Every now and then, usually when a Renewal bill arrives, I wonder whether it is worth renewing and maybe I should let this web page pass away with dignity. I started teaching the obvious absurdities of biophysical colloid osmotic pressure manipulations (‘therapies’ except that they don’t actually treat anything) about 2010. Then I had my own personal EUREKA moment when I discovered Levick and Michel’s heartfelt cry for recognition by clinicians and fellow physiologists and it all began to make sense. I can’t say it happened in my bath, and I don’t pretend the path to enlightenment was easy. For several days I could not explain how the infusion of 200ml of hyperoncotic albumin could increase the plasma volume by more than 200ml if –
microvascular absorption is transient in most tissues; slight filtration prevails in the steady state, even in venules.Microvascular fluid exchange and the revised Starling principle
March 2010. Cardiovascular Research 87(2):198-210
Mike Margarson and Neil Soni had found in 2004 that –
albumin 20%, 200 ml caused a secondary fluid resorption and volume expansion maximal at 30 min, equivalent to a 430 ml infusion in septic patients and 500 ml in controls.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.
I considered on what measurements they based that statement, and it was haemodilution. So we could now restate the conclusion as
albumin 20%, 200 ml caused a fall in haematocrit maximal at 30 min, which was greater than expected from the infused volume if we presumed that our blood sample was representative of the total intravascular volume.after Margarson & Soni 2004.
Then it struck me that Mike and Neil knew nothing of the intravascular endothelial surface layer that excluded red blood cells and within which infused albumin molecules could become entangled, and from within which a sudden change in COP of the circulating plasma could redistribute water. Their presumption of fluid reabsorption from the interstitium was not justified!
Now I have to jump forward a couple of years, I think it was 2015, when I met Mike at a meeting at the Royal College of Physicians in London. I told him how his paper had nearly caused me to reject practical applications of the revision of the Starling principle. Mike looked down on me (he is rather tall) and replied “We did not say where the resorption of fluid came from”. Which is true… We must also recall that Levick and Michel were talking about steady-state physiology, and were at pains to explain how up to 500 ml of “autotransfusion” is available to a euvolaemic adult when sudden changes in the Starling forces occur. The revised Starling principle is not contradicted by haemodilution studies.
My favoured albumin opinion leaders had always been Gilbert Park at Addenbrookes and Neil Soni at Westminster. Let me share an anecdote that I often recite about Neil. It was a sunny spring morning in Brussels, and I was drinking coffee at a street bar when I saw Neil hurrying along with a cassette loaded with diazo slides. I called him over and asked if he wanted to share a beer later. “Sorry mate, this morning I’m giving a lecture on Why I Use Albumin.” So I suggested meeting later. “Sorry, this afternoon I’m giving a lecture on Why I Don’t Use Albumin, same slides.”
Anyway, I digress. Ashley Miller, who posted the Tweet that I take for the title of this comment, is no mere mortal, he is a talented teacher and is currently a Candidate for office at the Intensive Care Society. My Twitter feed keeps reminding me that we still have a long way to go before we can be confident that most practicing physicians are conversant with Starling physiology, or indeed with modern fluid physiology more broadly. We talk about body water and its distribution, but we less often talk about the circulation of body water and we even more rarely measure or monitor it. The struggle goes on.