DOCSLIB.ORG

Hyponatremia and Hepatorenal Syndrome

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Hyponatremia and Hepatorenal Syndrome Hyponatremia and Hepatorenal Syndrome Arpan Mohanty, MD, and Guadalupe Garcia-Tsao, MD Dr Mohanty is a clinical fellow in the Abstract: Hyponatremia and hepatorenal syndrome are severe Section of Digestive Diseases at Yale complications in patients with cirrhosis and ascites resulting from University School of Medicine in New circulatory abnormalities (splanchnic and systemic vasodilata- Haven, Connecticut and is affiliated with tion) that develop with portal hypertension. Both conditions are the Section of Digestive Diseases at the Veterans Administration–Connecticut associated with an increased risk of death. Hyponatremia and Health Care System in West Haven, renal failure may develop in patients with cirrhosis due to causes Connecticut. Dr Garcia-Tsao is a professor other than portal hypertension. Making an accurate differential of medicine in the Section of Digestive diagnosis is important both therapeutically and prognostically. In Diseases at Yale University School of this article, we discuss the pathophysiology, diagnosis, differential Medicine and is the chief of the Section of diagnosis, and management of hyponatremia and hepatorenal Digestive Diseases at the Veterans Adminis- tration–Connecticut Health Care System. syndrome in patients with cirrhosis. Address correspondence to: Dr Guadalupe Garcia-Tsao Section of Digestive Diseases Yale University School of Medicine One Gilbert Street, TAC, #S241-B yponatremia and hepatorenal syndrome (HRS) are severe New Haven, CT 06510 complications that occur in patients with cirrhosis and Tel: 203-737-6063 ascites and are associated with lower survival than in Fax: 203-785-7273 Hpatients with decompensated cirrhosis (eg, those who have uncom- E-mail: [email protected] plicated ascites, variceal hemorrhage, or encephalopathy).1,2 There- fore, the development of these 2 complications represents a stage of further decompensation of cirrhosis. Dilutional hyponatremia and HRS (a type of renal failure unique to patients with cirrhosis) represent manifestations of a con- tinuum of pathophysiologic events stemming from portal hyperten- sion and the resultant vasodilatation, which are the main mecha- nisms responsible for the development of ascites.3 In a prospective inception cohort study of patients with cirrhosis and new-onset ascites who were followed for a mean of 41 months, hyponatremia developed in 28% of the patients, 11% developed refractory asci- tes, and 8% developed HRS, suggesting a sequential process (from ascites to hyponatremia to refractory ascites to HRS).4 Each of these processes was associated with increasing severity of liver disease, worsening vasodilatation evidenced by decreasing mean arterial pressure (MAP), and more avid sodium retention.3 However, it is important to recognize that hyponatremia and renal failure in the patient with cirrhosis may result from conditions Keywords Hyponatremia, hepatorenal syndrome, cirrhosis, that occur in noncirrhotic patients and that result from pathophysi- ascites ologic mechanisms different from worsening portal hypertension/ 220 Gastroenterology & Hepatology Volume 11, Issue 4 April 2015 HYPONATREMIA AND HEPATORENAL SYNDROME vasodilatation. Making an accurate differential diagnosis Cirrhosis is important both prognostically and therapeutically. We therefore review the pathophysiology, diagnosis, differ- ential diagnosis, and management of hyponatremia and Portal hypertension HRS in patients with cirrhosis. Splanchnic/systemic vasodilatation Pathophysiology of Hyponatremia and Hepatorenal Syndrome Eective arterial blood volume Vasodilatation of both the splanchnic and systemic cir- culations is one of the main factors contributing to the Activation of neurohumoral systems : development of hyponatremia and HRS in cirrhosis Renin- (Figure 1). Vasodilatation occurs after portal hyperten- Aldosterone AVP Angiotensin sion has led to the formation of portosystemic collaterals when factors that have not been well elucidated (vascular Sodium Water Renal endothelial growth factor being one of them) trigger the retention retention vasoconstriction production of nitric oxide and other vasodilators.5,6 This vasodilatation leads to decreased effective arterial volume Dilutional Hepatorenal Ascites and activation of various