Stewart-Figge Methodology Research Articles

Acid-base variables in patients with acute kidney injury requiring peritoneal dialysis in the pediatric cardiac care unit

We aimed to clarify the acid-base abnormalities of patients with acute kidney injury (AKI) requiring peritoneal dialysis (PD) in pediatric cardiac care units. A retrospective observational study was conducted in a pediatric cardiac care unit in a tertiary care university hospital. The subjects were 40 patients with AKI requiring PD between 2003 and 2005, and controls matched by type of surgery and body weight. Acid-base variables, including blood gas data and electrolytes, were assessed. The Stewart-Figge variables, including strong ion difference apparent (SIDa), strong ion difference effective (SIDe), and strong ion gap (SIG), were calculated. Blood gas analyses showed that the PD group was more acidemic, with a lower mean bicarbonate and a lower mean base excess, typical features of metabolic acidosis. The strong ion analyses revealed that the PD group had lower mean sodium and albumin concentrations. Based on the Stewart-Figge methodology, SIDa was smaller in the PD group than in the control group, but SIG was similar in the two groups. Receiver-operating characteristic curve analyses showed that serum albumin was the only prognostic factor associated with PCCU mortality, even after adjustment for PD treatment. Patients with AKI requiring PD in a pediatric cardiac care unit had significant metabolic acidosis compared to controls matched by the type of surgery and body weight. Hyponatremia and hypoalbuminemia were characteristics of these patients. The calculated SIDa was smaller in the PD than in the control group. Only the serum albumin had a significant prognostic value.

Acid-base Balance in Combined Severe Hepatic and Renal Failure: A Quantitative Analysis

Severe hepatic failure (SHF) commonly leads to major changes in acidbase balance status. However, the direct effects of liver failure per se on acid base balance are poorly understood because this condition is usually associated with acute renal failure (ARF). To assess the effect of SHF on acid-base balance. Retrospective laboratory investigation. Thirty-seven critically ill patients with SHF complicated by ARF, and 42 patients with severe ARF without liver failure prior to renal replacement therapy. Retrieval of clinical and laboratory data from prospective unit and laboratory databases. Quantitative acid-base assessment using Stewart-Figge methodology. Comparison of findings between the two groups. Comparison of demographic and clinical features. Patients with combined SHF and ARF were younger and had significantly higher mean bilirubin, ALT and INR levels (p<0.0001). Their mean lactate concentration was higher (6.4 vs. 2.1 mmol/L; p<0.0001) leading to a greater anion gap (25.8 vs. 16.1 mmol/L; p<0.0001). The ionized calcium concentration (1.00 vs. 1.15 mmol/L; p<0.0001) was lower but the strong ion difference apparent (SIDa) was greater (42.0 vs. 38.0 mEq/L; p<0.005) due to hypochloremia. The albumin concentration was low but higher than in control patients (28 vs. 24 g/L; p<0.01) and the calculated strong ion gap (SIG) was greater (12.6 vs. 9.3 mEq/L; p<0.01). The base excess was similar to controls and the pH was preserved in the near normal range by marked hypocapnea. Combined SHF and ARF is a syndrome with unique acid-base changes due mostly to lactic metabolic acidosis and, in smaller part, to the accumulation of unmeasured anions. This acidosis, like that of ARF, is attenuated by hypoalbuminemia, by a unique preservation of the SIDa due to hypochloremia, and by marked hypocapnea.

The Acid-Base Effect of Changing Citrate Solution for Regional Anticoagulation during Continuous Veno-Venous Hemofiltration

