Critical Care Therapies
The information contained in this page is intended for U.S. healthcare professionals only.
Baxter's critical care therapies includes albumin which is primarly used as plasma-volume replacement therapy for the treatment of hypovolemia, Hypoalbuminemia, Burns, Adult Respiratory Distress Syndrome, Nephrosis, Cardiopulmonary Bypass Surgery, Hemolytic Disease of the Newborn.
Human albumin is an essential protein found in human plasma and accounts for about 50%-60% of plasma proteins.1 Each molecule is composed of three units, or domains, which function together to give albumin its unique binding properties.3 It is the primary agent responsible for maintaining osmotic pressure of the blood, and for transport of fatty acids, hormones, enzymes, and therapeutic drugs.2
Albumin is primarily responsible for 75%-80% of plasma's normal colloid oncotic pressure.1 Albumin supplementation restores intravascular volume and maintains cardiac output and colloid osmotic pressure. When plasma volume is drastically reduced, albumin can help restore the losses.1
Hypovolemia is a possible indication for albumin. Its effectiveness in reversing hypovolemia depends largely upon its ability to draw interstitial fluid into the circulation. It is most effective with patients who are well hydrated.
When hypovolemia is long standing and hypoalbuminemia exists accompanied by adequate hydration or edema, 25% albumin is preferable to 5% protein solutions. However, in the absence of adequate or excessive hydration, 5% protein solutions should be used or 25% albumin should be diluted with crystalloid.
Although crystalloid solutions and colloid-containing plasma substitutes can be used in emergency treatment of shock, albumin has a prolonged intravascular half-life. When blood volume deficit is the result of hemorrhage, compatible red blood cells or whole blood should be administered as quickly as possible.4
Hypoalbuminemia can result from one or more of the following:
(1) Inadequate production (malnutrition, burns, major injury, infections, etc.)
(2) Excessive catabolism (burns, major injury, pancreatitis, etc.)
(3) Loss from the body (hemorrhage, excessive renal excretion, burn exudates, etc.)
(4) Redistribution within the body (major surgery, various inflammatory conditions, etc.)
When albumin deficit is the result of excessive protein loss, the effect of administration of albumin will be temporary unless the underlying disorder is reversed. In most cases, increased nutritional replacement of amino acids and/or protein with concurrent treatment of the underlying disorder will restore normal plasma albumin levels more effectively than albumin solutions. Occasionally hypoalbuminemia accompanying severe injuries, infections or pancreatitis cannot be quickly reversed and nutritional supplements may fail to restore serum albumin levels. In these cases, albumin human serum might be a useful therapeutic adjunct.4
An optimum regimen for the use of albumin, electrolytes and fluid in the early treatment of burns has not been established, however, in conjunction with appropriate crystalloid therapy, albumin may be indicated for treatment of oncotic deficits after the initial 24 hour period following extensive burns and to replace the protein loss which accompanies any severe burn.4
Adult Respiratory Distress Syndrome (ARDS)
A characteristic of ARDS is a hypoproteinemic state, which may be causally related to the interstitial pulmonary edema. Although uncertainty exists concerning the precise indication of albumin infusion in these patients, if there is a pulmonary overload accompanied by hypoalbuminemia, 25% albumin solution may have a therapeutic effect when used with a diuretic.4
Albumin may be a useful aid in treating edema in patients with severe nephrosis who are receiving steroids and/or diuretics4.
Cardiopulmonary Bypass Surgery
Albumin has been recommended prior to or during cardiopulmonary bypass surgery, although no clear data exist indicating its advantage over crystalloid solutions. 4
Hemolytic Disease of the Newborn (HDN)
Albumin may be administered in an attempt to bind and detoxify unconjugated bilirubin in infants with severe HDN.4
Protein C Deficiency Therapy
Other critical care therapies include Protein C for patients with severe congenital Protein C deficiency.
Protein C is an anticoagulant protein that plays an important role in the regulation of hemostasis, providing a natural mechanism to control the coagulation system response. A severe deficiency of Protein C causes a defect in the control mechanism and leads to unchecked coagulation activation, resulting in thrombin generation and intravasuclar clot formation with thrombosis.
Two types of congenital Protein C deficiency have been identified.
- Homozygous: Severe congenital Protein C deficiency is most often caused by a homozygous genetic defect, inherited as an autosomal recessive trait. It may result in thrombotic events in utero or manifest soon after birth with purpura fulminans and cerebral/retinal thrombotic complications. If left untreated, the thrombotic complications can result in blindness, severe brain damage, multi-organ failure, and death.5 Incidence of homozygous Protein C deficiency is approximately 1 to 2 for every 1,000,000 births.6
- Heterozygous: The incidence of heterozygous Protein C deficiency is estimated at 1 in every 200-300 births.7
Heterozygous Protein C deficiency is inherited in an autosomal dominant
mode and is a weak risk factor for thrombosis, which does not usually
become manifest until later in life.8
Double heterozygous defects can also result in severe congenital Protein C deficiency.5
Intravenous Beta Blocker
The portfolio also includes the very short-acting cardioselective β1-adrenergic blocker BREVIBLOC PREMIXED Injection (esmolol HCI) in ready-to-use bags and BREVIBLOC Injection (esmolol HCI) in vials.
1. Gonzalez ER, Kannewurf B. The clinical use of albumin. US Pharmacist. 1998;23:HS15-HS26.
2. Peters T, Jr. The Plasma Proteins: Structure, Function, and Genetic Control. Academic Press; 1975;1(2):133-181.
3. Doweiko JP, Nompleggi DJ. Role of albumin in human physiology and pathophysiology. Journal of Parenteral and Enteral Nutrition. 1991;15:207-11.
4. FLEXBUMIN Prescribing Information. Westlake Village, CA: Baxter Healthcare Corporation; February 2006.
5. Moritz B, Rogy S, Tonetta S, Schwarz HP, Ehrlich H and the CEPROTIN Study Group. Efficacy and Safety of a High Purity Protein C Concentrate in the Management of Patients with Severe Congenital Protein C Deficiency. In: Scharrer I, Schramm W, ed. 31st Hemophilia Symposium Hamburg 2000. Berlin Heidelburg: Springer-Verlag; 2002: 101-109.
6. Salonvaara M, et al. Diagnosis and treatment of a newborn with homozygous protein C deficiency. Acta Paediatr 2004; 93:137-139.
7. Miletich JP, Sherman LA, Broze GJ. Absence of thrombosis in subjects with heterozygous protein C deficiency. New England Journal of Medicine.
8. Dreyfus M, et al. Replacement Therapy with Monoclonal Antibody Purified Protein C Concentrate in Newborns with Severe Congenital Protein C Deficiency. Seminars in Thrombosis and Hemostasis. 1995; 21(4): 371-381.