vasoconstrictor and antinatri- hyponatremia syndrome uretic neurohumoral systems (the renin-angiotensin- aldosterone system and sympathetic nervous system), Figure 1. The pathophysiology of hyponatremia and hepa- leading to renal sodium and water retention and an torenal syndrome (HRS) in cirrhosis. Cirrhosis and portal hypertension lead to the development of splanchnic and sys- increase in intravascular volume, which in turn leads to a temic vasodilatation that causes a decrease in effective circula- hyper dynamic circulatory state. tory volume, which in turn leads to the activation of various In advanced stages of cirrhosis, progressive vasodila- vasoconstrictor and antinatriuretic neurohumoral systems tation leads not only to avid sodium retention (with for- (renin-angiotensin-aldosterone system, sympathetic nervous mation of ascites that is now refractory to diuretics) but system, and nonosmotic release of antidiuretic hormone). This also to the nonosmotic release of antidiuretic hormone or initially leads to water and salt retention increasing intravascular arginine vasopressin (AVP). The biological effects of AVP volume and allowing for the continuous formation of ascites. in increasing water reabsorption are mediated through However, with worsening cirrhosis (or with precipitant fac- G protein–coupled receptors, specifically vasopressin 2 tors), splanchnic/systemic vasodilatation worsens, leading to a (V2) receptors located on the basolateral membrane of significant increase in antidiuretic hormone release and water principal cells of the collecting ducts. When activated by retention (in excess of sodium retention) and, thereby, to dilu- tional hyponatremia. Maximal vasodilatation and activation of AVP, V2 receptors enable translocation of selective water vasoconstrictive systems (renin-angiotensin) lead to renal vaso- channels called aquaporins from the cytosol to the lumi- constriction and the development of HRS. nal plasma membrane of the collecting ducts, increasing water permeability. This increase in water reabsorption AVP, arginine vasopressin. exceeds that of sodium retention and leads to dilutional hyponatremia. V2 receptor antagonism has therefore event. However, more often than not, HRS is precipi- been a potential target for drugs used in the treatment of tated by factors that cause either a decrease in effective this dilutional hyponatremia. arterial blood volume, such as rapid fluid loss (eg, exces- Progressive vasodilatation also leads to further sive diuresis and gastrointestinal bleeding), or worsening activation of vasoconstrictive systems (mainly renin and vasodilatation induced by drugs (eg, nitrates, carvedilol, angiotensin), resulting in renal vasoconstriction and and angiotensin-converting enzyme inhibitors) or by a decreased renal blood flow. In addition, a relative decrease systemic inflammatory response (eg, infection). in cardiac output in this high-output cardiac failure state (or cirrhotic cardiomyopathy) may further contribute Hyponatremia in Cirrhosis to decreased renal blood flow.5,7,8 This decrease in renal blood flow leads to a decreased glomerular filtration rate Hyponatremia in cirrhosis has been arbitrarily defined as and a prerenal type of kidney injury (ie, HRS). a serum sodium level of less than 130 mEq/L and is pres- Hepatorenal physiology as described above may be ent in approximately one-fifth of patients with decom- present in many patients with advanced cirrhosis who pensated cirrhosis.9 It is important to note that, although may develop HRS without an obvious precipitating not meeting this definition, a serum sodium level of less Gastroenterology & Hepatology Volume 11, Issue 4 April 2015 221 MOHANTY AND GARCIA-TSAO than 135 mEq/L in patients listed for liver transplanta- mental component scores of the SF-36 questionnaire tion has been associated with increased mortality, inde- that assesses HRQOL.15 A recent study of the effect of pendent of Model for End-Stage Liver Disease (MELD) hyponatremia and hepatic encephalopathy on HRQOL score.1 In fact, the incorporation of serum sodium level demonstrated that patients with cirrhosis and hyponatre- into MELD (referred to as MELD-Na) has been shown mia but without hepatic encephalopathy have a poorer to predict survival more accurately than MELD alone10 HRQOL as measured by the Sickness Impact Profile, and will likely be used soon instead of MELD for organ despite better