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Hepatorenal syndrome


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Hepatorenal syndrome

  2. 2. INTRODUCTION PRE-RENAL type of renal failure seen in patients of liver disease (mostly cirrhosis, sometimes acute) ALTERED HAEMODYNAMICS FUNCTIONAL Renal Histology NORMAL
  3. 3.  DEFINITION BY INTERNATIONAL ASCITES CLUB:-Hepatorenal syndrome is a clinical condition that develops in patients with chronic/acute liver disease and advanced hepatic failure and portal hypertension.
  4. 4. Characterized by impaired renal function and marked abnormalities in the arterial circulation and activity of the endogenous vasoactive systems.
  5. 5. PATHOPHYSIOLOGYSystemic arterial vasodilationRenal arterial vasoconstrictionCardiac dysfunction
  6. 6. Systemic VasodilationEndogenous substances like NO, prostacyclin, adrenomedullinDecreased “effective” circulating volumeCompensatory - increase in heart rateHyperdynamic circulation
  7. 7. Renal artery vasoconstriction Compensatory in response to systemic vasodilation Stimulation of SNS, RAAS Role of endothelins, prostaglandins Result- Increased renal vascular resistance Decreased perfusion pressure & GFR
  9. 9. Cirrhosis with ascitesSerum creatinine level ≥ 1.5 mg/dLNo or insufficient improvement in serum creatinine level (remains ≥1.5 mg/dL) 48 hr after diuretic withdrawal and adequate volume expansion with intravenous albumin
  10. 10. Absence of shockNo evidence of recent use of nephrotoxic agentsAbsence of intrinsic renal disease
  11. 11. Major Criteria Low GFR indicated by S.creatinine > 1.5 mg/dL or creatinine clearance < 40 ml/min Absence of shock, ongoing bacterial infection, current treatment with nephrotoxic drugs No sustained improvement in renal function (decrease in serum creatinine to 1.5mg/dL or increase in creatinine clearance to 40 ml/min) after diuretic withdrawal & expansion of plasma volume with 1.5 L of a plasma expander Proteinuria < 500 mg/ dL & no USG evidence of obstructive uropathy or parenchymal renal disease
  12. 12. Additional criteria Urine volume < 500 ml/day Urine sodium < 10 mEq/L Urine osmolality > plasma osmolality Urine RBC < 50/hpf Serum sodium concentration < 130 mEq/L
  13. 13. NOTE:Decrease muscle mass inCLD, in turn result inreduced serum creatinineand blood urea nitrogenlevels- delaying recognitionof HRS.
  14. 14. Diuretics, lactulose may influence intravascular volume status & renal perfusion.HRS in 20 to 30% of SBP patients. Low threshold for evaluating cirrhotic patients with ascites for the presence of SBP needed.
  15. 15. CLINICAL FEATURESDue to liver diseaseDue to complications of cirrhosisDecreased urine output(Note: Oliguria may not be present initially in all cases of HRS)
  16. 16. HRS diagnosed in anindividual at risk on basisof the results oflaboratory tests, in theexclusion of othercauses.
  17. 17. TRIGGERSOver-diuresisDiarrhoea caused by lactuloseGI bleed from varices or hemorrhoidsLarge paracentesis without colloid administrationSBPBacteremia
  18. 18. Sometimes, Acute hepatic injury,superimposed on cirrhosis, may lead to liver failure and HRS
  19. 19. Acute viral hepatitisDrug-induced liver injury (acetaminophen, idiopathic drug-induced hepatitis)Flare of chronic hepatitis B virus infection by an emergent resistant viral strain or withdrawal of antiviral therapy or superimposed acute delta virus hepatitis.
  20. 20. Risk Factors for developing HRSPrevious episodes of ascitesPoor nutritional statusHigh plasma renin activity (>4 ng/mL per h)Low mean arterial pressure (<85 mm Hg)
  21. 21. Increased plasma norepinephrine (>500 pg/mL)Presence of esophageal varicesModel for End-Stage Liver Disease score
  22. 22. MELD SCOREMELD = 3.78[Ln serumbilirubin (mg/dL)] + 11.2[LnINR] + 9.57[Ln serumcreatinine (mg/dL)] + 6.43
  23. 23.  UNOS has made the following modifications to the score: If the patient has been dialyzed twice within the last 7 days, then the value for serum creatinine used should be 4.0 Any value less than one is given a value of 1 (i.e. if bilirubin is 0.8, a value of 1.0 is used)
  24. 24.  MELD scores of about 10 is associated with an 8% and 11% risk of HRS at 1 and 5 years, respectively. If the MELD score approaches 18, nearly 40% of patients develop HRS within 1 year..!!
