Hyponatremia In Cirrhosis Research Articles

THE CORRELATION BETWEEN SERUM SODIUM LEVELS AND THE SEVERITY OF CIRRHOSIS OF LIVER AND ITS COMPLICATIONS

Objective: The study aimed to assess the incidence of hyponatremia in cirrhosis of the liver and to evaluate the association between serum sodium levels and the severity of cirrhosis and its complications. Methods: Data on inpatients with cirrhosis of the liver were collected on the date of admission. The serum sodium levels on day 1 and the presence of complications and their severity in 100 patients were analyzed. Results: The incidence of dilutional hyponatremia, which was subdivided into three groups (mmol/L): A-≤130, B-131-135, and C-≥136, were 55%, 25%, and 20%, respectively. The severity of liver cirrhosis was assessed using the CTP score and the MELD score, with a higher score seen in Group A (p=0.011 and p=0.012), respectively. Furthermore in group A, higher grades of complications were seen: grade 3/gross ascites (p=0.001), grade lll/lV hepatic encephalopathy (p=0.007), spontaneous bacterial peritonitis (p=0.049), and hepatorenal syndrome (p=0.022). Even in group B with s.Na+level 131–135 mmol/L, the development of complications was no less common. Conclusion: Serum sodium levels must be closely monitored in cirrhotic patients as they suggest the possibility of a potentially negative impact on the clinical course of the disease.

Albumin: a comprehensive review and practical guideline for clinical use.

Nowadays, it is largely accepted that albumin should not be used in hypoalbuminemia or for nutritional purpose. The most discussed indication of albumin at present is the resuscitation in shock states, especially distributive shocks such as septic shock. The main evidence-based indication is also liver disease. In this review, we provided updated evidence-based instruction for definite and potential indications of albumin administration in clinical practice, with appropriate dosing and duration. Data collection was carried out until November 2023 by search of electronic databases including PubMed, Google Scholar, Scopus, and Web of Science. GRADE system has been used to determine the quality of evidence and strength of recommendations for each albumin indication. A total of 165 relevant studies were included in this review. Fluid replacement in plasmapheresis and liver diseases, including hepatorenal syndrome, spontaneous bacterial peritonitis, and large-volume paracentesis, have a moderate to high quality of evidence and a strong recommendation for administering albumin. Moreover, albumin is used as a second-line and adjunctive to crystalloids for fluid resuscitation in hypovolemic shock, sepsis and septic shock, severe burns, toxic epidermal necrolysis, intradialytic hypotension, ovarian hyperstimulation syndrome, major surgery, non-traumatic brain injury, extracorporeal membrane oxygenation, acute respiratory distress syndrome, and severe and refractory edema with hypoalbuminemia has a low to moderate quality of evidence and weak recommendation to use. Also, in modest volume paracentesis, severe hyponatremia in cirrhosis has a low to moderate quality of evidence and a weak recommendation. Albumin administration is most indicated in management of cirrhosis complications. Fluid resuscitation or treatment of severe and refractory edema, especially in patients with hypoalbuminemia and not responding to other treatments, is another rational use for albumin. Implementation of evidence-based guidelines in hospitals can be an effective measure to reduce inappropriate uses of albumin.

SODIUM AND CALCIUM LEVELS IN PATIENTS WITH CIRRHOSIS OF THE LIVER AND ITS CORRELATION WITH HEPATIC ENCEPHALOPATHY

Introduction: Patients with chronic liver disease have a specific susceptibility to an electrolyte imbalance that can deteriorate their condition to hepatic encephalopathy. It occursin about 57% of hospitalized patients with cirrhosis. Hyponatremia in cirrhosis is an in dependent risk factor for mortality and is common in patients with end-stage liver disease. These patients had a significantly higher incidence of hepatic encephalopathy, hepatorenal syndrome, and spontaneous bacterial peritonitis. Hepatic encephalopathy is worsened by the presence of hyponatremia and hypocalcemia. Aim:The aim of this study is to evaluate sodium and calcium levels in CLD patients and its correlation with hepatic encephalopathy. Methods: This cross-sectional study was conducted in SMHS Hospital,Govt.Medical College Srinagar, Jammu Kashmir,India, during a three-year period. 150 patients with chronic liver disease admitted to the general medicine and gastroenterology department were included. Data was entered in SPSS software version 20. Qualitative data were analyzed using chi-square, and quantitative data were analyzed using independent t-tests. A P-value <0.05 was considered significant. Results: Our study on 150 CLD patients showed that the serum sodium level and serum calcium level were significantly lower in patients with hepatic encephalopathy with P-Values of 0.0006 and 0.002, respectively. Conclusion: It seems that reducing serum sodium and calcium level can be predictive of hepatic encephalopathy inpatients with chronic liver disease.

