Metabolic Alkalosis

Causes

Metabolic alkalosis results from loss of acid, retention of base, or renal mechanisms associated with decreased serum levels of potassium and chloride.

Loss of acid

Causes of critical acid loss include vomiting, nasogastric tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid).

Hyperadrenocorticism is another cause of severe acid loss. Cushing's disease, primary hyperaldosteronism, and Bartter's syndrome, for example, all lead to retention of sodium and chloride and urinary loss of potassium and hydrogen.

Retention of base

Excessive retention of base can result from excessive intake of bicarbonate of soda or other antacids (usually for treatment of gastritis or peptic ulcer), excessive intake of absorbable alkali (as in milkalkali syndrome), administration of excessive amounts of I. V. fluids with high concentrations of bicarbonate or lactate, or respiratory insufficiency - all of which cause chronic hypercapnia from high levels of plasma bicarbonate.

Signs and symptoms

Clinical features of metabolic alkalosis result from the body's attempt to correct the acid-base imbalance, primarily through hypoventilation. Other man ifestations include irritability, picking at bedclothes (carphology), twitching, confusion, nausea, vomiting, and diarrhea (which aggravates alkalosis).

Cardiovascular abnormalities- such as atrial tachycardia-and respiratory disturbances-such as cyanosis and apnea-also occur. In the alkalotic patient, diminished peripheral blood flow during repeated blood pressure checks may provoke carpopedal spasm in the hand - a possible sign of impending tetany (Trousseau's sign). Uncorrected metabolic alkalosis may progress to seizures and coma. ifestations include irritability, picking at bedclothes (carphology), twitching, confusion, nausea, vomiting, and diarrhea (which aggravates alkalosis).

Cardiovascular abnormalities- such as atrial tachycardia-and respiratory disturbances-such as cyanosis and apnea-also occur. In the alkalotic patient, diminished peripheral blood flow during repeated blood pressure checks may provoke carpopedal spasm in the hand - a possible sign of impending tetany (Trousseau's sign). Uncorrected metabolic alkalosis may progress to seizures and coma.

Diagnosis

Metabolic alkalosis may be suspected based on symptoms, but often may not be noticeable. The condition is usually confirmed by laboratory tests on blood and urine samples. Blood pH above 7.45 confirms the condition. Levels of other blood components, including salts like potassium, sodium, and chloride, fall below normal ranges. The level of bicarbonate in the blood will be high, usually greater than 29 mEq/L. Urine pH may rise to about 7.0 in metabolic alkalosis.

Treatment

The goal of treatment is to correct the underlying cause of metabolic alkalosis. Therapy for severe alkalosis may include cautious administration of ammonium chloride I.V. to release hydrogen chloride and restore the concentration of extracellular fluid and chloride levels.

Potassium chloride and normal saline solution (except in the presence of heart failure) are usually sufficient to replace losses from gastric drainage. Electrolyte replacement with potassium chloride and discontinuing diuretics correct metabolic alkalosis resulting from potent diuretic therapy.

Prevention

Patients receiving tube feedings or intravenous feedings must be monitored to prevent an imbalance of fluids and salts, particularly potassium, sodium, and chloride. Overuse of some drugs, including diuretics , laxatives, and antacids, should be avoided.