In humans, albumin makes up for 4/5th of the normal Colloidal Oncotic Pressure which equates to 25 mmHg (1). The high colloidal osmotic pressure was due to its heavy molecular weight and its increased concentration in plasma. Present at a greater concentration than other plasma proteins and still has the greatest osmotic significance (2). This direct osmotic effect dispenses 60% of the oncotic pressure of albumin. The remaining 40% is a consequence of its negative charge, providing an attractive force for the intravascular retention of positively charged solute particles (3). It is the COP gradient across the capillary membrane which is of greater importance in determining fluid shift into the interstitium rather than the absolute plasma value (4). Excess albumin levels prevent the accumulation of excess colloid primarily through increased albumin degradation and albuminuria, rather than changes in albumin synthesis. The exact site of oncotic regulation in albumin synthesis is not clearly understood, but it has been hypothesized to reside within the hepatic interstitial volume (5). Decreased serum colloid osmotic pressure has been observed in critically ill patients post-operatively (6), and reduced colloid osmotic pressure is associated with higher rates of postoperative complications (morbidity and mortality) in surgical patients. (5).