Antidiuretic hormone (ADH) is secreted in excess as the normal balance is disrupted. The kidneys respond to the antidiuretic hormone by retaining additional fluid in the body, often in excess.
There are several mechanisms in which SIADH can develop. Besides increased secretion as a cause, the kidneys can develop increased sensitivity to ADH, as the cellular osmostat can be reset. Often, this is caused by medication administration, especially with chlorpropamide, tolbutamide, carbamazepine, mizoribine, nonsteroidal anti-inflammatory drugs, and cyclophosphamide.
Because this condition causes the normal blood volume to dilute with only free water, the overall osmolality decreases below normal, often less than 280 mOsm/kg. This decreased osmolality in the extracellular space causes fluid to enter the interstitial spaces, causing cellular swelling.
In severe cases of SIADH, there is a tremendous decrease in serum osmolality, leading to marked hyponatremia. If the serum sodium level becomes drastically low, patients are at risk for seizure, stupor, hallucinations and even coma.
As the extracellular blood volume is diluted with free water, the sodium level per liter of blood is reduced. This decrease causes many signs of hyponatremia, such as muscle cramps, weakness, fatigue, confusion, and changes in LOC. SIADH can only be diagnosed if serum sodium levels are below normal (<135 mEq/L).
Due to the hypoosmolar state that develops in SIADH, patients become hyponatremic. This electrolyte abnormality has several manifestations, which also include muscle cramping or tremor.
Patients typically have a normal overall fluid volume status (euvolemia) due to excessive free water reabsorption despite hyponatremia due to excessive secretion into the urine.
As hyponatremia worsens with more advanced SIADH, patients may exhibit confusion and personality changes. As sodium level drops below 110 mEq/L, they may progress to a comatose state.
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