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Kumar
13th May 2004, 06:52 AM
Hello all,

Can you please tell me the reasoning, differances & science of Edema-pitting & non-pitting, Swelling, Obesity? Why Edema is pitting & non-pitting types? Pls tell technical reasons of causes other than: http://www.medicinenet.com/Edema/article.htm

Thanks.

Pantastic
13th May 2004, 10:38 AM
I'm not clear what information you want to know. The link you provide seems a good overview of oedema (UK spelling) for the non-medically educated.

Kumar
13th May 2004, 08:29 PM
I want to know technical differance between pitting & non-pitting edema(oedema) i.e. how it is pitting & non pitting. How it is differanciated with swelling & obesity? Is there any differance between fluid & water retention/accumulation?

Camillus
14th May 2004, 06:16 AM
As Pantastic said the link you provided is a good overview of oedema. The definition that it gives of pitting oedema is the one that is used clinically: pressure is applied to the area and if an indentation is still visible a while after the pressure is removed then it is considered pitting oedema.

Once you've seen oedema you won't mistake it for fat (obesity) and it is almost always much more generalised than the kind of swelling that you get after say an insect bite.

Kumar
14th May 2004, 07:53 PM
Camillus, thanks for reply. Pitting & non pitting both are Oedema. What does then make it pitting or non pitting? Can we say swelling & obesity(as central obesity) by fluid retention & by excess fats differantly?

Corallinus
15th May 2004, 03:35 AM
For the differences between the two, you really need to look at the reasons why both happen. That is your answer.

Pitting oedema normally occurs due to fluid in the body being in the wrong compartments. The compartments are Intracellular Fluid (ICF) - the fluid within the cells, the Extracellular Fluid (ECF) - the fluid outside the cells and the Interstitial Fluid (ISF), which is really the fluid in the microscopic spaces between tissue cells. This also includes Plasma which is the fluid part of the blood.

You also have what is known as Osmotic pressure or osmolarity that is created, so that exchange can take place. This exchange takes place in different forms depending on the place in the body and can occur by osmosis, facilitated diffusion or active transport.

When osmolarity drops for any reason, then oedema will occur. Normally it is Albumin that creates osmolarity and albumin can become low in the course of chronic disease and dietary deficiency. In chronic liver disease, albumin levels will be low and also in renal failure, the same thing can happen.

In renal disease albumin levels are low and because albumin levels are low, fluid is unable to return to the correct compartments within the body and so causes a build up within the tissues of the body, thus creating pitting oedema. This is because there is low osmotic pressure because of the low albumin levels. This is why in patients with renal disease, if their albumin levels are low and they have more fluid weight on board, it is very hard to dialyse this off them without their blood pressure dropping, because all this fluid is all in the tissues. This is why at times, if a patient is dialysing it is advisable to give Albumin across dialysis. This raises the albumin levels and will help the fluid re-enter the correct comparments and this can then be dialysed out without such a dramatic fall in blood pressure and any risk to the patient.

Zep
15th May 2004, 04:05 AM
Corallinus, just a word of caution. Kumar usually trawls through here looking for all sorts of reasons to prop up his, erm, highly unusual and individual views on homeopathy and a thoroughly discredited 18th century remedy system known as "tissue salts". And one of his less endearing charms here is that he acknowledges all the scientific responses he gets from knowlegeable posters, but then completely ignores them and presses on with some incredibly illogical (and, at times, insane) conjectures about how the subject at hand relates to homeopathy and/or his beloved "tissue salts".

We have emplored him already to go find a decent library to pursue his research, either online or in real life, but that doesn't seem to be an option he cares to exercise.

Kumar is a very polite person, thank goodness. However I hesitate to use the words "blindly obsessive" but they are becoming more and more applicable to Kumar as time passes and he persists in repeating this strategy ad nauseum.

Just so you know.

Kumar
15th May 2004, 04:09 AM
Corallinus ,

Many thanks for explaination of pitting oedema. Pitting oedema normally occurs due to fluid in the body being in the wrong compartments. If pitting pretibial oedema is an example to the same? If non pitting oedema will occur due to excess fluid in body but in right compartment or otherwise?

