Albumin, the EGL, vascular permeability and trout fishing.

Jon-Emile Kenny is a New York physician who has recently joined the FOAMEd movement, and is opening his PulmCrit account with a blast around the steady-state Starling principle.

It seems JE has read RSE&GM 2012 and is concerned about his propensity to prescribe hyperoncotic albumin with furosemide to cirrhotic patients. I am sure he is not alone, so I offer a few thoughts on albumin as a biophysical osmotic therapy. I recall the moment during the writing of RSE&GM 2012 when I searched for an experiment in which plasma volume had been estimated before and after hyperosmotic albumin bolus. The experiment is a difficult one because in traditional clinical measurement the plasma volume is presumed to be the same as the volume of distribution of albumin. (1) My old friends Mike Margarson and Neil Soni had done this experiment at the Chelsea and Westminster Hospital and published in the watershed year of 2004. What they found shocked me; 200 ml of hyperoncotic albumin (20%) increased the plasma volume by 400 ml. (2) Had I been wrong to believe the no-reabsorption rule? I had a sleepless night, but then it occured to me that although the plasma-expanding water must have entered from the EGL, it did not follow that it must have flowed backwards up the transendothelial junction breaks. Eureka! With our RSE&GM glasses on, the fluid had been sucked from the EGL, causing it to compress.  The no-reabsorption rule had survived. In other experiments related to Mike’s Doctoral studies they had shown that albumin transfusion to patients with sepsis has no effect on the transcapillary escape rate of albumin (the Js of albumin in RESE&GM speak). I recall the charismatic Paul Marik telling us in a popular Podcast lecture that albumin is an integral EGL component that contributes to vascular permeability; it is, but as I have previously noted, once the plasma albumin reaches 10g / L the albumin contribution to vascular permeability has reached its maximum. Raising plasma albumin further has no worthwhile effect on vascular permeability, as was neatly demonstrated by Margarson & Soni in 2002. (3) If we are looking to heal the leak that ensues on over-infusion of resuscitation fluids, the answer may lie in PDE IV inhibitors. (4)

As luck would have it, Neil Soni & I are fishing the Rectory Beat today. The waving of ranunculus weed in clear flowing chalkstream can’t fail to convince you of the way EGL responds to free-flowing plasma!

I have also discovered the wonderfully-titled resource, which tells me that my Eureka moment is now accepted wisdom for examination sitters;

  1. Margarson MP, Soni NC. Plasma volume measurement in septic patients using an albumin dilution technique: comparison with the standard radio-labelled albumin method. Intensive Care Med. 2005;31:289-295.
  2. Margarson MP, Soni NC. Changes in serum albumin concentration and volume expanding effects following a bolus of albumin 20% in septic patients. Br J Anaesth. 2004;92:821-826.
  3. Margarson MP, Soni NC. Effects of albumin supplementation on microvascular permeability in septic patients. J Appl Physiol (1985). 2002;92:2139-2145.
  4. Lin YC, Adamson RH, Clark JF, Reed RK, Curry FR. Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume-expanded mice. J Physiol. 2012;590:309-322.


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