The symptoms of chronic syndrome of inappropriate antidiuresis are more vague, and may include cognitive impairment, gait abnormalities, or osteoporosis.
[2] The presence of cerebral edema, or other moderate to severe symptoms, may necessitate intravenous hypertonic saline administration with close monitoring of the serum sodium levels to avoid overcorrection.
The process occurs as follows: in some hypothalamic cells there are osmoreceptors which respond to hyperosmolality in body fluids by signalling the posterior pituitary gland to secrete ADH.
First, in the extracellular fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration – hyponatremia.
Swelling of brain cells – cerebral edema – causes various neurological abnormalities which in acute and/or severe cases can result in convulsions, coma, and death.
A confirmed diagnosis has seven elements: 1) a decreased effective serum osmolality – <275 mOsm/kg of water; 2) urinary sodium concentration high – over 40 mEq/L with adequate dietary salt intake; 3) no recent diuretic usage; 4) no signs of ECF volume depletion or excess; 5) no signs of decreased arterial blood volume – cirrhosis, nephrosis, or congestive heart failure; 6) normal adrenal and thyroid function; and 7) no evidence of hyperglycemia (diabetes mellitus), hypertriglyceridemia, or hyperproteinia (myeloma).
[1] There are nine supplemental features: 1) a low BUN; 2) a low uric acid; 3) a normal creatinine; 4) failure to correct hyponatremia with IV normal saline; 5) successful correction of hyponatremia with fluid restriction; 6) a fractional sodium excretion >1%; 7) a fractional urea excretion >55%; 8) an abnormal water load test; and 9) an elevated plasma AVP.
The hyponatremia caused by appropriate ADH release (from the kidneys' perspective) in both CHF and cirrhosis have been shown to be an independent poor prognostic indicator of mortality.
[15] Cerebral salt wasting syndrome (CSWS) also presents with hyponatremia, there are signs of dehydration for which reason the management is diametrically opposed to SIADH.
Management of SIADH includes:[5] 40% of all hospitalized adults aged 65 and older have hyponatremia, with an estimated 25–40% of those cases being due to inappropriate antidiuresis.
Patients with extra-renal salt losses complicated by hyponatremia were found to be common-place, and consistent with McCance's description, they excreted urine virtually free of sodium.
Their work suggested that a primary reduction in cellular osmolarity may be the initiating factor in the development of this new syndrome (later called SIADH).
An eosinopenia response to epinephrine and the ability to reduce the excretion of sodium on a regime free of salt aids in differentiating this syndrome from Addison's disease.
[23] Almost a century after the pioneering work of Claude Bernard (1813–1878) in animals, Peters et al, in 1950, reported three patients seen at Yale New Haven Hospital with hyponatremia associated with varying cerebral pathologies and severe dehydration.
They postulated that this provided evidence of an extra-pituitary cerebral structure mediating normal sodium metabolism but were unsure of its location or mechanism of action.
[24] In 1952, Welt et al, described another six patients with cerebral lesions exhibiting severe clinical dehydration, hyponatremia, a negative sodium balance, but no potassium retention.
The authors felt neither pituitary nor adrenal insufficiency was involved, but that direct neural control of renal proximal tubular reabsorption of sodium was disrupted.
[25] In 1953, Leaf et al, demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain.
Vasopressin-ADH administration to normal humans was shown to result in water retention and urinary loss of electrolytes (primarily sodium) in other studies at the time.
The first reports of hyponatremia and renal sodium loss corrected by fluid restriction in patients with bronchogenic carcinoma were published by Bartter.