Approach

The main goals of management are treating the primary condition causing the polydipsia and monitoring electrolytes.[3] If hyponatraemia is present, the onset (acute versus chronic), symptomatology (degree and duration), and risk factors for central nervous system (CNS) complications should be taken into account.[3][65]

Severe or symptomatic hyponatraemia: correction of serum sodium

Acute symptomatic hyponatraemia occurs in under 48 hours when fluid intake is rapid and far above normal levels, resulting in cerebral oedema.[1] Chronic hyponatraemia may be asymptomatic due to CNS adjustment to low sodium levels. Balancing the risk of hyponatraemia-associated complications and the risk of sodium correction, and customising treatment to the individual patient, is optimal. A nephrology consultation should be sought early.

Treatment should be initiated on the basis of symptoms.[66] An acute drop in sodium level of 10 mmol/L (10 mEq/L) over a few hours may be sufficient to produce clinical symptoms, including restlessness, salivation, ataxia, stupor, and coma.[67] Gastrointestinal (GI) symptoms (including nausea and vomiting) can be seen in patients with sodium levels between 125 and 130 mmol/L (125-130 mEq/L). Neurological symptoms (including restlessness, psychosis, ataxia, stupor, and coma) are predominant at serum sodium levels <125 mmol/L (<125 mEq/L).[54]

Correction strategies include the use of hypertonic saline (3%) infusions. Vigilant and frequent monitoring of serum sodium and electrolytes during this process is essential.[65] This minimises risk of central pontine myelinolysis and osmotic demyelination that can occur with very rapid correction.[1] With acute, severe symptoms, electrolytes should be monitored initially every 2-3 hours, progressing to every 6-12 hours when sodium levels are stabilised.

For patients with severe hyponatraemia (<125 mmol/L [<125 mEq/L]) or with neurological symptoms, rapid correction with hypertonic saline (3%) infusions is needed. Infusion rates range from 1 mL/kg/hour to 6 mL/kg/hour if severe neurological symptoms such as seizures are present.[41] Correction should continue until the patient is asymptomatic and serum sodium level is >118-120 mmol/L (>118-120 mEq/L), to minimise the risk of seizures. Once the patient is asymptomatic and sodium levels are >118 mmol/L (>118 mEq/L), correction should occur at a maximum of 8 mmol/L (8 mEq/L) in 24 hours, to achieve a target sodium level of 125 mmol/L (125 mEq/L).[68]

The goal is to limit correction to <12 mmol/L (<12 mEq/L) (1.5 to 2 mEq/L/hour or approximately 0.5 mmol/L/hour) on the first day and <6 mmol/L (<6 mEq/L) for every subsequent day until symptoms subside or serum sodium rises. Symptoms usually subside after a modest increase in sodium of 3-5 mmol/L (3-5 mEq/L).[29]

For patients with serum sodium between 125 and 130 mmol/L (125-130 mEq/L) or with GI symptoms, the goal is to limit correction to <12 mmol/L (<12 mEq/L) (1.5 to 2 mEq/L/hour, or approximately 0.5 mmol/L/hour) on the first day and <6 mmol/L (<6 mEq/L) for every subsequent day until symptoms subside or serum sodium rises. Symptoms usually subside after a modest increase in sodium of 3-5 mmol/L (3-5 mEq/L).

Fluid restriction and diuretics

Patients with chronic symptoms and no or mild hyponatraemia should be treated with fluid restriction. For those with dilute urine (urine osmolality <200 mOsm/kg H₂O), fluid restriction should begin at 1 to 1.5 L/day. However, for patients with a urine osmolality over 200 mOsm/kg H₂O, fluid restriction to 0.8 to 1.5 L/day is recommended.[29] Fluid restriction necessitates constant monitoring to prevent patients from seeking alternative water sources (e.g., bathroom taps).

Regular patient weights are often used to determine water intake diurnally. In a monitored setting (e.g., in a hospital or group home), patients may be weighed each morning and in the afternoon, as well as any time they are showing symptoms of polydipsia.[10] If body weight exceeds a pre-determined threshold, brief fluid restriction for 1-3 hours may help eliminate excess water through diuresis.[10] Differences in diurnal weight gain in patients with PPD can be much greater than those in controls (2.2% vs. 0.6%).[37]

In addition to fluid restriction, giving loop diuretics to enhance water excretion (e.g., furosemide) may be necessary.[29] This has been described in individuals with intellectual disabilities and behavioral disorders in the intensive care setting.[69] Furosemide preferentially causes water excretion over sodium excretion.[1]

Behavioural therapy

Behavioural intervention

  • Therapeutic fluid restriction is an inexpensive form of treatment, but high rates of non-compliance in patients with psychiatric disorders may pose challenges, and it may take several days for a clinical effect to appear.[41]

  • Group psychotherapy may improve adherence to fluid restriction.[70]

  • Reinforcement schedules using tokens for rewards and removing these tokens for non-adherence have been used with some success.[71]

  • Most behavioural intervention studies are reported in inpatients, often requiring close monitoring and a substantial time commitment from staff. In extreme cases of non-adherence, patients may be confined to an area where there are no water sources.

Behavioural modification

  • Therapists use cognitive techniques to address thoughts leading to drinking behaviour by implementing a behavioural programme to restrict water intake. The focus is on stimulus-control methods that include positive reinforcement and coping skills.

  • Patients are followed up weekly for 12 weeks. Delusions and fears related to drinking excessively are addressed. The patient maintains a log of the time, fluid amount, and mitigating situation for each beverage consumed.

  • For example, a 500 mL water jug is given to the patients as a stimulus-control device. The patient is instructed to fill it only 6 times daily, to achieve a goal of less than 3 litres for water restriction. The patient uses coping skills (substituting ice cubes for drinks, taking small sips, engaging in distracting activities) and positive feedback from the therapist, along with improvement of urinary frequency, to reinforce fluid restriction.[49]

Psychopharmacological therapy

Atypical antipsychotics have been reported to improve symptoms of PPD:

  • Clozapine has shown benefit in case reports and prospective trials.[1][10][72][73] A prospective 6-week study of clozapine in 8 patients with schizophrenia who had polydipsia and low plasma osmolality showed that clozapine normalised plasma osmolality and was well tolerated.[74] PPD is not a licensed indication for clozapine, and although clozapine has the most evidence for antipsychotic use in PPD, the use of clozapine and presence of hyponatraemia are both associated with a decreased seizure threshold. Therefore, this potential iatrogenic effect should be considered in clinical decision-making, especially when other comorbidities which increase the risk for epilepsy are present (e.g., traumatic brain injury, cerebrovascular accident).  

  • Risperidone and olanzapine improved polydipsia in case reports, but prospective double-blind studies have not shown any benefit with olanzapine.[75][76][77]

Use of this content is subject to our disclaimer