Reflex Sympathetic Dystrophy (RSD and CRPS) Reflex Sympathetic Dystrophy (Complex Regional Pain Syndromes Type I) and Causalgia (Complex Regional Pain Syndromes Type II)(RSD and CRPS)


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Old 09-09-2007, 05:45 PM #31
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Quote:
Originally Posted by jo55 View Post
I didn't realize that so many are in a HBOT treatment chamber at one time.
I thought { assumed} it was a one at a time personalized treatment.
I could see if so many with varying dx's were in one chamber for a tx - that many more attendants would be required to monitor everyone.



Hi jo,

There are some mono chambers around here but they are usually hired out by elite sports teams who can afford to have the appropriate staff on standby for just one person however the greater number of centres have chambers that take 6 or more people at once.
As this is the case the variance of needs from one patient to another in the chamber is often great. I have been in a chamber with an unconscious intubated accident victim at one stage so we actually were in longer to accommodate his needs. No harm done except from extreme boredom.
This is a costly treatment for sure so unfortunately the multiple use is by far the most common and because of that there are the appropriate staff available to treat any side effects that may occur.
I had oxygen toxicity on my first dive and in my months in the chamber I have seen 2 others. This problem resolves as soon as the patient is removed from the chamber but if there is nobody there to recognise or treat the seizures then there can be catastrophic problems.
I guess it is like any of our treatments where we must decide whether we are willing to take a risk no matter how miniscule it is to perhaps improve our situation.
Despite my first experience I continued my treatments with no other major problems other than a little claustrophobia and earache.
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Old 11-19-2007, 01:23 PM #32
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Just been catching up on this thread and have a real interest in one of the topics discussed in particular
Tayla, yourself and Vicc had a lengthy discussion about IRI / RSD and tourniquets
Am I right in thinking that there are studies that suggest that the use of tourniquets are not useful for RSD patients and may also lead to further IRIs
If that is the case, then I am seriously wondering if the tourniquet used during Alisons bier block is somehow directly linked to the worsening of her symptoms and the fact that her motor skills have been severley impeded in that leg since the block four months ago and have yet to recover
I always said at the time it was as though the RSD jumped from the sympathetic to the motor nerves whilst she was in theatre, although her PMT suggest that this is a confidence issue which is somehow a psychological and protective reaction to the fact that the block did not relieve the pain
Any thoughts....?
Andrea
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Old 11-19-2007, 02:38 PM #33
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Hi again, Andrea,

I hope you are prepared for another lengthy Vic reply, because here it comes.

First, it slipped my mind that bier blocks involved tourniquets, which are the worst possible procedures for people with RSD (assuming, of course, that this is an IRI), because current belief about IRI is that it always and only begins with the use of a toruniquet.

My hypothesis that RSD is an IRI rests entirely on my contention that this view is incorrect, and that the ischemia mediated by the immune response to trauma is sufficient; that tourniquet ischemia is not necessary to initiate IRI.

I will have much more to say about this in my long-promised series of posts on IRI, so I'll limit my discussion here to saying that that it is folly to beleive everything is known about anything: That there is more to learn about IRI.

The disease was discovered in 1963, a century after Weir Mitchell reported the new disease he called causalgia. The discovery came about after the heart-lung machine made open-heart surgery possible by maintaining circulation while stopping the heart. But open-heart surgery required that arterial blood-flow into the heart be blocked, creating ischemia.

Not long after the first successful open-heart surgeries, patients began dying following apparently successful surgeries. Researchers began looking for the cause and discovered that the microvascular systems (MVS), the arterioles, capillaries and venules that deliver arterial blood to the cells and return "used" blood to the veins, were being plugged by white blood cells in the venules.

(If you dip a straw into a liquid and then remove it, the liquid drains out, but it you plug one end, the liquid is trapped in the straw. This is similar to IRI, in that blocking blood from leaving the MVS prevents fresh blood from entering).

The cells of the heart muscle died from oxygen deprivation (hypoxia), and when enough cells died, the heart stopped and the patient died.

Later researchers discovered that other internal organs were also affected by IRI following surgeries (which always involve tourniquet ischemia). In the late 1980s, other researchers discoverd IRI in skeletal muscle (including arms and legs), but again, tourniquet ischemia was involved: Limb transplants in which ischemia lasted for hours, and surgical procedures, which can last minutes to hours.

No one involved in IRI research has ever learned of a disorder like IRI in which tourniquet ischemia isn't involved, and they won't learn about it by reading the literature on RSD, because the only clue for ischemia is cyanosis, and that word simply can't be found in the literature. (I'll explain why this is so in that series I keep promising).

So, we have one group of experts who know about RSD, but not IRI, and another group who know about RSD, but not IRI, and me. I've studied both disorders and believe than anyone familiar with one who learns about the other will agree with me. I haven't come across anyone who has studied both, but it will happen

All that is necessary for the diagnosis of RSD to be changed to one of IRI is recognition that tourniquet ischemia is not essential. That is more difficult to prove than you might imagine, since I can't tell IRI experts that cyanosis is common in RSD. They would rather trust the literature than a bed-confined social worker in rural Kansas.

