Hi Liz,

It certainly is a 'chicken and the egg' situation. For me my RSD/CRPS was well and truly established before I ever had a tourniquet applied and certainly know many who have RSD/CRPS who have never had a tourniquet anywhere near them
I am certain that the use of a tourniquet is surely going to complicate matters ( apart from the fact it hurts like crazy ) The interruption of blood flow to already compromised tissue can't be good in the long term even thought the resultant pain relief from a bier block may make it seem to be a successful procedure.
Cheers Tayla

Well im a bit biased lol, but only because I know how I got RSD, and it was from ischemia.

Besides that, I do remember that survey but I think it was waayy back on BT1. At least I think it was.

If you look at the history of RSD you will find alot of reference to tourniquets resulting in what we now call RSD. There even is some inference about RSD following low to no blood surgeries.

My vascular surgeon told me that every vascular surgeon knows that RSD follows certain ischemic conditions, but usually dont start treatments for it, or even tell the patient it may happen to them. They are more intent on fixing the problem at hand, not something they cant fix.

I'll post replies to some of the replies on this thread, but won't begin trying for at least a few hours, but I've been waiting for an opportunity to talk about this:

Hey Liz,

I don't know if I talked about this here at NT, but I think I mentioned it twice at BT:

I have been a history buff since jr hi school, and over the years began to focus on U.S. Military history and the Civil War. The soldiers back then had it really rough; bad food, harsh discipline and about half the military deaths during that war came from disease.

Civil War medics were mainly cooks and bandsmen with no medical training at all; they would scour the battlefield for the wounded and carry them back to aid stations where they would wait hours (often without shade) until a doc could treat them. Because battles sometimes went on for two or three days, many of the wounded died alone in bloody fields.

They couldn't do anything about most of that, but they eased their fears a little by carrying tourniquets into the battle and this might help preventing them from bleeding to death. The tourniquet was the most common form of battlefield first aid in that war.

Realizing this makes it a little easier to understand how Weir Mitchell was able to treat enough causalgia patients to write a book about it. He had lots more RSD patients than most docs have seen.

It is obviously much easier to develop RSD following a tourniquet ischemia (TI), which is why I took a bold leap and posted on another thread that anyone who develops RSD following surgery has an diagnosable ischemia-reperfusion injury (IRI). Nobody seemed to pick up on that.

Explaining how RSD develops without TI is much more difficult, since IRI experts believe it is an essential factor, but they know that once blood flow is restored, the patient continues to suffer from waves of compression ischemias (CI) as inflammation swells the tissue, which compresses the tiny arteries that feed the microvascular systems.

They know that the bulk of ischemic damage is done following CIs, as the disease continues to spread throughout all or part of an organ. I know that no one really understands what I'm saying when I talk about IRI, but I hadn't intended to begin a major discussion on it; all of this is the result of my reply to a question about whether a person might have RSD.

I haven't managed much work on the second post to my thread titled Facts you may not know about RSD. That post will describe how ischemia is the most practical and logical explanation for cold RSD, I don't mind being diverted, because I think debates like this allow me to offer information in bite-size packets rather than my long and relatively dry "educational" posts.

Still, I didn't expect this sort of sustained response to a few simple words: All I can say is that you would be a real exception to the rule if your warm, red skin is RSD; 16 months is just too long.

Anyway, I can't complain: I wanted the opportunity to talk about why I believe RSD is an IRI, and I have had plenty of opportunities to do that here...Vic

what about surgical touniquets?

would you even know if they were used?

Surgical tourniquets prevent blood flow to a limb and enable surgeons to work in a bloodless operative field. This allows surgical procedures to be performed with improved precision, safety and speed. Tourniquets are widely used in orthopedic and plastic surgery, as well as in intravenous regional anesthesia (Bier block anesthesia) where they serve the additional function of preventing local anesthetic in the limb from entering general circulation.

http://en.wikipedia.org/wiki/Surgical_tourniquet

i only copied part of the post on wiki.

Hey Flippnut,

You didn't raise any questions I felt needed my reply, but I do have some comments about the State of the Science [on RSD] published by the National Institute for Neurological Disorders and Stroke (NINDS).

