Primary Polydipsia

Primary polydipsia is excessive fluid intake without an osmotic stimulus, producing polyuria with dilute urine and, in extreme cases, hyponatraemia.

• Types: psychogenic polydipsia (schizophrenia, up to 6–20% of chronic psychiatric inpatients), dipsogenic polydipsia (abnormal thirst mechanism from hypothalamic disease, sarcoidosis, tuberculosis, head trauma), iatrogenic or habitual (health beliefs, "drink more water"), drug-induced (anticholinergic, phenothiazines, carbamazepine).
• Water intake over 3 L/day (often 5 to 15 L); ADH suppressed appropriately.
• Chronic polydipsia causes renal medullary washout and impaired concentrating ability, mimicking partial nephrogenic DI.
• Complications: hyponatraemia (water intoxication) with seizures, coma, cerebral oedema, rhabdomyolysis; hydronephrosis, bladder dilatation.

• Polyuria, polydipsia, nocturia, thirst, usually described as pleasant or compulsive.
• Psychiatric history (schizophrenia, intellectual disability, eating disorders), medications, restless drinking behaviours.
• Acute water intoxication: headache, nausea, vomiting, confusion, seizures, coma.
• Chronic: mild hyponatraemia (125 to 135 mmol/L), fatigue, hydronephrosis, urinary incontinence.

• Polyuria (over 3 L/day) with low urine osmolality (under 300 mOsm/kg), low-normal serum sodium (135–140) and serum osmolality under 285 mOsm/kg.
• Plasma copeptin low (under 4.9 pmol/L baseline) or appropriate suppressed ADH; hypertonic saline-stimulated copeptin over 4.9 pmol/L at sodium over 149 mmol/L supports primary polydipsia (accuracy 95%).
• Water deprivation test with caution (risk of hypernatraemia in DI, but may unmask partial concentration defect from washout); urine osmolality rises toward 500–800 mOsm/kg gradually but may be blunted by medullary washout.
• Exclude diabetes mellitus, hypercalcaemia, hypokalaemia, central DI, nephrogenic DI, adrenal insufficiency, thyroid disease.
• Review medications and psychiatric history, MRI pituitary and hypothalamus if suspected organic dipsogenic polydipsia.
• Hypertonic saline stimulation test in specialised centres.

• Behavioural therapy: fluid restriction (1.0–1.5 L/day, gradual reduction to avoid thirst), structured fluid diaries, weight monitoring (daily weight gain over 2–3 kg indicates excess intake).
• Never give desmopressin (risk of severe hyponatraemia).
• Treat underlying psychiatric disorder: clozapine 150 to 450 mg daily may reduce polydipsia in schizophrenia; naltrexone, demeclocycline, propranolol, ACE inhibitors, and risperidone have been tried with variable evidence.
• Cognitive behavioural therapy, supervised fluid regimens, mouth care, sugar-free gum.
• Acute hyponatraemia with symptoms: hypertonic saline 3% 100 to 150 mL IV over 10 to 20 minutes, repeated up to twice, aiming for a 4–6 mmol/L rise in the first 6 hours; limit correction to 8–10 mmol/L in 24 hours (risk of osmotic demyelination, lower with water diuresis: monitor sodium hourly, consider desmopressin clamp if overcorrection).
• Mild asymptomatic hyponatraemia: fluid restriction.
• Dipsogenic polydipsia: treat primary cause (sarcoid steroids, antituberculous therapy).
• Long term monitoring of sodium, bladder function, renal ultrasound; psychiatric follow-up.