Management of Ascites and Hepatorenal Syndrome. Florence Wong University of Toronto. June 4, /16/ Gore & Associates: Consultancy

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1 Management of Ascites and Hepatorenal Syndrome Florence Wong University of Toronto June 4, /16/ Disclosures Gore & Associates: Consultancy Sequana Medical: Research Funding Mallinckrodt Pharmaceutical: Research Funding 1

2 Ascites is the Most Common Form of Decompensation in Cirrhosis 0.75 Decompensation Ascites Bleeding Encephalopathy Jaundice months Months Ascites occurs at the rate of 7-10% per year (D Amico et al, J Hepatology 2006) Natural History of Ascites in Cirrhosis 2

3 Pathophysiology of Ascites Formation in Cirrhosis Pathophysiology of Ascites Formation in Cirrhosis 3

4 Stepwise Approach to Treatment of Ascites Sodium restriction Diuretics Large volume paracentesis TIPS Liver transplantation How Do We Deliver the Ascites Care? Care Management Check Up Group Team consists of consultant hepatologists dedicated nurses residents Standard lab tests Ultrasound if none in last 6 M Gastroscopy if last one of 2 years ago showed no varices Detection of alcohol for patients with alcoholic etiology of cirrhosis CP score of 9: check for minimal HE Dietary advice given Update all medications Standard of Care Group Care entrusted to primary care physicians Consultant hepatologists available on demand (Morando F, et al, J Hepatology 2013) 4

5 How Do We Deliver the Ascites Care? Both groups had equal access to Day care unit for large volume paracentesis Day care unit for transfusion of blood products Endoscopy unit for band ligation of varices Case Management Check-up Group patients always had the same hepatologist Standard of care patients can have any hepatologist on duty (Morando F, et al, J Hepatology 2013) Comprehensive Care is Better for Patient Outcomes Survival (%) Day Emergent Hospital Admission Care Management Program P<0.01 Standard of Care (Morando F, et al, J Hepatology 2013) 5

6 Comprehensive Care Reduces Ascites Admission (%) 45 P< Care Management Plan Standard Of Care Ascites HE SBP HRS GI Bleed (Morando F, et al, J Hepatology 2013) Comprehensive Care is Cost Saving Specialist Day Care Unit (Morando F, et al, J Hepatology 2013) 6

7 Refractory Ascites Diuretic-resistant Weight loss 1.5kg/week while on 30mg of amiloride or 400mg of spironolactone one week plus 160mg of furosemide daily Dietary sodium restriction 50mmol per day Diuretic-intolerant Patients with ascites who cannot have their diuretic doses increased because of the development of complications (Int Ascites Club, Liver Int 2010) Sodium Restriction Mainstay of treatment in fluid overload in cirrhosis is sodium restriction Recommended at all stages of ascites in order to reduce its accumulation Consultation with dietitian important Diet sheets listing low sodium food items and suggested meal plans are very helpful Provide a list of shops where low sodium food items may be purchased Literature on low sodium cook books is readily available 7

8 Treatment of Refractory Ascites OR Large volume paracentesis Transjugular Intra-hepatic Porto-systemic Stent Shunt Large Volume Paracentesis is Safe (Gines P, et al, Gastroenterology 1987) 8

9 Large Volume Paracentesis Removing large volume of ascites will lower the intraabdominal pressure This will exaggerate the pressure difference between the portal system and the abdomen Portal hypertensio n Albumin This has the tendency to reduce the intravascular volume further and refill the abdominal cavity faster Patients are at greater risk for developing hyponatremia and renal failure Use of Albumin in the Management of Ascites Following LVP (Bernardi M et al, Hepatology 2012) 9

10 Adequate Albumin During LVP Can Reduce the Deleterious Renal Effects (Tan H, et al, Dig Dis Sci 2016) Post- Paracentesis Circulatory Dysfunction (Tan H, et al, Dig Dis Sci 2016) 10

11 Transjugular Intrahepatic Porto-systemic Stent Shunt (TIPS) in Refractory Ascites Procedure performed by interventional radiologist Indicated as a treatment for refractory ascites It bridges a branch of the hepatic vein with a branch of the portal vein Effective in reducing sinusoidal portal pressure which is one of the pathogenetic mechanisms of ascites formation in cirrhosis Gradually eliminates ascites even in the absence of diuretic therapy Hepatic vein Final position of TIPS Portal vein Age, bilirubin and serum sodium predict survival after TIPS for refractory ascites Probability*of*death* P r e d I c t e d M o r t a l i t y age 60 yrs bilirubin 3 mg% Na130 meq/l age 55 yrs bilirubin 2 mg% Na135 meq/l age 50 yrs bilirubin 1 mg% Na140 meq/l Months Young patients with refractory ascites and minimal liver dysfunction will do well after TIPS insertion with elimination of ascites and good survival (Salerno F, et al, Gastroenterology 2007) 11