That report is more than 6 years old; here is information from the NINDS Fact Sheet on CRPS, published in 2006 [1]:

Complex regional pain syndrome (CRPS) is a chronic pain condition that is believed to be the result of dysfunction in the central or peripheral nervous systems. This confirms what I said about no agreement about which nervous system is damaged in RSD. They just don't know; but they're neurologists, so they're committed to the idea that it MUST be the result of a nerve injury.

NINDS is part of the big lie pretending that cyanosis doesn't exist in RSD; in their list of key symptoms of this disease, they include: changes in skin temperature: warmer or cooler compared to the opposite extremity. This is distinctly different from what their Fact Sheet on RSD said in 1996 [2]: One visible sign of RSDS near the site of injury is warm, shiny red skin that later becomes cool and bluish.

Their 1996 version avoided using the word cyanosis, but certainly described it, and that was obviously going too far; so they changed it to a collection of words that don't accurately describe what happens in RSD.

Even though they begin by talking about dysfunctions in either the peripheral or central nervous systems. later in the text they frankly admit: The cause of RSDS is unknown. Those who insist on believing that RSD must be caused by nerve damage do so in spite of the facts.

The Oaklander study you posted in your 2nd reply has intrigued me for some time: If you read my first post in Facts you may not know about RSD, you saw how I demonstrated that ischemia alone can cause allodynia. I reported that neurons (nerve cells) have no energy reserves, so they are the first to show signs of hypoxic stress, and would be the first to die in ischemic hypoxia.

Oaklander reported: The skin biopsies showed that, the density of small-fiber nerve endings in CRPS-I patients was reduced from 25 to 30 percent in the affected areas compared with unaffected areas. The A-fibers I discussed in Facts, are commonly referred to as small nerve fibers.

Oaklander had no explanation for what caused this huge reduction in small nerve fibers; finding no evidence of physical nerve damage, but when cells die from hypoxia, the body reabsorbs them without leaving a trace of evidence as to what killed them. Ischemic hypoxia killed those small nerve fibers, not some sort of physical injury that left no damage to tissue surrounding those fibers.

I know this won't offer much comfort for those who argue that the "experts" are right and RSD is the result of physical nerve damage, but science is science; at least when "experts" don't pretend that obvious signs of RSD aren't even there...Vic

(I don't include you in the group that believes this must be the result of physical nerve damage; it is obvious you're struggling to learn the facts).

A [ ] with a number inside means I will email you a copy of the article cited. Just click the “rsd_hbot” link at the bottom of the page and type in the title of the post and the number(s) you want to receive.

Amber,

In your last post (#8, dated 09/05 at 7:54 PM). you're probably talking about my remark that this is all good fun: This isnt fun for me to do and rather be reading stuff from the boards. Please consider the possibility that my words were my way of hiding my frustration at having to repeatedly say "I didn't say that" in response to your and Tayla's repeated misrepresentations of what I actually said.

I would much rather be working on my post about cold pain than constantly repeating "I didn't say that". I thought my reply (#6 09/04 at 4:30 PM). in which I cited six times when I referred to the warm or inflammatory stage of RSD, {which was in direct response to a post you made), would finally put an end to your accusations that I said RSD pain is always cold pain.

I went even further, stating that: RSD begins with the warm, red skin of inflammation, which later becomes cold (and usually cyanotic). I hopt this clears up any questions you have...and then you repeat your accusation again in your last post:

I am not harping on you either.. but you are saying 2 different things and even admitted [on another forum] to haveing "warm" stage RSD when you say that RSD is only cold??

Then you say; and im NOT asking you to repeat your self over and over!!! I would love to know why you say that..

I say it because you continue to misrepresnt what I've said. and I don't want people to remember your representations of my words as my actual words. Every time you misquote me, I'm forced to repeat "I didn't say that", and then repeat what I actually said;.again and again.

I researched IRI and i only find stuff on ishecmic bowl and liver disease.. nothing about RSD or any peripheral disase. Medline shows that there are 19,007 documents matching IRI; PubMed shows 20,980 (almost all of them duplicating those found at Medline).

I have more than 100 abstracts on IRI in my computer files, and I estimate I read five for every one that I saved. You have to dig for the facts, not give up because the first couple of abstracts don't seem to fit what you're looking for.

...why go on a crusade or what ever and say its IRI when even the docs right now dont know IRI [?] IRI experts know what IRI is, but they don't know anything about RSD. I'm on a "crusade" because I knew about RSD when I began investigating IRI, and I concluded that they are one and the same.

but dont get all ..... i dont want to say preachy but thats all i can come up with right now, but preachy about something and not take any considerations or back it up. I don't understand exactly what you're saying here but I don't need to back up what I say by citing research: I say things that are found in commonly known facts about science and medicine; anyone can go online and look for science that contradicts what I say.

