Case Presentation: A 40 year old man was brought in by ambulance after having a 30 second tonic-clonic seizure witnessed by his mother. He was intubated on route to the hospital for airway protection. On arrival he was afebrile and hemodynamically stable. Neurological exam was notable for GCS of 8. Pupils were mildly anisocoric and sluggishly reactive to light. CT brain was unremarkable. EEG showed diffuse slowing, but no evidence of active seizure activity. Routine laboratory analysis yielded a sodium of 121 mmol/L. On further history, it was revealed that he had a history of bipolar type 1 disorder and was currently in a manic phase, during which he drinks copious amounts of water. Medications include lithium, oxcarbazepine, and olanzepine. There had been no recent changes in his medication. He had no history of seizure in the past. He was treated with 3% normal saline and sodium increased to 128 mmol/L. He was subsequently extubated. Urine studies revealed osmolality of 106 MoM/kg and sodium of 25 mmol/L. He was subsequently diagnosed with hyponatremia secondary to psychogenic polydipsia. He was initially placed on fluid restriction of 1.5 L daily, but his sodium corrected rapidly to 143 mmol/L. Due to this rapid correction he was monitored closely for signs of osmotic demyelination syndrome, but remained asymptomatic and was discharged home.
Discussion: Psychogenic polydipsia is a rare diagnosis, in which an individual drinks excessive amount of water, thus overwhelming the kidney’s ability to maintain an osmotic balance in the blood. This is caused by an abnormality in the hypothtlamic-pituitary axis not associated with abnormal ADH activity. Many causes are hypothesized, including dysregulation of the dopaminergic axis. This could suggest why the condition is most prevalent in those with concurrent psychiatric diagnosis, including schizophrenia and bipolar disorder. Iatrogenic rapid correction of sodium in this circumstance is relatively common, as patients are often more limited to access to free water than necessary. The major risk of rapid sodium correction is osmotic demyelination syndrome, (previously known as central pontine myelinolysis). Presentation varies depending on the area of the brain effected, but may include ataxia, dysphagia, catatonia, and flaccid quadriplegia.
Conclusions: This case illustrates a rare cause of hyponatremia that must be considered, especially in the hospitalized psychiatric patient. Additionally, it serves to educate readers on the dangers of rapid correction of hyponatremia. Luckily, this patient exhibited a desirable outcome and was unaffected by the iatrogenic rapid correction.