You probably learned in high school that our cells combine oxygen (O2) with glucose (Gl), to generate the energy that keeps them alive: No Gl and no O2 = no energy. You probably also learned that our cells also create all of the heat necessary to keep the body at a constant 98.6 degrees. Heat is a by-product of cells transforming matter into energy.

Without any O2 or Gl, the cells would die, if enough cells die, the body temp would begin its drop to the temp of the air around it. There is a mid-range, however, when the cells aren’t getting enough 02 or Gl to function properly, but still survive. But the temperature will drop.

The only explanation I have found for our painful hyper-sensitivity to cold and lowered skin temperatures is that the cells aren’t getting enough O2, or Gl, or both. This is that mid-range I just talked about.

I’ll talk more about exactly why RSD falls into this mid-range in future posts, but my purpose here is to show how ischemic hypoxia: blood flow to cells and organs that is not sufficient to maintain their normal function.* explains these symptoms, while nerve injury does not.

The only way to stop or decrease cell metabolism is by reducing the amount of O2 or Gl reaching it.

We can know we suffer from tissue hypoxia simply by looking at our blue to purplish skin. That is the color defined as cyanosis: a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*

Our skin is supposed to be a normal, healthy color; you know: “Skin color”, so why isn’t it? Cyanosis is a bluish or purplish discoloration (as of skin) due to deficient oxygenation of the blood.*It is visible proof of hypoxia. If our skin is cyanotic, our cells are hypoxic.


When we see cyanosis, we are actually looking at millions of microvascular systems (MVS) filled with oxygen depleted blood, and that blood isn’t moving. Our MVS are part of the circulatory system and blood is supposed to be constantly moving, never stopped. Those MVS are ischemic. A low oxygen state usually due to obstruction of the arterial blood supply or inadequate blood flow leading to hypoxia in the tissue.*

MVS are the arterioles, capillaries, and venules that deliver “fresh” arterial blood to the cells and return “used” blood to the veins. The blue color means that blood is not flowing through the arterioles and into the capillaries that supply everything the cells need. When this happens, our cells do what they are programmed to do to:

They switch from aerobic metabolism to glycolysis; generating energy without using O2, but glycolysis doesn’t generate any heat, and isn’t nearly as efficient as aerobic metabolism. It does provide enough energy for the cells to survive, but not enough for them to function properly.

They also release chemical neurotransmitters (Nts) that tell the brain that they aren’t getting enough 02; and they tell other nearby cells the same thing: Nearby cells may be served by functioning MVS, and if they are, they transfer some O2 and Gl to the needy ones. This helps keep those cells alive, but it also means the donor cells now don’t have enough of either to function properly. Now they aren’t able to generate enough heat to keep the limb warm.

This works pretty well during an emergency, but if crisis lasts very long, all of the cells suffer. In RSD, the crisis lasts too long. Many, if not most of the cells in the affected area are now dysfunctional and the temperature of the affected limb begins to fall.

The temp doesn’t need to drop much before the cells begin releasing Nts telling the brain they’re cold. Our bodies are designed to maintain a constant temp of about 98.6 degrees; a drop of one degree can cause the cells to begin complaining, 96.6 degrees feels bitterly cold, and a core temperature of 95.6 degrees will produce violent shivering.

When the air temp in my room drops to 68 degrees, it gets too cold for my feet: They start screaming that they’re freezing. Other things may be contributing to the cold pain I’m experiencing; my “pain nerves”, C-fibers (Cfs), aren’t getting enough 02 either, and they may be amplifying the cold messages from the cells.

The bottom line is that when cells don’t get enough O2 and Gl, they can’t generate enough heat to warm themselves, much less the tissue around them. They start sending out frantic signals because this is a real crisis.

They send signals telling the brain they aren’t getting enough O2, so the brain tells the sympathetic nerves to increase blood flow, and this aggravates things because one of the things the SNS does to increase blood flow is to stimulate the release of adrenalin. Adrenalin increases the burning pain of RSD.

We know that adrenalin does this because if you inject norepinephrine (artificial adrenalin) just below the site of a recent sympathetic block; the burning pain comes back. That is what sympathetically maintained pain (SMP) is, and it is why blocks work: They are blocking normal sympathetic release of adrenalin, NOT blocking some abnormal SNS activity.

