Albumin; let’s Bust another Myth today.

Earlier today I encouraged my Twitter followers to revisit Gilbert Park’s BJA 2000 Review entitled The role of albumin in critical illness. It was a timely response to Cochrane Injuries Group Albumin Reviewers. Human albumin administration in critically ill patients: systematic review of randomised controlled trials. Br Med J 1998; 317: 235–40.

Gilbert was an early anti-HAS therapist and a very entertaining lecturer. He delivers some great points that every clinical EM/ICU clinician needs to be applying and teaching even today;

“The function of circulating albumin in critical illness is not fully understood. It may differ significantly from that in healthy subjects.”

Never truer than in the story of albumin! But Gilbert, like the rest of us, was yet to appreciate the consequences of revisions of the Starling Principle;

“Each day, 120–145 g of albumin is lost into the extravascular space. Most of this is recovered back into the circulation by lymphatic drainage.”

We have to forgive Gilbert this error, for he knew not that the capillary barrier is asymmetric and that there is a vital circulation of interstitial fluid and albumin from capillary to lymph node or thoracic duct. Extravascular albumin must not be thought of as Lost to the circulation. He then raised this point, which I must admit I had not given much credence to;

“Measurement of total circulating and total exchangeable albumin pools shows a 30% reduction with major surgery, consistent with sequestration of albumin into non‐exchangeable sites, such as wounds, the intestine and extra‐abdominal sites.”

I was recently contacted by a retired anesthesiologist of no small repute who is agonising over what to do with his data set which appears to illustrate the loss of albumin to such a non-exchangeable site, and appears to suggest that choice of anaesthetic technique might influence the extent of such loss. It now looks like we can account for this hypothesised “sequestration of albumin into non‐exchangeable sites” by the fact that colorimetric albumin assay (BCG) greatly underestimates the true albumin concentration during oxidative stress. (doi:10.1371/journal.pone.0159839.g001) The albumin does not get lost in stressful conditions, it just becomes unmeasured. And hence colloid osmotic pressure is higher than we would expect from the lab’s reported [Alb]. Let’s end with two important and Still True statements from Gilbert;

“There is no significant correlation between serum albumin concentration and COP in these patients. Drug binding by albumin is important in critically ill patients, but the increased free fraction of drugs in patients with hypoalbuminaemia does not necessitate treating the decreased serum albumin concentration.”

 

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