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What is SIADH syndrome and definition
The SIADH is characterized by enormous release of antidiuretic hormone from the posterior pituitary gland. It is the most common cause of euvolemic hyponatremia in hospitalized patients. The syndrome is associated with patients that have pneumonia, brain tumors, head trauma, strokes, meningitis, encephalitis, small-cell carcinoma of the lung, Hodgkin disease, or with patients that use drugs as thiazide diuretics, paracetamol, indomethacin, karbamazepin, SSRI and many others.
ADH (antidiuretic hormone) is produced by cells in ncl. supraopticus and ncl. paraventricularis in hypothalamus. Produced hormone is transported via axonal transport to nerohypophysis, from which it is secreted into bloodstream. The secretion is directed by osmoreceptors in hypothalamus. ADH increase permeability in distal tubules and collecting tubules in kidneys. The ADH receptors in tubules are called aquaporins. These receptors transport water from primary urine back to the body.
Increased secretion of ADH cause higher reabsorption in the tubules and the result is increased volume in intravascular and extravascular space. As a response the ANP (atrial natriuretic peptide) is released. Therefor patients have increased natriuresis, lower natremia.
Clinical picture: Symptoms of brain edema. There is lethargy, apathy, disorientation, nausea, vomiting, cramps, Cheyne-Stokes breathing. Symptoms respond to the velocity of falling natremia, not to the absolute level of natrium in blood. Rapidly falling natremia is typical for acute stadium. In chronic stadium natremia decreases gradually.
Diagnosis: Laboratory findings in diagnosis of SIADH include: hyponatremia, hypoosmolality, metabolic acidosis.
- The main goal is to stabilized natremia. The plan depends on stadium of SIADH.
- acute stadium – hypertonic solutions are applied + furosemide.
- chronic stadium – fluid restriction
- Other alternative is using vaptans