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Hyponatremia Precipitated by Psychogenic Polydipsia Triggers Hypercarbic Respiratory Failure: A Case Report FREE TO VIEW

Kovid Trivedi, MD; Jen-Chieh Cheng, MD; Raul Gazmuri, MD
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Chicago Medical School/Rosalind Franklin University of Medicine & Science, North Chicago, IL

Chest. 2013;144(4_MeetingAbstracts):968A. doi:10.1378/chest.1705194
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SESSION TITLE: Miscellaneous Student/Resident Case Report Posters II

SESSION TYPE: Medical Student/Resident Case Report

PRESENTED ON: Tuesday, October 29, 2013 at 01:30 PM - 02:30 PM

INTRODUCTION: Psychogenic polydipsia is a frequent cause of hyponatremia. Hyponatremia is associated with CNS symptoms such as headache, seizures, lethargy, and coma. Restriction of excess water intake is the mainstay of treatment prompting effective reversal of hyponatremia and the associated manifestations.

CASE PRESENTATION: A 53 year old male nursing home resident with history of psychogenic polydipsia, COPD, OSA, diabetes mellitus, morbid obesity, active smoking, and paranoid schizophrenia was found to be lethargic with altered mental status. Patient was transferred to the ED and physical examination revealed a lethargic obese male in no acute distress and without focal neurological deficits. Chest examination showed good bilateral air entry with bibasilar crackles. Laboratory investigations revealed serum sodium of 119 mEq/l, pH 7.23, PCO2 87 mmHg, PO2 58 mmHg, and HCO3 35 mmol/l. A chest radiograph showed cardiomegaly with mild pulmonary congestion and mild pleural effusion. Patient was intubated, started on mechanical ventilation, and transferred to ICU for further management. Without access to excessive water intake the serum sodium increased to 121 mEq/l on the day 2 and to 129 mEq/l on day 3. His mental status improved as the sodium level increased enabling successful on day 3. The episode described above is representative of multiple similar episodes in which hyponatremia precipitates hypercarbic respiratory failure with prompt reversal after fluid restriction and correction of hyponatremia. In none of these episodes and additional cause of respiratory failure could be identified. The concomitant presence of OSA is likely to be contributor.

DISCUSSION: As for the pathogenic mechanism, the possibility of cerebral edema caused by hyponatremia blunting the respiratory center responsiveness to hypercarbic acidosis is an attractive - yet unproven - possibility.

CONCLUSIONS: The association between hyponatremia and hypercarbic respiratory failure has been described in post-neurosurgery cases but not - to the best of our knowledge - in the medical setting herein described.

Reference #1: Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure. Ayus JC, Arieff AI. Chest. 1995 Feb;107(2):517-21.

DISCLOSURE: The following authors have nothing to disclose: Kovid Trivedi, Jen-Chieh Cheng, Raul Gazmuri

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