Hyponatremia and its Clinical Outcome Among Patients with Hepatic Encephalopathy Due to Liver Cirrhosis Presenting to ATH Abbottabad

Introduction: Hepatic encephalopathy (HE) is a potentially reversible complication of liver cirrhosis causing significant mortality. Hyponatremia in cirrhosis is caused by hampered renal function to eliminate free water that results in water retention disproportionate to sodium retention leading to reduced plasma osmolality and is associated with significant morbidity and mortality. The purpose of study was to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy. Methods: The design of this study was an observational study design which was hospital-based survey and was conducted on 130 patients of liver cirrhosis. A specialized questionnaire was designed to collect all the study information. All data was analyzed using SPSS Statistics version 24. Chi-square test and Spearman's rank test were employed to correlate hyponatremia with HE and its severity. A p-value of <0.05 was considered statistically significant. Results: Among the patients, 92 (71%) males and 38 (29%) females; the mean age of the patients was 56±11.3 years. Hyponatremia was present in 48 (36.9%) patients. Among these, 25 (52%) were male and 23 (48%) were female; 12 (25%) patients had mild Hyponatremia, 28(58.3%) had moderate, and 8 (16.6%) had severe Hyponatremia. HE was significantly associated with hyponatremia with p value of lea than 0.001. Practical Implication: The benefit of our study was undertaken to determine the frequency of hyponatremia among patients of liver cirrhosis with hepatic encephalopathy to provide evidence for hyponatremia as a prognostic factor in HE so that early detection and management of hyponatremia in such patients will help reduce disease burden and mortality in liver cirrhosis. Conclusion: Patients with lower levels of sodium had higher grades/severity of HE. Significant association of hyponatremia was seen with liver cirrhosis and encephalopathy. Keywords: Abbottabad, Cirrhosis, Hepatic encephalopathy, Hyponatremia, Liver.

The Impact of Hyponatremia on Severity of Decompensated Chronic Liver Disease

Introduction: Hyponatremia in cirrhosis is low sodium concentration in the blood. It has been additionally reported that hyponatremia occurs when serum sodium concentration in the blood is less than 135mmol/L, with severe hyponatremia being below 120 mmol/L. In general, two kinds of hyponatremia may be found in patients with cirrhosis, such as hypovolemic and hypervolemic hyponatremia. Complications may arise in case of correcting hyponatremia too quickly. The study aims to investigate the impact of hyponatremia on the severity of decompensated chronic liver disease. Methods: A Prospective cross-sectional study was carried out Department of Gastroenterology and Hepatology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Shabagh, Dhaka, from March 2014 to February 2015. A total of 100 patients (N=100) for one year were enrolled in this study following the inclusive criteria. Data were collected using the predesigned semi-structured questionnaire. Verbal consent was taken before recruiting the study population. Completed data forms were reviewed, edited, and processed for computer data entry. Result: Among hundred patients (N=100) with decompensated chronic liver disease observe the impact of hyponatremia with the severity of complications. Of them, it was observed that more than one-third of the patients (37, 37.0%) belonged to age 31-40 years. The mean age was found 42.2±SD years. It was observed that almost two-thirds of the patients (63, 63.0%) were male and thirty-seven (37,37.0%) patients were female. Among the study population, the majority of the patients (90, 90.0%) belonged to serum sodium ≤135 mmol/l (Hyponatremia). The mean serum sodium was found 124.7±SD mmol/l. The majority of patients (57,57.0%) had moderate ascites, nineteen patients (19,19.0%) had mild and about one-fourth of the patients (24,24.0%) had severe ascites. Conclusion: Hyponatraemia should be accomplished by dipping diuretics and increasing the plasma volume with fluid resuscitation.

Prevalence of hyponatremia in Cirrhosis and its correlation with severity of the disease

Prevalence of hyponatremia in Cirrhosis and its correlation with severity of the disease

Hyponatremia in Cirrhosis: Role of Vasopressors.

Hyponatremia in Cirrhosis: Role of Vasopressors.

