Year : 2012 | Volume
: 5 | Issue : 2 | Page : 193--195
Intracranial hypertension secondary to psychogenic polydipsia
Vanessa M Gleason1, Niels D Martin2,
1 Department of Pharmacy, Division of Acute Care Surgery, Thomas Jefferson University, Philadelphia, PA, USA
2 Department of Surgery, Division of Acute Care Surgery, Thomas Jefferson University, Philadelphia, PA, USA
Niels D Martin
Department of Surgery, Division of Acute Care Surgery, Thomas Jefferson University, Philadelphia, PA
Psychogenic polydipsia, in its most severe form, can lead to acute water intoxication by way of extreme hyponatremia. This results in cerebral edema, mental status deterioration and can lead to life threatening intracranial hypertension if not identified and treated urgently. However, this treatment rarely involves surgical intervention. Herein, we describe a 47-year-old man who presented to our emergency department who was found down with a decline in mental status and generalized tonic clonic seizures. He was comatose with glasgow coma score of 5. His exam was notable for sluggishly reactive pupils, absence of corneal reflexes, decorticate posturing, and globally increased tone and hyper-reflexia with upgoing toes bilaterally. Lab work revealed sodium of 107 mmol/L. CT scan of the head showed global cerebral edema with sulcal effacement. A ventriculostomy was placed with an opening pressure of 35-cm H 2 O, and cerebrospinal fluid was drained to maintain normal intracranial pressure. Fluid restriction and hypertonic saline were used to carefully correct the hyponatremia. The patient improved and at day five was neurologically intact. His history later revealed schizophrenia and a predilection for drinking greater than 8 L of diet cola daily.
|How to cite this article:|
Gleason VM, Martin ND. Intracranial hypertension secondary to psychogenic polydipsia.J Emerg Trauma Shock 2012;5:193-195
|How to cite this URL:|
Gleason VM, Martin ND. Intracranial hypertension secondary to psychogenic polydipsia. J Emerg Trauma Shock [serial online] 2012 [cited 2020 Jul 15 ];5:193-195
Available from: http://www.onlinejets.org/text.asp?2012/5/2/193/96496
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, it is still poorly understood, leading to delayed or even missed diagnosis.
Hyponatremia (serum Na<135 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. These findings could lead a practitioner to suspect even trauma.
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. Only later was his history of PPD elicited. 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. Two self-limited generalized tonic-clonic seizures were witnessed by ED staff. He was intubated for airway protection. No additional history was available. 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 vital signs were normal. Prior to intubation his glasgow coma scale (GCS) was 5. 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. He initially was unresponsive, but later exhibited decorticate posturing to painful stimuli. Tone was increased and hyper-reflexia with upgoing toes, was present bilaterally. The remainder of his physical examination was unremarkable.
Routine laboratories revealed hyponatremia (107 mmol/L, normal 135-146) and hypochloremia (76 mmol/L, normal 98-109). His other electrolytes, blood gas and urine drug screen were unremarkable. 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 H 2 0, normal <20 cm H 2 0). In the first 48 hours, 270 cc drained out of the ventriculostomy to maintain an ICP below 15 cm H 2 0. 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. He ultimately was discharged to a rehab facility with extensive psychiatry follow-up.
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 mmol/L.  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.
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