It is sometimes said as; fluid retention or water retention. Are these two are same terms? If non conversion of fluid in water can be a cause of oedema eg. carbohydrate's partial metabolism.

Corallinus
15th May 2004, 04:30 AM
Fluid and water retention refer to the same thing.

Remember also that the inflammatory process is another cause of oedema. Inflammation will cause tissues to swell, where you then get heat, pain, redness, swelling and in some cases, loss of function.

Chronic or Ischaemic heart disease can cause oedema, live disease and renal disease.

Cerebral oedema is also possible and this can follow CVA's of both kinds and trauma. Cerebral trauma can cause bleeding, swelling and raised Intracranial Pressure, which can prove fatal in not controlled and treated.

Also, neurosurgery can cause this too with inflammation occuring following the surgery.

Badly Shaved Monkey
15th May 2004, 05:12 AM
Originally posted by Corallinus
For the differences between the two, you really need to look at the reasons why both happen. That is your answer.

Pitting oedema normally occurs due to fluid in the body being in the wrong compartments. The compartments are Intracellular Fluid (ICF) - the fluid within the cells, the Extracellular Fluid (ECF) - the fluid outside the cells and the Interstitial Fluid (ISF), which is really the fluid in the microscopic spaces between tissue cells. This also includes Plasma which is the fluid part of the blood.

You also have what is known as Osmotic pressure or osmolarity that is created, so that exchange can take place. This exchange takes place in different forms depending on the place in the body and can occur by osmosis, facilitated diffusion or active transport.

When osmolarity drops for any reason, then oedema will occur. Normally it is Albumin that creates osmolarity and albumin can become low in the course of chronic disease and dietary deficiency. In chronic liver disease, albumin levels will be low and also in renal failure, the same thing can happen.

In renal disease albumin levels are low and because albumin levels are low, fluid is unable to return to the correct compartments within the body and so causes a build up within the tissues of the body, thus creating pitting oedema. This is because there is low osmotic pressure because of the low albumin levels. This is why in patients with renal disease, if their albumin levels are low and they have more fluid weight on board, it is very hard to dialyse this off them without their blood pressure dropping, because all this fluid is all in the tissues. This is why at times, if a patient is dialysing it is advisable to give Albumin across dialysis. This raises the albumin levels and will help the fluid re-enter the correct comparments and this can then be dialysed out without such a dramatic fall in blood pressure and any risk to the patient.

Corallinus

This is a competent description of the mechanisms of oedema, but the choice of clinical example is an odd one. You wouldn't be NaturalHealth/Homeoskeptic by any chance?

Corallinus
15th May 2004, 06:06 AM
Why should renal failure be an odd example? I would have thought it was a perfect example of what can happen?

The reason that I chose renal failure as an example was because I had a brother who was diabetic and went into End Stage Renal Failure. He was diagnosed with this as a teenager and of course, being a normal teenage boy, could not cope with it. He just wanted to ignore it and go out with his mates. He would only take his insulin injections if forced to do so by my parents, so consequently, he spent many years with his blood sugars being very poorly controlled.

As a result of all this poor control early on, he went onto develop a lot of the other manifestations of diabetes, which included neuropathy and nephropathy. His renal function started to decrease, until he needed dialysis. He was started on CAPD and did ok on this for a few years, until he started to get repeated infections and they then had to pull his tube and put him onto haemodialysis. He did not do that well on haemodailysis at all and his condition started to deteriorate. I saw him on dialysis many times when he had too much fluid on board. They could not take any of this fluid off until they had given him some albumin across dialysis, as a lot of the time, his albumin levels were so low. He did not really want to eat at all and was not getting enough nourishment because the dialysis normally made him feel so unwell.

My brother was on the transplant list, but a kidney never became available and there were times when he had to be removed from the list because he was just too unwell and would not have survived surgery.

My brother died four years ago now as a direct result of the complications of diabetes, which in his case was ESRF.

This is the reason that I used renal failure as an example, because I have direct experience of this, that was very close to home.

Badly Shaved Monkey
15th May 2004, 07:33 AM
Originally posted by Corallinus
Why should renal failure be an odd example? I would have thought it was a perfect example of what can happen?