  25. 25. TYPES OF HRS Type 1 : Cirrhosis with rapidly progressive acute renal failure Type 2 : Cirrhosis with sub-acute renal failure Type 3 : Cirrhosis with types 1 or 2 HRS superimposed on CKD or AKI Type 4 : Fulminant liver failure with HRS
  26. 26. TYPE 1Creatinine level doubles to greater than 2.5 mg/dL within 2 weeksRapid progression & high mortalityMedian survival - 1 to 2 weeksTRIGGERS
  27. 27. TYPE 2Creatinine increases slowly and gradually (several weeks or months )Reciprocal gradual reduction in GFR.Median survival - 6 monthsWithout triggersMay transform to type 1 if trigger
  28. 28. TYPE 3 85% of end-stage cirrhotics have intrinsic renal disease on renal biopsy Patients with pre-existing renal disease do not meet traditional diagnostic criteria for HRS They have not been included in therapeutic clinical trials.
  29. 29. . Given the absence of diagnostic markers for HRS, the evaluation of a cirrhotic patient with multiple causes of renal failure is complexIt is unclear whether a chronically reduced baseline GFR, from chronic intrinsic renal disease, predisposes cirrhotic patients to develop HRS
  30. 30. TYPE 4More than half of patients with ALF develop HRSSuperimposed on already poor prognosisMECHANISM ??
  32. 32. PREVENTION (TRIALS) Prospective RCTs, Triggers Norfloxacin for primary prophylaxis for SBP reduced the 1- year probability of HRS to 28%, compared with 41% in controls not administered antibiotic prophylaxis Study strongly suggested that HRS can be prevented in patients with advanced cirrhosis and ascites with a low protein content (< 1.5
  33. 33. Albumin (1 g/kgintravenously) at diagnosisand at day 3 in patientswith SBP significantlyreduced the incidence oftype 1 HRS and the 3-month mortality
  34. 34. Pentoxifylline, 400 mg three times a day, to patients with severe acute alcoholic hepatitis was associated with a marked reduction in HRS incidence and in-hospital mortality
  35. 35. Not yet been confirmed by subsequent large studies.In context of poor prognosis of HRS, however, broad acceptance of these prophylactic measures
  36. 36. TREATMENT - MEDICALVasoconstrictorsTerlipressin , Ornipressin- V1 receptor agonist (splanchnic circulation)Octreotide – Somatostatin analogueMidodrine – alpha-adrenergic agonist
  37. 37. Trial on 376 patients –using terlipressin alone/with albuminusing octreotide plus albuminusing noradrenalin plus albumin
  38. 38. RESULT: Terlipressin + albumin - short-term mortality reduction in type 1 HRS, but no such reduction in patients with the type 2Octreotide & noradrenaline therapies indicated neither harmful nor beneficial effects
  39. 39. VOLUME EXPANSIONSTOP NEPHROTOXIC DRUGS (ACEi, ARBs, NSAIDs, Diuretics)Prevent variceal bleed – medical, surgical
  40. 40. ROLE (?)Misoprostol – synthetic analogue of PGE1 (based on low urinary vasodilatory PGs)Dopamine – low dose, improve renal blood flowN-acetylcysteine
  42. 42. TIPSSLowers portal pressure & splanchnic pooling of blood(pathophysiology)Increased venous returnAggravate cardiac dysfunctionHepatic ENCEPHALOPATHY!!
  43. 43. Role of TIPSSExperimentalIf no response to vasoconstrictor/volume expansionChild-Pugh class A or BMeet criteria for TIPSS
  44. 44. Peritoneo-venous shuntingplasma volume expansion & improvement of circulatory functionRole in type 2 HRS who often have refractory ascitesNo proven role in type 1
  46. 46. BEST AVAILABLE (?) TREATMENTcan potentially permanently reverse HRS + other complications of CLDPatients with HRS undergoing transplantation, however, have a MORE perioperative morbidity & mortality
  47. 47. More practical in type 2Absence of precipitating eventsLonger clinical courseRelatively less severe renal failure
  48. 48. THANK YOU