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RRI_as_diagnostic_and_follow_up_indicator_in_cirrhosis_.pptx
- 1. RRI as diagnostic and follow up indicator in cirrhosis of the liver with hepatorenal syndrome and refractory ascites by DR. K ANANYA MODERATOR :DR KIRAN MD Journal of The Association of Physicians of India : volume 67 :April 2019
- 2. INTRODUCTION • Hepatorenal syndrome(HRS) is defined as unexplained kidney failure in patients with liver disease due to renal vasoconstriction. • The Renal resistive index(RRI) derived from intrarenal arterial doppler is a non-invasive tool to know the extent of vasoconstriction. • Large volume paracentesis is the first line therapy for refractory ascites in cirrhosis patients but the dreaded complication of LVP is Paracentesis induced circulatory dysfunction(PICD)
- 3. • Albumin is the commonly used plasma expander to reduce incidence of PICD and to prevent HRS. • In this study a combination of noradrenaline and albumin infusion have been tried to increase the GFR and renal plasma flow in order to improve renal function and reverse HRS.
- 4. • In a study done by Moshin et al it was seen that patients with RRI> 0.77 had massive ascites compared to patients with RRI<0.77,similar findings are seen in studies done by Gotzberger et al, Celebi et al and Rivolta et al. • A study by Goyal et al revealed that patients with cirrhosis and ascites have significantly increased RRI(0.72 +/-0.02) compared to cirrhosis without ascites (0.62+/-0.06).
- 5. OBJECTIVES 1. To determine usefulness of RRI in diagnosis and follow up of HRS. 2. To determine if large volume paracentesis, noradrenaline and albumin infusion can prevent patients from going into Hepatorenal syndrome. In this study we used LVP, Noradrenaline and albumin infusion for treating cirrhosis with refractory ascites and HRS while monitoring with RRI.
- 6. MATERIALS AND METHODS • The study was a descriptive observational prospective study conducted in MVJ Medical College and Hospital Hoskote, Bangalore over a period of two years (2014 –2016). • Duplex doppler ultrasound of renal arteries(interlobar and arcuate) are done with fasting period of 4 hours prior to the ultrasound to reduce masking by intestinal gas.
- 7. • The RRI was calculated with the formula (peak systolic velocity – end diastolic velocity)/peak systolic velocity • LVP(4 lit) was done over 1-2 hrs, albumin(5g/L) was given noradrenaline infusion rate adjusted to maintain SBP at 110 mmHg for 24 hrs ,post paracentesis RRI was measured on day 2,day 7 and after 2 months.
- 8. Inclusion criteria • Patients > 18 years diagnosed to have cirrhosis of liver with refractory ascites clinically and sonologically. • Patients with RRI > 0.7
- 9. Exclusion criteria • Patients with acute infections, cardiovascular instability, diabetes, hypertension, suspected or overt malignancies. • Patients with nephropathies, decreased kidney size or reduction of renal parenchymal width and significant renal parenchymal hyper echogenecity. • Patients with peripheral vascular thrombosis, mesenteric vascular thrombosis, INR>2 after repeated correction with FFP, hypotension, hypersensitivity to adrenaline.
- 10. RESULTS
- 14. DISCUSSION • Hepatorenal syndrome is a form of renal failure without renal pathology that occurs in about 10% of patients with advanced cirrhosis or acute liver failure. • It represents the end – stage of a sequence of reductions in renal perfusion induced by severe hepatic injury.
- 15. PATHOGENESIS • Arterial vasodilation in the sphlanchnic circulation triggered by portal hypertension plays key role in the hemodynamic changes and decline in kidney function in cirrhosis. • The presumed mechanism is increased production or activity of vasodilators in the splanchnic circulation.
- 17. • As the hepatic disease progresses, there will be rise in cardiac output and fall in systemic vascular resistance despite of local increase in renal vascular resistance due to hypotension induced activation of renin-angiotensin-aldosterone system and sympathetic nervous system. • The renal vasoconstriction causes decreased renal perfusion associated with reductions in GFR and sodium excretion and fall in mean arterial pressure.
- 18. CLINICAL FEATURES • Hepatorenal syndrome is characterized by following features in a clinically evident acute or chronic liver disease patient a. A progressive rise in serum creatinine b. An often normal urine sediment c. No or minimal proteinuria(less than 500 mg per day) d. A very low rate of sodium excretion (urine sodium concentration less than 10 mEq/L) e. Non oliguria or oliguria, depending upon the severity
- 19. • Based upon rapidity of decline in kidney function, there are two forms of hepatorenal syndrome 1. Type 1 hepatorenal syndrome : It is defined as at least a twofold rise in serum creatinine (reflecting 50% reduction in creatinine clearance in 24 hrs <20 ml/min) to a level greater than 2.5 mg/dL during a period of less than two weeks, some have urine output < 400 –500 ml per day, its severe type with high mortality with 10% surviving more than 2 months.
- 20. 2. Type 2 hepatorenal syndrome : Patients satisfy the criteria of HRS but renal failure doesn't progress rapidly as type 1.They have relatively preserved hepatic function with refractory ascites. survival is reduced compared ascites with normal renal function. • The onset of HRS is insidious but sometimes may be precipitated by bacterial infection, GI bleeding, spontaneous bacterial peritonitis
- 21. DIAGNOSIS • Hepatorenal syndrome is diagnosed based on clinical criteria, there is no specific test • It is a diagnosis of exclusion, meaning that other potential etiologies of acute or subacute kidney injury in liver failure should be ruled out
- 22. • The following criteria are considered for diagnosis Major criteria: 1. low glomerular filtration rate(serum creatinine> 1.5mg/dl or creatinine clearance < 40 ml/min) 2. Absence of shock, ongoing sepsis, fluid loss, nephrotoxic drugs. 3. No sustained improvement in renal function after diuretic therapy stopped and expansion of plasma volume with 1.5 lit of plasma expander. 4. Proteinuria <500mg/day;no ultrasound evidence of renal tract obstruction or renal disease.