12 Renal Function Post TIPS Urinary sodium excretion 120 mmol/day * * * 20 0 Baseline 1 month 3 months * p < vs baseline 6 month 12 months (Tan HK, J Gastro Hepatol 2015) Clinical Response Post TIPS Response after TIPS Complete response Partial or no response Proportion month 3 months 6 months 12 months > 12 months (Tan HK, J Gastro Hepatol 2015) 12

13 Survival Post TIPS Post TIPS survival by response Percent survival Complete responder Partial responder Non-responder p < vs partial or non-responder p = 0.42 vs non-responder Months Complete responder Partial responder Non-responder (Tan HK, J Gastro Hepatol 2015) Treatment of Ascites- Future Directions The ALFA Pump Automatically and continually moves ascites from the abdominal cavity to the bladder, where it is excreted naturally from the body. Significantly reduces the need for paracentesis Improves patient quality of life 6/16/

14 6/16/ Pathophysiology of Hepatorenal Syndrome 14

15 Renal Dysfunction in Cirrhosis GFR Normal or Decompensation of cirrhosis GFR Normal or GFR GFR Hepatorenal syndrome Type I AKI Subtle sodium retention Obvious sodium retention Avid sodium retention Functional Renal failure Pre-ascites Diuretic Diuretic Hepatorenal responsive ascites refractory ascites syndrome Risk of AKI Type II Intercurrent illness Infection is the most Common Precipitant of AKI in Cirrhosis n=62 (Wong F, Liver Transplantation, 2015) 15

16 Hepatorenal Syndrome Type 1 Diagnostic Criteria 1. Cirrhosis and ascites; 2. Serum creatinine > 1.5 mg/dl; 3. No improvement of serum creatinine (decrease of creatinine equal to or less than 1.5 mg/dl) after at least 48 hours of diuretic withdrawal and volume expansion with albumin (1 g/kg b.w./day for 2 days); 4. Absence of hypovolemic shock or severe infection requiring vasoactive drugs to maintain arterial pressure; 5. No current or recent treatment with nephrotoxic drugs; 6. Proteinuria <500 mg/day and no microhematuria (<50 RBCs/ml). (International Ascites Club, Liver Int 2010) The Evolving Concept of Renal Dysfunction in Cirrhosis AKIN modified RIFLE criteria IAC defined HRS 1 IAC modified diagnosis of HRS 1 IAC further defined AKI diagnostic criteria ADQI defined RIFLE criteria IAC & ADQI defined AKI for cirrhosis KDIGO modified AKIN & RIFLE criteria KDIGO criteria For AKI Biomarkers: Susceptibility Diagnosis Prognosis 16

17 Diagnosis of Renal Dysfunction in Cirrhosis (Angeli P et al, International Ascites Club, Gut 2015) 17

18 Rate of confirmed HRS reversal Treatment of HRS type 1 - Terlipressin Pooled data (%) n=56 P=0.01 n=153 n=97 n=56 n=99 n=155 (Sanyal AJ et al. Abstract 241, AASLD 2014) Midodrine/Octreotide versus Terlipressin for HRS 1 (Cavallin M, Hepatology, 2015) 18

19 Norepinephrine vs. Terlipressin for HRS Type 1 (Singh V. et al. J Hepatology, 2012) Progression of AKI has Negative Impact on Prognosis (Belcher J. et al. J Hepatology, 2012) 19

20 Regression of AKI Stage is Associated With Improved Survival (Wong F. et al. [Abstract] Nephrology Dialysis Transplantation, 2015) Liver Transplantation All patients with refractory ascites should be referred for liver transplant assessment Liver transplantation will eliminate - portal hypertension - liver dysfunction - hemodynamic abnormalities Ascites will disappear as the patient recovers from liver transplant surgery Transient persistence of renal dysfunction post-transplant May require short-term dialysis 20

21 HRS1 Reversal Post Liver Transplantation ( Wong F. et al, Liver Transplantation 2015) The Future - Biomarkers Complications Normal Increased GFR Damage Kidney Death risk failure Window for early targeted intervention Biomarkers identify susceptibility Biomarkers for diagnostic criteria including creatinine, decreased urine output Biomarkers identify injury mechanisms Biomarkers to track progression ( Murray P. et al, Kidney Int 2013) 21

22 Potential Role of Biomarkers in the Management of AKI ( Murray P. et al, Kidney Int 2013) Summary Acute Kidney Injury in cirrhosis has now been re-defined Acute of type 1 HRS is a special form of AKI Minor changes in serum creatinine are relevant in patients with decompensated cirrhosis The proposed new definitions of AKI, once validated, will help improve treatment strategies The development of renal biomarkers will help to finetune diagnosis and guide management of renal dysfunction in cirrhosis Early treatments can be life saving 22

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