Schwartz-Barter syndrome: causes, symptoms, diagnosis, treatment

Schwartz-Bartter syndrome is a syndrome of inappropriate secretion of antidiuretic hormone. Clinical symptoms depend on the degree of water intoxication and the degree of hyponatremia. The main signs of this disease are hyponatremia, a decrease in the osmotic pressure of blood plasma and other body fluids with a simultaneous increase in the osmotic pressure of urine. Despite the fact that the water content in the body increases, symptoms such as edema and hypertension are absent (the presence of edema syndrome is possible with a significant increase in water consumption only with simultaneous kidney disease with impaired sodium secretion or heart failure).

Causes of Schwartz-Barter syndrome

Schwartz-Bartter syndrome most often occurs subclinically, is quite rare, but is diagnosed even less often, and can accompany numerous CNS diseases (both diffuse and local). Laboratory testing of blood sodium levels allows for a correct diagnosis and the necessary measures. Various causes leading to the syndrome of inappropriate secretion of antidiuretic hormone are explained by the fact that the predominant inhibitory effect of antidiuretic hormone secretion is carried out by suprahypothalamic formations. Thus, in CNS diseases of various nature and localization, a kind of "denervation" hyperactivation of the hypothalamic-pituitary structures with subsequent hypersecretion of antidiuretic hormone may occur. In some cases, the causes of the disease cannot be established, then idiopathic syndrome of inappropriate secretion of antidiuretic hormone is diagnosed.

Pathogenesis of Schwartz-Bartter syndrome

As a result of hypersecretion of antidiuretic hormone, fluid accumulation and a progressive decrease in the concentration of substances dissolved in the body occur.

With a 10% increase in water volume, sodium excretion with urine increases. Natriuresis somewhat reduces hypervolemia, but increases hyponatremia, while the decrease in osmotic pressure of body fluids progresses even more. Hypersecretion of antidiuretic hormone is associated with hyperactivation of the supraoptic nuclei of the hypothalamus and neurohypophysis, which develops, as a rule, as a result of a violation of extrahypothalamic inhibitory mechanisms in relation to antidiuretic hormone.

According to the severity, a mild or chronic form, moderate and severe are distinguished depending on the severity of hyponatremia. For the mild or chronic form, complaints of decreased appetite, fatigue, nausea are characteristic. Most often, this form is subclinical. In severe cases, with a decrease in the sodium concentration to 120 mEq/l, vomiting, drowsiness, and confusion occur. With a further decrease in the sodium concentration to 100 mEq/l and below, paresis, convulsions, and coma may be observed. These cerebral phenomena are due to the development of hyperhydration and symptoms of cerebral edema. It should be emphasized that the clinical manifestations of the disease directly depend on the amount of fluid consumed.

Differential diagnosis. Should be performed with ectopically located tumors secreting antidiuretic hormone (bronchogenic cancer, thymoma, pancreatic cancer, ureteral cancer, duodenal cancer, Ewing's sarcoma), with non-neoplastic pulmonary diseases (pneumonia, fungal diseases, tuberculosis), drug intoxications (vasopressin, oxytocin, vincristine, chlorpropamide, chlorothiazide, tegretol, nicotine, phenothiazines, cyclophosphamide), endocrinopathies (myxedema, Addison's disease, hypopituitarism), somatic diseases (heart failure, liver cirrhosis).

Treatment of Schwartz-Barter syndrome

The main treatment tactics consist of strict restriction of fluid intake. Its total consumption should not exceed 0.5 l/day. In emergency conditions with cerebral symptoms, infusion of hypertonic sodium chloride solution (3-5%) is used, which is administered at a rate of 3 ml/kg per hour with simultaneous intravenous administration of furosemide. In moderate and mild forms, furosemide is not used due to pronounced natriuria. Quite effective are drugs that inhibit the effect of vasopressin on the kidneys, such as demeclocycline (declomycin). It is prescribed for the chronic form of the syndrome at a dose of 1.2 g/day. When used, it is possible to induce a reversible form of nephrogenic diabetes insipidus. The use of lithium carbonate for the same purpose is hardly justified, since it is highly toxic and has pronounced side effects.