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Hyponatremia as a Result of Posttraumatic Primary Polydipsia

Published:December 29, 2014DOI:https://doi.org/10.1016/j.amjmed.2014.12.013
      To the Editor:
      Primary polydipsia is a condition of compulsive water consumption that is etiologically associated with psychiatric disorders. The association between primary polydipsia and head trauma is a rare one that has seldom been reported in the literature.

      Objective

      We present a case of primary polydipsia without major psychiatric features in a patient with head trauma.

      Case Report

      A 58-year-old male patient with a history of alcohol abuse was admitted to the medical intensive care unit for management of delirium tremens.
      He improved with benzodiazepines and was transferred to the medical floor, where he was observed to display compulsive water-drinking behavior. Chart review revealed the onset of compulsive water drinking with hyponatremia, concurrent with bilateral frontal hemorrhage from head trauma a few months prior.
      Evaluation revealed euvolemic hypotonic hyponatremia with appropriate low urine osmolality (<100 mOsm/kg). This suggests that the main mechanism contributing to the development of hyponatremia was primary polydipsia.
      Time relationships between compulsive water intake, development of acute episodes of hyponatremia, and intracranial hemorrhage suggest a traumatic etiology of primary polydipsia. Continuous thorough psychiatric evaluation did not reveal psychotic or major psychiatric features.
      Management of the patient entailed housing with fluid restriction, behavioral modification with rewards for Na level >135 mEq/L, and a trial of propranolol and olanzapine.

      Discussion

      Primary or psychogenic polydipsia was first reported in the literature in 1938 as a case of water intoxication in a schizophrenic patient.
      • Barahal H.S.
      Water intoxication in a mental case.
      Three-quarters of a century has elapsed and the exact pathophysiology is still unclear. Many anatomical sites have been proposed as the foci of dysregulation that lead to abnormality in fluid homeostasis. The cholinergic, dopaminergic, and hippocampal systems are most commonly implicated.
      • Zafonte R.D.
      • Watanabe T.K.
      • Mann N.R.
      • Ko D.H.
      Psychogenic polydipsia after traumatic brain injury. A case report.
      The literature contains sparse description of any relationship between primary polydipsia and traumatic brain injury. However, given the various models proposed, it is reasonable to believe that brain injury puts a patient at risk of developing this condition by disruption of one or more of the anatomical sites involved in the maintenance of fluid homeostasis.
      • Zafonte R.D.
      • Watanabe T.K.
      • Mann N.R.
      • Ko D.H.
      Psychogenic polydipsia after traumatic brain injury. A case report.
      Hyponatremia can occur after traumatic brain injury, but it is usually linked with the Cerebral Salt Wasting Syndrome or the Syndrome of Inappropriate Antidiuretic Hormone. Hyponatremia due to psychogenic polydipsia as a consequence of head trauma is rare. The etiology of hyponatremia must be determined in the patient with head injury, as the treatment of one disorder could worsen the other, if present.
      • Zafonte R.D.
      • Watanabe T.K.
      • Mann N.R.
      • Ko D.H.
      Psychogenic polydipsia after traumatic brain injury. A case report.
      • Dundas B.
      • Harris M.
      • Narasimhan M.
      Psychogenic polydipsia review: etiology, differential, and treatment.
      • Chang C.H.
      • Liao J.J.
      • Chuang C.H.
      • Lee C.T.
      Recurrent hyponatremia after traumatic brain injury.
      Evaluation of hyponatremia is based on the history, physical examination, and laboratory tests. This patient presented with intermittent episodes of hypotonic euvolemic hyponatremia. Undetectable levels of antidiuretic hormone (ADH; <1 ug/uL) and urine osmolality below 100 mOsm/Kg with serum sodium <135 mEq/L (Tables 1 and 2) suggest normal ability to excrete free water, indicating appropriate suppression of ADH.
      Table 1The Relationship Between Serum Osmolality, Urine Osmolality, Serum Sodium Concentration, and Urine Sodium Concentration
      Serum Osmolality (mosm/kg)Urine Osmolality (mosm/kg)Serum Sodium (mmol/L)Urine Sodium (mmol/L)
      2697412423
      2526811924
      281414137153
      2739412513
      2927212711
      28745214077
      30230213579
      28247813878
      Table 2ADH Concentration in Response to Serum Sodium
      ADH (pg/uL)Serum Sodium (mmol/L)
      1.2137
      <1.0133
      <1.0131
      ADH = antidiuretic hormone.
      Conditions that cause hyponatremia despite appropriate suppression of ADH are: advanced renal failure, primary polydipsia, and low dietary solute intake. This patient did not have renal failure, but compulsive water intake and low serum urea levels suggest primary polydipsia with low dietary solute intake component.
      Various pharmacological agents have been proposed for use in primary polydipsia with varying levels of success. These include atypical antipsychotic agents such as clozapine, beta-blockers such as propranolol and angiotensin-converting enzyme inhibitors. Newer agents such as aquaretics that antagonize ADH have also been found to be of benefit in some patients. Fluid restriction and behavioral modification are, however, the mainstay of treatment of these patients.
      • Dundas B.
      • Harris M.
      • Narasimhan M.
      Psychogenic polydipsia review: etiology, differential, and treatment.

      Acknowledgment

      The authors thank Dr. Donald Hutcheon of British Columbia, Canada.

      References

        • Barahal H.S.
        Water intoxication in a mental case.
        Psychiatr Q. 1938; 12: 767-771
        • Zafonte R.D.
        • Watanabe T.K.
        • Mann N.R.
        • Ko D.H.
        Psychogenic polydipsia after traumatic brain injury. A case report.
        Am J Phys Med Rehabil. 1997; 76: 246-248
        • Dundas B.
        • Harris M.
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        Psychogenic polydipsia review: etiology, differential, and treatment.
        Curr Psychiatry Rep. 2007; 9: 236-241
        • Chang C.H.
        • Liao J.J.
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        Recurrent hyponatremia after traumatic brain injury.
        Am J Med Sci. 2008; 335: 390-393