Hyperchloremic Acidosis Medication
- Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
The goals of pharmacotherapy are to correct the acidosis, to reduce morbidity, and to prevent complications. Alkalinizing agents, electrolytes, diuretics, mineralocorticoids, and vitamin D supplements can be used against acidosis.
These are used as gastric, systemic, and urinary alkalinizers and have been used in the treatment of acidosis resulting from metabolic and respiratory causes, including diarrhea, kidney disturbances, shock, and diabetic coma.
Sodium bicarbonate is indicated for the treatment of metabolic acidosis. It increases renal clearance of acidic drugs.
Sodium citrate treats metabolic acidosis and is used as an alkalinizing agent when long-term maintenance of alkaline urine is desirable.
Electrolytes are used to correct disturbances in fluid and electrolyte homoeostasis or acid-base balance and to reestablish the osmotic equilibrium of specific ions.
Potassium chloride is essential for the transmission of nerve impulses, the contraction of cardiac muscle, the maintenance of intracellular tonicity, skeletal and smooth muscle function, and the maintenance of normal renal function.
Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Depletion usually results from diuretic therapy, primary or secondary hyperaldosteronism, diabetic ketoacidosis, severe diarrhea (if associated with vomiting), or inadequate replacement during prolonged parenteral nutrition.
Potassium depletion sufficient to cause a 1-mEq/L decrease in serum potassium requires the loss of approximately 100-200 mEq of potassium from total body stores.
Diuretics are used to overcome fluid overload. They increase the distal delivery of sodium by rendering the collecting tubule impermeable to chloride and increase the exchange of sodium for hydrogen and potassium.
This agent increases water excretion by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. The dose must be individualized to patient.
Bumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs following administration, renal vascular resistance decreases, and renal blood flow is enhanced. Bumetanide is roughly four times as potent as furosemide on a milligram basis. Depending on the response, administer bumetanide at small dose increments (0.5-5 mg) until desired diuresis occurs.
Torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the sodium, potassium, and chloride carrier system. It increases urinary excretion of sodium, chloride, and water, but does not significantly alter the glomerular filtration rate, renal plasma flow, or acid-base balance. Torsemide is roughly twice as potent as furosemide on a milligram basis. Depending on the response, administer furosemide at small dose increments (10-100 mg) until desired diuresis occurs.
Mineralocorticoids may be useful for aldosterone deficiency. Combine mineralocorticoid therapy with sodium loading and diuretics to prevent heart failure.
Fludrocortisone promotes increased sodium reabsorption and potassium loss in renal distal tubules.
Vitamin D Supplements
Vitamin D is a fat-soluble vitamin that promotes the absorption of calcium and phosphorus in the small intestine. It also promotes renal tubule phosphate resorption.
This is the active form of vitamin D. It is used in pRTA as multitherapy with large quantities of alkali and potassium supplementation.
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