Hiponatremia en niños con cirrosis hepática: Estrategias de tratamiento

Hyponatremia is a common hydroelectrolytic disorder in pediatric patients with advanced cirrhosis. This complication is related to the alteration in the renal capacity to eliminate free water with solutes such as sodium, which leads to disproportionate water retention, a condition known as dilutional hyponatremia. The main pathogenic factors are the non-osmotic secretion of antidiuretic hormone and the activation of the renin-angiotensin-aldosterone axis and the sympathetic nervous system. Given that hyponatremia in cirrhosis is associated with an increase in morbidity and mortality, the objective of this review is to propose a systematic approach, based on the level of serum sodium, assessment of hemodynamic status and diuresis, which allows precise modifications that minimize negative impacts on survival and neurological sequelae.

P: 72 Hyponatremia Correction in Cirrhosis May Increase the Speed of Complex Information Processing

BACKGROUND: Hyponatremia is frequent in patients with advanced cirrhosis and ascites. A decrease in plasma osmolality exacerbates astrocyte swelling and through this mechanism may worsen cognitive function. Our objective was to determine whether, in patients with cirrhosis and ascites, an increase in plasma sodium (spontaneous or induced by an aquaretic) leads to an improvement in cognitive function. METHODS: 250 patients with liver cirrhosis and ascites were included in two double-blind, randomised, multicentre clinical studies of satavaptan (a vasopressin V2 antagonist). Patients were included after a "wash-out period" (one week on controlled sodium intake and spironolactone 100 mg/d) and received either placebo (n = 61) or satavaptan (n = 189) at three different doses (5, 12.5, 25 mg/d). Patients completed the trail-making test (TMT) at baseline and at 5–7 and 14–28 days of follow-up. The TMT (scored in seconds) assesses speed of information processing and is considered a test of simple (part A) and complex attention (part B). Improvement of hyponatraemia was defined as an increase in plasma sodium >5 mmol/l or to a value >135 mmol/l. RESULTS: At inclusion into the studies, patients with normonatremia exhibited better results on the TMT-A and TMT-B that could not be explained by differences on age. This group also exhibited better parameters of liver function (Table 1). Improvement of hyponatremia was associated with shortening on the time needed to complete TMT-B: −20 s vs −6.5 s (P = 0.02), but not TMT-A: −10 s vs −5 s (P = 0.16). Increase in serum osmolality was also associated with better TMT-B scores (P < 0.001 at Day 5-7 and P = 0.033 at Day 14–28), but this was not shown for TMT-A. Liver function parameters remained stable in both groups of patients. Improvement of hyponatremia at Day 5 was most commonly seen in patients that received satavaptan (59.7%, n = 82) than in those treated with placebo (18.5%, n = 28). Median changes in TMT scores with satavaptan (all doses pooled) compared to placebo were: TMT-A −10 s vs 0 s (P = 0.08) and TMT-B −20 s vs −7.5 s (P = 0.12). CONCLUSIONS: Improvement of hyponatremia in cirrhosis was associated with an increase in the speed of complex information processing. Improvement of hyponatremia was achieved more frequently with satavaptan treatment, which showed a trend towards better results on cognitive function.

Improvement of hyponatremia in cirrhosis is associated with improved complex information processing.

Hyponatremia, a cause of brain dysfunction and risk factor for hepatic encephalopathy, is frequent in patients with advanced cirrhosis and ascites. The interdependence of liver failure and hyponatremia makes it difficult to separate the effects of each on cognitive function. The objective was to assess whether an increase in plasma sodium in patients with cirrhosis and ascites leads to an improvement in cognitive function. This is a post-hoc analysis of 250 cirrhosis patients without overt hepatic encephalopathy randomized to receive either placebo or satavaptan, a vasopressin V2 antagonist. The exposure was plasma sodium, and the outcome was the trail-making test (TMT) parts A and B, which assesses speed of information processing, performed before the study starts and after 14days. The results were analyzed by initial and change to final sodium concentration. At entry, the patients with normonatremia exhibited better results on both the TMT-A (median 56 vs 77.5s for patients with sodium ≤130mmol/L [P=0.0059]) and the TMT-B (median 127 vs 170s for patients with sodium ≤130mmol/L [P=0.0066]), unrelated to age. Improvement of hyponatremia was more common in patients who received satavaptan (59.7%) than placebo (18.5%). Correction of hyponatremia did not shorten the simple TMT-A but markedly improved the complex TMT-B by an average of 20s compared with 6.5s in those with continuing hyponatremia (P=0.02). Liver status measures remained stable during the period reported. These data suggest that improvement of hyponatremia in patients with cirrhosis leads to an increase in the speed of complex information processing.

