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Abstract

Introduction: Hyponatremia, characterized by serum sodium levels <135 mM/L, is a common electrolyte disorder affecting 15–22% of hospitalized patients. The clinical manifestations of hyponatremia stem from intracellular water shift. It causes cerebral edema and primarily manifests as neurological symptoms. The etiology of hyponatremia can be identified through a comprehensive history, physical examination, and assessment of volume status. Hypoxia emerges as a significant factor in brain damage among individuals with hyponatremic encephalopathy.

Methodology: The study enrolled 100 consenting inpatients with hyponatremia (<135 mEq/L) from the Department of General Medicine.

Results: The mean age was 49.4 ± 17.15 years, with an equal male-to-female ratio. The most common presentation was decreased appetite (45%). Plasma osmolality showed hyposmolar levels in 96% of subjects. Euvolemic, hypervolemic, and hypovolemic states were observed in 48%, 33%, and 19% of subjects, respectively. SIADH (27%) and chronic liver disease (21%) were the predominant etiologies. Tuberculosis was the leading cause of SIADH. The overall mortality rate was 9%, primarily associated with moderate and severe hyponatremia, with a higher mortality observed in males. A weak positive correlation was found between serum sodium levels and pO2 levels (coefficient 0.233, p-value 0.019), while a negative correlation was observed with pCO2 levels (coefficient –0.206, p-value 0.04).

Conclusion: These findings highlight the interplay between hyponatremia and respiratory status, highlighting the potential impacts of hyponatremia on blood oxygen and carbon dioxide levels.

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