Health & Medical intensive care

Acid-Base Status of Critical Patients With Acute Renal Failure

Acid-Base Status of Critical Patients With Acute Renal Failure
Introduction: 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.
Materials and Methods: 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.
Results: 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).
Conclusions: 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.

Acute renal failure (ARF) is a common complication of critical illness. Patients with ARF and critical illness present with a variety of disorders of acid–base homeostasis, which are poorly understood and have not yet been formally studied. Furthermore, it is difficult to separate the acid–base effects of critical illness per sefrom those of ARF. Understanding the contribution of ARF to acid–base disorders and gaining insight into the nature of such disorders are likely to help clinicians in making the correct physiological diagnosis.

The extent and nature of acid–base disorders in critically ill patients with ARF might be better understood if quantitative biophysical methods are applied to its assessment and if control groups are used to appreciate which features might be unique to ARF. Accordingly, we compared a cohort of critically ill patients with ARF with two control groups: a matched control group, an Acute Physiology and Chronic Health Evaluation (APACHE) II-matched cohort without ARF; and an intensive care unit (ICU) control group, a group of consecutive critically ill patients without ARF. We then assessed the acid-base status using quantitative biophysical principles (Stewart–Figge methodology).

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