Chronic liver disease (CLD) is a progressive disorder characterized by persistent hepatic injury that leads to fibrosis, architectural distortion, and ultimately cirrhosis. [1] The disease process involves chronic inflammation and hepatocellular injury, which progressively impair essential hepatic functions such as protein synthesis, detoxification of metabolic by-products, and bile secretion. Cirrhosis represents the terminal stage of CLD and is marked by nodular regeneration, vascular remodeling, extracellular matrix deposition, and activation of hepatic stellate cells that promote fibrogenesis. [1] Liver disease constitutes a major global health burden, accounting for over two million deaths annually worldwide. In 2019, approximately 290 million individuals were affected by chronic liver disease globally, contributing substantially to morbidity and mortality across different age groups. [2] In India, liver diseases have emerged as a significant public health concern and account for nearly 18.3% of global liver disease–related mortality. [3] Decompensated chronic liver disease (DCLD) represents the advanced stage of cirrhosis and is associated with considerable morbidity and mortality. It is clinically characterized by complications such as ascites, jaundice, hepatic encephalopathy, variceal bleeding, and hepatorenal syndrome. [4, 5] These complications arise from progressive deterioration of hepatic function in patients with underlying CLD. They may be precipitated by infections, gastrointestinal bleeding, alcohol-related hepatitis, or drug-induced liver injury; however, in a substantial proportion of cases no identifiable precipitating factor is found. [4, 5] In the absence of liver transplantation, the five-year mortality rate among patients with decompensated cirrhosis may reach up to 85%. [6] The liver plays a vital role in maintaining metabolic homeostasis, including the regulation of fluid and electrolyte balance. In advanced liver disease, several mechanisms contribute to electrolyte disturbances. These include portal hypertension, impaired renal perfusion, activation of the renin–angiotensin–aldosterone system (RAAS), and increased secretion of antidiuretic hormone (ADH). Together, these processes promote sodium and water retention and disrupt normal electrolyte regulation. [7, 8] Consequently, abnormalities in key electrolytes such as sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺), and magnesium (Mg²⁺) are frequently observed in patients with DCLD. Hyponatremia is the most common electrolyte disturbance in decompensated cirrhosis and is associated with serious complications including hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome. Disturbances in potassium homeostasis, particularly hypokalemia, may occur due to diuretic therapy, renal dysfunction, and secondary hyperaldosteronism. These abnormalities can exacerbate hepatic encephalopathy and lead to cardiac and neuromuscular complications. [9-12] Additionally, hypocalcemia and hypomagnesemia may develop due to hypoalbuminemia, impaired vitamin D metabolism, poor nutritional status, and increased renal losses, contributing to metabolic and neuromuscular disturbances. [13, 14] Electrolyte abnormalities serve as important indicators of disease severity and prognosis in patients with decompensated chronic liver disease. However, their pattern and clinical significance are often under-recognized in routine clinical practice. Therefore, the present study was undertaken to evaluate serum electrolyte levels (Na⁺, K⁺, Ca²⁺, and Mg²⁺) in patients with decompensated chronic liver disease and to assess their clinical significance.

Study Design A cross-sectional observational study was conducted to evaluate serum electrolyte levels (Na⁺, K⁺, Ca²⁺, and Mg²⁺) and their clinical significance in patients with decompensated chronic liver disease (DCLD). The study assessed the association between electrolyte disturbances, disease severity, and related complications at a single point in time. Study Setting and Population The study was conducted in the Department of General Medicine at a tertiary care teaching hospital during the study period. A total of 95 patients diagnosed with decompensated chronic liver disease and admitted during this period were included. Eligible patients were enrolled consecutively. Inclusion Criteria Patients diagnosed with decompensated chronic liver disease based on clinical evaluation, laboratory parameters, and radiological findings were included in the study. Exclusion Criteria The following patients were excluded: • Patients who did not provide informed consent • Patients with a history of heart failure • Patients with chronic kidney disease • Patients receiving medications known to affect neuropsychiatric status or hepatic function, including selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs), or cytotoxic drugs Data Collection Data were collected using a structured and predesigned proforma documenting