TAILIEUCHUNG - Chapter 048. Acidosis and Alkalosis (Part 10)

Differential Diagnosis To establish the cause of metabolic alkalosis (Table 48-6), it is necessary to assess the status of the extracellular fluid volume (ECFV), the recumbent and upright blood pressure, the serum [K+], and the renin-aldosterone system. For example, the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or that the hypertensive patient is receiving diuretics. Low plasma renin activity and normal urine [Na+] and [Cl–] in a patient who is not taking diuretics indicate a primary mineralocorticoid excess syndrome. The combination of hypokalemia and alkalosis in a normotensive, nonedematous patient can be. | Chapter 048. Acidosis and Alkalosis Part 10 Differential Diagnosis To establish the cause of metabolic alkalosis Table 48-6 it is necessary to assess the status of the extracellular fluid volume ECFV the recumbent and upright blood pressure the serum K and the renin-aldosterone system. For example the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or that the hypertensive patient is receiving diuretics. Low plasma renin activity and normal urine Na and Cl- in a patient who is not taking diuretics indicate a primary mineralocorticoid excess syndrome. The combination of hypokalemia and alkalosis in a normotensive nonedematous patient can be due to Bartter s or Gitelman s syndrome magnesium deficiency vomiting exogenous alkali or diuretic ingestion. Determination of urine electrolytes especially the urine Cl- and screening of the urine for diuretics may be helpful. If the urine is alkaline with an elevated Na and K but low Cl- the diagnosis is usually either vomiting overt or surreptitious or alkali ingestion. If the urine is relatively acid and has low concentrations of Na K and Cl- the most likely possibilities are prior vomiting the posthypercapnic state or prior diuretic ingestion. If on the other hand neither the urine sodium potassium nor chloride concentrations are depressed magnesium deficiency Bartter s or Gitelman s syndrome or current diuretic ingestion should be considered. Bartter s syndrome is distinguished from Gitelman s syndrome because of hypocalciuria and hypomagnesemia in the latter disorder. The genetic and molecular basis of these two disorders has been elucidated recently Chap. 278 . Table 48-6 Causes of Metabolic Alkalosis I. Exogenous HCO3- loads A. Acute alkali administration B. Milk-alkali syndrome II. Effective ECFV contraction normotension K deficiency and secondary hyperreninemic hyperaldosteronism A. Gastrointestinal origin 1. Vomiting 2. Gastric aspiration 3. .

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