Aetiology

The exact cause of PPD is not known. Occurring in 6% to 20% of psychiatric patients, PPD is most commonly seen in people with schizophrenia, but may also present in those with other psychiatric disorders and neurodevelopmental disorders.[1][2][3][4][5][6][7] Affective disorders, anxiety disorder, anorexia nervosa, obsessive compulsive disorder, and personality disorders have all been associated with PPD. Polydipsia can also occur in the absence of underlying medical or psychiatric conditions.[10] Increasing popularity of lifestyle programmes that advocate water drinking to improve overall health have led to a rise in polydipsia among the general population.[10]

PPD seen in adolescents and young adults is often associated with anorexia nervosa, possibly as a coping strategy and/or to reduce hunger.[13][14]

People with schizophrenia report drinking in the absence of thirst to alleviate dysphoria, or in response to delusional beliefs.[10] Individuals with schizophrenia or cognitive impairment have also reported drinking excessive amounts of fluids to 'feel better', comparing the effects of excessive fluid intake to drinking alcohol.[17]

Nicotine stimulates antidiuretic hormone release, and, in some studies, up to 70% of patients with self-induced polydipsia were cigarette smokers.[18][19] In a study of psychiatric patients with compulsive water-drinking, symptomatic hyponatraemia developed only in those who were heavy smokers.[20]

Pathophysiology

Water homeostasis in healthy people

  • In healthy people, antidiuretic hormone (ADH), also known as arginine vasopressin, primarily exerts a hydro-osmotic effect by promoting the reabsorption of water from the tubular fluid along the course of the distal tubule and collecting duct. Secondarily, a pressor effect causes arteriolar vasoconstriction and a rise in arterial blood pressure. ADH has no significant effect on the rate of sodium reabsorption.

  • Secretion of ADH is suppressed at plasma osmolalities <280 mOsm/kg H₂O. The thresholds for ADH suppression and suppression of thirst are set near each other.[21] These linked set points suppress thirst before or at the same time as ADH is completely suppressed.

  • Renal excretion of dilute urine, along with intake of solutes, normally protects against profound hyponatraemia. Symptomatic hyponatraemia occurs when the kidney's short-term capacity to excrete urine is overwhelmed.[22]

Mechanism of polydipsia in PPD

  • The aetiopathogenesis of PPD is multifactorial.

  • Patients with PPD have a difference in the set points of ADH suppression and thirst suppression. They feel thirsty and drink excessive water even when ADH is fully suppressed.[23][24]

  • Hippocampus-mediated neuroendocrine dysregulation during acute psychotic episodes may reset the osmostat for ADH secretion, leading to transient impairments in water excretion.[10][25]

  • Some patients with schizophrenia drink excessive water in the absence of thirst to alleviate dysphoria, or in response to delusional beliefs.[10] Individuals with schizophrenia or cognitive impairment have also reported drinking excessive amounts of fluids to 'feel better', comparing the effects of excessive fluid intake to drinking alcohol.[17]

Hyponatraemia in PPD

  • In 3% to 6% of patients, PPD leads to low plasma sodium (hyponatraemia).[10][12] Symptomatic hyponatraemia is more likely after an acute 3- to 4-litre fluid ingestion (e.g., in urinary drug testing and before radiological examinations) or if patients continue to drink excessively (>10 litres daily) after reaching their limit of urine dilution (100 mOsm/kg H₂O in osmolality) and ADH suppression.[4][22]

  • Co-existing syndrome of inappropriate secretion of ADH (SIADH; central hypersecretion or increased renal sensitivity) can also precipitate hyponatraemia. Failure to maximally suppress ADH secretion is the foundation of SIADH. Increased ADH secondary to stress or nausea can also contribute to impaired water excretion. It is often these patients with paradoxically higher ADH effect, in the face of heavy fluid intake, who develop profound hyponatraemia.

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