The reason that I chose renal failure as an example was because I had a brother who was diabetic and went into End Stage Renal Failure. He was diagnosed with this as a teenager and of course, being a normal teenage boy, could not cope with it. He just wanted to ignore it and go out with his mates. He would only take his insulin injections if forced to do so by my parents, so consequently, he spent many years with his blood sugars being very poorly controlled.

As a result of all this poor control early on, he went onto develop a lot of the other manifestations of diabetes, which included neuropathy and nephropathy. His renal function started to decrease, until he needed dialysis. He was started on CAPD and did ok on this for a few years, until he started to get repeated infections and they then had to pull his tube and put him onto haemodialysis. He did not do that well on haemodailysis at all and his condition started to deteriorate. I saw him on dialysis many times when he had too much fluid on board. They could not take any of this fluid off until they had given him some albumin across dialysis, as a lot of the time, his albumin levels were so low. He did not really want to eat at all and was not getting enough nourishment because the dialysis normally made him feel so unwell.

My brother was on the transplant list, but a kidney never became available and there were times when he had to be removed from the list because he was just too unwell and would not have survived surgery.

My brother died four years ago now as a direct result of the complications of diabetes, which in his case was ESRF.

This is the reason that I used renal failure as an example, because I have direct experience of this, that was very close to home.

Fair enough. And I'm sorry that the basis for the experience was so sad.

Kumar
15th May 2004, 08:17 AM
Corallinus,

Sorry, it is so sad to read it. Somethig to be done for this, is badly required. I have also seen similar cases but here this albunim theory seen to be not much in practice. However, one big hospital has given human albunim to one diabetic patient on start of dialysis, but I don't know how much this has effected, but patients was better afterwords. Now coming to the point, what do you say that what can be the effect if carbohydrates are partly metabolized & not converted in CO2+water. Can it be one cause of fluid retention? Oxygen defficiency/availability due to current environment can be a reason for this improper metabolism of carbs. Btw, if acidity as in lactic,keto or uremia are linked to diabetes & root cause may be O2 deficiency/bio-availability.

Just for this:


One diabetic patient with central obesity, excess weight, persistance high blood sugar levels got pre-tibial edema after he started insulin & oral medicines. All other possible kidney,liver, heart etc. tests were normal. Doctors told it is due to diabetic medications. Other related agencies could not tell any other reasons. After studying tissue salts--one remedy was for ' it creates water in system' by metabolizing lactic acid into CO2 & water. When he taken this remedy-- his pretibial edema got cleared, 7/8 kg weight reduced, central obesity reduced, BS levels improved, urine out put increased, breathing, acidity improved etc.

Corallinus
15th May 2004, 09:16 AM
Kumar,

Firstly, thank you. Yes, this was a very sad event for me and the rest of my family.

Unfortunately, we still do not really know for sure what causes diabetes. There is definitely a genetic link and in Type II diabetes, their are dietary links and obesity too that can be factors. It is thought that some viruses may cause it, with Type I diabetes being an auto-immune disorder, where the Islets in the pancreas responsible for insulin production are attacked and killed by the body's own cells.

Anyway, renal anemia is caused because there is no EPO to stimulate the production of red blood cells. EPO is produced by the kidney as a direct response to falling oxygen levels in the blood. This EPO then stimulates the bone marrow to produce more red blood cells. It does this and the oxygen levels rise again, so EPO production is then 'switched' off. This is a very good example of a negative feedback system within the body. Blood sugar control and regulation is an example of a negative feedback system too.

Basically, the low oxygen levels that you mention are controlled within the body by the kidneys. Oxygen levels fall and this is sensed by receptors. The kidney then releases EPO. EPO then stimulates the bone marrow to produce more red blood cells. This is done, so oxygen levels then rise.

What you are talking about, low levels of oxygen in the environment is a different matter altogether. This is to do with pressure and the levels that you live at. If you live somewhere that is at sea level, then you are ok. If you live somewhere that is above, then oxygen levels are likely to be low. It is to do with altitude and that is why athletes go and train at high altitude because there is less oxygen and they can then adapt and increase their fitness levels. They come back a couple of weeks before an event and because they have trained at high altitude, they are fitter and can run faster. This is to do with the body's adaptation mechanisms. It is the same process, where the oxygen levels are low, so the kidneys produce more EPO in response to this and new red blood cells are made and this then produces more oxygen within the body.