To compare the acid-base balance effects of two different citrate doses for regional citrate anticoagulant (RCA) for continuous veno-venous hemofiltration (CVVH). We used a commercial citrate fluid (citrate concentration: 11 mmol/L) from July 2003 to July 2004 (period A) in 22 patients; then changed to a new citrate fluid (citrate concentration: 14 mmol/L) from July 2004 to Feb 2005 (Period B) in 21 patients. Replacement fluid rate was fixed at 2,000 ml/h. We measured all relevant variables for acid-base analysis according to the Stewart-Figge methodology. After commencement of RCA-CVVH, there was a change in bicarbonate and base excess (BE) toward acidosis for both fluids. This change was significantly different between period A and B at 6 and 12 hours (pH: p<0.01, BE: p<0.05) with greater decreases with the 11 mmol/L citrate fluid. These changes were mostly secondary to an increase in the strong ion difference (SID) and occurred despite an increased strong ion gap (SIG) (+0.5 mEq/L vs. +1.5 mEq/L; p<0.01) in the higher citrate concentration fluid. Cessation of RCA-CVVH was associated with short-lived differences in bicarbonate and SIG which were similar to those seen on initiation of RCA-CVVH but in the opposite direction. A small increase This was partly offset by an increase in SIG, consistent with increased citratemia. Cessation of treatment showed a differential improvement in SIG also consistent with disposal of therapy-associated citrate. These observations might assist clinicians in interpreting acidbase changes during RCA-CVVH.in citrate infusion rate caused an alkalinizing increase in SID.

Acid-Base Balance during Continuous Veno-Venous Hemofiltration: The Impact of Severe Hepatic Failure

Continuous renal replacement therapy (CRRT) affects acid-base balance but the influence of severe hepatic failure (SHF) on this effect is unknown. To assess the effect of SHF on acid-base balance in patients receiving CVVH. Retrospective laboratory investigation. Forty patients with SHF and acute renal failure (ARF) treated with CVVH and 42 critically ill patients with severe ARF but no liver disease also treated with CVVH (controls). Retrieval of clinical and laboratory data from prospective unit and laboratory databases. Quantitative acid-base status assessment using the Stewart-Figge methodology. Comparison of findings between the two groups. Although CVVH had a major effect on acid base balance in both groups, patients with SHF had a higher mean lactate concentrations (4.8 vs. 3.1 mmol/L; p<0.0005), a greater base deficit compared to controls (-1 vs. 4.1 mEq/L; p<0.0001) and a lower PaCO 2 tension (36.8 vs. 42.5 mmHg; p<0.0001), despite the use of bicarbonate replacement fluid. The acidifying effect of hyperlactatemia was slightly worsened by an increased strong ion gap (9.3 vs. 4.9 mEq/L; p<0.0001). It was, however, attenuated by an increased strong ion difference apparent (SIDa) (43.6 vs. 41.9 mEq/L; p<0.05) secondary to hypochloremia (96 vs. 100 mmol/L; p<0.0001) and by hypoalbuminemia, although hypoalbuminemia in SHF patients (26 vs. 23; p<0.005) was less pronounced than in controls. The use of CVVH does not fully correct the independent acidifying effect of liver failure on acid-base status. Increased lactate and strong ion gap values maintain a persistent base deficit despite the alkalinizing effects of hypoalbuminemia and hypochloremia. The correction of acidosis in SHF patients may require more intensive CVVH.

Low-dose Citrate Continuous Veno-venous Hemofiltration (CVVH) and Acid-base Balance

To evaluate the acid-base effect of low-dose regional citrate anticoagulation (RCA) during continuous veno-venous hemofiltration (CVVH). Prospective observational study. ICUs of tertiary public and private hospitals. Thirty critically ill patients with acute renal failure at risk of bleeding or with a major contraindication to heparin-CVVH and/or short filter life. We used a commercial citrate-based fluid (11 mmol/L, sodium: 140 mmol/L, chloride: 108 mmol/L and 1 mol/L of potassium) as pre-dilution replacement fluid during CVVH. Further potassium was added according to serum potassium levels. We measured all relevant variables for acid-base analysis according to the Stewart-Figge methodology. Before treatment, study patients had a slight metabolic acidosis, which worsened over 6 hours of RCA-CVVH (pH from 7.39 to 7.38, p < 0.005; bicarbonate from 23.2 to 21.6 mmol/L, p < 0.0001 and base excess from -2.0 to -3.0 mEq/L, p < 0.0001) due to a significant increase in SIG (from 5.8 to 6.6 mEq/L, p < 0.05) and a decrease in SIDa (from 37.5 to 36.6 mEq/L, p < 0.05). These acidifying effects were attenuated by hypoalbuminemia and a decrease in lactate (from 1.48 to 1.34 mmol/L, p < 0.005) and did not lead to progressive acidosis. On cessation of treatment, this acidifying effect rapidly self-corrected within six hours. Low dose RCA-CVVH induces a mild acidosis secondary to an increased strong ion gap and decreased SIDa which fully self-corrects at cessation of therapy. Clinicians need to be aware of these effects to correctly interpret changes in acid-base status in such patients.

