Correlation of Serum Sodium with Severity of Hepatic Encephalopathy in Liver Cirrhosis Patients Presenting at Tertiary Care Hospital, Lahore

Aleena  Ali; Asad Ullah  Mahmood; Bilal  Ahmed; Ali  Gohar

doi:10.54112/bcsrj.v6i2.1581

Authors

Aleena Ali Doctors Hospital and Medical Center, Lahore, Punjab, Pakistan
Asad Ullah Mahmood Lahore General Hospital, Lahore, Punjab, Pakistan
Bilal Ahmed Lahore General Hospital, Lahore, Punjab, Pakistan
Ali Gohar Lahore General Hospital, Lahore, Punjab, Pakistan

DOI:

https://doi.org/10.54112/bcsrj.v6i2.1581

Keywords:

Hepatic Encephalopathy, Cirrhosis, Hyponatremia, Serum Sodium, Neurological Dysfunction, Liver Disease

Abstract

Hepatic encephalopathy (HE) is a serious complication of liver cirrhosis, characterized by cognitive impairment and neurological dysfunction. Emerging evidence suggests that hyponatremia plays a critical role in the pathophysiology of HE, potentially exacerbating its severity. However, the relationship between serum sodium levels and the severity of HE remains an area of ongoing investigation. Objective: To evaluate the correlation between serum sodium levels and the severity of hepatic encephalopathy in cirrhotic patients. Methods: This descriptive cross-sectional study was conducted at the Department of Gastroenterology, Doctors Hospital and Medical Center, Lahore, over a period of six months. A total of 120 patients diagnosed with HE were enrolled using non-probability consecutive sampling. Clinical history, laboratory investigations, and serum sodium levels were documented. The severity of HE was graded using the West Haven classification system. Pearson’s rank correlation test was applied to assess the relationship between serum sodium levels and HE severity, and the Chi-square test was used to evaluate categorical associations. Data analysis was performed using SPSS Version 24, with a p-value of ≤0.05 considered statistically significant. Results: Among the 120 patients, 55 (45.8%) were men and 65 (54.2%) were women, with a mean age of 59.84 ± 7.93 years. Hyponatremia (serum sodium <135 mEq/L) was present in 99 patients (82.5%). A statistically significant inverse correlation was observed between serum sodium levels and the severity of HE (Pearson’s R = -0.285, p = 0.002). Additionally, the Chi-square test confirmed a strong association (p < 0.001) between hyponatremia and HE severity. Conclusion: Hyponatremia is significantly correlated with increased severity of hepatic encephalopathy in cirrhotic patients. Routine monitoring of sodium levels and early corrective interventions may help prevent HE progression and improve patient outcomes. Further research is required to assess the prognostic implications of hyponatremia in HE management.

Downloads

Download data is not yet available.

References

Nazish Z, Inayatullah M, Nasir SA, Arshad M, Tanveer S, Naqvi AB. Liver cirrhosis: clinical presentation. Prof Med J. 2002;9(3):207-12.

Swaminathan M, Ellul MA, Cross TJ. Hepatic encephalopathy: current challenges and future prospects. Hepat Med. 2018;10:1-11.

Elwir S, Rahimi RS. Hepatic encephalopathy: an update on the pathophysiology and therapeutic options. J Clin Transl Hepatol. 2017;5(2):142-51.

Poudyal NS, Chaudhary S, Kc S, et al. Precipitating factors and treatment outcomes of hepatic encephalopathy in liver cirrhosis. Cureus. 2019;11(4):e4363.

Tapper EB, Henderson JB, Parikh ND, Ioannou GN, Lok AS. Incidence of and risk factors for hepatic encephalopathy in a population-based cohort of Americans with cirrhosis. Hepatol Commun. 2019;3(11):1510-9.

Mumtaz K, Ahmed US, Abid S, Baig N, Hamid S, Jafri W. Precipitating factors and the outcome of hepatic encephalopathy in liver cirrhosis. J Coll Physicians Surg Pak. 2010;20(8):514-8.

Shawcross DL, Dunk AA, Jalan R, Kircheis G, de Knegt RJ, Laleman W, et al. How to diagnose and manage hepatic encephalopathy: a consensus statement on roles and responsibilities beyond the liver specialist. Eur J Gastroenterol Hepatol. 2016;28(2):146-52.

Riggio O, Efrati C, Catalano C, Pediconi F, Mecarelli O, Accornero N, et al. High prevalence of spontaneous portal-systemic shunts in persistent hepatic encephalopathy: a case-control study. Hepatology. 2005;42(5):1158-65.

Patidar KR, Bajaj JS. Covert and overt hepatic encephalopathy: diagnosis and management. Clin Gastroenterol Hepatol. 2015;13(12):2048-61.

Heron MP. Deaths: leading causes for 2016. Natl Vital Stat Rep. 2018;67(5):1-77.

Afridi MAR, Ali Z, Muhammad R, Asghar M, Afridi MF, Alam AB, et al. Hyponatremia and its correlation with hepatic encephalopathy in patients with cirrhosis. J Postgrad Med Inst. 2017;31(3):243-6.

Guevara M, Baccaro ME, Torre A, Gómez-Ansón B, Ríos J, Torres F, et al. Hyponatremia is a risk factor for hepatic encephalopathy in patients with cirrhosis: a prospective study with time-dependent analysis. Am J Gastroenterol. 2009;104(5):1382-9.

Liu A, Perumpail RB, Kumari R, Younossi ZM, Wong RJ, Ahmed A. Advances in cirrhosis: optimizing the management of hepatic encephalopathy. World J Hepatol. 2015;7(21):2871-9.

Qureshi MO, Khokhar N, Saleem A, Niazi TK. Correlation of hyponatremia with hepatic encephalopathy and severity of liver disease. J Coll Physicians Surg Pak. 2014;24(3):135-7.

Bernardi M, Ricci CS, Santi L. Hyponatremia in patients with cirrhosis of the liver. J Clin Med. 2014;4(1):85-101.

John S, Thuluvath PJ. Hyponatremia in cirrhosis: pathophysiology and management. World J Gastroenterol. 2015;21(11):3197-205.