Approach

The main goals of management are treating the primary condition causing the polydipsia and monitoring electrolytes.[3] If hyponatremia 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][67]

Severe or symptomatic hyponatremia: correction of serum sodium

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

Treatment should be initiated based on symptoms.[68] An acute drop in sodium level of 10 mEq/L over a few hours may be sufficient to produce clinical symptoms, including restlessness, salivation, ataxia, stupor, and coma.[69] Gastrointestinal (GI) symptoms (including nausea and vomiting) can be seen in patients with sodium levels between 125 and 130 mEq/L. Neurologic symptoms (including restlessness, psychosis, ataxia, stupor, and coma) are predominant at serum sodium levels <125 mEq/L.[56]

Correction strategies include the use of hypertonic saline (3%) infusions. Vigilant and frequent monitoring of serum sodium and electrolytes during this process is essential.[67] This minimizes 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 stabilized.

For patients with severe hyponatremia (<125 mEq/L) or with neurologic symptoms, rapid correction with hypertonic saline (3%) infusions is needed. Infusion rates range from 1 mL/kg/hour up to 6 mL/kg/hour, if severe neurologic symptoms such as seizures are present.[43] Correction should continue until the patient is asymptomatic and serum sodium level is >118-120 mEq/L, to minimize the risk of seizures. Once the patient is asymptomatic and sodium levels are >118 mEq/L, correction should occur at a maximum of 8 mEq/L in 24 hours, to achieve a target sodium level of 125 mEq/L.[70]

The goal is to limit correction to <12 mEq/L (1.5 to 2 mEq/L/hour, or approximately 0.5 mmol/L/hour) on the first day and <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 mEq/L.[29]

For patients with serum sodium between 125 and 130 mEq/L or with GI symptoms, the goal is to limit correction to <12 mEq/L (1.5 to 2 mEq/L/hour, or approximately 0.5 mmol/L/hour) on the first day and <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 mEq/L.

Fluid restriction and diuretics

Patients with chronic symptoms and no or mild hyponatremia 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 >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 faucets).

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 predetermined 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%).[71]

In addition to fluid restriction, 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.[72] Furosemide preferentially causes water excretion over sodium excretion.[1]

Behavioral therapy

Behavioral intervention

  • Therapeutic fluid restriction is an inexpensive form of treatment, but high rates of noncompliance in patients with psychiatric disorders may pose challenges, and it may take several days for a clinical effect to appear.[43]

  • Group psychotherapy may improve adherence to fluid restriction.[73]

  • Reinforcement schedules using tokens for rewards and removing these tokens for nonadherence have been used with some success.[74]

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

Behavioral modification

  • Therapists use cognitive techniques to address thoughts leading to drinking behavior, by implementing a behavioral program 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 <3 liters 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.[51]

Psychopharmacologic therapy

Atypical antipsychotics have been reported to improve symptoms of PPD:

  • Clozapine has shown benefit in case reports and prospective trials.[1][10][75][76] A prospective 6-week study of clozapine in 8 patients with schizophrenia who had polydipsia and low plasma osmolality showed that clozapine normalized plasma osmolality and was well tolerated.[77] 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 hyponatremia 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.[78][79][80]

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