Albumin -Key Points

1. Albumin is the most abundant extracellular protein, it’s distribution is primarily intravascular.

2. Albumin has a role in maintaining COP, binding and transport, free radical scavenging, acid base balance, coagulation and vascular permeability.

3. Albumin is measured using BCG or BCP. This overestimates a low serum albumin.

4. Serum albumin concentration falls due to decreased synthesis, increased catabolism, increased loss and redistribution.

5. The serum albumin falls when patients become sick, and comes back up when patients get better. The liver stops producing albumin in critical illness: low albumin is a non specific marker of disease.

6. Edema formation is determined by the rate of fluid flux: COP is determined by  total protein concentration, and the state of the lymphatic system.

7. Hypoalbuminemia is associated with liver and renal disease, PET, SIRS including burns, trauma and surgery.

8. Decreased albumin in adults is a marker of associated disease (a negative acute phase reactant) not a feature of isolated protein-energy malnutrition. It is a poor indicator of nutritional status (so too is prealbumin).

9. Low serum albumin is an independent indicator of (poor) outcome in critical illness.

10. There is no evidence that correcting hypoalbuminemia improves outcome, indeed therapeutic albumin administration may worsen outcome.

A number of strategies have utilized albumin as a therapeutic agent:

• Correcting hypoalbuminemia to improve outcome – no evidence of improvement.
• Using albumin as a hypertonic-hyperoncotic agent to reduce tissue prefusion, with or without diuretics – no evidence of improvement.
• For volume replacement in cirrhosis (spontaneous bacterial peritonitis) – some evidence.
• As the colloid of choice in infants – no evidence either way.
• In burns – no evidence either way.
• Following paracentesis for ascites – no evidence.
• To treat nephrotic syndrome – no evidence.
• As a colloid agent in critical illness: little supportive evidence.