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    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.