cognition, compared with those with con- allocation in the United States. comitant encephalopathy.16 Furthermore, in a prospective study, correction of hyponatremia was associated with Differential Diagnosis of Hyponatremia in Cirrhosis improvement in cognitive function and HRQOL.17 Hyponatremia in cirrhosis may be (1) hypervolemic or Pretransplant hyponatremia is an independent dilutional as a result of water retention (in excess of sodium predictor of short-term mortality after liver transplanta- retention) due to AVP activation secondary to vasodilata- tion.18,19 Rapid correction of hyponatremia in the postop- tion and decreased effective circulatory volume or (2) erative period can result in central pontine demyelinoly- hypovolemic as a result of sodium and fluid losses (mainly sis,20,21 a lethal neurologic complication that can result
Load more

Recommended publications
  • Ascites, Hepatorenal Syndrome, Portal HTN and SBP
    Ascites, Hepatorenal Syndrome, Portal HTN and SBP Sept 2014 Ascites Excessive free fluid in the peritoneal cavity. >1.5L before clinically apparent. Starling forces: ↑venous pressure, ↑capillary permeability, hypoproteinaemia, lymphatic obstruction Causes Liver cirrhosis (75%) Malignancy (15%) - Ca colon, other GI, Ca ovary (Meigs’ syndrome), Hepatic tumour, Lymphoma CCF (3%) TB (2%) Pancreatitis (1%) Constrictive pericarditis, Venous obstruction – e.g. Budd-Chiari, Renal failure, Myxoedema Examination Abdominal distension umbilicus down, Shifting dullness to percussion, Fluid thrill Stigmata of chronic liver disease Other masses: Ca colon/ovary, PR exam Lymphadenopathy Kussmaul’s sign for constrictive pericarditis Signs of CCF, hepatojugular reflex, Signs of IBD Kayser-Fleischer Rings (Wilson’s), Jaundice, Proteinuria Investigations Bloods: FBC, LFT, UEC, Coags, TFT, Hepatitis screen Imaging: USS, CT, CXR Paracentesis/Ascitic tap Paracentesis/Ascitic Tap Types Diagnostic - exudate vs transudate, ?infection, cancer, etc. Therapeutic or palliative – ↑comfort, ↓nausea, ↑pulmonary fn, ↓effect on venous return Procedure Pre-procedure: FBC, coags, but studies show no instances sig bleeding even if plts<50 & INR>1.5. Preparation – equipment, explain to patient Aseptic technique Choose site: lower flank (lateral to inf. Epigastric vessels) or midline 2cm below umbilicus (beware bladder) Withdraw 20-60ml for diagnostic tap or connect to a bag and allow as much as possible to drain over 4-6 hrs for therapeutic tap. Give 100ml albumin for every
    [Show full text]
  • Patients with Hepatorenal Syndrome Should Be Dialyzed? CON
    Kidney360 Publish Ahead of Print, published on December 16, 2020 as doi:10.34067/KID.0006872020 Patients with hepatorenal syndrome should be dialyzed? CON Hani M. Wadei Department of Transplantation, Mayo Clinic, Jacksonville, FL Address for Correspondence: Hani M. Wadei, MD Associate Professor of Medicine Department of Transplantation Department of Medicine, Division of Nephrology and Hypertension Mayo Clinic 4500 San Pablo Rd. Jacksonville, FL 32224 Fax: 9049563220 Email: [email protected] Copyright 2020 by American Society of Nephrology. Introduction AKI is a common and notorious complication that affects up to 20% of hospitalized cirrhotic patients 1. The incidence of AKI however increases in parallel with the progression of the liver disease. The incidence of AKI in cirrhotic patients also varies according to how AKI was defined. For example, if the updated International Ascites Club (IAC) definition of AKI in cirrhotic patients is utilized to define AKI, the risk of AKI in cirrhotic patients has been reported to occur in up to 30% of hospitalized cirrhotic patients 2, 3. Fortunately, almost two-thirds of AKI cases in cirrhotics respond to volume expansion especially with albumin infusion while the remaining one-third is attributed to either hepatorenal syndrome (HRS) or acute tubular necrosis (ATN) 1. HRS is a specialized functional type of pre-renal AKI that occurs exclusively in patients with advanced cirrhosis and those with fulminant hepatic failure. While the overall pathophysiology of HRS is complex, the main underlying mechanism of AKI is intense renal vasoconstriction and therefore HRS-AKI is resistant to volume expansion 4. Despite the continuous efforts to update the HRS diagnostic criteria, differentiating HRS from other causes of AKI, especially ATN, is often difficult in clinical practice 5.
