Is Stewart's approach useful in evaluation of acid–base disorders in septic shock patients?
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KeywordsSeptic Shock Metabolic Acidosis Prospective Observational Study Septic Shock Patient Base Equilibrium
Disorders of acid–base equilibrium are common in critically ill patients. The Stewart approach has been found useful in explaining these disorders, where conventional analysis was deficient. However, much uncertainty remains about the usefulness and clinical meaning of this new approach. The aim of our study was to compare the traditional method based on the analysis of standard base excess (SBE) and anion gap with the Stewart approach based on the analysis of the independent variables in septic shock.
A prospective observational study with all patients admitted to the ICU of our hospital for septic shock between September 2007 and July 2008. Na+, K+, Ca2+, Mg2+, Cl-, pH, PaCO2, lactate, phosphorus, albumin were measured at admission. Bicarbonate, SBE, anion gap corrected for albumin (AGc), Cl corrected for water excess/deficit (Clc), apparent and effective strong ion differences and strong ion gap (SIG) were calculated. Unmeasured anions were identified if SIG >6 mEq/l.
Thirty-one patients were included. Metabolic acidosis (SBE <-3 mEq/l) was found in 20 (64.5%) patients, while the Stewart approach identified metabolic acidosis in 27 (87%) patients. The traditional approach failed to identify seven cases of metabolic acidosis (five patients considered normal and two having an alkalosis).The inclusion of AGc in the traditional analysis based on SBE resulted in a different clinical interpretation of acid–base status than the Stewart method in only two (6.4%) patients. The Stewart approach did not identify one patient with metabolic acidosis observed with the use of SBE and AGc. Hyperlactatemia (lactate >2 mmol/l) was present in 18 (58%) patients. SIG and AGc were elevated in 25 (81%) and 24 (77.4%) patients. Hypoalbuminemia was found in all patients. Patients with normal SBE and high SIG had lower Clc than patients with low SBE (103.1 ± 2.3 vs. 108 ± 3.6; P = 0.03). Albumin was not different between these two groups. The normal SBE found with high SIG was almost completely explained by the alkalinizing effect of hypochloremia. AGc and SIG showed a very good self-correlation (r2 = 0.708; P = 0.001). Thirteen patients died before day 28. All metabolic acid–base variables failed to predict outcome.
The Stewart approach and traditional method associating the AGc are clinically interchangeable in identifying the acid–base disorders in septic shock patients. Because of its simplicity and very good correlation with the complex calculation of SIG, AGc must be used in clinic practice. Critically ill patients may present high SIG with a normal value of SBE as a result of associated hypochloremic alkalosis.
This article is published under license to BioMed Central Ltd.