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Definition and EtiologyTop
1. The sensation of thirst and the role of serum osmolality: The human body needs to maintain a serum osmolality between 280 and 295 mOsm/kg. This physiologic necessity is achieved by a combination of the sensation of thirst, secretion of antidiuretic hormone (ADH) (also referred to as arginine vasopressin [AVP]), and renal response to AVP. Thirst and AVP release are controlled by the central nervous system (CNS). The involved areas of the CNS lack the blood-brain barrier, which allows for direct sensing of the osmolality of circulating blood, so that large fluctuations can be detected and avoided or corrected if they occur.
If serum osmolality rises to ~285 mOsm/kg, below which AVP is essentially undetectable, AVP is released by neurons in the hippocampus. The exact serum osmolality that triggers thirst is debated but is thought to share the same threshold as AVP. Thirst leads to increased consumption of free water and AVP release leads to increased uptake of free water from the kidneys, both eventually resulting in lowering of serum osmolality to the narrowly controlled range. Abnormalities involving any of these steps (thirst, AVP release, or resistance to AVP at the kidney level) can lead to serious derangements in serum sodium levels and osmolality. It is difficult to establish volumes of fluid intake and output that would be considered abnormal, as this may depend on the personal and environmental factors (imagine a long-distance runner in a warm climate).
2. Etiology: Most frequently increased thirst is due to loss of water. Less often it results from a primary disturbance of water intake or reabsorption at the level of the kidneys. Excessive water loss may lead to hypertonic dehydration or less frequently to isotonic or hypotonic dehydration (see Dehydration).
1) Water loss through the skin, gastrointestinal (GI) tract, or respiratory tract: Vomiting, diarrhea, fistulas (various enteric and pancreatic fistulas; surgical and nonsurgical), excessive sweating, fever.
2) Water loss through the kidneys due to osmotic (solute) diuresis: Diabetes mellitus and new sodium-glucose cotransporter 2 (SGLT-2) inhibitors, urea diuresis (a mechanism partially responsible for increased water loss in recovering acute tubular necrosis in addition to tubular dysfunction in this condition), increased tissue catabolism, high-protein diet or feeds, administration of urea as treatment of syndrome of inappropriate antidiuretic hormone secretion (SIADH), sodium diuresis (administration of IV fluids and postobstructive diuresis), or mannitol.
3) Primary disturbance of water intake: Psychogenic polydipsia, pituitary diseases (sarcoidosis, histiocytosis), drug-induced xerostomia (mirtazapine, thioridazine, chlorpromazine, anticholinergic agents).
4) Water loss through the kidneys caused by arginine vasopressin deficiency or resistance: Neurogenic diabetes insipidus, nephrogenic diabetes insipidus.
Any diagnostic workup should start with a detailed history and physical examination. If an obvious cause is found, treating the underlying etiology or modification of pharmacotherapy can be considered. Additional studies: plasma and urine osmolality; urinalysis; plasma levels of creatinine, urea, glucose, sodium, potassium, total protein and calcium; urinary levels of sodium; complete blood count (CBC).
A detailed history, physical examination, and results of diagnostic studies are usually sufficient to diagnose polydipsia caused by water loss through the GI tract, skin, or lungs, or through the kidneys due to osmotic diuresis. Once these causes have been excluded, nephrogenic or neurogenic diabetes insipidus or psychogenic polydipsia should be suspected and further testing performed (water deprivation test, vasopressin stimulation test [see Diabetes Insipidus]).
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