15% oxygen free radicals (OFRs), and these thingies do all the cell damage in IRI. Reports of patients who enjoy dramatic improvement in the first few sessions, then catastrophically relapse a few days after HBO, certainly suggest that secondary damage from this massive influx of OFRs may be the problem.

I have strongly urged people to take GSE during and after HBO, and no one that I know of who has taken an oral antioxidant has reported that sort of relapse.

The main reason I believe HBO should be delivered at less oxygen and a much lower ATA is the evident mechanism of action: stimulation of production of VEGF.

Someone with full body RSD has lost millions of MVS, and these can't be rebuilt overnight. It will take a lot of VEGF, then a lot of time to build new MVS and allow them to mature. Current HBO practices don't take this into account; which makes sense, because the operators don't know that RSD is IRI.

I haven't described the role of OFRs in RSD/IRI, much less how MVS are destroyed, but if you want to learn more you can go to Medscape or PubMed and look up IRI and start reading research abstracts; or you can wait until I take another swing at describing the IRI process: from initial physical trauma through the destruction of MVS.

I think HBO is the only therapy that addresses the problem in RSD, and it is certainly the safest and most cost effective way to treat this disease...Vic

I just wanted to say that I have had success with the blocks and I have several friends here that have. One of my friends is a nurse at the hospital and she has RSD in her right foot and she told me that when she sees it starts coming out she goes to get a block. She has worked at the hospital for at least 15 years and has had the RSD for as long.

I had 3 blocks to help put the RSD into remission and it worked for me. The surgeries I had brought it back out and then I started asking for blocks with the surgeries and the Drs. did them with no argument. I do believe that the blocks work for many people. Maybe not all but many.

As far as PT. I spent over 3 years in PT. It didn't heal me but it helped to get me moving better then I was. I went twice a week for over 3 years to deal with my back which I was bed ridden at the time and they got me walking, then I went for the TOS and got somewhat better but had to have the surgery anyway. Then I went for the RSD and Fibro and I saw a world of difference as far as movement was concerned.

I worry about people saying that the blocks don't work, I believe that they are one of the best ways to help the RSD if they do work for the person getting them. They do sometimes become useless to certain people with RSD but I think people should let the Drs. try them if they offer them to a person.

Ada

Vicc,
Here is where you wrote about the RSD expert writing about IRI... I'd love the article... could you PM it to me? Thanks.

Quote:

Originally Posted by Vicc (Post 69154)

Hi Roz,

As you already know, I'm an advocate for HBO in treating RSD. In fact, I believe it is the only available therapy that offers any hope for ending the ravages of RSD, yet I never talk about it here. I guess it's time I started.

I haven't begun until now because I have focused on showing why is actually an ischemia-reperfusion injury (IRI), a disease that wasn't even discovered until 1964 and thus wasn't in the running when Weir Mitchell attributed this to a nerve injury a century earlier.

I won't try to explain IRI here, limiting myself to pointing out that the IRI process ends with the plugging of millions of microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to the cells and return used blood to the veins.

Blood can't pass through a plugged MVS: Used blood must empty into veins in order for fresh arterial blood to enter the MVS. Block one end of the tunnel and the other is blocked too.

Because our cells get everything they need in order to function properly from arterial blood delivered by the capillaries, IRI explains every sign and symptom of RSD, from abnormal pain (oxygen deprived sensory nerves); to cyanosis (visible proof of IRI: cyanosis is only seen when blood is not flowing through capillaries); to patchy osteoporosis (bones need calcium, which is delivered by the capillaries); to inhibited hair and nail growth. IRI explains it all.

Plugged MVS' can't be unplugged. They don't make Roto-rooters tiny enough to ream them out. Even if they could, we have millions of plugged MVS and cleaning all of them this way would take years.

HBO doesn't fix plugged MVS', it replaces them. It stimulates production of what is called vascular endothelial growth factor (VEGF), and VEGF is necessary to stimulate production of veins, arteries and MVS. Ever since it was discovered that HBO stimulates VEGF, people have been trying to find a way to make it stop.

Increased stimulation of production of VEGF can be harmful for those who don't need it, but not for those who do. Interestingly, some physicians have been fond of calling HBO 'a cure in search of a disease', so its nice to know we can help it find its way home. HBO is the most effective way known to "grow" new MVS.