demographic characteristics, clinical history, physical examination findings, and laboratory and radiological investigation results. Clinical Evaluation All patients underwent a comprehensive clinical evaluation including vital parameters (blood pressure, pulse rate, respiratory rate, peripheral oxygen saturation [SpO₂], and temperature), general physical examination (pallor, icterus, pedal edema, clubbing, cyanosis, and lymphadenopathy), anthropometric measurements (height, weight, body mass index, and abdominal girth), and systemic examination with particular emphasis on manifestations of chronic liver disease. Laboratory Investigations Blood samples were collected for the following investigations: • Serum electrolytes: sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺), and magnesium (Mg²⁺) • Liver function tests: total bilirubin, direct bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), serum albumin, serum globulin, and albumin–globulin ratio • Renal function tests: blood urea and serum creatinine Radiological Investigations All patients underwent abdominal ultrasonography to evaluate liver morphology and identify features of portal hypertension, splenomegaly, and ascites. Additional Investigations Additional investigations were performed when clinically indicated, including ascitic fluid analysis for spontaneous bacterial peritonitis (SBP) and urine examination with culture to detect urinary tract infections. Assessment of Disease Severity Disease severity was assessed using the Child–Pugh classification and the Model for End-Stage Liver Disease (MELD) score. Ascites was graded as Grade I (detectable only on imaging), Grade II (moderate and clinically evident), and Grade III (gross ascites with marked abdominal distension). Hepatic encephalopathy was graded according to the West Haven criteria. Ethical Considerations The study was conducted after obtaining approval from the Institutional Ethics Committee. Written informed consent was obtained from all participants prior to enrollment, and the study adhered to the principles of the Declaration of Helsinki. Data Collection Procedure Eligible patients fulfilling the inclusion criteria were enrolled consecutively. Demographic details, clinical findings, laboratory results, and radiological findings were recorded in the structured proforma. Disease severity and associated complications were documented systematically. Statistical Analysis Data were entered into Microsoft Excel and analyzed using the Statistical Package for the Social Sciences (SPSS). Continuous variables were expressed as mean ± standard deviation, while categorical variables were presented as frequencies and percentages. Comparisons between quantitative variables were performed using the independent Student’s t-test, and categorical variables were analyzed using the Chi-square test where appropriate. A p value <0.05 was considered statistically significant.

Table 1. Baseline Characteristics of Patients (N = 95) Variable Value n (%) Age (years), mean ± SD 52.8 ± 11.4 Gender Male 68 (71.6%) Female 27 (28.4%) Etiology Alcoholic 44 (46.3%) Viral 30 (31.6%) NASH 12 (12.6%) Others 9 (9.5%) Child–Pugh class A 10 (10.5%) B 30 (31.6%) C 55 (57.9%) MELD score, median (IQR) 18 (13–24) Table 1 summarizes the baseline demographic and clinical characteristics of the study population. The mean age of the patients was 52.8 ± 11.4 years, indicating that most participants were middle-aged adults. A clear male predominance was observed, with 68 males (71.6%) and 27 females (28.4%) included in the study. Regarding the underlying etiology of chronic liver disease, alcohol-related liver disease was the most common cause (46.3%), followed by viral hepatitis (31.6%), non-alcoholic steatohepatitis (NASH) (12.6%), and other causes (9.5%). Assessment of liver disease severity using the Child–Pugh classification revealed that the majority of patients had advanced disease, with 55 patients (57.9%) classified as Child–Pugh class C, while 31.6% were class B and only 10.5% were class A. The median MELD score was 18 (IQR: 13–24), reflecting a significant burden of hepatic dysfunction among the study participants. Table 2. Serum Electrolyte Levels (N = 95) Electrolyte Mean ± SD Range Normal Cases n (%) Abnormal Cases n (%) Sodium (mmol/L) 130.7 ± 6.4 116–145 33 (34.7%) 62 (65.3%) Potassium (mmol/L) 3.95 ± 0.62 2.8–5.8 74 (77.9%) 21 (22.1%) Corrected Calcium (mg/dL) 8.16 ± 0.78 6.4–9.6 57 (60.0%) 38 (40.0%) Magnesium (mg/dL) 1.61 ± 0.33 0.9–2.3 52 (54.7%) 43 (45.3%) Table 2 presents the serum electrolyte levels among the study participants. The mean serum sodium level was 130.7 ± 6.4 mmol/L, which was below the normal reference range, and 65.3% of patients had hyponatremia, making it the most common electrolyte abnormality observed. The mean potassium level was 3.95 ± 0.62 mmol/L, with the majority of patients (77.9%) maintaining potassium levels within the normal range, while 22.1% had abnormal potassium