Presence Of Unmeasured Anions Research Articles

Chloride:Sodium Ratio May Accurately Predict Corrected Chloride Disorders and the Presence of Unmeasured Anions in Dogs and Cats.

Disorders of chloride and mixed acid–base disturbances are common in veterinary emergency medicine. Rapid identification of these alterations and the presence of unmeasured anions aid prompt patient assessment and management. This study aimed to determine in dogs and cats if site-specific reference values for [Cl−]:[Na+] ratio and [Na+] − [Cl−] difference accurately identify corrected chloride abnormalities and to evaluate the predictive ability of the [Cl−]:[Na+] ratio for the identification of unmeasured anions. A database containing 33,117 canine, and 7,604 feline blood gas and electrolyte profiles was generated. Institution reference intervals were used to calculate site-specific reference values for the [Cl−]:[Na+] ratio and the [Na+] − [Cl−] difference. Contingency tables were used to assess the ability of these values to correctly identify corrected chloride disorders. Unmeasured anions were estimated by calculating strong ion gap (SIG). Continuous variables were compared using the Mann–Whitney U test. Correlations between continuous variables were assessed using Spearman’s rho (rs). In dogs, site-specific reference values for the [Cl−]:[Na+] ratio correctly identified 94.6% of profiles as hyper-, normo-, or hypochloremic. For dogs with normal sodium concentrations, site-specific reference values for the [Na+] − [Cl−] difference correctly identified 97.0% of profiles. In dogs with metabolic acidosis (base deficit > 4.0), [Cl−]:[Na+] ratio and SIG were moderately but significantly negatively correlated (rs −0.592, P < 0.0001). SIG was significantly greater in dogs with metabolic acidosis and hypochloremia compared to those without hypochloremia (P < 0.0001). In cats, site-specific reference values for the [Cl−]:[Na+] ratio correctly identified 93.3% of profiles as hyper-, normo-, or hypochloremic, while site-specific reference values for [Na+] − [Cl−] difference correctly identified 95.1% of profiles. In cats with metabolic acidosis [Cl−]:[Na+] ratio and SIG were moderately significantly negatively correlated (rs −0.730, P < 0.0001). SIG was significantly greater in cats with metabolic acidosis and hypochloremia compared to those without hypochloremia (P < 0.0001). Site-specific values for [Cl−]:[Na+] ratio and [Na+] − [Cl−] difference accurately identify corrected chloride disorders in both dogs and cats and may aid identification of the presence of unmeasured anions.

The nature of unmeasured anions in critically ill patients

We read with interest the commentary of Venkatesh and Morgan in the February issue of Critical Care [1], in which they discuss the continuing need for clarification of the nature of unmeasured anions in critically ill patients. The questions asked in this commentary arise from the study of Bruegger and colleagues in a previous issue of this journal [2]. The main issue discussed is the ongoing uncertainty about the contribution of intermediates of the tricarboxylic acid (TCA) cycle to the strong ion gap (SIG). As Venkatesh and Morgan accurately point out, the extremely high concentrations of acetate and citrate found by Bruegger and colleagues may very well be confounded by the exogenous administration of resuscitation fluids and blood products in the animal model described. In the March issue of Critical Care Medicine, we published our study conducted in critically ill patients with a metabolic acidosis with and without an increased SIG, representing the absence or presence of unmeasured anions [3]. We explored the presence of and contribution to the SIG of a large variety of compounds, largely organic acids and amino acids, by use of several laboratory techniques such as ion-exchange column chromatography and gas chromatography. In addition, proton nuclear magnetic resonance (1H-NMR) spectroscopy was used to quantify intermediates of the TCA cycle. Despite our elaborate attempt, only 7.9% of the difference in SIG between the low and high SIG groups could be explained by the presence of high concentrations of amino acids, uric acid, and organic acids. As a single compound, uric acid was responsible for the largest relative contribution to the SIG, namely 2.2%. Our study excludes many other potent unmeasured anions, such as uremic toxins and pyroglutamic acid, as major contributors to the SIG. As to the presence of TCA cycle intermediates, only succinic acid was significantly elevated in the high SIG group but it accounted for only 0.07% of the increased SIG. Furthermore, concentrations of isocitrate and citrate obtained by gas chromatography were not relevantly elevated in the high SIG group and all intermediates of the TCA cycle quantified with 1H-NMR spectroscopy, including acetic acid, corresponded to the published reference ranges. As outlined in our discussion, these findings are in contradiction to a recent human study [4]. The accumulation of TCA cycle intermediates by the mechanism of accelerated amino acid catabolism would imply distinct patterns of altered amino acid concentrations, which also was not supported by the results of our study. Our research enables us to answer the last question posed in the commentary of Venkatesh and Morgan. Raised concentrations of (iso)citrate and acetate do not clarify the SIG in the critically ill. Thus, a significant contribution of TCA cycle intermediates to the SIG in human acidosis is excluded. However, given the small percentage of the SIG that was represented by the measured anions, a largely unclarified portion of the strong anion gap remains to be explored.

Avaliação da acidose metabólica em pacientes graves: método de Stewart-Fencl-Figge versus a abordagem tradicional de henderson-hasselbalch

To review strategies of assessment of metabolic acidosis giving emphasis to the of Stewart-Fencl-Figge method versus the traditional method of Henderson-Hasselbalch. Metabolic acidosis is a common issue in critically ill patients, an important cause of myocardial contractility depression and sensible marker of impaired tissue oxygenation. Traditionally, is evaluated by the Henderson-Hasselbalch approach in which an arterial blood sample provides information about the presence and type of acid base disturbance. However, this method is not always capable to explain the causes of the metabolic acidosis and, therefore, several studies have explored mechanisms to improve its interpretation. The Stewart-Fencl-Figge method calculated through a mathematical formula, where in addition to arterial blood gas levels, serum levels of electrolytes, lactate and albumin are used, supplies trustworthy information allowing detection of mixed metabolic abnormalities and quantification of the magnitude of each component, mainly in patients with multiple organic dysfunctions. In these individuals, the presence of unmeasured anions in the plasma is an important mechanism of metabolic acidosis and its early detection fundamental to avoid deleterious effect on the organism. The traditional Henderson-Hasselbalch approach fails in analyzing the underlying mechanisms of metabolic acidosis and possesses many variables that intervene with its result especially in the critically ill patient. The Stewart-Fencl-Figge method offers a broader analysis of metabolic acidosis, indicating its mechanisms and guiding a better therapeutically strategy. As an alternative, the albumin-corrected and lactate-corrected anion gap seems to be as useful as the Stewart approach in identifying the unmeasured anions.