So what went wrong when you tried HBO?

Right now, most HBO chamber operators use the "one size fits all" model of treatment. If it works for the "bends"; for severe carbon monoxide poisoning, and sometimes works for RSD, why change? And why change when there is no research showing a different percentage of oxygen at a different pressure might help more RSD patients?

Well, common sense has to fit into the equation somewhere, but there are a lot of areas in medicine where common sense is considered unscientific. Better to wait for proof than try something different just because it seems to make sense. RSD and HBO seem particularly affected by these "values". We get a "double-whammy": neither group of experts has any sense.

Common sense tells us that if we need enough VEGF to stimulate the production of millions (or even more) MVS, it will probably take some time; but the "one size fits all" model of HBO demands as few sessions as possible (usually 30 to 40). If you don't want VEGF in the first place, fewer sessions even makes sense.

VEGF is just the start of the process: our bodies need time to assemble the materials to create these new MVS; they don't come pre-built, so it takes time to build all of them. This means that most of our cells aren't going to see reperfusion (restoration of normal blood flow) for a while, so they will need to be resupplied with oxygen at least if we are to prevent further damage during reconstruction.

Using emergency protocols that "push" as much oxygen into the body in as short a time as possible is the right way to treat the "bends" or carbon monoxide poisoning, where people die quickly if not treated dramatically, but it doesn't appear to make much sense when it comes to rebuilding several million (and sometimes several hundred million) MVS.

I'm only guessing, but my guess is that you got 100% oxygen (O2) at 2.5 atmospheres (ATA). That is generally considered to be safe; especially when less could mean the patient's death.

My guess is based on the fact that another RSD patient went to Canada and received 100% O2 at 1.5 ATA, and improved dramatically, but several months later began to relapse. This time she went to Texas, got 100% at 2.5 ATA and during the "therapy" would call to tell me she was getting worse every day.

I told her to get the Hell out of there. Shoot her way out if necessary; that she didn't really have to shoot anyone, just a couple of light fixtures is enough to scare all but the bravest; but get out now. She didn't. She's now saving money for another trip to Canada.

In Texas, they told her that she must be having a reaction to Lyme's disease. They told you it must be pulmonary embolism. I suggest it was too much O2 at too high an ATA.

One size fits all doesn't fit every RSD patient. In fact, some have gone into HBO, gotten better, then catastrophically relapsed within a few days; some even ending up worse than before.

(I have read many reports of casastrophic relapses, and while there isn't space here to present the reasons, I can report that I know of no one who had begun taking the antioxidant grape seed extract prior to HBO who later reported this.

(In my next post about symptom migration: what causes it and how to prevent it [hint: buy grape seed extract], I will discuss the role of oxygen free radicals (OFRs) in both processes. And lest someone labels me a health food fanatic, I don't have enough money to buy vitamins. I urge everyone to take GSE because it works).

Here is another problem: The research necessary to find an optimal dosage of HBO for RSD/IRI will never be done. There is no way to license HBO, which means no one can have a monopoly on using it and make billions of dollars. If you can't make billions selling it, why spend millions researching it? It aint gonna happen.

What will happen is that those of us who advocate for HBO will finally find the backbone to talk about what we believe - and why - despite the fact that the experts only have to point out that they're experts and we're not. Hell, we aren't even scientists; just people who care enough to spend years researching something no one else is interested in unless they can make a buck from it.

Over time, as more RSD people hear from people who have successfully undergone HBO, more RSD people will try it. Some will get better and some will be like you and my other friend. I figure that in 15 to 20 years, people will have sorted out in their minds the O2 and ATA dosage they feel will best serve them.

Of course during this 15 to 20 years, most RSD people will wait for an answer from the experts; and suffer from the symptoms of this disease all that time.

You see, in RSD the experts have been 100% wrong for 100% of the time. They are still telling us that this is a neurological disorder, despite that fact that at least some of them know about IRI (one even wrote an article about it), and know that this makes more sense.

In the next few days I will publish a post showing why RSD can't be the result of a nerve injury; I expect two or three polite comments while no one pays any attention to what it says. It's going to be an interesting (albeit frustrating) next 15 to 20 years.