levels. The mean corrected calcium level was 8.16 ± 0.78 mg/dL, and 40% of patients had hypocalcemia. Similarly, serum magnesium levels averaged 1.61 ± 0.33 mg/dL, with 45.3% of patients demonstrating hypomagnesemia. These findings highlight the frequent occurrence of electrolyte disturbances in patients with chronic liver disease. Table 3. Prevalence of Electrolyte Abnormalities (N = 95) Abnormality Abnormal n (%) Normal n (%) Hyponatremia 62 (65.3%) 33 (34.7%) Hypokalemia 11 (11.6%) 84 (88.4%) Hyperkalemia 10 (10.5%) 85 (89.5%) Hypocalcemia 38 (40.0%) 57 (60.0%) Hypomagnesemia 43 (45.3%) 52 (54.7%) Table 3 illustrates the prevalence of different electrolyte abnormalities in the study population. Hyponatremia was the most prevalent abnormality, affecting 62 patients (65.3%), whereas 34.7% had normal sodium levels. Potassium disturbances were relatively less common; hypokalemia was present in 11.6% of patients, while hyperkalemia was seen in 10.5%. Hypocalcemia was detected in 40% of the patients, indicating a considerable burden of calcium imbalance. In addition, hypomagnesemia was observed in 45.3% of patients, suggesting that magnesium deficiency is also frequently encountered in chronic liver disease. Table 4. Major Clinical Complications (N = 95) Complication n % Ascites 78 82.1 Hepatic encephalopathy 32 33.7 Variceal bleeding 18 18.9 Renal dysfunction (AKI/HRS) 22 23.2 Infections (SBP/UTI/Sepsis) 25 26.3 Table 4 shows the distribution of major clinical complications among the study participants. Ascites was the most frequently observed complication, present in 78 patients (82.1%), reflecting advanced portal hypertension in the majority of cases. Hepatic encephalopathy was observed in 32 patients (33.7%), indicating a substantial prevalence of neuropsychiatric complications. Infections were reported in 25 patients (26.3%), including spontaneous bacterial peritonitis, urinary tract infections, and sepsis. Renal dysfunction, including acute kidney injury and hepatorenal syndrome, was present in 23.2% of patients, while variceal bleeding occurred in 18.9%, representing complications associated with portal hypertension. Table 5. Mean Electrolyte Levels by Child–Pugh Class Child–Pugh Class n Na⁺ K⁺ Ca²⁺ Mg²⁺ A 10 136.0 4.10 8.6 1.80 B 30 132.0 4.00 8.3 1.65 C 55 129.0 3.90 8.0 1.55 p value <0.001 0.041 0.018 <0.001 Table 5 demonstrates the relationship between electrolyte levels and the severity of liver disease based on the Child–Pugh classification. A progressive decline in electrolyte levels was observed with worsening liver function. Mean serum sodium levels decreased from 136.0 mmol/L in Child–Pugh class A to 129.0 mmol/L in class C, showing a highly significant association (p < 0.001). Magnesium levels also declined significantly across Child–Pugh classes, from 1.80 mg/dL in class A to 1.55 mg/dL in class C (p < 0.001). Similarly, serum calcium and potassium levels showed statistically significant reductions with increasing disease severity (p = 0.018 and p = 0.041 respectively). These findings indicate that electrolyte abnormalities become more pronounced as liver disease progresses. Table 6. Association of Electrolyte Abnormalities with Hepatic Encephalopathy Electrolyte HE Present n (%) HE Absent n (%) p value Hyponatremia 28 (45.2%) 34 (54.8%) 0.001 Normal sodium 4 (12.1%) 29 (87.9%) Hypocalcemia 20 (52.6%) 18 (47.4%) 0.002 Normal calcium 12 (21.1%) 45 (78.9%) Hypomagnesemia 22 (51.2%) 21 (48.8%) 0.001 Normal magnesium 10 (19.2%) 42 (80.8%) Table 6 presents the association between electrolyte abnormalities and hepatic encephalopathy (HE). Hyponatremia was significantly associated with the occurrence of HE, with 45.2% of hyponatremic patients developing encephalopathy compared to only 12.1% of patients with normal sodium levels (p = 0.001). Similarly, hypocalcemia showed a strong association with HE, as 52.6% of hypocalcemic patients developed encephalopathy compared to 21.1% of those with normal calcium levels (p = 0.002). Hypomagnesemia was also significantly associated with HE, with 51.2% of patients with low magnesium levels developing encephalopathy compared to 19.2% of those with normal magnesium levels (p = 0.001). Table 7. Association of Infection with Serum Magnesium Levels Magnesium Status Infection Present Infection Absent Total p value Hypomagnesemia 18 25 43 0.001 Normal Magnesium 7 45 52 Total 25 70 95 patients with infections, including spontaneous bacterial peritonitis, urinary tract infection, and sepsis, 18 patients (72%) had hypomagnesemia, while only 7 patients (28%) had normal magnesium levels. In contrast, among the 70 patients without infections, 25 patients (35.7%) had hypomagnesemia and 45 patients (64.3%) had normal magnesium levels. Statistical analysis revealed a significant association between hypomagnesemia and the presence of infections (p = 0.001), suggesting that magnesium deficiency may be linked to an increased risk of infections in patients with chronic liver disease.