RSD "experts" are so dedicated to the view that this is a neurological disorder, they aren't going to listen to me either. So I talk to RSD people, who know all about cyanosis, but must be taught about IRI.

I understand your frustration with Ali's physicians, and I'm beginning to understand their frustration with you: You ask too many questions they can't answer.

According to what is known about IRI today, every surgery that results in signs of tissue hypoxia: Cyanosis; lower skin temperature; painful hypersensitivity to cold; inhibited hair and nail growth; etc, should be viewed as a potential IRI. This includes RSD following carpal tunnel surgery or any other surgery in which blood flow to the surgical site is blocked.

Here is an interesting fact: When Weir Mitchell identified high-velocity impact wounds as the cause of causalgia, he knew that every soldier in that war carried with him a tourniquet: Thousands of soldiers bled to death while waiting for someone to carry them to surgeons, and they were determined not to die that way. I would bet that every causalgia patient Mitchell saw had used a tourniquet after being wounded.

Had he known about tourniquet ischemia and IRI, the history of RSD might be completely different, but he couldn't know that, of course: IRI wouldn't be discovered until a full century had passed.

Allen's RSD began when a surgeon inadvertantly looped a suture around an artery, where it blocked blood flow until the pain forced surgeons to re-enter the site and find that suture.

It is entirely possible (probable, certain), that any symptoms that followed that tourniquet on Ali were caused by it. That wouldn't be the case for worsening symptoms in her leg, however, as the tourniquet would not affect the leg. I'm afraid her worsening symptoms there are solely the result of the disease's progress.

IRI does not follow every surgery involving tourniquet ischemia; it is relatively rare. RSD does not follow every physical trauma, and is rarer than IRI, but both are preceded by the immune response to trauma (IRT), because it follows every trauma, no matter how minor. There is clearly some sort of pre-conditioning for both; it could be genetic, it could be environmental (lots of chemicals in our air), or it could be something else, but both disorders clearly require more that trauma and initial ischemia. We may never know what that is, but that isn't necessary; all we need to know is how to treat it. I'll talk about that in my upcoming series too.

I will have much more to say about IRI in the future, and after reading your question here, I suspect you will be reading those posts...Vic
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Last edited by Vicc; 11-19-2007 at 04:07 PM.
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Old 11-19-2007, 05:51 PM #34
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Thanks for the quick response Vicc - Much appreciated as always!!!
Just to clarify - you say It is entirely possible (probable, certain), that any symptoms that followed that tourniquet on Ali were caused by it. That wouldn't be the case for worsening symptoms in her leg, however, as the tourniquet would not affect the leg. I'm afraid her worsening symptoms there are solely the result of the disease's progress
This confuses me as the tourniquet was used on the leg and that is the area where we have seen marked loss of balance immediately after the block was completed. Am I right in thinking you belive the two are not connected???
As you have far more knowledge an research under you belt than myself I await clarification on this with interest
Yu are right that I must annoy the doctors as they never can answer my questions, though I mainly ask about there experiences with other patients and how this may be applied to helping Ali recover
Thanks again and I await you response with interest
Andrea
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Old 11-19-2007, 08:25 PM #35
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Hi Andrea,

The reason for your confusion is clear: I got confused. Instead of refreshing myself about what you wrote on another thread, I relied on my faulty memory and assumed that Ali's block involved her arm.

When I wrote the passage in question, I erred. Now that I actually reread what you wrote on that other thread, all I can say is that it is possible that the tourniquet aggravated the symptoms that were already present, but it doesn't appear likely.

The reason I must revise my remarks is that it would take a certain amount of time (days, at least, and possibly weeks), before an IRI caused by the tourniquet would develop symptoms. The stages of IRI are well defined and there is no evidence that I know of that would suggest that they would be bypassed even when the IRI had already begun to develop.

I'm afraid that you will probably never know why Alison suddenly worsened after the block, but I suspect that it was more likely the block itself rather than the tourniquet. It is possible that the well-intended weight bearing exercises were a factor, but there doesn't seem to be a way to confirm that either.

I know this doesn't answer any of your questions -- either here or on the other thread -- but, like her doctor, I have never heard of anything like this happening before.

There is more that is unknown about IRI than is known, especially in the way the brain and body responds to microvascular ischemia, and the role of blocks in this disease.

It is known that sympathetic blocks act to inhibit normal sympathetic function, as research has shown that injecting norepinephrine below the site of the block results in an instant resumption of symptoms [1], [2].

Research has also shown that production of adrenalin (aka: norepinephrine), is increased in RSD affected limbs (not sure if I have a copy of that research, so I haven't cited it). This is because the body's response to tissue hypoxia is to increase adrenaline, which is a vasodilator and increases blood flow in the affected limb. Increasing blood flow is useful in arterial ischemias such as late stage diabetes.

Since these blocks inhibit production of adrenalin while the body is increasing it, pain relief from blocks is understandable, but no one can explain why they often suppress visible cyanosis. There is still much to learn. But I digress.

