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Albumin as compared with nonprotein colloid or crystalloid solutions has not been well addressed in appropriately designed studies. Thus, albumin administration is based on an individual patient’s clinical status. Clinical situations where albumin is commonly administered include replacement fluid for therapeutic plasma exchange (TPE), ovarian hyperstimulation syndrome (OHSS), cirrhosis with spontaneous bacterial peritonitis (SBP), large-volume paracentesis (LVP), nephrotic syndrome, and fluid resuscitation in critically ill patients (e.g., sepsis, acute burns). Alternatives to albumin for plasma expansion include crystalloids (e.g., 0.9% sodium chloride [normal saline], Ringer’s lactate), alternate protein colloids (e.g., plasma protein fraction [PPF]), and nonprotein colloids (e.g., dextran, gelatin, and starches). Crystalloids and nonprotein colloids have not demonstrated a benefit over albumin but are less expensive; however, nonprotein colloids have been associated with adverse effects.
Albumin, the most abundant protein (50%–60%) in human plasma, accounts for 80%–85% of the plasma osmotic pressure and therefore maintains and regulates plasma volume. As a result, albumin infusions draw fluid from the extravascular to intravascular space. Albumin also acts as carrier for other physiologic molecules and administered drugs, provides antioxidant properties, and serves as a buffering molecule with an acidifying effect.
Albumin was initially used as a treatment for shock during World War II, and its use has expanded; however, advantages and disadvantages of albumin have not been well addressed in appropriately designed studies. The Cochrane Collaboration has published systematic reviews of, and recommendations for, albumin use in specific clinical circumstances. Clinical situations where albumin is commonly administered are described below.
Albumin is the primary replacement fluid used during TPE, except in clinical disorders that require specific factors, such as thrombotic thrombocytopenic purpura ( Chapter 73 ).
OHSS usually results from iatrogenic administration of human chorionic gonadotrophin (hCG) to induce ovulation. OHSS is typified by enlarged ovaries, which release vascular endothelial growth factor that can increase capillary permeability, leading to a fluid shift from the intravascular compartment to abdominal/pleural spaces. In the most severe form, OHSS is associated with tense ascites, oliguria, dyspnea, hemodynamic instability, and thromboembolism. Treatment includes fluid restriction, analgesics, and monitoring.
Mild OHSS occurs in ∼33% and moderate to severe OHSS in ∼5% of women receiving hCG. Increased risks include young age, low body weight, polycystic ovarian syndrome, high-dose hCG, high or rapid rise in estradiol level, and previous history of OHSS. In addition, the risk is proportional to the number of developing follicles and oocytes retrieved. Plasma expanders (albumin, hydroxyethyl starch [HES], and mannitol) reduce rates of moderate and severe OHSS in high-risk women; however, albumin may reduce pregnancy rates.
SBP is complicated by type 1 hepatorenal syndrome in 30% of patients. The pathophysiology may be secondary to increased intraperitoneal nitric oxide leading to systemic vasodilation and hypovolemia, resulting in renal vasoconstriction and renal failure. In a randomized trial, albumin infusion with antibiotics versus antibiotics alone decreased renal failure and improved mortality in cirrhotic patients with SBP. Current guidelines recommend albumin administration for all SBP patients at a dose of 1.5 g/kg on day 1 followed by 1 g/kg on day 3 (regimen used in trial).
Albumin is often used in cirrhotic patients undergoing LVP (removal of >5 L) for diuretic refractory ascites to prevent paracentesis-induced circulatory dysfunction. A recent meta-analysis found insufficient evidence that albumin infusion after LVP lowered mortality in patients without hepatocellular carcinoma but with advanced liver disease. Nevertheless, guidelines currently recommend albumin administration.
Nephrotic syndrome occurs secondary to increased permeability of glomerular capillary basement membranes, leading to increased urinary protein excretion and resultant hypoalbuminemia, edema, renal failure, and hyperlipidemia. Primary treatment is mitigation of the underlying cause, diuretic therapy, and a sodium-restricted diet. Albumin combined with diuretics has been used to increase glomerular vascular pressure to increase diuresis; however, recent studies have shown no benefit or worse outcomes including hypertension, respiratory distress, and electrolyte abnormalities. Thus, albumin replacement in nephrotic patients is currently considered second-line therapy.
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