What I wrote here offers a hint as to why I haven't finished writing my article for publication: I'm not a scientist and I have no research upon which my conclusions will be based. I expect that if it is published, I'm gonna get beat up pretty bad in the responses. That's ok, they can kill me, but the law says they can't eat me.

I will not be writing to the experts: my target audience are those conciencious HBO chamber operators who want their patient's to leave better than they came in. The ones who will be willing to try less O2 at lower ATA if it makes sense to them.

My only real hope for the immediate future is that some work comp insurance co will learn enough about HBO to investigate it. Right now they are fighting us with everything they have; because they know we aren't going to get better. If just one major company figures out how to treat us (and thus stop having to pay us), the future could change overnight.

Isn't HBO expensive? It is when we have to pay for it. People who work for insurance companies are very good bean counters, though; profits are everything lives mean nothing: so if their computers tell them that one spinal cord stimulator will pay for, say 100 HBO sessions (more than anyone ever gets today); and if their actuarials tell them that people who get HBO get better while people who get the SCS still get worse. we may see the day when they force RSD patients to undergo HBO.

When/if that day comes, I won't be surprised if they go with what works, rather than wait for experts to do research that will never be done...Vic

Vicc, I started a thread for you with questions about HBOT, because I do have more questions...

Here's the link:
http://neurotalk.psychcentral.com/sh...ad.php?t=13809

Thanks for being patient with me and answering all my questions, and responding to my comments. :)

I do understand why HBOT is the only treatment if you say RSD is an IRI. Thanks for explaining.

Hope to hear from you more soon.

Quote:

Originally Posted by Vicc (Post 69413)

Hi Roz,

I suppose I should look up the relationship between depth in feet and atmospheric pressure, but I can be a rigid old coot; 15 feet is not a scientific way to measure air pressure. It is a throwback to the days when HBO was used almost exclusively to treat divers who suffered the "bends" after rising to the sea surface too fast. I guess they understood depth, but couldn't get their minds around air pressure. I don't know what 15 feet means.

You don't seem to be having much luck in finding doctors: one tells you that he "guesses" the bruises were the result of a pulmonary embolism (was he guessing the embolism was acute or long-healed?). Either way, I think you should have been hospitalized for this severe reaction.

Another doc sees that your O2 level is "way below norm" and refers you to a pulmonary specialist, who tells you your O2 is 77%. In my not so humble opinion, the only explanation for the way you were maltreated is that you don't have medical insurance, or your insurance sucks.

I would have thought that widespread bruising would be enough to see you admitted to the hospital for testing, but there may be relatively benign explanations for that.

77% oxygen is an emergency. Hard to breathe? Hell, as I understand it, O2 that low makes it hard to live. My memory isn't as reliable as it used to be, but I remember when my daughter couldn't take in enough air.

I followed the ambulance to KU Med Center and by the time I got into the ER it seemed like everyone there was gathered around her bed. She was already on oxygen and I heard the words "hyperbaric oxygen" from someone in that group.

I think her O2 was in the high 70 to low 80 percent, and it was clear to me that they weren't sure she was going to live. When they took her to a room, I wondered if I would see her again. I don't know how people can get through stuff like that without God. (I could be wrong about the numbers, it's been many years and lots of oxycodone ago).

Since you're still alive, I won't bother to Google it, but as I recall, below 95% oxygen is not good. Perhaps one of the nurses here could help on that one.

You will be horrified to learn that in most states a person can be making french-fries one day and an HBO "technician" the next. Maybe LisaShea will add her experiences to your horror story.

Anyone contemplating HBO can only be assured of competent staff by making sure the chamber is certified by the Undersea and Hyperbaric Medicine Society.

The manufacture, sales and even advertising of hyperbaric chambers is closely monitored by the FDA. which (like much of the medical profession) suspects HBO is some sort of voodoo medicine. They don't seem to care about what happens to patient's, however, and I suspect that they don't mind a few dying each year; it reassures them that they're right: there is something amiss about HBO.

There are people in the business who are only in it for the money, so buyer beware...Vic

Hi, nurse here who will confirm that 77% oxygen sats would require intubation in most cases. If this did not occur and Roz was not treated as a medical emergency then I suggest she may have been misinformed regarding how low her sats were.
I have also had 90 "dives" of HBOT as a part of my wound (infected with MRSA) healing treament. It is paid for by my workcover providers.
It has not appeared to be too useful for may pain but certainly has helped my wound.
I feel I must share with you that in the months I have been "diving" and sharing a tank with 6 other people there has never been anyone who has had an adverse reaction to the HBOT.:)

(Originally posted on another thread by InHisHands)

Hello, Vicc

I appreciate your replies to my various questions. I have a few regarding HBOT, if you wouldn't mind answering them.

