The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure

Murphy, Nick; Auzinger, G.; Bernel, William; Wendon, Julia

doi:10.1002/hep.20056

Cited by 343 publications

(158 citation statements)

References 37 publications

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“…24 Finally, in patients with acute liver failure and grade IV hepatic encephalopathy, the administration of hypertonic saline to increase serum sodium concentration reduces the incidence and severity of intracranial hypertension compared with a control group of patients receiving the standard of care. 25 Hepatorenal syndrome was also strongly associated with low serum sodium concentration in our series (17% in patients with serum sodium Յ130 mmol/L compared with 10% in patients with serum sodium 130-135 mmol/L and only 6% in patients with normal serum sodium concentration) ( Fig. 2 and Table 5).…”

Section: Discussionsupporting

confidence: 53%

Hyponatremia in cirrhosis: Results of a patient population survey

et al. 2006

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and the CAPPS InvestigatorsLow serum sodium concentration is an independent predictor of mortality in patients with cirrhosis, but its prevalence and clinical significance is unclear. To evaluate prospectively the prevalence of low serum sodium concentration and the association between serum sodium levels and severity of ascites and complications of cirrhosis, prospective data were collected on 997 consecutive patients from 28 centers in Europe, North and South America, and Asia for a period of 28 days. The prevalence of low serum sodium concentration as defined by a serum sodium concentration <135 mmol/L, <130 mmol/L, <125 mmol/L, and <120 mmol/L was 49.4%, 21.6%, 5.7%, and 1.2%, respectively. The prevalence of low serum sodium levels (<135 mmol/L) was high in both inpatients and outpatients (57% and 40%, respectively). The existence of serum sodium <135 mmol/L was associated with severe ascites, as indicated by high prevalence of refractory ascites, large fluid accumulation rate, frequent use of large-volume paracentesis, and impaired renal function, compared with normal serum sodium levels. Moreover, low serum sodium levels were also associated with greater frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome, but not gastrointestinal bleeding. Patients with serum sodium <130 mmol/L had the greatest frequency of these complications, but the frequency was also increased in patients with mild reduction in serum sodium levels (131-135 mmol/L). In conclusion, low serum sodium levels in cirrhosis are associated with severe ascites and high frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome. (HEPATOLOGY 2006;44:1535-1542 I mpairment in body water homeostasis is a common feature of advanced cirrhosis. [1][2][3] This is characterized by a higher rate of renal retention of water in relation to sodium due to a reduction in solute-free water clearance. The consequent inability to adjust the amount of water excreted in the urine to the amount of water ingested leads to dilutional hyponatremia. In recent years, great advances have been made in the knowledge of the pathogenesis of reduced solute-free water clearance in patients with advanced cirrhosis. The inability to excrete an adequate amount of solute-free water in the urine is related to several factors, the most important of which is increased vasopressin release. A reduction of effective circulating volume due to arterial splanchnic vasodilation is considered the afferent factor leading to a baroreceptormediated nonosmotic stimulation of vasopressin release in cirrhosis. 4 Additional factors in the pathogenesis of hyponatremia in cirrhosis are thought to be reduced production of solute-free water due to a reduced sodium delivery to the distal tubule as a consequence of reduction of glomerular filtration rate and/or increase of sodium reabsorption in the proximal tubule. [4][5][6][7] Several studies in large cohorts of patients with cirrhosis have shown that the renal ability to...

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Section: Discussionsupporting

confidence: 53%

Hyponatremia in cirrhosis: Results of a patient population survey

et al. 2006

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“…35 About 25% of patients with ALF in a report from India had hyponatremia, which was prominent in patients with severe encephalopathy. 4 However pathogenesis of hyponatremia in ALF is unclear.…”

Section: Aggravating Factors Of Encephalopathy In Acute Liver Failurementioning

confidence: 99%

“…66 In a recent prospective randomized trial involving 30 patients with ALF, it was found that use of hypertonic (30%) sodium chloride infusion to maintain serum sodium levels between 145 and 155 mmol/L led to a significant decrease in ICP. 35 …”

