Published online Feb 27, 2020. doi: 10.4240/wjgs.v12.i2.45
Peer-review started: September 5, 2019
First decision: October 13, 2019
Revised: November 4, 2019
Accepted: December 14, 2019
Article in press: December 14, 2019
Published online: February 27, 2020
While hyponatremia has been studied in the context of other infectious and inflammatory disease states, sodium level has not yet been studied in a large-scale clinical study of patients with severe biliary disease. Serum sodium a common initial laboratory test for patients presenting with biliary disease, may serve as an important diagnostic tool for assessing the underlying severity of illness.
Despite advances in both laboratory and radiographic technologies, identifying patients with severe biliary disease remains a challenge for health care providers in the acute setting. We felt that serum sodium could serve as a critical tool in identifying patients with severe illness, accelerating their care, and improving patient outcomes.
We sought to clarify the relationship between serum sodium and severe biliary disease. Specifically, our goals were to determine if a correlation existed between serum sodium and both illness severity and the presence/location of biliary bacteria. We also sought to determine if such a correlation existed with other clinical factors including the presence of gangrenous changes, Charlson comorbidity score, and glucose level.
We utilized a prospectively collected, comprehensive quality outcomes database containing detailed patient demographics, clinical information, and outcomes spanning from March 1989 to October 2019 with 920 patients with gallstone disease. The lowest sodium level during the initial acute phase of illness, prior to therapeutic intervention was recorded. We determined illness severity based on pre-intervention findings and classified patients accordingly. The level of bacterial infection was determined using culture results from gallstones, bile, and blood; patients were stratified by the highest level of bacterial infection detected. Patients were also stratified by the Charlson Comorbidity Index.
We observed a progressive, statistically significant decrease in sodium level with worsening disease severity. We also observed an incremental decrease in serum sodium with ascending bacterial infection. Charlson Comorbidity Index and the presence of gangrenous changes were also independent predictors of decreased sodium on multivariate analysis.
This study is the first to describe an inverse relationship between serum sodium and severity of biliary disease. Furthermore, it reveals that both underlying medical morbidity and acute illness severity contribute to decreased sodium levels, and that the effects are additive. This study justifies the use of serum sodium as a clinical predictor of the severity of biliary disease.
The direction of future research regarding patients with low serum sodium and biliary disease should focus on the pathophysiologic cause of decreased serum sodium. The applications of this research have implications not only for patients with biliary disease, but with any inflammatory or infectious process.