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

Naka T, Bellomo R - Crit Care (2004)

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

ABSTRACT
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.

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Related in: MedlinePlus

Difference in pH between patients with acute renal failure (ARF) in an intensive care unit (ICU) and a control population of ICU patients.
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Figure 1: Difference in pH between patients with acute renal failure (ARF) in an intensive care unit (ICU) and a control population of ICU patients.

Mentions: Classically, metabolic acidosis in renal failure is described as a high anion gap metabolic acidosis. However, in the clinical setting, the anion gap is not always elevated. These findings might lead clinicians to diagnostic and therapeutic confusion. In these situations, quantitative analysis using the Stewart–Figge approach can be helpful. In this regard, Rocktaeschel and coworkers [9] recently examined the acid–base status of ARF patients using the Stewart–Figge methodology and demonstrated several features. First, critically ill patients with ARF were typically acidemic compared with control patients (Fig. 1). Second, this acidemia appeared secondary to metabolic acidosis with a mean base excess of approximately -7 mEq/l, which appeared secondary to the accumulation of lactate, phosphate, and unmeasured anions (possible candidates for these unmeasured anions include sulfate, urate, hydroxypropionate, oxalate, and furanpropionate [10]; Fig. 2). Third, in these patients there was also a marked failure to alter the apparent SID to achieve a degree of metabolic compensation (Fig. 3). Despite this finding, half of the ARF patients had an anion gap within the normal range. Furthermore, these acidifying disorders were attenuated by a concomitant metabolic alkalosis, which was essentially secondary to hypoalbuminemia. Hypoalbuminemia lowered the anion gap and masked the presence of acidifying anions to those clinicians using conventional acid–base analysis.


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

Naka T, Bellomo R - Crit Care (2004)

Difference in pH between patients with acute renal failure (ARF) in an intensive care unit (ICU) and a control population of ICU patients.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC420038&req=5

Figure 1: Difference in pH between patients with acute renal failure (ARF) in an intensive care unit (ICU) and a control population of ICU patients.
Mentions: Classically, metabolic acidosis in renal failure is described as a high anion gap metabolic acidosis. However, in the clinical setting, the anion gap is not always elevated. These findings might lead clinicians to diagnostic and therapeutic confusion. In these situations, quantitative analysis using the Stewart–Figge approach can be helpful. In this regard, Rocktaeschel and coworkers [9] recently examined the acid–base status of ARF patients using the Stewart–Figge methodology and demonstrated several features. First, critically ill patients with ARF were typically acidemic compared with control patients (Fig. 1). Second, this acidemia appeared secondary to metabolic acidosis with a mean base excess of approximately -7 mEq/l, which appeared secondary to the accumulation of lactate, phosphate, and unmeasured anions (possible candidates for these unmeasured anions include sulfate, urate, hydroxypropionate, oxalate, and furanpropionate [10]; Fig. 2). Third, in these patients there was also a marked failure to alter the apparent SID to achieve a degree of metabolic compensation (Fig. 3). Despite this finding, half of the ARF patients had an anion gap within the normal range. Furthermore, these acidifying disorders were attenuated by a concomitant metabolic alkalosis, which was essentially secondary to hypoalbuminemia. Hypoalbuminemia lowered the anion gap and masked the presence of acidifying anions to those clinicians using conventional acid–base analysis.

Bottom Line: 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.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Intensive Care, Austin Hospital, Heidelberg, Victoria, Australia.

ABSTRACT
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.

Show MeSH
Related in: MedlinePlus