    [Show full text]
  • Review Article: Hepatorenal Syndrome – Definitions and Diagnosis
    Aliment Pharmacol Ther 2004; 20 (Suppl. 3): 24–28. Review article: hepatorenal syndrome – definitions and diagnosis R. MOREAU & D. LEBREC Laboratoire d’He´modynamique Splanchnique et de Biologie Vasculaire, INSERM U-481 and sevice d’He´patologie, Hoˆpital Beaujon, Clichy, France criteria: (1) severe cirrhosis; (2) glomerular hypofiltra- SUMMARY tion; (3) no other functional or organic causes; (4) Hepatorenal syndrome (HRS) is a severe complication of failure of plasma volume expansion; (5) no proteinuria. cirrhosis that develops in the final phase of the disease. Additional diagnostic criteria may be present. The Two types of HRS exist. Type 1 is defined by a rapid diagnosis of HRS may be difficult in patients with severe reduction of renal function and in type 2 HRS the cirrhosis. Other types of acute renal failure may occur. reduction of renal function is slowly progressive. Type 1 For example, ischaemic or toxic tubular necrosis or HRS is diagnosed when the serum creatinine level sepsis may cause renal failure in these patients. increases by more than 50% of the baseline value to Furthermore, uncontrolled HRS may lead to ischaemic above 133 lmol/L. According to the International tubular necrosis; thus, these patients must be managed Ascites Club, HRS is defined by the presence of five as soon as possible in an intensive care unit. the baseline value or to above 133 lmol/L (1.5 mg/dL). INTRODUCTION In patients with pre-existing renal impairment, acute Renal failure is characterized by the association of a renal failure is diagnosed when serum
    [Show full text]
  • Hepatorenal Syndrome-Current Concepts in Pathophysiology
    Gastroenterology & Hepatology: Open Access Review Article Open Access Hepatorenal syndrome-current concepts in pathophysiology Abstract Volume 7 Issue 1 - 2017 Hepatorenal syndrome (HRS) is a functional renal impairment that occurs in advanced liver Piyush Mathur,1 Dinesh Agarwal2 cirrhosis or fulminant hepatic failure due to diminished renal blood flow in histological 1Consultant Nephrologist, Santokba Durlabhji Meorial Hospital, normal kidneys. The pathophysiologic hallmark of HRS is splanchnic vasodilation and India renal vasoconstriction leading to renal hypoperfusion and decline in glomerular filtration 2Consultant Gastroenterologist, Santokba Durlabhji Memorial rate. Two subtypes of HRS i.e. Type 1 and type 2 have been identified with type 1 carrying Hospital, India poor prognosis. Correspondence: Piyush Mathur, Consultant Nephrologist, Keywords: hepatorenal syndrome, splanchnic vasodilation, renal vasoconstriction, University: Santokba Durlabhji Meorial Hospital, Address: Jaipur, glomerular filtration rate India, Tel +91 7023333189, Email Received: March 30, 2017 | Published: June 23, 2017 Introduction decrease in effective arterial volume with activation of endogenous vasoactive systems. These hemodynamic changes ultimately lead to Hepatorenal syndrome (HRS) is a functional renal impairment renal hypoperfusion and decline in glomerular filtration rate (GFR). that occurs in advanced liver cirrhosis or fulminant hepatic failure Figure 1 shows pathophysiology of HRS. due to diminished renal blood flow in histological normal kidneys. This pathophysiologic correlation was first described by Hecker and Sherlock in 1958.1 The functional nature of HRS was confirmed further by the ability to transplant kidneys from patients with HRS and the normalization of renal function after liver transplantation.2,3 The pathophysiologic hallmark of HRS is splanchnic vasodilation and renal vasoconstriction which has been established in multiple studies.4-8 Here we present brief overview of current concepts in pathophysiology of HRS.