Several things can cause the kind of cyanosis we see in RSD: In late stage diabetes, the disease has damaged small arteries so badly that they can’t carry enough arterial blood to supply the cells; in Raynaud’s Disease, spasming of the arterioles in the MVS prevent arterial blood from getting into the MVS. In both of these disorders, too many cells die and gangrene can develop, making amputations necessary.

RSD patients sometimes end up with an amputated limb, but not because of gangrene: When microcirculation is impaired, wounds can’t heal properly and infections can develop; antibiotics are delivered in arterial blood, so the amount that reaches the site where they’re needed is too little to do the job.

Something else causes the cyanosis in RSD, and after ten years of research the only explanation I’ve found that makes sense is ischemia-reperfusion injury (IRI). It begins with a physical trauma, followed by inflammation and then by ischemia in which some cells still get enough O2 and Gl.

I’ll explain more about IRI in future posts, but before I get to that I need to prove that ischemia can cause every sign and symptom of this disease. I hope that once I’ve done that, you will be more open to the idea that this disease is NOT caused by nerve damage. My next post will talk about those other signs and symptoms…Vic

* Online Medical Dictionary (OMD)

Things I know

My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc.

My RSD WAS caused by nerve injury.

People who know me know the full story.

People who refuse to accept my account of how I contracted this don't know me at all and sure don't know my history (or maybe just choose to take the parts they want to hear).

In keeping on topic... this will be my only post on the subject.

Ladies, I hope you all have a wonderful day today. Keep up the good work

Hi Farm Wife,

You are no way alone with the aetiology of your RSD. As I have said in a previous post that if RSD can come from a paper cut or a mosquito bite then there is absolutely no restricted blood flow causing it.
Sorry, I don't know your history but you can be sure that there would be no reason why I would question your account of your injury, you sound like a very well educated and I would gather a resourceful women.
Wishing you heaps of luck
Tayla

Hi Farm Wife,

I try to avoid talking about the personal views of forum members, but I do think it appropriate to point out that in previous posts I have said that diagnoses of CRPS-II have not been discussed in the literature, that some tissue injuries can also injure nerves, and there is nothing in the literature that describes how a nerve injury can cause the signs and symptoms of this disease.

Also, I don't know how one can say: My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc. Unless tests have excluded IRI or tissue hypoxia. The absence of cyanosis does not exclude either of these, as cyanosis is only visible when the microvascular systems at the skin surface are ischemic.

Many people diagnosed with RSD don't present with cyanosis because the injury involves fractures, ligament injuries, nerve entrapments (which can initiate the immune response to trauma), etc, that don't involve blunt force trauma to the skin.

Finally, while I don't claim to have read all the literature on what might cause painful hypersensitivity to cold, I have look for other explanations for this symptom and couldn't find any that didn't involve diminished cell metabolism due to tissue hypoxia.

I am not arguing with you; I'm simply pointing out that a diagnosis of a nerve injury does not exclude tissue hypoxia. At this stage in my life, I would be relieved to learn that I am wrong about IRI. If that were to happen, I could refocus back to reading history and even possibly write a thesis that could earn a Master's degree in that subject.

Until and unless that happens, however, I feel compelled to explain why RSD is an IRI and that IRI is treatable...Vic

Hi Vic,
First, before I get in trouble, let me state that I enjoy everyone fo your postings and think you do lots and lots of homework. i agree with a lot of what you say and then there are times when i am confused my it. so that being said:
I would like you to explain something to me. i had hip surgery and awoke with nerve damage, unable to control my left foot and numbness here and there from the knee down, then the crmaps started and then the pain and the sweeling and the cyanosis, all within a matter of days. i was of course later diagnosed with RSD. so could you please explain to me, what you think the exact process was?
I ask you this because i can't quite connect the fact that i had a nerve damaged, that caused the nerve palsy, and then the RSD symptoms emerged, and i would like to fit this into your IRI theory and see how i feel about it because i do think you make a good point there.
i will say right out, i do not have a clue what rsd is, or how i got it, or how anyone gets it, or why, or what to do for the pain, or what a cure might be or when ...but i am intersted in your opinion.
thanks, joan

CRPS II is nerve damage, and it sounds like what you have experienced Joan. You might read up on that. That is what I have also, a known nerve damage.

That said, I wonder if anyone has thought about the relationship of the nerves and the vascular system? If you have nerve damage, wouldnt you think it would influence the vascular system?

I mean the nerves control the muscles, and that means all, even the muscles in the vascular system. It could be quite possible that the 2 camps are both "right" here. It seems logical to me that no matter how you got RSD, once you have it there would be complications with anything the nerves had anything to do with.

