Serum albumin and colloid osmotic pressure in survivors and nonsurvivors of prolonged critical illness

Abstract

SummaryWe retrospectively compared the changes in serum albumin concentration and colloid osmotic pressure between survivors and nonsurvivors of prolonged (Ն7 days) critical illness over a 2-year period from 1 July 1995. All patients had serum albumin measured daily, and colloid osmotic pressure measured 5 days a week, throughout their ICU admission. (survivors); p < 0.01]. Analysis of colloid osmotic pressure results showed no difference between the groups in mean, minimum or recovery mean. Regression analysis of mean colloid osmotic pressure and albumin revealed that albumin only contributed 17% of the colloid osmotic pressure in these patients. The similar decrease in albumin in nonsurvivors and survivors may reflect the acute inflammatory response and/or haemodilution. However, survivors showed an ability to increase serum albumin concentrations, possibly owing to resumption of synthesis. The colloid osmotic pressure varied little between or within either group of patients, possibly because of the use of artificial colloids. There was no relationship between death and colloid osmotic pressure.

Colloid Osmotic Pressure and Osmolality Monitoring

“…In this study, however, artificial colloids could be used as directed by the patients' physicians, and mean COP in all patients was 16.1 mm Hg. 9 This maintained the COP value above the cutoff that had previously been associated with increased mortality. Further research may find that through management of a patient's low COP with artificial colloids and albumin, this risk factor is eliminated in critically ill patients, and therefore the overall chance of survival is improved.…”

Evaluation of noninvasive determinants for capillary leakage syndrome in septic shock patients

“…COP was significantly lower in the CLS patients than in controls at study entrance and remained low after albumin administration, whereas in the controls there was a significantly higher increase in COP after albumin administration than in CLS patients. In normal subjects serum albumin is a main determinant of COP, but in critically ill patients with increased capillary permeability the correlation between serum albumin and COP is poor [24]. Thus implicates that the effect upon the transcapillary COP gradient and fluid shifts is not predictable from serum albumin levels [23].…”

Cytotoxic Edema in Posterior Reversible Encephalopathy Syndrome: Correlation of MRI Features with Serum Albumin Levels

“…However, its contribution toward COP is only 17% in critically ill individuals. 12 Reduction of COP alone would not cause edema in the normal brain tissue, which is largely due to the properties of capillary endothelium that constitute the BBB. 13 The failure of autoregulatory mechanisms involved in the maintenance of CBF might also lead to hyperperfusion and vasogenic edema in the presence of excessive elevations in systemic blood pressure.…”