Carbohydrate is only one source of energy that the body uses. It is a quick source of energy and is metabolised by the liver. You can also use fats and proteins as energy too and these are metabolised by the liver too.

In Type I diabetes, it is not to do with the carbohydrate metabolism as such, but the lack of insulin within the body to allow the cells to use this glucose as an energy form that is the problem.

Insulin needs to attach to carrier molecules, normally proteins to cross the cell membrane. If there is no insulin getting into the cells, then the body will be unable to utilise glucose as an energy source. In the absence of this energy source, the body then breaks down fats, proteins and at times muscle tissue as a source of energy - ATP.

This is why, before people are diagnosed, they can eat enormous quantities of food and will still lose weight, because their body cannot utilise this. They will eat fast amounts and still be hungry. They will also have increased thrist and polyurea due to the high levels of glucose cirulating in the system.

Badly Shaved Monkey
15th May 2004, 12:43 PM
Originally posted by Kumar
One diabetic patient with central obesity, excess weight, persistance high blood sugar levels got pre-tibial edema after he started insulin & oral medicines. All other possible kidney,liver, heart etc. tests were normal. Doctors told it is due to diabetic medications. Other related agencies could not tell any other reasons. After studying tissue salts--one remedy was for ' it creates water in system' by metabolizing lactic acid into CO2 & water. When he taken this remedy-- his pretibial edema got cleared, 7/8 kg weight reduced, central obesity reduced, BS levels improved, urine out put increased, breathing, acidity improved etc.

Are we finally getting somewhere? Is this your own history and is this the basis from which all these discussions spring? If so then we can talk in more specific terms than the wild speculations about silica and cosmic rays

Kumar
15th May 2004, 07:57 PM
Originally posted by Corallinus

..Anyway, renal anemia is caused because there is no EPO to stimulate the production of red blood cells. EPO is produced by the kidney as a direct response to falling oxygen levels in the blood. This EPO then stimulates the bone marrow to produce more red blood cells. It does this and the oxygen levels rise again, so EPO production is then 'switched' off. This is a very good example of a negative feedback system within the body. Blood sugar control and regulation is an example of a negative feedback system too.

Basically, the low oxygen levels that you mention are controlled within the body by the kidneys. Oxygen levels fall and this is sensed by receptors. The kidney then releases EPO. EPO then stimulates the bone marrow to produce more red blood cells. This is done, so oxygen levels then rise...

Thanks for explaination in detail. Relationship among Albumin-fluid , EPO-O2-RBC is a new information & it attracts me because it may be having some relations with calcium phosphate.

However I was willing to know relationship between-- partial/mis metobolism of carbs-acidosis-Oxygen levels-oedema & persistance of high blood sugar.

Furthur, is it true that a diabetic patients persist for high BS levels if their lipids are on lower side of normal range OR if blood is thin (hematocrit about 40) it persist BS at higher levels & likely to cause less diabetic complications?

BSM, This is one aspect. You can go ahead for the discussion on this in this thread or in other thread.

Kumar
19th May 2004, 01:26 AM
Originally posted by Corallinus
For the differences between the two, you really need to look at the reasons why both happen. That is your answer.

Pitting oedema normally occurs due to fluid in the body being in the wrong compartments. The compartments are Intracellular Fluid (ICF) - the fluid within the cells, the Extracellular Fluid (ECF) - the fluid outside the cells and the Interstitial Fluid (ISF), which is really the fluid in the microscopic spaces between tissue cells. This also includes Plasma which is the fluid part of the blood.

You also have what is known as Osmotic pressure or osmolarity that is created, so that exchange can take place. This exchange takes place in different forms depending on the place in the body and can occur by osmosis, facilitated diffusion or active transport.

When osmolarity drops for any reason, then oedema will occur. Normally it is Albumin that creates osmolarity and albumin can become low in the course of chronic disease and dietary deficiency. In chronic liver disease, albumin levels will be low and also in renal failure, the same thing can happen.

