Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been established that in conditions of intraoperative blood and plasma loss base deficiency is determined not only by hypocarbonatemia, but also by hypoproteinemia, hypophosphatemia and HCO3 metabolism disturbances caused by anemia. Correction of metabolic acidosis in such patients should include infusions of NaHCO3, protein preparations, blood, phosphates. Mellemgaard and Astrup's technique presupposes correction of the deficiency of all buffer bases only with NaHCO3, which dramatically increases its dosage. Thus, it is evident that the technique should be revised. The comparison of the results of metabolic acidosis correction using a conventional and adapted techniques (hydrocarbonate dose in mmol or ml of a 8.4% solution is 24-SB.body weight.0.2%) in statistically homogeneous groups has shown that differentiated "polybuffer" correction of metabolic acidosis with adapted NaHCO3 dose 1.7 times more frequently normalized acid-base balance parameters, reducing the risk of the onset of post-correction metabolic alkalosis to minimum.
 ...
PMID:[Characteristics of the dosage of sodium hydrocarbonate for correction of metabolic acidosis in surgical patients]. 133 43

Blood [base excess] ([BE]) is defined as the change in [strong acid] or [strong base] needed to restore pH to normal at normal PCO2. Some believe that [BE] is unhelpful because [BE] may be elevated with a "normal" [strong ion difference] ([SID]), where a strong ion is one that is always dissociated in physiological solution, and where [SID] = [strong cations]-[strong anions]. Using a computer simulation, the hypothesis was tested that [SID] = [SID Excess] ([SIDEx]), where [SIDEx] is the change in [SID] needed to restore pH to normal at normal PCO2. The most current version of the plasma [SID] ([SID]p) equation was used as a template, and an [SIDEx] formula, of the Siggaard-Andersen form, derived: [SIDEx]p = [HCO3-]p -24.72 + (pHp - 7.4) x (1.159 x [alb]p + 0.423 x [Pi]p). [SID] was compared to [SIDEx] over the physiologic range of plasma buffering, and it was found that [SIDEx] varied by approximately 15 mM at any given [SID], thereby faulting the hypothesis. It is concluded that [SID] can be "normal" with an elevated [SIDEx], the latter being an expression of the [BE] concept, and a more helpful quantity in physiology. The "metabolic" component of a given acid-base disturbance is usually estimated as whole blood [base excess] ([BE]WB), where [BE]WB is defined as the change in [strong acid] or [strong base] needed to restore plasma pH (pHp) to 7.4 at PCO2 of 40 Torr. However, the [BE] approach has been criticized as "inadequate for interpretation of complex acid-base derangements such as those seen in critically ill patients." The proposed alternative is the strong ion difference (SID) method, where a strong ion is one that is always dissociated in solution, and where [SID] = [strong cations] - [strong anions]. On the one hand, it does not seem possible, by the definitions of these entities, to change [SID] without also changing [BE]. On the other hand, a selected group of critically ill patients with hypoproteinemia has been reported in whom [SID] was "normal" (i.e. approximately 40 mEq.l-1) but [BE]WB clearly increased. The idea was that hypoproteinemia caused the alkalosis, due to a deficiency of plasma weak acid buffer, necessitating increased [HCO3-]p to maintain electrical neutrality. How could [SID] be "normal," but [BE] increased? The purpose of the current exercise was to address this question. An [SID excess] ([SIDEx]) formula was developed, conceptually identical to Siggaard-Andersen's [BE], and [SID] was compared to [SIDEx] over the physiological range of plasma [albumin] ([alb]p), plasma [phosphate] ([Pi]p), and plasma pH (pHp).
 ...
PMID:[Base excess] vs [strong ion difference]. Which is more helpful? 926 15

The purpose of this study was to compare traditional and quantitative approaches in analysis of the acid-base and electrolyte imbalances in horses with acute gastrointestinal disorders. Venous blood samples were collected from 115 colic horses, and from 45 control animals. Horses with colic were grouped according to the clinical diagnosis into 4 categories: obstructive, ischemic, inflammatory, and diarrheic problems. Plasma electrolytes, total protein, albumin, pH, pCO2, tCO2, HCO3-, base excess, anion gap, measured strong ion difference (SIDm), nonvolatile weak buffers (A(tot)), and strong ion gap were determined in all samples. All colic horses revealed a mild but statistically significant decrease in iCa2+ concentration. Potassium levels were mildly but significantly decreased in horses with colic, except in those within the inflammatory group. Additionally, the diarrheic group revealed a mild but significant decrease in Na+, tCa, tMg, total protein, albumin, SIDm, and A(tot). Although pH was not severely altered in any colic group, 26% of the horses in the obstructive group, 74% in the ischemic group, 87% in the inflammatory group, and 22% in the diarrheic group had a metabolic imbalance. In contrast, when using the quantitative approach, 78% of the diarrheic horses revealed a metabolic imbalance consisting mainly of a strong ion acidosis and nonvolatile buffer ion alkalosis. In conclusion, mild acid-base and electrolyte disturbances were observed in horses with gastrointestinal disorders. However, the quantitative approach should be used in these animals, especially when strong ion imbalances and hypoproteinemia are detected, so that abnormalities in acid-base status are evident.
 ...
PMID:A comparison of traditional and quantitative analysis of acid-base and electrolyte imbalances in horses with gastrointestinal disorders. 1635 83