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Clinical Approach to Metabolic Alkalosis

Obtain historical data to pinpoint the nature of the disease causing metabolic alkalosis.

* Ask the patient about history of vomiting, other gastric fluid loss, and diuretic use. Loss of gastric fluid and HCl due to vomiting is the most common cause of metabolic alkalosis.
  • Vomiting may be caused by pyloric stenosis or ulcers. Occasionally, it may be self-induced.
  • Significant gastric fluid loss can occur via long-term nasogastric (NG) tube drainage.
  • Diuretic use may lead to increased chloride losses.
* Obtain information about specific disease states such as primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, and deoxycorticosterone (DOC) excess syndromes.
* Because hypokalemia may lead to metabolic alkalosis, ask about the use of diuretics because these lead to potassium loss.
An algorithm for metabolic alkalosis
Increased neuromuscular excitability sometimes causes tetany or seizures. Generalized weakness may be noted if the patient also has hypokalemia. Signs and symptoms observed with metabolic alkalosis usually relate to the specific disease process that caused the acid-base disorder.

* Patients who develop metabolic alkalosis from vomiting can have symptoms related to severe volume contraction, with signs of dehydration that include tachycardia, dry mucous membranes, decreased skin turgor, postural hypotension, poor peripheral perfusion, and weight loss.
* Although diarrhea typically produces a hyperchloremic metabolic acidosis, diarrheal stools may rarely contain significant amounts of chloride, as in the case of congenital chloride diarrhea. Children with this condition present at birth with watery diarrhea, metabolic alkalosis, and hypovolemia.
* Weight gain and hypertension may accompany metabolic alkalosis that results from a hypermineralocorticoid state.

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