    [Show full text]
  • Cirrhosis and Chronic Liver Failure: Part II. Complications and Treatment JOEL J
    Cirrhosis and Chronic Liver Failure: Part II. Complications and Treatment JOEL J. HEIDELBAUGH, M.D., and MARYANN SHERBONDY, M.D. University of Michigan Medical School, Ann Arbor, Michigan Major complications of cirrhosis include ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, portal hyper- tension, variceal bleeding, and hepatorenal syndrome. Diagnostic studies on ascitic fluid should include a differential leukocyte count, total protein level, a serum-ascites albumin gradient, and fluid cultures. Therapy consists of sodium restriction, diuretics, and complete abstention from alcohol. Patients with ascitic fluid polymorphonuclear leukocyte counts of 250 cells per mm3 or greater should receive empiric prophylaxis against spontaneous bacterial peritonitis with cefotaxime and albumin. Patients who survive an episode of spontaneous bacterial peritonitis should receive long-term prophylaxis with norfloxacin or trimethoprim/sulfamethoxazole. Patients with gastrointestinal hemorrhage and cir- rhosis should receive norfloxacin or trimethoprim/sulfamethoxazole twice daily for seven days. Treatment of hepatic encephalopathy is directed toward improving mental status levels with lactulose; protein restriction is no longer recom- mended. Patients with cirrhosis and evidence of gastrointestinal bleeding should undergo upper endoscopy to evaluate for varices. Endoscopic banding is the standard treatment, but sclerotherapy with vasoconstrictors (e.g., octreotide) also may be used. Prophylaxis with propranolol is recommended in patients
    [Show full text]
  • Complications of Chronic Liver Disease
    Complications of Chronic Liver Disease By Rima A. Mohammad, Pharm.D., BCPS Reviewed by Paulina Deming, Pharm.D.; Marisel Segarra-Newnham, Pharm.D., MPH, FCCP, BCPS; and Kelly S. Bobo, Pharm.D., BCPS Learning Objectives and most patients are given a diagnosis of cirrhosis in the presence of these complications. Decompen- 1. Apply results from clinical studies and guidelines to the management of hepatic encephalopathy. sated (or unstable) liver disease occurs in 2% to 10% of 2. Design evidence-based treatment and prevention patients with viral hepatitis and in about 25% of patients regimens for patients with ascites or complications with alcoholic liver disease. of ascites such as spontaneous bacterial peritonitis The severity of cirrhosis is important to assess and hepatorenal syndrome. because it serves as a predictor of patient survival, sur- 3. Given recent guidelines on the management of gical outcomes, and the risk of complications such as portal hypertension, justify the need for primary variceal bleeding. Assessment tools commonly used and secondary prophylaxis of variceal bleeding in in patients with cirrhosis include the model for end- patients with cirrhosis. stage liver disease (MELD), which has a score ranging 4. Assess and apply the role of the pharmacist in pro- from 0 to 40; and the Child-Pugh classification system, viding appropriate treatment recommendations which has a score ranging from 0 to 15. Patients with a to health care providers and drug education to higher MELD score have a greater risk of dying within patients regarding the management of complica- 3 months than patients with a lower score. The Child- tions caused by chronic liver disease.
    [Show full text]
  • Hepatorenal Syndrome 2018
    Hepatorenal Syndrome 2018 Warren Kupin, MD FACP Professor of Medicine Miami Transplant Institute Katz Family Division of Nephrology and Hypertension University of Miami Miller School of Medicine Case Presentation U.S. Prevalence 60 year male with Diabetes 3.9 million with liver disease Cirrhosis : NASH 633,000 cases of Cirrhosis Stable : well compensated New cases of Cirrhosis / yr 30,000 10 yrs Deaths / yr (58% of all cases) Portal HTN 20-40,000 Ascites Stable : well compensated 1 -5 yrs (20 – 40% of all cases) 60 creat Hepatorenal GFR Syndrome years years Outline of Discussion Topics • What are the diagnostic criteria for Hepatorenal Syndrome (HRS) ? • Does a patient with HRS have Acute Kidney Injury or Chronic Kidney Disease or Both ? • Or is it Fake News and there is no “True” kidney disease ? • What is the pathophysiology behind the development of HRS ? • What therapeutic options are available for HRS ? • Does a patient with Cirrhosis and HRS need a Liver Transplant only or a combined Liver and Kidney Transplant ? • Will we finish this topic before noon ? Importance of Accurate Assessment of Renal Function in Liver Disease Determine drug dosing Determine the need Calculate the for combined MELD score liver / kidney Transplantation Diagnosis / Treatment response of HRS Serum Creatinine • Creatine • Synthesized in the liver and stored in muscle • Also ingested orally and localized to muscle • Creatinine • Cyclic anhydride of creatine (nonenzymatic) • End product of muscle metabolism • Renal excretion of creatinine – GFR - filtration – Tubular secretion Origin of Oral Ingestion-Meat (creatine) Creatinine Muscle (Energy source- Metabolized) 50% Creatinine 50% Hepatic Synthesis (creatine) Range of Creatinine Values in the Population Male Female 60 0.95 1.15 The normal creatinine level is 50 relative to muscle mass Women < 1.2 mg/dl 40 Men < 1.5 mg/dl (represents 2 SD above the mean) 30 20 10 0 < 0.7 0.7 - 0.8 0.9 - 1.0 1.1 - 1.2 1.3 - 1.4 1.5 - 1.6 1.7 - 1.8 1.9 - 2.0 Creatine Production in Patients with Cirrhosis Gliedman et al.
