Why are colloids such as albumin given to produce volume expansion then?
The physiology of albumin and colloid osmotic pressure is a long and complicated and still widely misunderstood story.
About a century ago Starling pointed out that the flux of water from plasma to and from tissues would depend on hydrostatic and osmotic pressures across blood vessel walls and wrote the 'Starling equation'. The medical community misread what he said and assumed that normal people do not have oedema because the equation was in balance. In fact the equation is never anywhere near balanced.
The implications of this are very complicated but the most misunderstood is that the protein level in the blood (which is almost half albumin) makes very little difference to oedema. The oedema seen with low albumin levels is due to other reasons - probably chiefly vessel permeability in renal disease and venous obstruction in liver disease.
Because doctors thought that oedema was due to low albumin they often would infuse albumin to 'correct' this. And since albumin is a blood product they the changed to artificial colloids. However, about twenty years ago, if my memory is right, a Canadian intensive care unit decided to do a study to see how much albumin infusions contributed to improved survival. They found it made survival significantly worse. It is true that infused colloid will stay in the circulation a bit longer than just saline, but the effect is lost after just a few hours so for most situations it is a waste of time. The problem is that fewer than 1% of doctors know enough about fluid balance physiology to understand the reasoning behind this so colloids still get given in lots of situations where they are no use. (I know all this partly because I spent five years working on fluid transport in joint tissue and got involved in the detailed analysis of what experiments actually show.)
Testing for albumin levels comes as part of the most standard chem path screen and is traditionally listed under 'liver function tests' because a low albumin tends to indicate liver disease, although it can also indicate kidney disease. Low levels indicate that the liver is not synthesising enough albumin to keep levels up. This is probably usually due to a change in the liver feedback control so there is no point in giving albumin - the liver will just destroy it. And destroying albumin will raise urea (giving uremic coma for renal failure) or ammonia (hepatic coma for hepatic disease).
High albumin levels do not mean much in terms of chronic disease - I cannot think of an example. However, albumin levels will go high if a person becomes
relatively dehydrated in comparison to
what they were a day or two before. So it is not an indication of continuous dehydration and certainly not of hypovolaemia, which is something different. It indicates short term drying out. If albumin is high for more than a day or two the liver will bring it down again.
The bottom line is that serum albumin is really of no interest at all in ME, as far as I can see. It can be an indication of dehydration in old people found alone after a stroke who have drunk nothing for two days but that's about it. And dehydration is not really the issue - the issue is whether it is associated with functional hypovolaemia - i.e. blood volume less than suited to the blood vessel tone. The best ways to tell that are a clinical JVP measurement, backed up by CVP line if there is concern, and urine output and concentration in the face of known fluid intake.
Forget albumin folks!