Hyperchloremic Acidosis Treatment & Management

Treatment of GI causes of hyperchloremic acidosis is aimed at the underlying cause and includes (1) administration of saline solutions to repair the volume losses and (2) early administration of potassium.

Treatment of acidosis with bicarbonate-containing solutions is accompanied by potassium replacement to avoid severe hypokalemia, with its possible associated cardiac arrhythmias and muscular paralysis due to the rapid introduction of potassium into the cells.

Patients with chronic acidosis secondary to diarrhea benefit from long-term therapy with sodium and potassium citrate solutions.

Once the underlying disease entity behind hyperchloremic acidosis has been identified, specific therapy is needed to control the primary problem. However, therapy for the hyperchloremic acidosis itself is still needed. Depending on the type of RTA, the goals of therapy are to decrease the rate of progressive renal insufficiency by preventing nephrocalcinosis and nephrolithiasis; to neutralize metabolic bone disease; and, in children, to improve growth.

Go to Metabolic Acidosis, Pediatric Metabolic Acidosis, and Emergent Management of Metabolic Acidosis for complete information on these topics.

In cases of pRTA, multitherapy with large quantities of alkali, vitamin D, and potassium supplementation is required. (Depending on the degree of renal dysfunction, renal activation of vitamin D to the active calcitriol metabolite may be impaired, and administration of calcitriol may be preferred over other vitamin D preparations.)

The usual range of bicarbonate administration is 5-15 mEq/kg/d, and the administration must be accompanied or preceded by the administration of large amounts of potassium.

Proximal RTA can be difficult to treat, because alkali administration results in prompt and marked bicarbonaturia and potassium wasting.

The use of diuretics to induce extracellular volume depletion that enhances proximal tubular bicarbonate reabsorption can be effective but is usually accompanied by worsening of the hypokalemia. Thus, diuretics must be used with caution, and they require additional potassium or the addition of potassium-sparing agents.

In hypokalemic dRTA, treatment consists of long-term alkali administration in amounts sufficient to counterbalance endogenous acid production and any bicarbonaturia that may be present.

Fortunately, the alkali requirements of these patients are minimal compared with the requirements needed to treat patients with pRTA. A daily dose of 1-2 mEq/kg of NaHCO₃ is usually sufficient in most cases and can be provided in the form of citrate solutions (eg, Shohl solution), which is well tolerated because it causes less abdominal distention and aerophagia than does sodium bicarbonate (tablet or solution).

Providing bicarbonate via citrate salts that are metabolized to bicarbonate in the liver provides the additional advantage of exogenous citrate from the portion escaping hepatic metabolism.

Potassium supplements are indicated in the presence of hypokalemia. Hypokalemia can be severe, and patients can be symptomatic. Spironolactone can be used to maintain normokalemia.

Corrective alkali therapy results in normal growth in children with dRTA if therapy is started early.

Hypercalciuria, nephrolithiasis, and nephrocalcinosis are also prevented when alkali therapy is started in the early stages of dRTA.

With hyperkalemic dRTA, entities amenable to intervention, such as obstructive uropathy, must be identified.

In general, distal sodium delivery is increased if patients increase their ingestion of dietary salt, taking into account that many of these patients have concomitant cardiorenal compromise.

Fluid overload can be overcome with the addition of furosemide to a high-salt diet. This combination encourages distal delivery of sodium by rendering the collecting tubule impermeable to chloride, and it increases the exchange of sodium for hydrogen and potassium.

Mineralocorticoid therapy (ie, fludrocortisone in daily doses of 0.1-0.2 mg) is sometimes useful for aldosterone deficiency, but care needs to be taken when combining mineralocorticoid therapy with diuretics (in order to prevent precipitation of heart failure).

Foods with a high potassium content and drugs that may aggravate hyperkalemia (eg, ACE inhibitors, potassium-sparing diuretics, beta blockers) must be avoided.

Cation-exchange resins (eg, sodium polystyrene sulfonate [Kayexalate], alkalinizing salts) can be helpful in controlling hyperkalemia.

In many instances, careful evaluation of iatrogenic offenders (eg, beta blockers, ACE inhibitors) can explain persistently high potassium levels in the absence of moderate to severe renal failure.

A variety of drugs can aggravate or cause hyperchloremic acidosis is important.

Drugs that increase GI bicarbonate loss include calcium chloride, magnesium sulfate, and cholestyramine.

Drugs or toxins that can induce pRTA include streptozotocin, lead, mercury, arginine, valproic acid, gentamicin, ifosfamide, and outdated tetracycline.

Drugs or toxins that can cause dRTA include amphotericin B, toluene, nonsteroidal anti-inflammatory drugs, lithium ^[15] , and cyclamate.