Category: Professional Posters
Reported in up to twenty percent of psychiatric patients, psychogenic polydipsia, or compulsive water drinking, involves a disturbance in thirst control not attributed to impaired production or release of antidiuretic hormone. The etiology of psychogenic polydipsia is unclear. Complications include hyponatremia (sodium less than 135 mEq/L), and water intoxication that can lead to seizures, coma, and death. Treatment for psychogenic polydipsia includes a combination of behavioral modifications, such as fluid restriction and cognitive behavioral therapy, and pharmacologic modalities. Atypical antipsychotics such as aripiprazole, clozapine, risperidone, and olanzapine improved psychogenic polydipsia in case reports. Beta-blockers, clonidine, diuretics, angiotensin-converting enzyme inhibitors, and angiotensin receptor blockers have been shown to decrease water consumption. Naltrexone, a mu-opioid receptor antagonist FDA approved for the treatment of alcohol dependence and the prevention of relapse in opioid dependence, modulates the mesolimbic dopaminergic pathway, preventing the increased dopamine release responsible for the pleasurable reinforcing effects of substance abuse. Limited evidence supports the safe and effective use of naltrexone as monotherapy or as an augmentation agent in treating patients with compulsive behaviors. Naltrexone may offer an alternative treatment option for psychogenic polydipsia.
This case report describes the use of naltrexone in a thirty one year-old male with a history of schizoaffective disorder-bipolar type, polysubstance abuse disorder (dextromethorphan, cannabis, nicotine) and hyponatremia attributed to psychogenic polydipsia. The patient has a history of numerous inpatient psychiatric hospitalizations due to an inability to remain safe in the community. He drinks excessive amounts of fluid in an effort to get high, because he feels numb, or due to a feeling of anxiety in his chest. The current admission has been characterized by the need for emergent care on two occasions due to hyponatremia. Interventions have included placing the patient on constant observation, a fluid restriction, limiting bathroom access, and initiating sodium supplementation. Sodium levels are monitored on a regular basis. In the hope of reducing the craving and the pleasurable reinforcing effects the patient was experiencing from hyponatremia attributed to psychogenic polydipsia, naltrexone was initiated at an oral dose of 50mg daily. Since beginning naltrexone, the patient reports that it has been helpful in reducing his craving for excessive fluid. Sodium levels have remained within normal limits. The patient was enthusiastic about the addition of naltrexone, thinking that it may also help reduce the urge to drink alcohol after discharge. The patient is no longer on constant observation, and the fluid restriction has been eased. Discharge planning has been initiated.