Treatment

Serum electrolytes should be monitored in patients with CKD for the development of metabolic acidosis. Metabolic acidosis in patients with CKD is generally characterized by an elevated anion gap greater than 17 mEq/L (17 mmol/L), due to the accumulation of phosphate, sulfate, and other organic anions.

Nonpharmacologic Therapy

Treatment of metabolic acidosis in CKD requires pharmacologic therapy. Other disorders that may contribute to metabolic acidosis should also be addressed. Altering bicarbonate levels in the dialysate fluid in patients receiving dialysis may assist with the treatment of metabolic acidosis, although pharmacologic therapy may still be required.

Pharmacologic Therapy

Pharmacologic therapy with sodium bicarbonate or citrate/citric acid preparations may be needed in patients with stage 3 CKD or higher to replenish body stores of bicarbonate. Calcium carbonate and calcium acetate, used to bind phosphorus in sHPT, also aid in increasing serum bicarbonate levels, in conjunction with other agents.

Sodium bicarbonate tablets are administered in increments of 325 and 650 mg tablets. A 650 mg tablet of sodium bicarbonate contains 7.7 mEq (7.7 mmol) each of sodium and bicarbonate. Sodium retention associated with sodium bicarbonate can cause volume overload, which can exacerbate hypertension and chronic heart failure. Patient tolerability of sodium bicarbonate is low because of carbon dioxide production in the GI tract that occurs during dissolution.

Solutions that contain sodium citrate/citric acid (Shohl's solution and Bicitra) provide 1 mEq/L (1 mmol/L) each of sodium and bicarbonate. Polycitra is a sodium/ potassium citrate solution that provides 2 mEq/L (2 mmol/L) of bicarbonate, but contains 1 mEq/L (1 mmol/L) each of sodium and potassium, which can promote hyperkalemia in patients with severe CKD. The citrate portion of these preparations is metabolized in the liver to bicarbonate, while the citric acid portion is metabolized to CO2 and water, increasing tolerability compared to sodium bicarbonate. Sodium retention is also decreased with these preparations. However, these products are liquid preparations, which may not be palatable to some patients. Citrate can also promote aluminum intoxication by augmenting aluminum absorption in the GI tract.

When determining the dose of bicarbonate replacement, the goal for therapy is to achieve a normal serum bicarbonate level of 24 mEq/L (24 mmol/L). The dose is usually determined by calculating the base deficit: [0.5 L/kg x (body weight)] x [(normal CO2) - (measured CO2)]. Because of the risk of volume overload resulting from the sodium load administered with bicarbonate replacement, the total base deficit should be administered over several days. Once the goal serum bicarbonate level is attained, a maintenance dose of bicarbonate is necessary and should be titrated to maintain serum bicarbonate levels.

Outcome Evaluation

Monitor serum electrolytes and arterial blood gases regularly. Correct metabolic acidosis slowly to prevent the development of metabolic alkalosis or other electrolyte abnormalities.

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