    [Show full text]
  • Guidelines on the Management of Ascites in Cirrhosis Gut: First Published As 10.1136/Gutjnl-2020-321790 on 16 October 2020
    Guidelines Guidelines on the management of ascites in cirrhosis Gut: first published as 10.1136/gutjnl-2020-321790 on 16 October 2020. Downloaded from Guruprasad P Aithal ,1,2 Naaventhan Palaniyappan,1,2 Louise China,3 Suvi Härmälä,4 Lucia Macken ,5,6 Jennifer M Ryan,3,7 Emilie A Wilkes,2,8 Kevin Moore,3 Joanna A Leithead,9 Peter C Hayes,10 Alastair J O’Brien ,3 Sumita Verma5,6 ► Additional material is ABSTRACT 2.2. A diagnostic paracentesis should be per- published online only. To view, The British Society of Gastroenterology in collaboration formed in patients with GI bleeding, shock, please visit the journal online fever or other signs of systemic inflammation, (http:// dx. doi. org/ 10. 1136/ with British Association for the Study of the Liver has gutjnl- 2020- 321790). prepared this document. The aim of this guideline is to gastrointestinal symptoms, hepatic encephalop- review and summarise the evidence that guides clinical athy, and in patients with worsening liver or For numbered affiliations see renal function. (Quality of evidence: moderate; end of article. diagnosis and management of ascites in patients with cirrhosis. Substantial advances have been made in Recommendation: strong) 3 Correspondence to this area since the publication of the last guideline in 2.3. Ascitic neutrophil >250/mm count re- Professor Guruprasad P Aithal, 2007. These guidelines are based on a comprehensive mains the gold standard for the diagnosis of SBP NIHR Nottingham Biomedical literature search and comprise systematic reviews in the and this can be performed either by manual mi- Research Centre, Nottingham croscopy or using automated counts, based on University Hospitals NHS key areas, including the diagnostic tests, diuretic use, Trust and the University of therapeutic paracentesis, use of albumin, transjugular flow cytometry for counting and differentiating Nottingham, Nottingham NG7 intrahepatic portosystemic stent shunt, spontaneous cells.
    [Show full text]
  • Budd-Chiari Syndrome
    Prague Medical Report / Vol. 118 (2017) No. 2–3, p. 69–80 69) Budd-Chiari Syndrome Tomáš Grus1, Lukáš Lambert2, Gabriela Grusová3, Rohan Banerjee2, Andrea Burgetová2 12nd Department of Surgery – Department of Cardiovascular Surgery, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic; 2Department of Radiology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic; 34th Department of Medicine – Department of Gastroenterology and Hepatology, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic Received October 10, 2016; Accepted August 28, 2017. Key words: Budd-Chiari syndrome – Thrombosis – Hepatic vein – Inferior vena cava – Cirrhosis – Liver Abstract: Budd-Chiari syndrome (BCS) is a rare disease with an incidence of 0.1 to 10 per million inhabitants a year caused by impaired venous outflow from the liver mostly at the level of hepatic veins and inferior vena cava. Etiological factors include hypercoagulable conditions, myeloprolipherative diseases, anatomical variability of the inferior vena cava, and environmental conditions. Survival rates in treated patients range from 42 to 100% depending on the etiology and the presence of risk factors including parameters of Child-Pugh score, sodium and creatinine plasma levels, and the choice of treatment. Without treatment, 90% of patients die within 3 years, mostly due to complications of liver cirrhosis. BCS can be classified according to etiology (primary, secondary), clinical course (acute, chronic, acute or chronic lesion), and morphology (truncal, radicular, and venooclusive type). The diagnosis is established by demonstrating obstruction of the venous outflow and structural changes of the liver, portal venous system, or a secondary pathology by ultrasound, computed tomography, or magnetic resonance.