Corallinus,

You have told that " Pitting oedema normally occurs due to fluid in the body being in the wrong compartments". Can you pls tell me that pitting oedema occurs due to excess fluid in which compartment out of ICF, ECF & ISF compartments. I think excess NaCl & blood gulucose are two main causes of fluid retention(don't take organs problem as kidney, liver, heart etc. here). Can any other body's biochemical also cause fluid retention?

Corallinus
19th May 2004, 02:13 AM
The pitting oedema is a result of the fluid being in the tissues when it should not be. The fact that this fluid can leak out is due to the reduced osmotic pressure which keeps it in the correct compartments.

Also remember that salt and water follow each other.

Rolfe
19th May 2004, 02:21 AM
Can somebody clarify something for me? (I should know this, but it's a small blind spot.) As far as I know, there's no such thing as "non-pitting oedema". Oedema pits, that's how you recognise it. If it doesn't pit, it's swelling, inflammation, haematoma, something else.

The two main causes are hypoproteinaemia, where lack of the osmotic pressure normally provided by the plasma proteins means that water isn't being retained in the circulation but collects in the tissues; and congestive heart failure, where the circulation is so poor that again water pools in the tissues. And as Corallinus said, salt balance is very important too. You can also get localised oedema due to impaired local circulation, such as a touriquet, and horses will show it if they're inactive for a whole as their circulation relies quite a lot on movement of muscles to keep things moving.

But so far as I know, the definition of oedema is that it pits.

Rolfe.

Pantastic
19th May 2004, 04:16 AM
Originally posted by Rolfe
Can somebody clarify something for me? (I should know this, but it's a small blind spot.) As far as I know, there's no such thing as "non-pitting oedema". Oedema pits, that's how you recognise it. If it doesn't pit, it's swelling, inflammation, haematoma, something else.

The two main causes are hypoproteinaemia, where lack of the osmotic pressure normally provided by the plasma proteins means that water isn't being retained in the circulation but collects in the tissues; and congestive heart failure, where the circulation is so poor that again water pools in the tissues. And as Corallinus said, salt balance is very important too. You can also get localised oedema due to impaired local circulation, such as a touriquet, and horses will show it if they're inactive for a whole as their circulation relies quite a lot on movement of muscles to keep things moving.

But so far as I know, the definition of oedema is that it pits.

Rolfe.

You do indeed get pitting and non-pitting oedema. Oedema itself is simply an accumulation of fluid in the tissues, such as by the mechanisms you describe, and is pitting. However, oedema caused by damage, obstruction, or loss of the lymphatic channels causes lymphoedema, which does not pit, which is how you tell it apart. I don't know the precise mechanism, but I do know it's very complicated.

Badly Shaved Monkey
19th May 2004, 04:28 AM
Originally posted by Rolfe
But so far as I know, the definition of oedema is that it pits.

Rolfe.

Now you've gone and spoilt things, but I do agree with you.

"...and congestive heart failure, where the circulation is so poor that again water pools in the tissues....You can also get localised oedema due to impaired local circulation, such as a touriquet, and horses will show it if they're inactive for a whole as their circulation relies quite a lot on movement of muscles to keep things moving."

I think the generic term for this would be hydrostatic. There are three mechanisms at work- osmosis acting on concentration via a semi-permeable membrane, membrane permeability and pressure. Everything else is a subset of one of these classes or a combination thereof.

(An example of increased permeability leading to oedema would be in an inflammatory response like a classic urticarial reaction- increased membrane permeability but COP constant. There may also be a pressure component because of microvascular dilatation, but we'd need an expert to confirm that).

Badly Shaved Monkey
19th May 2004, 04:36 AM
Originally posted by Pantastic


You do indeed get pitting and non-pitting oedema. Oedema itself is simply an accumulation of fluid in the tissues, such as by the mechanisms you describe, and is pitting. However, oedema caused by damage, obstruction, or loss of the lymphatic channels causes lymphoedema, which does not pit, which is how you tell it apart. I don't know the precise mechanism, but I do know it's very complicated.

Well, in that case I've learnt something new.

