Which potential cause would the nurse associate with a patients diagnosis of metabolic acidosis?

Alkali Treatment of Metabolic Acidosis

Treatment of metabolic acidosis usually involves either sodium bicarbonate or citrate34 [Table 12.2]. NaHCO3 can be taken orally as tablets or powder or given intravenously as a hypertonic bolus or an isotonic infusion, which can be created by adding 150 mmol NaHCO3 to 1 liter of 5% dextrose in water [D5W]. This solution is useful if treatment requires both volume expansion and alkali administration.

Citrate may be taken orally as a liquid, as sodium citrate, potassium citrate, or citric acid, or a combination. Many patients find citrate-containing solutions more palatable than oral NaHCO3 as a source of oral alkali therapy. Oral citrate therapy should not be combined with medications that include aluminum. Citrate, which has a −3 charge under normal conditions, can complex with aluminum [Al3+] in the intestinal tract, resulting in an uncharged moiety that is rapidly absorbed across the intestinal tract and then can dissociate to release free aluminum. This can increase the rate of aluminum absorption dramatically and in some patients, particularly those with severe CKD, has resulted in acute aluminum encephalopathy.

The dose of alkali therapy administered is based on both the total body bicarbonate deficit and the desired rapidity of treatment. Under normal circumstances, the volume of distribution [VD] for bicarbonate is approximately 0.5 l/kg total body weight. Thus the bicarbonate deficit, in millimoles, can be estimated from the following formula:

Bicarbonate deficit=[0.5×LBWkg]×[24−HCO3−]

whereLBWkg is the lean body weight in kilograms and24 is the desired resultant bicarbonate concentration.

Several caveats regarding this equation should be understood. First, edema fluid contributes to the volume of distribution of bicarbonate. Accordingly, an estimation of the amount of edema fluid should be included in this calculation. Second, the volume of distribution for bicarbonate increases as the severity of the metabolic acidosis worsens. When serum [HCO3−] is 5 mmol/l or less, the volume of distribution may increase to 1 l/kg or more.

When acute treatment is desired, 50% of the bicarbonate deficit should be replaced during the first 24 hours. If hypertonic NaHCO3 is administered, the increase in serum [HCO3−] will be mirrored by an increase in serum [Na+]. After the initial 24 hours of therapy, the response to therapy and the patient's current clinical condition are reevaluated before future therapy is decided. Acute hemodialysis solely for the treatment of metabolic acidosis, other than that associated with renal failure, is rarely beneficial.

Renal Tubular Acidosis in Chronic Kidney Disease

Metabolic acidosis in advanced CKD is caused by failure of the tubular acidification process to excrete the normal daily acid load. As functional renal mass is reduced by disease, there is an adaptive increase in ammonia production and H+ secretion by the remaining nephrons. Despite increased production of ammonia from each remaining nephron, overall production may be decreased secondary to the decrease in total renal mass. In addition, there is less delivery of ammonia to the medullary interstitium secondary to a disrupted medullary anatomy.17 The ability to lower the urinary pH remains intact, reflecting the fact that the impairment in distal nephron H+ secretion is less than that in ammonia secretion. Quantitatively, however, the total amount of H+ secretion is small, and the acidic urine pH is the consequence of very little buffer in the urine. The lack of ammonia in the urine is reflected by a positive value for the UAG. Differentiation of RTA from type 4 RTA can be difficult as it is based on the clinician's determination of whether the severity of metabolic acidosis is out of proportion to the degree of renal dysfunction.

Patients with CKD may develop a hyperchloremic normal gap metabolic acidosis associated with normokalemia or mild hyperkalemia as GFR decreases to less than 30 ml/min. With more advanced CKD [GFR