Section: Ammonia Lowering Strategiesmentioning

confidence: 99%

Management in Acute Liver Failure

Shalimar

Acharya

2015

Journal of Clinical and Experimental Hepatology

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Acute liver failure (ALF) is a rare, potentially fatal complication of severe hepatic illness resulting from various causes. In a clinical setting, severe hepatic injury is usually recognised by the appearance of jaundice, encephalopathy and coagulopathy. The central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique and multifactorial. Ammonia plays a central role in the pathogenesis. The role of newer ammonia lowering agents is still evolving. Liver transplant is the only effective therapy that has been identified to be of promise in those with poor prognostic factors, whereas in the others, aggressive intensive medical management has been documented to salvage a substantial proportion of patients. A small fraction of patients undergo liver transplant and the remaining are usually treated with medical therapy. Therefore, identification of the complications and causes of death in such patients, and use of appropriate prognostic models to identify those who need liver transplant and those who can be managed with medical treatment is a vital component of therapeutic strategy. In this review, we discuss the various pathogenetic mechanisms and treatment options available. ( J CLIN EXP HEPATOL 2015;5:S104-S115)A cute liver failure (ALF) can be a fatal complication of acute hepatic injury and occurs unpredictably. It is a rare clinical entity marked by the sudden loss of hepatic function and a severe life-threatening course in a person with no prior history of liver disease. ALF represents a syndrome rather than a specific disease, having multiple causes that vary in course and outcome. ALF is difficult to identify in its early stages, resulting in frequent delays in initiation of treatment. The causes of ALF include viral hepatitis, drug induced and toxin-induced liver damage, metabolic errors, ischemia, and miscellaneous rare causes.ALF is defined by three criteria: (1) rapid development of hepatocellular dysfunction (jaundice, coagulopathy), (2) encephalopathy, and (3) absence of a prior history of liver disease. 1 However, the interval between onset of acute hepatic injury (jaundice) and onset of liver failure (encephalopathy with or without coagulopathy) in such patients (icterus-encephalopathy interval; IEI) has been described to be between 4 weeks (Indian definition) 2-4 to 24 weeks (AASLD-ALF study group). 5 Further, due to the diverse natural course, ALF has been sub-classified as hyperacute (IEI # 7 day), acute (IEI # 4 weeks) and sub-acute ALF (IEI $ 5 week to #12 weeks) by British authors. 6 Despite these differences in definitions, the central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique an...

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“…Low sodium levels are related to the impairment of renal solute-free water excretion most likely due to an increased vasopressin secretion, which results in increased sodium retention and reduced renal free water clearance, which predispose to life threatening conditions in the cirrhotic such as HRS and refractory ascites [36] . Also, hyponatremia represents an independent risk factor for brain edema, a fatal complication of acute liver failure [37,38] . Interestingly, we found that low sodium levels were associated with mortality at 30 and 90 d. Also, HRS was associated to mortality in the univariate and multivariate analysis.…”

Section: Discussionmentioning

confidence: 99%

Model for end-stage liver disease-Na score or Maddrey discrimination function index, which score is best?

Amieva-Balmori¹,

Mejia-Loza²,

Ramos-González³

et al. 2015

WJH

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AIM:To compare the ability of model for end-stage liver disease (MELD)-Na and Maddrey discrimination function index (DFI) to predict mortality at 30 and 90 d in patients with alcoholic hepatitis (AH). METHODS:We prospectively assessed 52 patients with AH. Demographic, clinical and laboratory parameters were obtained. MELD-Na and Maddrey DFI were calculated on admission. Short-term mortality was assessed at 30 and 90 d. Receiver operating characteristic curve analysis was performed. RESULTS:Thirty-day and 90-d mortality was 44% and 58%, respectively. In the univariate analysis, sodium levels was associated with mortality at 30 and 90 d (P = 0.001 and P = 0.03). Child stage, encephalopathy, ascites, or types of treatment were not associated with mortality. MELD-Na was the only predictive factor for mortality at 90 d. For 30-d mortality area Core tip: Alcoholic hepatitis (AH) is a severe condition associated with high mortality. The model for end-stage disease (MELD) score is widely used to predict mortality in end-stage liver disease, and the addition of sodium (MELD-Na) increase its utility. However, few studies have evaluated the utility of MELD-Na in AH. In this study, we found that MELD-Na is useful for predicting 90-d mortality in patients with AH and preserve prognostic advantage over Maddrey discrimination function index score. It represents a valuable tool to stratify patients by risk, however further studies are required to validate the prognostic utility of MELD-Na score in patients with AH. EVIDENCE-BASED MEDICINEAmieva-Balmori M, Mejia-Loza SMI, Ramos-González R, Zamarripa-Dorsey F, García-Ruiz E, Pérez y López N, Juárez-Valdés EI, López-Luria A, Remes-Troche JM. Model for end-stage liver disease-Na score or Maddrey discrimination function index, which score is best? World

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The effect of hypertonic sodium chloride on intracranial pressure in patients with acute liver failure

Cited by 343 publications

References 37 publications

Hyponatremia in cirrhosis: Results of a patient population survey

Hyponatremia in cirrhosis: Results of a patient population survey

Management in Acute Liver Failure

Model for end-stage liver disease-Na score or Maddrey discrimination function index, which score is best?

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