Badly Shaved Monkey
19th May 2004, 04:45 AM
Pantastic

Except, without wanting to turn this into an exercise in semantics, I think in my casual clinical usage 'oedema' is pitting oedema whereas non-pitting oedema would always be better describe by some other term.

I feel this could descend into more pedantry than I want to engage in on a sunny day with the garden and a glass of beer beckoning.

Rolfe
19th May 2004, 04:53 AM
Originally posted by Badly Shaved Monkey
Except, without wanting to turn this into an exercise in semantics, I think in my casual clinical usage 'oedema' is pitting oedema whereas non-pitting oedema would always be better describe by some other term.I think Pantastic is probably right, strictly and technically, but so are you in a general sense.

If you meant lymphoedema, or myxoedema come to that, you'd usually say that specifically. Just using the term "oedema" unqualified would normally mean the pitting sort. I think.

Where does myxoedema fit here anyway? I'm not in hypothyroidism gear right now.

Rolfe.

Pantastic
19th May 2004, 05:08 AM
I would agree that oedema used on its own would invariably refer to the pitting variety, and lymphoedema etc would be used for those specific types.
The question was asking specifically if oedema was defined by the fact that it pits, which it's not.

Rolfe
19th May 2004, 05:27 AM
Originally posted by Pantastic
I would agree that oedema used on its own would invariably refer to the pitting variety, and lymphoedema etc would be used for those specific types.
The question was asking specifically if oedema was defined by the fact that it pits, which it's not. I wasn't very clear in my question, and you've clarified this very well. Thank you.

Rolfe.

Kumar
19th May 2004, 07:19 AM
Hello all,

Thanks for postings. Oedema can be pitting & non pitting types. Lymphedema is a seprate issue. Just read at:

http://www.nlm.nih.gov/medlineplus/ency/article/003103.htm

http://www.nlm.nih.gov/medlineplus/ency/article/001117.htm

But I want to know that why it is pitting & non pitting. I think fluid in differant compartments may be a valid logic for the same. But fluid in which compartment causes which type of oedema is important to know. Furthur which substance is responsible for which type of oedema is another aspect to know it. If Acidosis is linked to oedema?

Corallinus
19th May 2004, 10:53 AM
Kumar,

There are lots of substances that can be involved in oedema. For example, the inflammatory process can cause oedema, so inflammatory factors that migrate to the area of inflammation in the tissues will cause oedema. That is the inflammatory process with heat, redness, swelling (oedema), pain and loss of function.

Kumar
20th May 2004, 03:05 AM
Corallinus,

It is okay but I am not asking the causes of oedema but I am asking the cause of pitting & non pitting oedema i.e. fluid in which compartment is responsible for showing pitting or non pitting oedema. As per my thinking : there should be three conditions; 1. excess ECF--may be linked to pitting type. 2. Excess ISF--??. 3. Excess ICF--may be linked to non pitting type. I can't say much but just varify it. Just also varify if NaCl can be responsible for excess ICF( can be ISF also) hypertension, heart problems or organic problems, alkaliosis etc. AND gulucose or partial metabolism of carbohydrates is responsible for excess ECF(can be ISF also) diabetes, acidosis etc.

Rolfe
20th May 2004, 04:20 AM
Kumar, ECF = interstitial fluid + lymph + blood plasma. Pitting oedema is caused by an excess of interstitial fluid, though usually there will be some excess of all three components involved.

Pantastic has explained, I think, that oedema caused by an accumulation of lymph is non-pitting - lymphoedema (is that right, Pantastic, I'm slightly rusty on that aspect).

Excess of intracellular fluid ain't gonna happen in this context, if it does to any significant extent I have this horrible vision of cells swelling and bursting all over the place and it's very messy and very fatal. Certain nasty things can happen to the brain due to hyponatraemia or hypernatraemia or over-enthusiastic correction of these, due to sudden and catastrophic fluid shifts between compartments, but that's a separate issue I think.

Honestly, if you want to understand this stuff, there are some very good basic physiology and biochemistry textbooks around, why not get hold of one and have a good read? You might be better-informed than me by the time you got to the end!

Rolfe.

