METABOLIC ALKALOSIS DEFINITION A primary rise in plasma bicarbonate concentration to greater than 28 mEq/L. This may be due to: * loss of acid from extracellular fluid in the urine or stool, or in acid-containing gastric juice (e.g. vomiting) or transfer of H+ ions into cells * excessive bicarbonate load (e.g. alkali given to patients with renal failure) * rapid contraction of the extracellular space due to excessive diuretic treatment TOXIC CAUSES Bicarbonate Loop diuretics (furosemide, ethacrynic acid) Mercurial diuretics (now obsolete). Any poisoning that results in severe vomiting may cause secondary metabolic alkalosis. NON-TOXIC CAUSES Administration of excessive bicarbonate in renal failure. Removal by suction of acid gastric contents. Vomiting from any cause, especially in patients with pyloric stenosis. CLINICAL FEATURES History of recent excessive loss of gastric contents, high-dose loop diuretic administration or alkali overload in patients with renal failure. Irritability, hyperexcitability, mental confusion, sometimes resembling that of alcohol intoxication, bradypnoea (even down to 6 to 8 respirations per minute), cyanosis, sometimes extreme. Muscular weakness, impaired gastrointestinal peristalsis (gastric retention, paralytic ileus), and polyuria suggest associated K+ depletion. Tetany may occur due to a fall in the serum ionized calcium fraction. RELEVANT INVESTIGATIONS Arterial blood gases. Significant hypoventilation may be associated with PaCO2 over 50 or even 60 mm Hg. Urine pH. Urine is alkaline but might be paradoxically acidic in cases with severe K+ depletion. Electrolytes. Hypokalaemia and hypochloraemia are usually present. ECG. May show evidence of hypokalaemia. TREATMENT When possible, the underlying cause must be corrected. Usually, oral or intravenous replacement of extracellular volume will suffice. In more severe cases, particularly with marked hypokalaemia and ECG abnormalities, an intensive care setting is necessary. In severe potassium deficiency, alkalosis cannot be corrected until potassium is repleted. In severe cases, unresponsive to other measures, ammonium chloride may be given (1 to 2 g orally every 4 to 6 hours to a maximum of 4 g every 2 hours; or by intravenous infusion of 100 to 200 mEq dissolved in 500 to 1000 ml of isotonic saline) in addition to potassium replacement. CLINICAL COURSE AND MONITORING Arterial blood gases and serum electrolytes should be monitored until normal. In severe metabolic alkalosis, cardiac and respiratory monitoring is needed. Urine output should be measured. LONG-TERM COMPLICATIONS Hypovolaemia, K+ deficiency, and persistent adrenal steroid excess are consequences of chronic metabolic alkalosis. AUTHOR(S)/REVIEWERS Author: Dr Janusz Szajewski, Warsaw Poisons Control Centre, Szpital Praski, Poland. Peer Review: Rio de Janeiro 9/97: J.N. Bernstein, E. Birtanov, R. Fernando, H. Hentschel, T.J. Meredith, Y. Ostapenko, P. Pelclova, C.P. Snook, J. Szajewski. London, 3/98: T. Della Puppa, T.J. Meredith, L. Murray, A. Nantel.