Pediatric Metabolic Alkalosis Clinical Presentation

Updated: Oct 19, 2017
  • Author: Lennox H Huang, MD, FAAP; Chief Editor: Timothy E Corden, MD  more...
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Presentation

History

Obtain clinical historical data to pinpoint the nature of the disease causing the patient's metabolic alkalosis. Symptoms usually relate to the specific disease process that caused the acid-base disorder. Ask about vomiting, other gastric fluid loss, and diuretic use. Loss of gastric fluid and hydrochloric acid (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. It may also result in potassium loss, and hypokalemia may lead to metabolic alkalosis.

Obtain information about specific disease states such as primary hyperaldosteronism, reninism, hyperglucocorticoidism, Bartter syndrome, and deoxycorticosterone (DOC) excess syndromes. [11, 12]

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Physical Examination

Signs observed with metabolic alkalosis usually relate to the specific disease process that caused the acid-base disorder. Increased neuromuscular excitability (eg, from hypocalcemia) sometimes causes tetany or seizures. Generalized weakness may be noted if the patient also has hypokalemia.

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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