I may have an opportunity to access HBOT, at an alternative medicine Doctor's office. My younger brother has autism, and so my family has worked with this Dr. before. If he feels comfortable treating someone with HBOT that has RSD, then I might give it a go.

I understand now a lot better why you feel HBOT is the only treatment for RSD if you are looking at it from an IRI standpoint.

In order to completely heal I understand that you need more than a few treatments. But, approx. how many? And how often? Is it a long term thing (months and months of treatment) or 4 weeks will do the job?

You speak of setting the HBOT chambers at certain depths... how do you tell a Dr. (who knows or at least thinks he knows what he is doing) not to set it at certain depths or to set it at a certain depths?

Since you claim it has been successful in others with RSD, how many others do you know who have had it and are doing better from it? Can you put me in contact with any? Are any here on this board?

Thanks again... I am willing to try just about anything about now... and HBOT sounds hopeful.

Hi again, IHH,

I’m sorry for the long delay in responding to your questions, it’s been a really difficult week but I’m recovering and at least able to type again.

I hope what you read here will be of some use to you, but I don’t think anyone will find it persuasive until you understand more about ischemia reperfusion injury, so I plan to devote most of my time and energy into a series of posts describing what it is and how it explains the signs and symptoms of RSD. I hope that after reading some of them, what I say here will be more useful in making informed decisions about treatment.

As I said earlier, IRI destroys microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to all of our cells and returned “used” blood to the veins. It doesn’t destroy every MVS; if it did the result would be death by gangrene in a very short time as none of our cell would receive either of those essentials, but it randomly destroys enough to seriously affect cell functioning throughout the affected area(s).

Those areas with the most widespread damage show the most serious symptoms, which explains why some of us experience more pain than others and some of the rarer symptoms (such as hyperhydrosis), can be severe in some and absent in others. The fact that almost all of us are extremely hypersensitive to cold is one of the most significant signs that this is an IRI, and I will explain why in one of the first few posts in my campaign to show why the medical world is wrong.

Now, in response to your questions: the apparent mechanism of action of HBO is stimulation of vascular endothelial growth factor VEGF. This is why it is approved for the treatment of IRI, making it one of a very short list of disorders the FDA and the Dept of Health and Human Services (HHS) will allow hospitals to treat with HBO.

There is no research describing the long term effects of stimulation of VEGF by HBO, but there is enough science to warrant some basic assumptions, among them: The body may not have the ability to create unlimited supplies of VEGF on demand despite intense stimulation, and that artificial stimulation of VEGF could result in an adaptive response to the increased stimulation (the body may not respond to normal stimulation after prolonged artificial stimulation)

It is also likely that the creation of new MVS is limited by the body’s ability to marshal the necessary materials where they are needed and that it is reasonable to view new MVS as similar to new plant growth; that it takes time to mature and become fully functional.

These assumptions are based partly on what is known about the healing process in general, but are also upon the fact that little is known about the long-term effects of HBO in people who have undergone the therapy. We could expect that if the results were overwhelmingly successful the news would have gotten around by now. Some of the successful ones would have taken time out of their restored lives to tell others about their continuing remission.

.Since RSD/IRI, means that millions, or even more that a billion, MVS have been plugged and functionally destroyed, the assumptions I cite mean it will take time to create enough VEGF to begin the process of replacing all of them; time to marshal the necessary material, and; time for the new MVS to fully establish themselves.

This is why I believe that the delivery of 100% oxygen (O2) at 2.5 atmospheres (ATA) for 20 to 30 daily sessions – not an industry standard, but pretty typical for most free standing chambers - may actually be harmful to RSD/IRI patients in the long run: even the most intense stimulation of VEGF would be useless if the body simply can’t produce enough in just 30 days. If the body adapts to require increased stimulation in order to respond, this would mean less VEGF during the time directly following the end of HBOT.

There is an added problem with treating RSD/IRI using HBO: Oxygen free radicals (OFRs).