Approach to Hyponatremia in Cirrhosis.

The patient in the case presented with hypervolemic hyponatremia associated with ascites and edema. The sNa concentration of 120 mmol/L is bordering severe hyponatremia and is associated with renal insufficiency. The management of this patient includes free water restriction, holding diuretics, and consideration of albumin infusion (Fig. ​(Fig.1).1). Tolvaptan is not recommended in patients with liver disease. Furthermore, hyponatremia and renal dysfunction are associated with poor prognosis. If the hyponatremia is persistent, liver transplant evaluation should be considered. Open in a separate window Figure 1 Algorithm depicting suggested management of hyponatremia in the patient with cirrhosis.

Hyponatremia in Cirrhosis: Implications for Liver Transplantation.

Hyponatremia in cirrhosis is defined as a serum sodium level ≤130 mEq/L and occurs in approximately 22% of patients with cirrhosis. The appearance of hyponatremia in patients with cirrhosis portends a poor prognosis before liver transplantation (LT), independent of the Model for End-Stage Liver Disease (MELD) score. With the development of the MELD-sodium score, the management of hyponatremia has become more relevant than ever before. Overcorrection of hyponatremia before LT or perioperatively can lead to the devastating neurologic condition known as osmotic demyelination syndrome, which is often irreversible and fatal. Therefore, the most important tenet of hyponatremia is to avoid correcting the serum sodium by ≥8 mEq/L in a 24-hour period. Treatment of hyponatremia is highly challenging. The vast majority of patients with cirrhosis have chronic hypervolemic hyponatremia. Fluid restriction increases serum sodium levels, but tolerance and compliance are significant barriers. Diuretic withdrawal is helpful but contributes to worsening fluid overload. There are limited data to support use of intravenous concentrated albumin solutions. The use of the arginine vasopressin antagonists ("vaptans") is contentious; however, they may have a limited role. Risk factors for intraoperative overcorrection of serum sodium include increased utilization of packed red blood cell and fresh frozen plasma transfusions, which are often unavoidable. Intraoperative management is evolving, and more data are needed in regard to the use of sodium-reduced continuous venovenous hemofiltration and the use of trishydroxymethylaminomethane (Tris) to avoid excess sodium rebound. A thorough discussion of the current treatment options before and during LT is given in this review.

A case of cirrhosis with severe hyponatremia

Cirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors such as infection. Hyponatremia in cirrhosis is associated with increased morbidity and mortality. we report a case of52 year old man with a history of alcoholic cirrhosis presented to the hospital with symptomatic profound hyponatremia (serum sodium concentration of 102 meq/L). The patient was treated with antibiotics, diuretics and hypertonic saline and was placed on a fluid restricted diet. The serum sodium level corrected slowly over four days with symptomatic improvement occurring after five days. In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring. Key words: hyponatremia, cirrhosis, liver

Limited Efficacy of Tolvaptan in Patients with Cirrhosis and Severe Hyponatremia: Real-Life Experience

BackgroundVaptans, vasopressin selective V2-receptor antagonists, represent the first pharmacologic approach to the treatment of hypervolemic hyponatremia in cirrhosis. However, information on the use of vaptans for patients with cirrhosis and hyponatremia in a real-life scenario is limited. Therefore, this study evaluated the effect of tolvaptan on serum sodium in patients with cirrhosis and severe hypervolemic hyponatremia. MethodsNine patients with cirrhosis and serum sodium ≤125 mEq/L were included. ResultsOnly 2 of the 9 patients (22%) gained an increase in serum sodium >130 mEq/L that persisted throughout treatment. In the remaining patients, serum sodium did not change or increased during the first days but decreased thereafter despite continuation of treatment. Only 1 patient developed hyperkalemia as a side effect. ConclusionsThe efficacy of tolvaptan in patients with cirrhosis and severe hypervolemic hyponatremia seems to be limited.

The Changing Role of Sodium Management in Cirrhosis.

Hyponatremia may occur in patients with cirrhosis and ascites mainly due to water retention and an inability of the kidney to excrete free water. The main reason for this abnormality is related to the fact that these patients have portal hypertension and this leads to systemic vasodilation that in turn activates sodium-retaining and water-retaining systems such as the renin-angiotensin-aldosterone system and arginine vasopressin (AVP). AVP increases solute-free water retention by acting on the V2 receptors of the kidney-collecting tubes. Hyponatremia in cirrhosis is defined as a serum sodium level less than 130meq/L. The appearance of hyponatremia in patients with advanced cirrhosis portends a poor prognosis before and after liver transplantation. Treatment of hyponatremia is difficult; fluid restriction rarely increases serum sodium levels and other therapies are associated with important drawbacks. A thorough discussion of the underlying mechanisms leading to hyponatremia and hypernatremia in cirrhosis and current treatment options including the use of vaptans (V2 receptor antagonists) are discussed in this review.

