- Adequate free water intake (without salt) to compensate for water loss
and avoid dehydration and hypernatraemia. - Thiazide diuretic may help. The mechanism is mostly through
induction of hypovolaemia. This will increase proximal tubular water
reabsorption and thus reduces the amount of urine reaching to the
distal nephron (the site of abnormality).
B. Water Retention:
This is usually caused by drugs increasing sensitivity of distal
nephron to ADH leading to excess water reabsorption which will lead to
dilutional hyponatraemia. These drugs are: cyclophosphamide,
indomethacin, sulfonylureas (chlorpropamide, tolbutamide),
acetaminophen, oxytocin and vasopressin.
Clinical Features and Diagnosis:
The picture is similar to that of the syndrome of inappropriate
secretion of ADH (SIADH) but with low plasma ADH level. There is
euvolaemic or hypervolaemic state (oedema, high blood pressure,
decreased haematocrit ratio), dilutional hyponatraemia and hypoosmolality
(irritability, disorientation, lethergy, twitching, nausea, seizures, and even
coma), mortality is 10% in chronic hyponatremia and 50% in acute
hyponatremia.
Treatment:
Withdrawal of the causative drug. If this is not possible, give
demeclocycline 200-600 mg/d.