DOCSLIB.ORG

Review the Hepatorenal Syndrome

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read 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. which renal failure occurs spontaneously in patients with severe liver disease and is rapidly progressive. It is char- PATHOPHYSIOLOGY acterised by marked reduction of renal function, as The hallmarks of HRS are reversible renal vasoconstriction defined by doubling of the initial serum creatinine to a and mild systemic hypotension.5 The kidneys are structur- level greater than 225 µM, or a 50% reduction in initial ally normal and at least in the early part of the syndrome, 24 hour creatinine clearance to <20 ml/min within two tubular function is intact, as reflected by avid sodium weeks. The development of type 1 HRS has a poor retention and oliguria. Moreover, kidneys from patients prognosis with 80% mortality at two weeks.2 Renal with HRS transplanted into a patient with end stage renal function may recover spontaneously following improve- failure and a healthy liver resumed normal function.6 ment in liver function.2 This is most frequently observed The cause of renal vasoconstriction is unknown but may in acute liver failure or alcoholic hepatitis, or following involve both increased vasoconstrictor and decreased http://gut.bmj.com/ acute decompensation on a background of cirrhosis. vasodilator factors acting on the renal circulation.7 There These patients are usually jaundiced with a significant are three factors predominantly involved in its pathogen- coagulopathy. Death often results from a combination of esis. These are: hepatic and renal failure or variceal bleeding. (1) Haemodynamic changes that decrease renal perfusion x Type 2 hepatorenal syndrome usually occurs in patients pressure. with diuretic resistant ascites. Renal failure has a slow (2) Stimulated renal sympathetic nervous system. course, in which it may deteriorate over months. It is (3) Increased synthesis of humoral and renal vasoactive associated with a poor prognosis3 although the survival mediators. on September 27, 2021 by guest. Protected copyright. time is longer than that of patients with type 1 HRS. The emphasis of each of the three pathogenic pathways probably varies from patient to patient, and between the EPIDEMIOLOGY acute (type 1) and chronic (type 2) forms of the syndrome. HRS occurs in about 4% of patients admitted with decom- Each of these pathways are interrelated and in practice the pensated cirrhosis, the cumulative probability being 18% at pathophysiology of this process is more complicated. How- one year, increasing to 39% at five years.2 Retrospective ever, this outline provides a simple framework with which studies indicate that HRS is present in ∼17% of patients to understand the mechanisms involved. admitted to hospital with ascites and in >50% of cirrhotics Table 1 Major criteria for a diagnosis of hepatorenal syndrome Haemodynamic changes Systemic vasodilatation of varying severity is the predomi- (1) Chronic or acute liver disease with advanced hepatic failure and portal nant haemodynamic abnormality in portal hypertension or hypertension acute liver failure, and accounts for several important (2) Low GFR, as indicated by serum creatinine >225 µM or creatinine 8 clearance <40 ml/min complications. Vasodilatation increases regional blood (3) Absence of shock, ongoing bacterial infection, or recent treatment with flow to the splanchnic circulation and a compensatory nephrotoxic drugs. Absence of excessive fluid losses (including increase in cardiac output. This leads to a fall in mean gastrointestinal bleeding) (4) No sustained improvement in renal function following expansion with arterial pressure and reflex activation of the sympathetic 1.5 litres of isotonic saline (5) Proteinuria <0.5 g/day, and no ultrasonagraphic evidence of renal tract disease Abbreviations used in this paper: HRS, hepatorenal syndrome; Additional criteria NOT required for diagnosis but commonly present SBP, spontaneous bacterial peritonitis; RBF, renal blood flow; GFR, (1) Urine volume <500 ml/day glomerular filtration rate; NO, nitric oxide; TNF, tumour necrosis (2) Urine sodium <10 mM factor; RAAS, renin-angiotensin-aldosterone system; NSAIDs, (3) Urine osmolality >plasma osmolality non-steroidal anti-inflammatory drugs; TIPS, transjugular (4) Urine RBC <50 per high per field (5) Serum sodium <130 mM intrahepatic portosystemic stent shunt; ET-1,endothelin 1; TXA2, thromboxane A2; MARS, molecular adsorbent recirculating system; GFR, glomerular filtration rate; RBC, red blood cells. OLT, orthotopic liver transplantation. www.gutjnl.com 730 Dagher, Moore nervous system.8 Several studies have consistently shown a resistance in the collateral portal circulation in animals progressive decrease in mean arterial pressure with hepatic with portal hypertension.41 42 While there was much enthu- decompensation, with the lowest values (typically 60–65 siasm for a primary role of NO in peripheral vasodilatation, Gut: first published as 10.1136/gut.49.5.729 on 1 November 2001. Downloaded from mm Hg) observed in patients with HRS.9 Prognostic stud- there is still considerable controversy as to the importance ies in patients with cirrhosis have shown that arterial pres- of NO in the hyperdynamic circulation of cirrhosis.32 sure is one of the best predictors of survival in patients with 10 cirrhosis and ascites, with low arterial pressure being Prostacyclin associated with a poor prognosis and increased risk of 11 Prostacyclin is a systemic vasodilator. Its secretion might developing HRS. be stimulated by shear stress in the arterial system.30 32 Uri- It is a common misconception that modest reductions in nary excretion of both systemic and renal metabolites of blood pressure are insignificant in humans, and that renal prostacyclin are high in decompensated cirrhosis, and autoregulation exists to prevent fluctuations in renal blood plasma levels (undetectable by available analytical meth- flow (RBF). However, autoregulation of the renal circula- ods) are presumably elevated.43 44 Nevertheless, administra- tion ensures a stable RBF during changes in renal 12–14 tion of indomethacin to cirrhotic patients increases perfusion pressure above 70–75 mm Hg. Below this systemic vascular resistance as well as pressor sensitivities pressure, RBF is directly proportional to perfusion to angiotensin II, suggesting that prostacyclin may have a pressure. Patients developing HRS have an activated sym- facultative role in the vasodilatation of cirrhosis.45 pathetic system, and increased synthesis of several renal vasoconstrictors. Several studies have shown that these cause a rightward shift in the autoregulatory curve,15 mak- Potassium channels ing RBF much more pressure dependent. Thus even mod- There are three major types of potassium channels which est decreases in mean blood pressure may result in a control the flux of potassium from the intracellular to the marked fall in RBF. Understanding this important princi- extracellular environment. The ATP sensitive potassium ple is essential in targeting pressor treatment. As a result, channels are opened during low ATP:ADP ratios, or by there is an interest in drugs which increase blood pressure, agonist induced activation of G protein dependent and over the years all have been reported to increase urine pathways. The second type is the delayed rectifier channel output, sodium excretion, or glomerular filtration rate opened by membrane depolarisation, and the third type is (GFR) with variable success in patients with severe liver the calcium activated potassium channel, which is activated disease and HRS.16–21 by increases in intracellular calcium and in a similar man- The presence of modest arterial hypotension raises the ner to that for ATP dependent potassium channels. Activa- question about its cause. It is well established that severe tion of potassium
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]
  • 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]
  • 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.
    [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]