    [Show full text]
  • Review the Hepatorenal Syndrome
    Gut 2001;49:729–737 729 Review Gut: first published as 10.1136/gut.49.5.729 on 1 November 2001. Downloaded from The hepatorenal syndrome Introduction dying from liver failure.3The most frequent cause of renal The hepatorenal syndrome (HRS) is defined as the devel- failure in cirrhosis is spontaneous bacterial peritonitis opment of renal failure in patients with severe liver disease (SBP). Approximately 30% of patients with SBP develop (acute or chronic) in the absence of any other identifiable renal failure.4 cause of renal pathology. It is diagnosed following There is still some contention as to whether patients who exclusion of other causes of renal failure in patients with develop renal failure following the treatment of complica- liver disease such as hypovolaemia, drug nephrotoxicity, tions of liver diseases such as sepsis or bleeding should be sepsis, or glomerulonephritis. A similar syndrome may also classified as having HRS. Many authors include patients occur in the setting of acute liver failure. with “successfully treated” SBP or other precipitants as hav- ing HRS and yet there are many patients who develop renal DIAGNOSTIC CRITERIA failure spontaneously and who have no objective criteria The International Ascites Club (1996) group defined the for a precipitating event other than progressive liver failure diagnostic criteria for hepatorenal syndrome1 and these are (for example, alcoholic hepatitis or acute liver failure). In listed in table 1. the future it may be useful to subdivide HRS type 1 into Two patterns of HRS are observed in clinical practice two categories—that is, those with and those without a and these were defined by the International Ascites club.1 precipitant event—but this will require further inter- x Type 1 hepatorenal syndrome is an acute form of HRS in national consensus.
    [Show full text]
  • Spontaneous Bacterial Peritonitis (Sbp) Prophylaxis in Ucdhs Patients with End Stage Liver Disease (Esld)
    SPONTANEOUS BACTERIAL PERITONITIS (SBP) PROPHYLAXIS IN UCDHS PATIENTS WITH END STAGE LIVER DISEASE (ESLD) SBP prophylaxis is appropriate in ESLD patients meeting any of the following criteria: 1. Prior history of SBP 2. No history of SBP, but with ascitic fluid protein levels <1.5gm/dL 3. Hospital admission for upper GI bleed Due to recent unavailability of norfloxacin as a result of discontinuation by the manufacturer, the recommended regimen for long term prophylaxis is TMP/SMX 1 double strength (DS) tablet PO daily.1-2 In patients with a documented history of true sulfa allergy, the recommended agent is levofloxacin 250mg PO daily. For patients to be treated as outpatients and lacking insurance coverage for levofloxacin, ciprofloxacin 500mg PO once daily can be used as an alternative.3 In patients admitted for GI bleeding, the recommended regimen is ceftriaxone 1gm IV q24H for 7 days, after which long term prophylaxis can be considered if patients meet criteria 1 or 2 listed above.1-2 A note on resistance: Intermittent use of prophylactic antibiotics (i.e. once weekly) is associated with increased bacterial resistance. Long term use of prophylactic antibiotics has also led to shifts in gastrointestinal flora and resistance to antibiotics.4-5 The use of intermittent antibiotics for SBP prophylaxis should be avoided if possible and long term prophylactic antibiotics should be reserved for patients at highest risk for infection as outlined above. The use of other restricted antibiotics for prophylaxis will require ID approval. References: 1. Runyon, B A. (2013). Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012.
    [Show full text]
  • Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012
    © 2012 The American Association for the Study of Liver Diseases, All rights reserved. rights All Diseases, Liver of Study the for Association American The 2012 © FORWARD REFERENCES FULL TEXT FULL RECOMMENDATIONS CONTENTS Jump to: Jump PRACTICE GUIDELINE PRACTICE Bruce A. Runyon A. Bruce Update 2012 Update with Ascites Due to Cirrhosis: Cirrhosis: to Due Ascites with Management of Adult Patients Patients Adult of Management AASLD Management of Adult Patients with Ascites PRACTICE GUIDELINE Due to Cirrhosis: Update 2012 CONTENTS RECOMMENDATIONS FULL TEXT REFERENCES WEB SITE Contents (click section title or page number) Recommendations and Rationales .......................... 3 Full-text Guideline ..................................... 56 Abbreviations ........................................ 57 Preamble ........................................... 58 Introduction ......................................... 58 Evaluation and Diagnosis ............................... 59 Ascitic Fluid Analysis ................................... 62 Differential Diagnosis ................................... 63 Treatment of Ascites ................................... 64 Refractory Ascites ..................................... 70 Spontaneous Bacterial Peritonitis .......................... 74 Prevention of SBP ..................................... 79 Hepatorenal Syndrome ................................. 81 Additional Considerations ................................ 84 Hepatic Hydrothorax ................................... 85 References .........................................
    [Show full text]