Siadh ( Syndrome Of Inapproperiate Antidiuretic Hormone Secretion)

SIADH

WHAT IS ADH? AND FROM WHERE IT IS SECRETED? AND FUNCTIONS OF ADH. • Anti diuretic hormone. Secreted by posterior pituitary or neurohypophysis to the distal convoluted tubules and collecting tubules of the nephron. • Functions:-function of ADH on the kidneys is to control the amount of water reabsorbed by kidney nephrons and causes the retention of water, but not solute. Hence, ADH activity effectively dilutes the blood.

hypothalamus( osmoreceptors) posterior pituitary ADH aquaporins (DCT and CT) urine out put

• ADH is secreted to prevent water loss in the kidneys. When water is ingested, it is taken up into the circulation and results in a dilution of the plasma. This dilution, otherwise described as a reduction in plasma osmolality, is detected by osmoreceptors in the hypothalamus of the brain and these then switch off the release of ADH. • The decreasing concentration of ADH effectively inhibits the aquaporins in the collecting ducts and distal convoluted tubules in the nephrons of the kidney. Hence, less water is reabsorbed, thereby increasing urine output, decreasing urine osmolality, and increasing (normalization of) blood osmolality.

WHAT IS SIADH AND ITS CAUSES AND CLINICAL FEATURE. • This is a syndrome characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland. • The result is hyponatremia, and sometimes fluid overload

Some common causes of SIADH include: • • • • • • • • • • •

meningitis (treated with fluid restriction and diuretics) Head injury Subarachnoid hemorrhage Cancers Lung cancer (especially small cell lung cancer, as well as other small-cell malignancies of other organs) Infections Brain abscess Drugs Carbamazepine Selective serotonin reuptake inhibitors (SSRIs, a class of antidepressants) Methylenedioxymethamphetamine (MDMA)

c/f • In general, increased ADH causes water retention and extracellular fluid volume expansion without edema or hypertension, owing to natriuresis (retention of water and passing of sodium in urine). • The water retention and sodium loss both cause hyponatremia, which is a key feature in SIADH. Hyponatremia and concentrated urine (UOsm >300 mOsm) are seen, as well as no signs of edema or dehydration. • When hyponatremia is severe (sodium <120 mOsm), or acute in onset, symptoms of cerebral edema become prominent (irritability, confusion, seizures, and coma).

WHAT IS THE DIANGNOSIS AND MANAGEMENT OF SIADH

Dx ( c/f and lab findings) • •

Hyponatremia <130 mEq/L, and POsm <270 mOsm/kg. Other findings include-

•

Urine sodium concentration >20 mEqlL (inappropriate natriuresis) Maintained hypervolemia Suppression of renin-angiotensin system No equal concentration of atrial natriuretic peptide Low blood urea nitrogen (BUN) Low creatinine Low uric acid Low albumin

• • • • • • •

management • Treating underlying causes when possible. • Fluid restriction to 800-1,000 ml/d should be obtained to increase serum sodium. • Intravenous saline - For very symptomatic patients (severe confusion, convulsions, or coma) hypertonic saline (5%) 200-300 ml IV in 3-4 h should be given.

• Drugs • Demeclocycline can be used in chronic situations when fluid restrictions are difficult to maintain; demeclocycline is the most potent inhibitor of AVP action. • Conivaptan - an approved antagonist of both V1A and V2 vasopressin receptors. Its indications are "treatment of euvolemic hyponatremia (e.g. the syndrome of inappropriate secretion of antidiuretic hormone, or in the setting of hypothyroidism, adrenal insufficiency, pulmonary disorders, etc.) in hospitalized patients."[1]