The Management of Hyponatremia in Cirrhosis: Should it Be Pharmacologic?

Hyponatremia is a common complication of patients with advanced cirrhosis that is associated with increased morbidity and mortality. Patients with cirrhosis may develop two types of hyponatremia: hypovolemic or hypervolemic hyponatremia. Hypervolemic hyponatremia is the most frequent type of hyponatremia that develops in patients with advanced liver disease and is the consequence of impairment in the renal capacity to eliminate solute-free water. The pathogenesis of these increased solute-free water retention involves several factors, but the most important one is a non-osmotic hypersecretion of vasopressin. The treatment of choice for hypervolemic hyponatremia is fluid restriction. Vaptans, drugs that are selective antagonists of vasopressin V2 receptors, emerged as the first pharmacological treatment of hypervolemic hyponatremia in cirrhosis with promising results. However, satavaptan was withdrawn from development for safety reasons and tolvaptan is not recommended in patients with liver disease. Therefore, currently there is no effective and safe pharmacological approach available for the management of hypervolemic hyponatremia in cirrhosis.

Hyponatremia in cirrhosis: pathophysiology and management.

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. The development of ascites in patients with cirrhosis is multi-factorial. Portal hypertension and the associated systemic vasodilation lead to activation of the sodium-retaining neurohumoral mechanisms which include the renin-angiotensin-aldosterone system, sympathetic nervous system and antidiuretic hormone (ADH). The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume resulting in the development of ascites. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and ascites leads to impairment of the kidneys to eliminate solute- free water. This leads to additional compensatory mechanisms including non-osmotic secretion of ADH, also known as arginine vasopressin, further worsening excess water retention and thereby hyponatremia. Hyponatremia is associated with increased morbidity and mortality in patients with cirrhosis, and is an important prognostic marker both before and after liver transplant. The management of hyponatremia in this setting is a challenge as conventional therapy for hyponatremia including fluid restriction and loop diuretics are frequently inefficacious. In this review, we discuss the pathophysiology and various treatment modalities, including selective vasopressin receptor antagonists, for the management of hyponatremia in patients with cirrhosis.

Incidence of Dilutional Hyponatemia in Hospitalized Patients with Liver Cirrhosis

Background: Dilutional hyponatremia in cirrhosis is defined as a reduction in serum sodium concentration in the setting of an expanded extracellular fluid volume as evidenced by the presence of ascites and/or edema. The incidence of dilutional hyponatremia in cirrhotic patients treated for an episode of ascites is 35%; it is one of the most important prognostic factors in these patients.

Low-dose tolvaptan for the treatment of dilutional hyponatremia in cirrhosis: a case report and literature review.

Dilutional hyponatremia is common in decompensated cirrhosis and can be successfully treated by tolvaptan, a vasopressin V2-receptor antagonist. Data were lacking regarding the effects of tolvaptan on cirrhotic patients with a Child-Pugh score of >10 and a serum sodium concentration of <120 mmol/L. We report a case of forties man with a 20-year history of chronic hepatitis B presenting with yellow urine and skin. Laboratory tests demonstrated prolonged prothrombin time, markedly elevated total bilirubin, severe hyponatremia, and a Child-Pugh score of >10. The patient was diagnosed with dilutional hyponatremia and was treated with recommended dosage tolvaptan at first. The serum concentration of sodium recover but the patient felt obviously thirsty. As the dosage of tolvaptan was decreased accordingly from 15 mg to 5 mg, the patient still maintained the ideal concentration of serum sodium. This case emphasizes that cirrhotic patient with higher Child-Pugh scores and serum sodium concentration of <120 mmol/L can be treated with lower dose of tolvaptan.

Letter in Response to the Recently Published Review: Hyponatremia in Cirrhosis and End-Stage Liver Disease—Treatment with the Vasopressin V2-Receptor Antagonist Tolvaptan

Letter in Response to the Recently Published Review: Hyponatremia in Cirrhosis and End-Stage Liver Disease—Treatment with the Vasopressin V2-Receptor Antagonist Tolvaptan