Corallinus
20th May 2004, 04:35 AM
Yes, books that I would recommend are Elaine N Marieb Human Anatomy and Physiology and also Netter's Atlas of Human Physiology. The Netter will give you diagrams with all the biochemistry included and Marieb is great for good all round and uncomplicated explanations of things. Good diagrams too.

Pantastic
20th May 2004, 05:21 AM
Originally posted by Rolfe
Pantastic has explained, I think, that oedema caused by an accumulation of lymph is non-pitting - lymphoedema (is that right, Pantastic, I'm slightly rusty on that aspect).


Indeed it is. Impaired lymphatic drainage = lymphoedema. This is non-pitting and hence distinguishable from other causes of oedema.

Badly Shaved Monkey
20th May 2004, 06:53 AM
Originally posted by Pantastic


Indeed it is. Impaired lymphatic drainage = lymphoedema. This is non-pitting and hence distinguishable from other causes of oedema.

But I think that Kumar is actually asking why the non-pitting type doesn't pit.

Why any of this matters to him is a mystery known only to him, but I'd also be quite interested in knowing what makes one type pit and not another.

Kumar
21st May 2004, 11:43 AM
Originally posted by Kumar
Corallinus,

It is okay but I am not asking the causes of oedema but I am asking the cause of pitting & non pitting oedema i.e. fluid in which compartment is responsible for showing pitting or non pitting oedema. As per my thinking : there should be three conditions; 1. excess ECF--may be linked to pitting type. 2. Excess ISF--??. 3. Excess ICF--may be linked to non pitting type. I can't say much but just varify it. Just also varify if NaCl can be responsible for excess ICF( can be ISF also) hypertension, heart problems or organic problems, alkaliosis etc. AND gulucose or partial metabolism of carbohydrates is responsible for excess ECF(can be ISF also) diabetes, acidosis etc. Just refine it again.

Rolfe
21st May 2004, 01:40 PM
Originally posted by Rolfe
Kumar, ECF = interstitial fluid + lymph + blood plasma. Pitting oedema is caused by an excess of interstitial fluid, though usually there will be some excess of all three components involved.

Pantastic has explained, I think, that oedema caused by an accumulation of lymph is non-pitting - lymphoedema (is that right, Pantastic, I'm slightly rusty on that aspect).

Excess of intracellular fluid ain't gonna happen in this context, if it does to any significant extent I have this horrible vision of cells swelling and bursting all over the place and it's very messy and very fatal. Certain nasty things can happen to the brain due to hyponatraemia or hypernatraemia or over-enthusiastic correction of these, due to sudden and catastrophic fluid shifts between compartments, but that's a separate issue I think.

Honestly, if you want to understand this stuff, there are some very good basic physiology and biochemistry textbooks around, why not get hold of one and have a good read? You might be better-informed than me by the time you got to the end!

Rolfe. Interstitial fluid is a part of the ECF, not a separate compartment, for a start. And you can forget about excess intracellular fluid in this context, it's not relevant.

Rolfe.

Kumar
21st May 2004, 11:26 PM
Thanks all for trials but things are not yet clear. Rolfee, do you say that there can not be any possibilty of excess fluid in IC? Can it be possible to retain more fluid due to its more association(water not disassociated due to any reason) with other body substances & remained attached in form of fluid OR due to presence of excess cells.

Water & Fats seems to be two major substances in body which makes or look like a person 'fat'.

Corallinus
22nd May 2004, 12:48 AM
Kumar,

If there was excesss fluid inside cells, then they would swell so much that they would burst.

Also, you are not likely to have any cells which are excess. Have you ever heard of apoptosis? This is programmed cells death and happens in the body. Cells are replicating all the time so you are never likely to have excess cells as you call them.

One instance where you would get uncontrolled replication of cells and excess cells would be in cancer. This is a disease state though and in a normal state of health, this would not happen.

Kumar
28th May 2004, 02:27 AM
Corallinus,

If it is not, then the question is still there --what makes one type pit and not another?

Kumar
29th May 2004, 08:31 AM
Originally posted by Corallinus
Kumar,

If there was excesss fluid inside cells, then they would swell so much that they would burst.



