The Case for Albumin as Volume Expander and beyond
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Hypoalbuminemia
Serum Albumin
Intravascular volume status
Oncotic pressure
Whether or not the rapid reduction in serum albumin concentration in acute surgical patients without evidence of pre-existing energy deficit correlates with outcome has yet to be studied. In this study, we attempted to determine whether albumin infusion or nutritional supplementation can improve outcome for patients with hypoalbuminemia.We retrospectively reviewed 80 non-calorie-deficient patients newly admitted to the surgical intensive care unit of the Veterans General Hospital-Taipei with complete data for serum albumin concentration and APACHE II score within 24 hours from August, 1998, to February, 1994. The relationships between age, sex, diagnosis, reason for intensive care, albumin infusion, hyperalimentation, APACHE II score, serum albumin concentration, days in intensive care and prognosis within three months were analyzed.Univariate statistical analysis showed that the serum albumin concentration and APACHE II score correlated well with patient survival (p = 0.002 and p = 0.025, respectively). Multivariate analysis showed that hypoalbuminemia was independently associated with patient outcome (p = 0.003). Simple albumin infusion or hyperalimentation for patients with hypoalbuminemia did not improve survival.The results suggest that serum albumin concentration appears to be a good prognostic marker for acute surgical patients. While decreased serum albumin concentration may also reflect poor nutritional status, for patients with moderate to severe hypoalbuminemia due to other causes, simple albumin infusion and/or nutritional support did not significantly improve survival. Consequently, aggressive treatment of the underlying disease is far more important.
Hypoalbuminemia
Serum Albumin
Univariate analysis
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Following onset of acute cardiogenic pulmonary edema in 21 patients, increases in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with decreases in plasma volume. Accordingly, there was a loss of hypo-oncotic fluid into the extravascular spaces. Following treatment with oxygen, furosemide, and morphine sulfate and reversal of clinical and radiographic signs of pulmonary edema, declines in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with increases in plasma volume. Hypo-oncotic edema fluid was therefore reabsorbed into the vascular compartment. The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema. During reversal of acute pulmonary edema with diuresis, there was re-expansion rather than contraction of blood volume.
Oncotic pressure
Intravascular volume status
Vascular permeability
Peripheral edema
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Hypoalbuminemia can be caused by decreased production, increased loss, redistribution, or dilution of albumin. In patients with moderate to severe hypoalbuminemia, fluid accumulation, decreased plasma volume, and thromboembolism may result. Treating the underlying disease process responsible for hypoalbuminemia is the most important factor in manag- ing hypoalbuminemic patients. However, nutritional support, adjustment of medications, prevention of thromboembolism, and maintenance of ade- quate colloid oncotic pressure are important as well. ABSTRACT:
Hypoalbuminemia
Oncotic pressure
Serum Albumin
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Albumin can quickly expand fluid and maintain a stable plasma colloid osmotic pressure in patients with hypovolemia.However,when various diseases cause the increase of the permeability of capillaries,albumin may not play such a role or even counteract.Considering the facts that albumin has a long half-life in human body,that it can be used only when it metabolizes into amino acids,and that it contains limited number of essential amino acids,its nutrition value is limited.However,albumin can improve the gut tolerance when patients with severe hypoalbuminemia undergo enteral nutrition supports.
Hypoalbuminemia
Oncotic pressure
Hypovolemia
Serum Albumin
Human albumin
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Following onset of acute cardiogenic pulmonary edema in 21 patients, increases in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with decreases in plasma volume. Accordingly, there was a loss of hypo-oncotic fluid into the extravascular spaces. Following treatment with oxygen, furosemide, and morphine sulfate and reversal of clinical and radiographic signs of pulmonary edema, declines in hematocrit, plasma protein concentration, and colloid osmotic pressure were associated with increases in plasma volume. Hypo-oncotic edema fluid was therefore reabsorbed into the vascular compartment. The concept that acute heeart failure with pulmonary edema is associated with an increase in intravascular volume is therefore not supported. To the contrary, there is a reduction of blood volume during acute pulmonary edema. During reversal of acute pulmonary edema with diuresis, there was re-expansion rather than contraction of blood volume.
Oncotic pressure
Intravascular volume status
Vascular permeability
Peripheral edema
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The theoretical basis for the rapid normalization of hypoalbuminemia is contingent on recognition of those clinical circumstances requiring rapid and prolonged repair of colloid oncotic pressure. Standard total parenteral nutrition (TPN) solutions repair serum protein only after prolonged periods of therapy. Nutritionists have empirically observed that adding albumin to TPN solutions can quickly normalize hypoalbuminemia for sustained periods. Infusion of similar quantities of albumin without TPN results in no prolonged normalization. The mechanism of the rapid normalization of serum albumin with albumin-modified TPN solutions has yet to be determined, as has its relationships to prevention of hypoalbuminemia-associated morbidity and mortality.
Hypoalbuminemia
Oncotic pressure
Serum Albumin
Normalization
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Most veterinarians are aware of the importance of this molecule in maintaining colloid oncotic pressure, but albumin has many other less commonly recognized functions as well. The clinical consequences of hypoalbuminemia are reflections of the many functions albumin fulfills. Understanding the functions, synthesis, and degradation of the albumin molecule can improve understanding of the causes, consequences, and treatment of hypoalbuminemia.
Hypoalbuminemia
Oncotic pressure
Serum Albumin
Human albumin
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Hypoalbuminemia may cause interstitial edema and hemodilution, which we hypothesized may influence serum sodium levels. Our purpose was to compare serum sodium levels of hospitalized adults with or without hypoalbuminemia. All sodium and albumin serum levels of 142 adults hospitalized at general medical wards over a six-month period were searched at a University Hospital mainframe computer. Relevant laboratory data and clinical details were also registered. Hypoalbuminemia was defined by serum albumin concentration < 3.3 g/dl Fisher, Mann-Whitney, and Student's t tests were applied to compare groups with or without hypoalbuminemia. Ninety-nine patients, classified as hypoalbuminemic, had lower blood hemoglobin (10.68 ± 2.62 vs. 13.54 ± 2.41), and sodium (135.1 ± 6.44 vs. 139.9 ± 4.76mEq/l) and albumin (2.74 ± 0.35 vs. 3.58 ± 0.28g/dl) serum levels than non-hypoalbuminemic (n=43). Pearson's coefficient showed a significant direct correlation between albumin and sodium serum levels (r=0.40) and between serum albumin and blood hemoglobin concentration (r=0.46). Our results suggest that hypoalbuminemic adults have lower serum sodium levels than those without hypoalbuminemia, a phenomenon that may be at least partially attributed to body water retention associated with acute phase response syndrome.
Hypoalbuminemia
Serum Albumin
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The question raised by Dr. Johnson concerning the conclusions of the paper "Albumin Metabolism in Cystic Fibrosis" is whether or not there is a causal relationship between the demonstrable change in plasma volume and hypoalbuminemia, or merely a correlation between the two. Dr. Johnson cites evidence that alterations in colloid osmotic pressure may result in hypoalbuminemia by (1) primarily affecting albumin synthetic rate, and by (2) causing an expansion of the plasma volume. Let us accept, for purposes of this discussion, that increased colloid osmotic pressure does indeed have these effects, and, further, that these patients with cystic fibrosis had an increased colloid osmotic pressure.
Hypoalbuminemia
Oncotic pressure
Plasma volume
Serum Albumin
Osmotic pressure
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Hypoalbuminemia
Oncotic pressure
Hyperlipidemia
Serum Albumin
Pathogenesis
Hypoproteinemia
NEFA
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