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Metabolic alkalosis – a case study report
Summarized from Taimur D, Garimella P, Strom J. Quiz: An unusual case of metabolic alkalosis in a patient with CKD. AJKD 2017; 69: A13-A16
Monitoring patient acid-base status is one of three principal clinical utilities of blood gas analysis (the other two are monitoring patient oxygen and ventilation status).
Three parameters generated during blood gas analysis (pH, pCO2 and bicarbonate) allow this acid-base assessment and classification of all acid-base disturbances to one of four broad groups: respiratory acidosis; metabolic acidosis; respiratory alkalosis; and metabolic alkalosis.
Metabolic alkalosis, which is characterized by increased pH and bicarbonate along with secondary (compensatory) increase in pCO2, is the subject of this recently published case study report. It provides a reminder that prescribed drugs can be the primary or a contributory cause of acid-base disturbance.
The case concerns an 83-year-old lady with moderately severe chronic kidney disease (e-GFR 36 mL/min) and a history of chronic hyperkalemia, osteoporosis and gastro-esophageal reflux disease (GERD). Recent complaints of chest pain and breathlessness, along with recent weight gain and pitting edema prompted hospital admission.
Blood gas analysis on admission revealed pH 7.55; pCO2 52 mmHg (6.6 kPa) and bicarbonate 45 mEq/L (45 mmol/L), and thereby confirmation of metabolic alkalosis. Other abnormal findings included severe hypokalemia (plasma potassium 2.0 mmol/L) and hypochloremia (plasma chloride 82 mmol/L).
The cause of metabolic alkalosis was attributed to drugs the lady had been prescribed. Specifically, the coadministration of sodium polystyrene (to treat her chronic hyperkalemia), calcium carbonate for osteoporosis and the antacid magnesium oxide used to treat GERD.
In discussion, the authors explain the mechanism of development of metabolic alkalosis from interaction between antacids (calcium carbonate and magnesium oxide in this case) and sodium polystyrene. They also discuss the role of potassium in acid-base balance and the notion that hypokalemia can contribute to metabolic alkalosis.
Adjustments to the dosing and timing of the lady’s prescribed drug regime restored normal acid-base and plasma potassium concentration.
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