I'm "preachy" because I know that RSD is IRI and I know that properly administered HBO can bring significant relief for almost everyone here. What should I do? Keep silent when I know something will help someone? Can't do that.

I guess that's all I have to say for now...Vic

Vicc,

I am guessing that when you feel up to it you will comment on my post and if you do I was wondering if you could comment on what you mean by 'properly administered HBOT"?
Have you experienced improperly administered HBOT?
HBOT as you know is a complex treatment that requires highly trained technicians, doctors and nursing staff to firstly to assess you for the treatment, to ascertain the timing and depth of the dive and then to medically supervise the dive. There are far too many restrictions in place here to allow for anything other than properly administered HBOT so I am wondering whether perhaps you work to completely different guidelines in the US?
Our medicare here requires each patient to have a proven hypoxic illness or wound caused by hypoxia or infection before they will ok the payment of treatment.
I know people who have been assessed with me who were knocked back for treatment as their TCOM (Trans cutaneous Oxygen Measurement) revealed no hypoxia in their tissue yet they have been diagnosed as having RSD/CRPS.
Can you possibly explain how you feel that this can be the case?
Thank you
Regards Tayla

Hi Curious,

I'm not surprised that you missed the one time I mentioned that tourniquet ischemia (TI) is surgical tourniquet ischemia. I just looked for that reference and couldn't find it; guess it got buried in the mass of words these three thread have become.

I didn't actually use the words surgical tounrniqueat ischema: I simply said something like iatrogenic ischemia followed by surgery. I was pointing out that IRI experts currently believe that TI, followed by surgery, is the only way one can develop this disorder. My argument with this view is that the known signs and symptoms of IRI and the predictive signs for RSD are identical, and the only the idea that TI is a prerequisite for an IRI stands in the way of linking the two.

IRI experts know that compression ischemia (CI) is the reason the disease spreads, and I take the position that CI (a part of the immune response to trauma), not only spreads IRI, but that it can cause it; that TI is NOT a prerequisite.

I probably shouldn't have even mentioned TI here, but I guess I felt it was necessary at the time. It is just a distraction at this point...Vic

Tayla,

Thank you for your diascussion of TCOM, I suspect it is known under another acronym here as I seem to recall a similar sounding test used in an experiment involving RSD patients. (Now I will have to look it up and learn whether it measures arterial or microvascular oxygenation: If it is the former, it isn't useful in understanding what is happening in RSD, but if it is the latter I might be a good diagnostic test for this disease).

The abstract you posted isn't really very useful as it doesn't contain any information about the dosage of oxygen or the atmospheric pressure (ATA) at which it was delivered. Both are critical in treating RSD.

I know that all modern folks call RSD, CRPS. but I think both taxonomies are unrealistic: RSD representing the discredited view that damage to the SNS causes this disease, and CRPS implying that this is only a pain disorder. Given that neither are accurate, I prefer the one that involves typing fewer letters.

Referencing your last reply: I am not prepared to get involved in a protracted discussion about HBO at this time, preferring to present my views in an organized manner in a single post.

Anyway, these discussions have already travelled far from their starting place: Steff's question to me and my reply to her. I don't want to get involved in another long discussion of something else. I'll try to limit my replies here to questions about what has already been introduced or to provocations I must refute. I want to get back to work on posts I've already promised...Vic

Vicc,

I respect the fact that you do not wish to answer my queries now but l look forward to when you can take the time.
I agree we have strayed somewhat from Steff's original post but as you have a new thread devoted to your hypothesis then I thought this was the most appropriate place to discuss things with you.
I do have one more query--you mentioned that the dose of oxygen and the ATA are critical in the treatment of RSD, I was wondering that seeing as the dose is always 100% oxygen the only differential being the ATA by what criteria do the doctors choose what ATA to use?
Here, unless you are lucky enough to have a chamber to yourself then that ATA is one that will suit the majority of the patients in the chamber.
I have had varying pressures for my dives depending on whether I was being treated for infection or my oedema and hypoxic tissue damage of RSD. The most usual being 2ATA.
Look forward to your response
Regards Tayla