Hypoalbuminemia in Critical Illness

Hypoalbuminemia in critical illness is caused by:

1. Decreased hepatic production.

2. Redistribution into the extravascular space.

3. Dilution due to fluid administration.

Low serum albumin is a non specific marker of disease. A fall in the albumin concentration appears to reflect deterioration, and a rise, recovery. Very low levels of albumin appear to reflect a poor outcome. The relevance of low albumin on ligand binding is unknown.

The serum albumin falls when patients become sick, and comes back up when patients get better.

What is the role of a low serum albumin in the acute inflammatory response? Are there any other markers that behave in a similar way?

The liver stops producing albumin in critical illness: low albumin is a non specific marker of disease.

In critical illness there is a reduction in the production of albumin, due to favored hepatic production of acute phase proteins such as globulins, fibrinogen and haptoglobin. Other proteins whose levels fall in this situation include pre-albumin, retinal-binding protein, transferring and somatomedian C. Although all intensive care patients are essentially different, the inflammatory cascade in many patients leads to a common pathway, causing a generalized increase in vascular permeability (“capillary leak syndrome”). This leads to leakage of protein rich fluid into the interstitium. This appears to be the primary cause of decreased serum albumin in sepsis.

Soni “serum albumin may be considered a non-specific marker of disease process and changes to its value are the result of pathological events rather than the cause of them.” So a low serum albumin (and probably prealbumin) is a negative acute phase response.

Does a low serum albumin mean that the patient will become edematous?

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

The formation of edema is determined by:

1. The rate of fluid flux
2. The clearance of fluid by lymphatics.

In critical illness, there is a stronger correlation between colloid oncotic pressure and total protein than with albumin. In these patients the decreased albumin is compensated for by an increase in acute phase proteins.  Nonetheless, there is increased leakage of albumin and this drags fluid with it. The overall fluid flux is less than would be predicted if albumin was the only protein responsible for oncotic pressure in the Starling equation.

Lymphoid function is important - if it is overwhelmed by increased capillary permeability or fluid flux, then edema will occur. It is likely that lymphoid dysfunction plays a significant role in edema formation in critical illness. There has been some speculation that lymphoid dysfunction is caused by free radicals

In summary: low serum albumin does not necessarily mean low plasma oncotic pressure, and does not always cause edema.

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