- 23. Additional criteria(not necessary for diagnosis) : 1. Urine volume <500 ml/day. 2. Urine sodium <10 mmol/day. 3. Urine osmolarity >plasma osmolarity. 4. Urine red cells <50/high-power field. 5. Serum sodium <130mmol/l.
- 24. DIFFERENTIAL DIAGNOSIS • Kidney injury associated with infection such as spontaneous bacterial peritonitis. • Diabetic Nephropathy • Parenchymal kidney disease(such as glomerulonephritis)
- 25. TREATMENT • The ideal treatment is management of cirrohsis and preventing its complications by Balanced diet with low salt intake(<2g/day) and protein intake of 1- 1.5 g/day. Abstinence of alcohol Effective antiviral therapy in viral hepatitis Corticosteroids in autoimmune hepatitis Interferon alpha and gama, antioxidants, colchicine Diuretic therapy, salt and fluid restriction Ursodeoxycholic acid to treat jaundice
- 26. Non selective Beta blockers like propanolol for primary prophylaxis of variceal bleeding. Octreotide and midodrine can also be used for prophylaxis of variceal bleeding and also in HRS. Endoscopic banding, sclerotherapy balloon tamponade are done for bleeding varices. Rifaximin, l-ornithine l-aspartate, lactulose are used in hepatic encephalopathy.
- 27. • The management of HRS includes 1 .Noradrenaline (0.5 to 3 mg/hr) as continuous infusion with a goal of raising mean arterial pressure by 10 mmHg and albumin(1g/kg/day max 100g)for at least two days 2. Vasopressin may also be effective starting at 0.01 units/min 3. Terlipressin IV bolus (1 to 2mg every 4-6 hrs) and albumin for two days.
- 28. 4. When terlipressin is not available a combination of midodrine, octreotide and albumin are given. 5. Midodrine orally starting at 7.5mg and increasing the dose 8 th hourly to a max of 15 mg (TID) 6. Octreotide by continuous IV infusion (50 mcg/hr) or subcutaneously (100-200mcg TID)
- 29. • In Patients with serum creatinine > 1.5mg/dL even after 2 weeks of medical treatment, Transjugular intrahepatic portosystemic shunt may be considered but not feasible in all cases. • In patients who fail to respond renal replacement therapy is done. • Definitive treatment is liver transplantation.
- 30. • Refractory ascites can be defined as ascites that persists even with maximum dose of diuretics(spironolactone 400-600mg/d and furosemide 120-160mg/d) and salt restriction. • Large volume paracentesis(4L or more) and albumin can be considered in case of refractory ascites along with diuretics.
- 32. • In this study the cases are treated with LVP adrenaline and albumin infusion while the controls are treated with salt restriction, diuretics and aldosterone antagonists without further treatment. • The results when monitored with RRI and eGFR, serum creatinine, sodium and portal vein diameter are better improved in cases compared to controls. • No other studies have used RRI as diagnostic tool and follow up of cirrhosis. • The value of RRI > 0.7 is taken based on Goyal's study.
- 33. CONCLUSION • RRI is an affordable, noninvasive and easily available tool that can be included as part of evaluation in liver cirrhosis, early detection and follow up of HRS. • LVP with noradrenaline and albumin infusion is effective in treating refractory ascites and to prevent HRS.
- 34. REFERENCES 1. Sheila Sherlock's Textbook of Liver and Biliary System, 12th Edition, May 2011; 224-229. 2. Pere Gaines, Monica Guevara, Vincente Arroyo, Juan Rode's; Hepatorenal syndrome. Lancet 2003;362:1819-27. 3. Arroyo V, Guevara M, Genes P; Hepatorenal syndrome in cirrhosis: pathogenesis and treatment. Gastroenterology 2002; 122:1658-76. 4. Salerno F, Gerbes A, Gines P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut 2007; 56:1310-18. 5. Carlow Alessandria, Chiara Elia, Lavinia Mezzabtta, Alessandro Rissio, Alinda Andrealli, Maurizio Spandre, Anna Morgando, Alfredo Marazano, Mario Rizzetto Digestive and liver disease(2011), doi:10. 1016/j.did.2011.06.001
- 35. 6. Aslam M, Ram SA, Krishnamurthy A. The renal resistive index is a non-invasive indicator of hepatorenal syndrome in cirrhotics. J Adv Clin Res Insights 2016; 3:23-27. 7. Gotzberger M, Singer J, Kaiser C, Gulberg V. Intrarenal resistive index as a prognostic parameter in patients with liver cirrhosis compared with other hepatic scoring systems. 8. Harika Celebi, Emir Donder, Huseyin Celiker. Renal Blood Flow Detection with Doppler Ultrasonography in patients with Hepatic Cirrhosis. Arch Intern Med 1997; 157:564-566. 9. Singh V, Ghosh S, Singh B, Kumar P, Sharma N, Bhallal A. Noradrenaline vs terlipressin in the treatment of Hepatorenal syndrome: a randomized study. J Hepatol 2012; 56:1293-1298. 10. Goyal s, Dixit VK, Jain AK, Shukla RC, Ghosh J, Kumar V. Intrarenal resistance index as a predictor of early renal impairment in patients with liver cirrhosis. Trop Gastroenterol 2013; 34;235-9.
- 36. Thank you