psychogenic polydipsia ( ppd ) , a clinical disorder characterized by polyuria and polydipsia , is defined by hyponatremia found in 10 - 20% of those presenting with compulsive drinking . symptoms are not typically seen until the patient reaches their limit of maximal urine dilution ( 100 mosmol / kg with minimum urine osmolality ) . once this point of water intoxication has been reached , the symptoms generally exhibited are confusion , lethargy , psychosis , cerebral edema , increased intracranial pressure ( icp ) , seizures or death . polydipsia occurs frequently among chronic psychiatric patients , particularly those with schizophrenia . even though this phenomenon was noted three quarters of a century ago , meq / l ) is one of the most common electrolyte abnormalities in hospitalized patients , and therefore may be overlooked on presentation to the emergency department ( ed ) . while acute hyponatremia ( < 48 hours ) is generally hospital - acquired , chronic hyponatremia ( > 48 hours ) usually develops outside the hospital and is generally better tolerated . the clinical distinction between acute and chronic hyponatremia , however arbitrarily defined , is crucial with regard to the optimal management of the hyponatremic patient . in the chronically hyponatremic patient , the brain has adapted to hypo - osmolar conditions ; while in the acute hyponatremic , adaptation to osmotic swelling has not yet been completed . the latter is most notably the case with self - induced water intoxication or ppd . multiple factors contribute to the lack of clinical information available to make informed clinical diagnoses in these patients . with a psychiatric history , many times these patients are unable to give a reliable medical history , and may present obtunded or with diminished cerebral function due to the hyponatremia . herein , we describe a case of a man who was found down after a presumed fall . he was initially treated as a trauma patient and was noted to have severe hyponatremia associated with cerebral edema . he underwent a surgical ventriculostomy for cerebrospinal fluid ( csf ) drainage for icp control . although at the time of ventriculostomy the etiology of his elevated icp was not known , his condition warranted csf draining . herein , we describe this interesting case of ppd resulting in cerebral edema severe enough to clinically require ventriculostomy placement for icp treatment . a 47-year - old man with a history of schizophrenia presented to our ed after a fall from standing , followed by a change in mental status . the patient was admitted to the trauma service with concern for a possible traumatic brain injury due to a history of fall with subsequent onset of mental status changes and seizure . on examination , his pupils were 3 mm and sluggishly reactive bilaterally , with a downward gaze preference . corneal reflexes were absent , occulocephalic reflexes were suppressed ; however , a gag reflex was present . routine laboratories revealed hyponatremia ( 107 mmol / l , normal 135 - 146 ) and hypochloremia ( 76 mmol / l , normal 98 - 109 ) . he had a low serum osmolarity ( 230 mosmol / kg , normal 275 - 295 ) and urine sodium ( 10 mmol / l , normal 50 - 150 ) which supported a diagnosis of hypervolemic hyponatremia . a non - contrast ct scan of his head showed loss of gray - white differentiation and sulcal effacement , consistent with cerebral edema . given his poor neurological examination , abnormal cranial nerve function , gcs upon arrival , among various other factors , there was concern for intracranial hypertension associated with the cerebral edema . a ventriculostomy was placed to allow for measurement of icp and treatment via csf drainage . opening pressure was elevated ( 35 cm h20 , normal < 20 cm h20 ) . in the first 48 hours , 270 cc drained out of the ventriculostomy to maintain an icp below 15 cm h20 . the drainage slowly tapered off with maintenance of normalized icp until the catheter was discontinued 8 days after admission . the sodium level was corrected over the first 5 days of admission with a combination of fluid restriction and hypertonic saline . after a detailed history was obtained from the family , it was discovered that the patient consistently consumed greater than 8 l of diet cola daily . he had been diagnosed with schizophrenia in his 20 's after a psychotic break and had been treated with several medications with varying success , including haldol and fluoxetine . the patient was seen by psychiatry and was diagnosed with ppd . within 2 weeks of presentation , the patient returned to a normal motor exam and was awake , alert and oriented to person , place and time . polydipsia is a problem for 6 - 20% of psychiatric patients , but more common among those with chronic schizophrenia . water intoxication leading to hyponatremia can result from both psychogenic and environmental fators . while hyponatremia is defined as plasma sodium levels below 135 mmol / l , symptoms such as lethargy , restlessness and disorientation do not typically develop until plasma levels fall to the range of 115 - 120 severe hyponatremia can result in seizures , coma , permanent brain damage , respiratory arrest , brain stem herniation and possibly death . polydipsic schizophrenics demonstrate both arginine vasopressin - dependent and independent defects in renal water excretion . symptoms rarely occur unless the patient drinks excessively ( > 10 l per day ) after they reach their maximum urine dilution ( 100 mosm / kg with minimum osmolality ) and full antidiuretic hormone suppression . the renal excretory capacity is 12 l per day . in our patient , treating the cerebral edema required correction of the hyponatremia . controlled osmolar therapy was imperative to prevent over correction and central pontine myelinosis . however , fluid restriction , diuretics and hypertonic saline , in a controlled fashion were too limited in their ability to decrease icp while only slowly correcting the hyponatremia . a clinical decision was made to perform a ventriculostomy and drain csf to control the icp . this was done per brain trauma foundation guidelines given his low gcs and evidence of cerebral edema on head ct . while hyponatremia is associated with cerebral edema , the ability of hyponatremia - induced cerebral edema to increase icp is not well - characterized . based on the clinical severity of our patient 's cerebral edema , he underwent early treatment with a ventriculostomy . his icp was elevated and he required drainage of a significant amount of csf during the first two hospital days in order to maintain an appropriate icp . in this setting of voluntary water intoxication , there have not been any cases , to our knowledge , that reported the need for external ventricular drainage in the management of the increased icp associated with hyponatremia . ppd is a known cause of hypervolemic hyponatremia . in the acute setting , severe hyponatremia has been reported to cause elevated icp and even signs of herniation . in the absence of an accurate history , patients with water intoxication may present in a manner consistent with that of a trauma patient . while there have not been any cases to our knowledge that reported using an external ventricular drain in the management of the increased icp associated with hyponatremia , in this case it proved to be a successful treatment modality for a patient with elevated icp secondary to acute water intoxication .