Colloid Solutions (Natural and Synthetic)

Mechanism

Human Albumin (4% and 20%)

Albumin is a soluble natural colloid synthesized exclusively by the liver. It represents approximately 75-80% of the total colloidal oncotic pressure of normal human plasma.

• 4% albumin (Iso-oncotic): It exerts an oncotic pressure of approximately 20 mmHg, equivalent to that of human plasma. Its administration expands the intravascular volume equivalently 1:1 with respect to the infused volume.
• 20% albumin (Hyper-oncotic): Exerts an oncotic pressure of approximately 100 mmHg. When administered, it exerts a powerful trans-interstitial hydrophilic effect, rapidly attracting 4 to 5 milliliters of free water from the interstitial space into the bloodstream for each milliliter of infused solution.

Indicators and dose

Evidence-Based Indications for Albumin

Albumin should not be used routinely as an initial volume expander in general critically ill patients. Its preferred clinical use is limited to indications in decompensated cirrhotic patients with underlying portal hypertension:

1. Large Volume Evacuative Paracentesis: Administer 8 grams of albumin for each liter of ascitic fluid extracted, as long as the total extraction exceeds 5 liters. This prevents post-paracentesis circulatory dysfunction (PPCD), which causes extreme splanchnic vasodilation and secondary prerenal renal failure.
2. Spontaneous Bacterial Peritonitis (SBP): Mandatory infusion of albumin at a dose of 1.5 g/kg of weight at diagnosis (day 1) followed by 1 g/kg of weight on day 3 of clinical evolution. It drastically prevents the development of hepatorenal syndrome and reduces in-hospital mortality.
3. Hepatorenal Syndrome Type 1 (HRS-AKI): Combined treatment with albumin (loading dose of 1 g/kg body weight on the first day followed by 20-40 g/day) together with intravenous terlipressin, closely monitoring the appearance of clinical signs of fluid overload or acute lung edema.

Synthetic Colloids (Starches, Gelatin and Dextrans)

Synthetic colloids, especially hydroxyethyl starches (HES 130/0.4), were designed to mimic the hemodynamic properties of albumin with lower production costs. However, multicenter randomized controlled clinical trials (VIAS, 6S, and CHEST studies) have consistently demonstrated an unacceptable safety profile in critically ill and septic patients.

Security

Toxicity Alert: Renal Failure and Coagulopathy due to HES

The administration of Hydroxyethyl starches (HES) in critically ill patients is formally contraindicated and has an alert of absolute restriction of use by regulatory agencies (EMA and FDA) due to two major adverse effects:

• Nephrotoxicity due to Accumulation of Macromolecules: Unfiltered starch molecules are taken up by pinocytosis by the epithelial cells of the proximal convoluted tubule. Since they cannot be degraded, they accumulate cytoplasmically, inducing osmotic vacuolization, cellular swelling and necrosis of the tubular architecture, significantly increasing the need for renal replacement therapy (dialysis) and 90-day mortality.
• Coagulopathy due to Dilution and Interference of Factors: HES physically interfere with the normal polymerization of fibrin and reduce the plasma availability of the von Willebrand factor complex and factor VIII, inducing a hemorrhagic diathesis that is difficult to reverse.