Bench-to-bedside review: Treating acid–base abnormalities in the intensive care unit – the role of renal replacement therapy

Acid–base disorders are common in critically ill patients. Metabolic acid–base disorders are particularly common in patients who require acute renal replacement therapy. In these patients, metabolic acidosis is common and multifactorial in origin. Analysis of acid–base status using the Stewart–Figge methodology shows that these patients have greater acidemia despite the presence of hypoalbuminemic alkalosis. This acidemia is mostly secondary to hyperphosphatemia, hyperlactatemia, and the accumulation of unmeasured anions. Once continuous hemofiltration is started, profound changes in acid–base status are rapidly achieved. They result in the progressive resolution of acidemia and acidosis, with a lowering of concentrations of phosphate and unmeasured anions. However, if lactate-based dialysate or replacement fluid are used, then in some patients hyperlactatemia results, which decreases the strong ion difference and induces an iatrogenic metabolic acidosis. Such hyperlactatemic acidosis is particularly marked in lactate-intolerant patients (shock with lactic acidosis and/or liver disease) and is particularly strong if high-volume hemofiltration is performed with the associated high lactate load, which overcomes the patient's metabolic capacity for lactate. In such patients, bicarbonate dialysis seems desirable. In all patients, once hemofiltration is established, it becomes the dominant force in controlling metabolic acid–base status and, in stable patients, it typically results in a degree of metabolic alkalosis. The nature and extent of these acid–base changes is governed by the intensity of plasma water exchange/dialysis and by the 'buffer' content of the replacement fluid/dialysate, with different effects depending on whether lactate, acetate, citrate, or bicarbonate is used. These effects can be achieved in any patient irrespective of whether they have acute renal failure, because of the overwhelming effect of plasma water exchange on nonvolatile acid balance. Critical care physicians must understand the nature, origin, and magnitude of alterations in acid–base status seen with acute renal failure and during continuous hemofiltration if they wish to provide their patients with safe and effective care.

Acid-base status of critically ill patients with acute renal failure: analysis based on Stewart-Figge methodology.

The aim of the present study is to understand the nature of acid-base disorders in critically ill patients with acute renal failure (ARF) using the biophysical principles described by Stewart and Figge. A retrospective controlled study was carried out in the intensive care unit of a tertiary hospital. Forty patients with ARF, 40 patients matched for Acute Physiology and Chronic Health Evaluation II score (matched control group), and 60 consecutive critically ill patients without ARF (intensive care unit control group) participated. The study involved the retrieval of biochemical data from computerized records, quantitative biophysical analysis using the Stewart-Figge methodology, and statistical comparison between the three groups. We measured serum sodium, potassium, magnesium, chloride, bicarbonate, phosphate, ionized calcium, albumin, lactate and arterial blood gases. Intensive care unit patients with ARF had a mild acidemia (mean pH 7.30 +/- 0.13) secondary to metabolic acidosis with a mean base excess of -7.5 +/- 7.2 mEq/l. However, one-half of these patients had a normal anion gap. Quantitative acid-base assessment (Stewart-Figge methodology) revealed unique multiple metabolic acid-base processes compared with controls, which contributed to the overall acidosis. The processes included the acidifying effect of high levels of unmeasured anions (13.4 +/- 5.5 mEq/l) and hyperphosphatemia (2.08 +/- 0.92 mEq/l), and the alkalinizing effect of hypoalbuminemia (22.6 +/- 6.3 g/l). The typical acid-base picture of ARF of critical illness is metabolic acidosis. This acidosis is the result of the balance between the acidifying effect of increased unmeasured anions and hyperphosphatemia and the lesser alkalinizing effect of hypoalbuminemia.