Corallinus,

I read this:

"Reversible Cell Damage

This is where the pathologic changes may be reversed when the stimulus is removed.


Cellular Swelling

This is usually an early and common manifestation of non-lethal hypoxic injury.
This is caused by the failure of Na+, K+-ATPase; resulting in sodium entering the cell and potassium leaving, and an isosmotic gain of water.
The endoplasmic reticulum balloons out as does the mitochondria.
This increase in water volume is known as "hydropic change" or "vacuolar change" if there is a formation of vacuoles.
These changes are reversible if oxygenation is restored. "

Can you comment on this in consideration of your above quote.

flume
29th May 2004, 09:03 AM
Originally posted by Kumar
This is caused by the failure of Na+, K+-ATPase; resulting in sodium entering the cell and potassium leaving, and an isosmotic gain of water.


Have you read about what Na+/K+ ATPase is and where it's located and why it is important to cell function?
Have you read about the cell membrane and about the different concentrations of Na+ and K+ inside the cells compared to outside the cells?

Kumar
29th May 2004, 10:46 AM
Flume,

It is mentioned here. (http://www.geocities.com/medinotes/response_cell_injury.htm)

flume
29th May 2004, 11:21 AM
Originally posted by Kumar
It is mentioned here. (http://www.geocities.com/medinotes/response_cell_injury.htm)
Yes, but do you yourself understand what Na+/K+ATPase is and what it does in cell membranes?

In another thread you were asking about the amount of Na+ and K+ in different tissues. The important difference is between the amounts inside the cells and outside the cells. If you're interested in the role of Na+ and K+ in the body, you would want to know what different things are involved in keeping the intracellular concentrations different from the extracellular concentrations, and at the right amounts. Na+/K+ ATPase is one of those things. (And you might want to read about the control mechanisms for keeping the Na+ and K+ at their normal level in the plasma.)

You asked for a comment, but I don't see the point of a comment, if you don't know how the system works.

Corallinus
29th May 2004, 11:24 AM
Kumar,

What you have just described is commonly known as the sodium/potassium pump. It is an active transport mechanism as it goes against a concentration gradient, going from an area of low concentration to an area of high concentration. It also uses ATP. Sodium would readily enter the cells and potassium would leak out, which is why the concentration must be kept and the sodium/potassium pump pumps out three Na+ to every 2 K+.

However, it is still possible for cells to rupture.

Kumar
29th May 2004, 09:14 PM
Flume, Corallinus,

I am just intresting to know what makes oedema one type pit and not another? If cellular swelling is related to oedema(may be non pitting) or not? I got a related referance & mentioned here for your comments on the same.

What does it mean?

Chronic Leg Edema (Brawny edema)
Tissue becomes fibrotic and fails to pit.


See here. (http://www.fpnotebook.com/REN15.htm)

Corallinus
30th May 2004, 02:16 AM
Kumar,

Fibrosis is something that is different. When trauma occurs the body will try to re-generate. It some cases, re-generation can be achieved and is successful, however, in other cases this is not possible, so the next best thing to do is repair. Repair will cause fibrosis from the fibrin that is used to heal.

Fibrin is a hard and collagenous material, so because of this it is likely to cause oedema that feels hard, but does not pit, as there is no fluid involved. It is normally the excess fluid that will make the oedema pit. If the excess fluid is not there, then oedema can be present, but without the pitting.

Trauma is an example of this, where the inflammatory process is involved. This would cause oedema without the pitting due to the inflammatory process. Cellulitis of the calf could be a cause of this also.

Kumar
30th May 2004, 03:18 AM
Originally posted by Corallinus
Kumar,

Fibrin is a hard and collagenous material, so because of this it is likely to cause oedema that feels hard, but does not pit, as there is no fluid involved. It is normally the excess fluid that will make the oedema pit. If the excess fluid is not there, then oedema can be present, but without the pitting.

Trauma is an example of this, where the inflammatory process is involved. This would cause oedema without the pitting due to the inflammatory process. Cellulitis of the calf could be a cause of this also. If no fluid is involved as you mentioned how it can be called as oedema?

Are you sure that trauma, inflamation or cellulitis do not causes pitting oedema & are these intracellular effects or EC?