All that I can add to what I've said is that the overwhelming evidence is that blocks only provide temporary relief, and they eventually stop working entirely. If my RSD became unendurably painful, I would present for blocks, but with the understanding that they would only provide a brief vacation from that pain.

I suppose I should add that before I conluded that my time would be better spent watching daytime TV than studying the professional literature on RSD, I learned that some "experts" believe that all of the relief provided by blocks are placebe effect [3]. [4]. I find it hard to believe that they are right, as too many people have reported remarkable (but temporary) relief from these procedures.

I wish this reply could have been more useful to your immediate needs, but as I said before, there is just not much research into any aspect of RSD, so answers just aren't there...Vic
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Last edited by Vicc; 11-19-2007 at 08:46 PM.
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Old 11-19-2007, 10:52 PM #36
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To those who may have read this entire thread today:

The first several posts on this thread were originally posted on another thread, then transferred here by KimmieDawn, so when you read references to previous posts, those posts are on the thread from which this was transplanted.

Post #16 here was originally posted on that other thread, so the posts I referenced in it are actually found in Steffs thread, PN board suggested I post here,

As I reviewed this thread today I saw how my references to those posts would lead anyone reading it today to wonder what in the Hell I was talking about. Sorry for the confusion; Kimmie wanted to restore the original thread to focus on the issues Steff raised there...Vic
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Old 11-20-2007, 12:14 AM #37
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Default Stirring the pot . . .

Alright, I am a newbie here, but I have had RSD since I was 11. (Gymnastics is an evil sport!) But beyond that, I am a neuroscientist. Fancy degree and all. So my understanding of the nervous system doesn't quite match a lot of what I am hearing in this post. Norepinephrine is not produced in reaction to only hypoxia- in fact this would not be the first neurotransmitter produced in response to hypoxic conditions. NE is produced in response to any noxious stimuli as detected by the Sympathetic division of the ANS. Nitric oxide would actually be the NT of choice in response to a hypoxic condition- its your primary vasodialator. That and histamine, which is a hormone. There are very compelling and highly tested reasons as to why this is a disorder of the peripheral sympathetic nervous system. It's probably a cop out not site a lot of highly reputable studies, but there are literally thousands of papers that establish a body of work that points in this direction. Science in never infallible- we should remember that- but all of these papers and studies are equivalent to a giant arrow pointing in this direction. (Sympathetic causation.) I have honestly never heard of any process through which the coagulation cascade recruits the nervous system as part of its pathology. And randomly enough I have suffered from major ischemic events- my first pulmonary embolism was 4 years ago. I'm now on coumadin and have clots here and there. But this really isn't based upon my personal experience. I just don't think that the science supports hypoxia as being the cause of RSD.
In its early days RSD was known as causalgia- literally meaning "on fire". But to jump from the original trauma to tourniquet application as the causal factor is a big jump. This used to be the disorder of gun shot victims- that is how it was known. These are big traumatic events, and it is the job of the Sympathetic nervous system to mediate the response to such an event. This is the primary injury and the primary response. At least this is what my scientific endeavors have shown me . . .
Linnie
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Old 11-20-2007, 12:33 AM #38
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"But to jump from the original trauma to tourniquet application as the causal factor is a big jump."

There is more in the literature which suggests lack of blood flow in the initiating event; specifically ice application is associated.

It seems from suffering from this condition that it is a result of infection. Of course this is hardly scientific and evidence still is weak.
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Old 11-20-2007, 01:54 AM #39
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Old 11-20-2007, 05:07 AM #40
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Quote:
Originally Posted by ali12 View Post
Just been catching up on this thread and have a real interest in one of the topics discussed in particular
Tayla, yourself and Vicc had a lengthy discussion about IRI / RSD and tourniquets
Am I right in thinking that there are studies that suggest that the use of tourniquets are not useful for RSD patients and may also lead to further IRIs
If that is the case, then I am seriously wondering if the tourniquet used during Alisons bier block is somehow directly linked to the worsening of her symptoms and the fact that her motor skills have been severley impeded in that leg since the block four months ago and have yet to recover
I always said at the time it was as though the RSD jumped from the sympathetic to the motor nerves whilst she was in theatre, although her PMT suggest that this is a confidence issue which is somehow a psychological and protective reaction to the fact that the block did not relieve the pain
Any thoughts....?
Andrea


Hi Andrea,
IRI occurs when there is tissue damage to an area that is reperfused after a period of ischaemia--whether it be from trauma or possibly a tourniquet.
IRI is extremely rare and as Ali had already been diagnosed before her Bier Block it is unlikely that there is an IRI cause to her RSD.
The damage tissue area from an IRI is quite obvious to see and whilst Ali has very obvious oedema and dystonia she does not appear to have trophic skin changes due to a substantial hypoxic event.
I must admit I do believe there may have been some mismanagement with regards to her Guanethidine block and her aftercare but it is so hard to pinpoint and even harder to find out from the doctor if he did the procedure correctly
Wishing you and Ali well
Tayla
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