(OFRs are oxygen molecules that are missing one or more electrons. This makes them highly unstable and the only way to restore stability is to steal the needed electrons from a nearby molecule; turning that molecule into a free radical (FR) that must in turn steal electrons from another molecule.

(This chain reaction of thefts is what damages cells, and it can only be ended by a FR coming into contact with an antioxidant, which can surrender electrons without becoming a FR itself, or by two FRs coming into contact, which results in one being restored and the other becoming an entirely different molecule.

(OFRs always initiate these chain reactions. They are the weapon the immune system uses to destroy cells and pathogens during the non-specific immune response (NSIR) to pathogens and cell debris. In high concentrations, OFRs produce so many chain reactions the target is literally ripped apart. Our cells are attacked by OFRs as many as hundreds of times per day, but the cells are able to repair themselves when this happens. A significant increase of OFRs could destroy newly created MVS’ before they are fully established).

Most of the research into OFRs during HBO reports that as much as 15% of the O2 delivered in this way is or becomes OFRs. This has been recently disputed and is the source of some controversy among HBO researchers, but even if the percentage turns out to be much lower, I believe that the increase in OFRs is directly responsible for reports from many RSD/IRI patients who suffered catastrophic relapses after reporting initial improvement during HBO

This alone is sufficient to demand that the maximum ATA for us be no more than 1.5. I would point out, however, that those people who have undergone HBO after talking to me have taken the antioxidant grape seed extract (GSE) and none have suffered a catastrophic relapse. A sample of five is too tiny to mean anything, but the precaution of taking antioxidants before, during and after HBO seems wise to me.

I don’t think we will ever know the best therapeutic application of HBO for RSD/IRI, I certainly don’t know today. Based on the assumptions I’ve make, however, I can say what I would demand if I were able to access it.

I would begin at 100% O2 at 1.5 ATA for five days, then 50% at 1.5 ATA twice weekly for at least seven weeks (20 sessions) and would be prepared to continue even longer if significant symptoms remained, and to repeat HBOT if I began to show evidence of relapse at any time in the future.

It might be that RSD/IRI requires an even more conservative approach, but if the assumptions I’ve made do apply, a lower O2 percentage at a lower ATA should result in longer periods of remission.

Why would anyone want to consider such a time-consuming and expensive process if relapse is possible or even probable?

The short answer is that if RSD is IRI, the only route to recovery is replacement of those lost microvascular systems, and HBO is the only available treatment that specifically addresses this problem.

Also, compared with other procedures, HBO is relatively inexpensive: prices fluctuate wildly even in areas where several chambers are available, but it can still be obtained for about $350.00 per session. 20 sessions would cost $7,000.00 plus incidental costs of less than $500.00.

When you contrast this with the cost of other procedures, most of which reported significant initial successes that could not be replicated by later clinicians or researchers, 40 sessions for about $15,000.00 is not really that expensive.

This is only true, of course, if RSD really is IRI. You will be better able to judge this for yourself after reading just a few posts in my planned series…Vic

Thanks Vicc, you answered my question of what is the right amount in terms of frequency of visits. I can only do 60 minutes at a time 90 makes me clautrophobic and edgy.

I was doing HBOT after my TOS surgery. Then I stopped doing HBOT and the RSD symptoms are rearing up

I am close to HBOT therapy and am thinking anout starting it again. I am going to print this off and talk to HBOT doc about it and trying your protocol.

I will let you know what he says.

:hug: to you Vicc. God Bless

Since my views on HBO seem to have attracted interest, it seems best to me to bump this thread in order to allow those who want to comment about them to read what I actually wrote.

I've said several times that my goal is to get people interested in learning about ischemia-reperfusion injury (IRI). I'm not so arrogant as to believe that anyone will rush right out and sign up for HBO because I tell them to, but I do hope that by discussing a mechanism of action for HBO, someone will take the time and effort necessary to learn whether IRI might make sense.

In RSD, it really does boil down to which view makes more sense: Those who believe this is the result of a nerve injury and that the success rate of ketamine therapy seems attractive will choose it. Those who take the time to learn for themselves whether IRI is a better explanation for our signs and symptoms will look to HBO.

The best way to make an informed decision is to gather information. I can't provide enough information about IRI to convince anyone; I can only hope to give people a reason to learn about it for themselves...Vic