FRAWLEY—COMPLICATIONS OF ACTH AND CORTISONE THERAPY

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potassium may prove fatal if an absolute or even relative hyperpotassemia develops.
The readjustment of the serum electrolyte abnormality should be made promptly
but not too rapidly and preferably by the oral route (chart 2).
Patients treated with ACTH and cortisone tend to retain sodium and water,
so that edema develops. This is particularly undesirable in situations where con­
gestive heart failure is imminent or already exists. To a large extent it may be
prevented by restricting the patient to a low sodium diet (less than 1.5 Gm. daily)
and limiting fluids to 1,000 to 1,500 ml. daily. In spite of these measures, it is
occasionally necessary to administer a mercurial in order to force diuresis. Since
this diuresis increases potassium excretion, it can prove serious to the edematous
patient who may already be hypopotassemic. It therefore is extremely important
before using diuretics to have a nearly normal serum potassium level or to protect
the potassium level with supplementary potassium.
Finally, it should be stated that a spontaneous diuresis occasionally occurs during
prolonged ACTH or cortisone therapy and that one invariably follows 48-72 hours
after withdrawal of treatment. At the end of the period of diuresis the patient may
complain of headache, weakness, drowsiness and a “washed-out” feeling. Additional
fluids by mouth, such as broths or fruit juices, will correct this situation if it is not
too severe.
In summary, the most important electrolytic change associated with the use of
ACTH and cortisone is the reduction in serum potassium. This is easily detected
chemically or with the electrocardiogram and is readily prevented and corrected with
potassium chloride. A varying degree of sodium and water retention is observed
in some patients receiving these hormones. Any edema which develops clears when
treatment is withdrawn.
Metabolic Changes.—Characteristically, ACTH and cortisone significantly
affect the intermediary metabolism of protein, carbohydrate and fat (table 2). The
effect most commonly observed clinically is on carbohydrate metabolism. Hyper­
glycemia and glycosuria accompany treatment with these hormones, but it rarely
becomes necessary to institute insulin therapy. The glycosuria is in a large measure
due to a reduction of renal threshold and alone is not sufficient reason for giving
insulin. If the fasting blood sugar is increased more than twofold and the treatment
is to be prolonged, it may be wise to start insulin using the blood sugar to determine
the dosage needed. Thus far, permanent diabetes following ACTH or cortisone has
not been reported. In the diabetic patient who must be treated with ACTH or
cortisone, the change in insulin requirement is most easily handled by the addition of
small increments of crystalline insulin to the daily insulin dosage., The amount of
crystalline insulin required may be determined by following the blood sugar. This
is a much more accurate procedure to follow, but the increase in glycosuria may be
used. It is important to emphasize the necessity of administering larger amounts
of crystalline insulin than are..customarily given to reduce glycosuria. This is . in
part due to the antagonism which exists between adrenal cortical steroids and insulin.
Any increase in the severity of the diabetes never reaches alarming proportions.
In the diabetic patient receiving ACTH or cortisone it is most important to reduce
the insulin dosage immediately on discontinuing hormone treatment. Otherwise,
severe hypoglycemic episodes may develop, due to temporary adrenal cortical insuf­
ficiency and increased insulin sensitivity. It is much better to be safe and cut back
the insulin to the previous maintenance level immediately rather than make graded
reductions.