Abstract
We had a case of syndrome of inappropriate secretion of antidiuretic hormone induced by hemorrhage in the right caudate nucleus.
The patient was a 67 year old man. His chief complaints were left hemiplegia and gait disturbance. His present illness and its course prior to admission to our hospital were as follows : Left hemiparesis and gait disturbance were first noticed on the morning of Oct. 14, 1978. Therapy after admission was done at another hospital, and he was able to walk very well by himself in about one month. He was followed up as an outpatient after discharge, but gait distur-bance gradually became exaggerated again from January, 1980, so he visited our hospital on April 1, 1980.
After his admission to our hospital, rehabilitation through training and drug therapy improved his condition, but he suffered two attacks of cerebral thrombosis on Oct. 25, 1980 and on Dec. 23, 1980, respectively. For the purpose of protecting him from a reccurrence, anticoagulants had been administered to him since January 20, 1981. The gait disturbance and dysarthria caused by transient cerebral ischemic attacks, however, frequently occurred. Rigidity of the whole body and an excess of sweat were noticed by his wife at noon on March 31, 1981. A CT scan of the brain showed the high density area of the right caudate nucleus, the lateral ventricle and the third ventricle. These findings meant the hemorrhage in the right caudate nucleus had perforated the cerebral ventricular system.
As hyponatremia and hypokalemia were observed after the cerebral hemorrhage, hyperosmotic saline infusion was performed. Hyponatremia, however, continued for about three weeks. On the other hand, a potassium drug soon normalized hypokalemia. The chief laboratory data obtained during hyponatremia were composed of serum osmorality 262 mOsm/L, urinary osmorality 440 mOsm/L, urinary sodium excretion 5.2 g/day (the same as before cerebral hemorrhage) and blood pH 7.48. The concentration of ADH in perpheral venous blood was 1.5 pg/ml. The normal value of ADH would be caused by the blood sampling at the beinning of serum sodium normalization.
As no pretibial edema was pinpointed in this case and hypoosmotic fluid transfusion was not given to correct dehydration, the hyponatremia induced by cerebral hemorrhage belonged to neither hypervolemic nor hypovolemic hyponatremia. Therefore, in this case, hyponatremia was categorized as normovolemic. Generally there are many causes of pathogenesis of hyponatremia, and SIADH is one cause. This case fits Schwartz's criteria of SIADH except for renal dysfunction. As the attack of cerebral hemorrhage didn't influence the renal function, it seemed that renal dysfunction had not been a cause of hyponatremia in this case. After all, there was no discrepancy with Schwartz 's criteria of SIADH in this case, but whether secretion of ADH was appropriate or inappropriate could not be confirmed.
Conclusively this case was diagnosed as SIADH induced by hemorrhage in the right caudate nucleus.