This study evaluated serum electrolyte abnormalities in patients with decompensated chronic liver disease (DCLD) and their association with disease severity and clinical complications. The mean age was 52.3 ± 11.6 years, with male predominance (71.6%), consistent with previous reports by Namala AV et al. (2025) [15] (50.11 ± 10.22 years) and Shetty VN et al. (2023) [9] (49.69 years, 93.8% males), highlighting the higher susceptibility of middle-aged males to chronic liver disease, largely due to alcohol exposure. Alcohol was the leading etiology (46.3%), followed by viral hepatitis (31.6%) and NASH (12.6%), in agreement with findings by Shetty VN et al. (2023) [9] and Singh Y et al. (2022) [11], reflecting patterns observed in Indian and global populations. Electrolyte disturbances were highly prevalent. Hyponatremia was the most frequent abnormality (65.3%), resulting from systemic vasodilation, activation of the renin–angiotensin–aldosterone system, and increased antidiuretic hormone secretion, which impairs renal free-water excretion. Hyponatremia was significantly associated with hepatic encephalopathy (p = 0.001), consistent with Singh Y et al. (2022) [11]. Potassium abnormalities were observed in 22.1% of patients (hypokalemia 11.6%, hyperkalemia 10.5%), likely due to diuretics, secondary hyperaldosteronism, gastrointestinal losses, and renal dysfunction. Cai JJ et al. (2019) [16] reported significantly elevated potassium levels in hyperkalemic patients (p < 0.001), and Singh Y et al. (2022) [11] noted potassium >5.4 mEq/L was associated with increased mortality, highlighting its prognostic relevance. Hypocalcemia (40%) and hypomagnesemia (45.3%) were also common, attributable to hypoalbuminemia, malnutrition, impaired vitamin D metabolism, and altered renal handling. Singh Y et al. (2022) [11] observed hypocalcemia in 16% and hypokalemia in 30%, while hyponatremia ranged from 14.9–47%, reflecting differences in population characteristics, disease severity, and clinical management. Electrolyte disturbances correlated significantly with disease severity. Serum sodium, calcium, and magnesium levels declined progressively across Child–Pugh classes (p < 0.05), with most patients in class C (57.9%), indicating worsening hepatic dysfunction. Shetty VN et al. (2023) [9] similarly reported lower sodium levels in patients with higher MELD scores. Electrolyte imbalances were associated with clinical complications. Hyponatremia and hypomagnesemia were significantly linked to hepatic encephalopathy (p < 0.05), while hypomagnesemia was associated with infections (p = 0.001), likely due to impaired immune function. Ascites was the most common complication (82.1%), consistent with Namala AV et al. (2025) [15], reflecting advanced portal hypertension. Overall, electrolyte disturbances are highly prevalent in DCLD, correlate with disease severity, and contribute to major complications. Early recognition, regular monitoring, and timely correction are essential to reduce morbidity and improve outcomes. Limitations This study was limited by its single-center design and modest sample size, which may affect generalizability. The cross-sectional design precludes causal inference, and potential confounders such as diuretic use, nutritional status, and comorbidities were not fully controlled. Serial electrolyte measurements and long-term outcomes were not assessed.

The present study highlights the high prevalence and clinical significance of electrolyte abnormalities in patients with decompensated chronic liver disease (DCLD). Hyponatremia was the most frequent disturbance, followed by hypomagnesemia and hypocalcemia. Serum electrolyte levels showed a significant decline with increasing disease severity as assessed by the Child–Pugh classification. Hyponatremia, hypocalcemia, and hypomagnesemia were significantly associated with the occurrence of hepatic encephalopathy, while hypomagnesemia was also linked to a higher risk of infections. These findings suggest that electrolyte disturbances are common in DCLD and closely correlate with disease severity and major clinical complications. Early recognition and appropriate correction of these abnormalities may contribute to improved clinical outcomes and better management of patients with advanced liver disease.

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