In my case I got CRPS II from ischemia, which in turn caused nerve damage.
Now there is symptoms of both going on in my body. Kinda like everything is spiraling out of control. Now if we can get blood oxygen flowing in to the damaged areas it would make sense that the nerves could have a chance at healing. Maybe the nerves are not allowing enough oxygen to flow in enough to get any healing, and after a length of time the damage is so far gone nothing is working properly?

I think we should all keep an open mind since even the experts cannot agree completely on the hows or whys of RSD. In my mind the two, nerve damage and vascular go hand in hand, and can both be resultant in RSD no matter which came first.

Tayla,

If you would take the time to learn about the immune response to trauma (IRT), you would know that both paper cuts and mosquito bites are trauma, and the immune response always involves ischemia: blockage of arterial blood flow.

It happens this way: White blood cells respond to the site of the trauma, where they release reactive molecules called oxygen free radicals (OFRs), OFRs are responsible for the inflammation and swelling that are obvious in injuries such as hitting your thumb with a hammer, but even if unnoticed, is present in the IRT to a paper cut.

Swelling compresses the tiny nearby arteries and veins that deliver blood to the capillaries and return "used" blood to the veins. This compression is ischemia.

IRI is a disorder that involves an IRT that doesn't end as it's supposed to; instead, the inflammation and swelling (ischemia) spreads over an increasingly widening area. The second stage of IRI is the blockage of arterial blood flow to the capillaries, which means that the cells no longer receive the O2 and Gl they need in order to function properly.

As I have said before, IRI is a complex series of events which I can't possibly explain in just a few hundred words. In fact, I haven't been able to explain IRI and OFRs in less than several thousand words. I am working on a briefer explanation, which would make it easier to understand, but necessarily means that I won't be able to provide all the information necessary to describe how all of this takes place.

If you are unwilling to accept this necessarily brief discussion of the IRT and IRI, I suggest you should learn for yourself what takes place. With your nursing education and experience, it should take you less time to learn than it took me...Vic

Hi Joan,

I just want you to know I will reply to your questions, but I've been awake all night, and my brain simply refuses to help me out right now. I really do appreciated your questions, because they give me the opportunity to explain a little more about IRI...Vic

Vicc,

Just wondering also how you can get your statement below..

"Also, I don't know how one can say: My RSD was NOT caused by restricted blood flow, IRI, lack of oxygen to the arm etc etc etc unless tests have excluded IRI or tissue hypoxia. The absence of cyanosis does not exclude either of these, as cyanosis is only visible when the microvascular systems at the skin surface are ischemic..."

I had a neuroma removed from my foot. Now a neuroma is a growth on the nerve and i had that removed and just like Joan my symptoms started after the surgery. Cramps, swelling, color changes, skin temp changes, and skin changes and then my foot started to invert. I did not have any thing on my leg during surgery that would cause restricted blood flow or lack of oxygen. My total surgery time was 9 mins. What else would cause RSD expecially since they removed sometihng from the nerve itself and I have nerve damage on 2 toes due to the surgey. (it was expected damage, just a result of the neuroma surgey, i knew that this would happen before the surgery.. just not that RSD was also part of it)

Now I may be repeating my self but cant go back a reread all the other posts, but what test are there to test for IRI??

Amber

I must say that Vicc you have your point of view as I said befor you may be right, who knows but I still have to say that it is just your theory, I do not agree with saying all docs who study this are wrong. Vicc my friend you cannot say that, based on what? your theory that is why more money must be made to study this, and why it is called COMPLEX so many diffrent things happen with RSD/CRPS and why no one test can prove it and diffrent people have a wide range of symptoms, it seems as if one patient has symptoms 1,3,5 patient # 2 has 2,4,6 see it is complex that is why they changed the name.
Again Vicc you should argue this with the medical field first, but do not call the docs who study this all wrong your research material you have did come from the medical field you say are wrong, and are you a doc? please to give some respect to men and women who do study this most with a MD with PHD's in front
I'm not targeting you, or flaming you just disagreeing with you thats all and it is healthy to disagree friend.
I also feel it is wrong to target this site on a another board, I wish you well and please if you can stay here it is good that you are here
sorry if I miss spell it is getting very hard to remember as of late and pain is way up,I may have to have another surgery everyone wich in a way I have nothing to lose, this one deals with my TOS and may help a little so I wish you all well.