Sub acute hepatic failure

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Sub acute hepatic failure

  1. 1. SUB ACUTE HEPATIC FAILURE DR.SARATH MENON.R DIVISION OF GASTROENTEROLOGY MGM MEDICAL COLLEGE ,INDORE
  2. 2. INTRODUCTION  severe devastating medical conditon with high mortality even in medically treated  Difference between fulminant hepatic failure  Clinical entity seen in Indian subcontinent  Revised criteria for diagnosis  Clinical symptoms & lab.evaluation  Management
  3. 3. HISTORY OF SAHF  reported from India in 1982  Series of similar cases reported by Tandon et al  Coined the term SAHF -Persistent jaundice 10 weeks after onset of icterus -development of ascites with/without encephalopathy - absence of pre-existing liver disease -Biochemical evidence of hepatocellular necrosis - Sub massive or bridging necrosis on liver biopsy
  4. 4. DEFINITION & TERMINOLOGY  Gimson et al( King’s college )- term LOHF - evidence of hepatic decompensation - 8 – 24 weeks from onset of icterus O’ Grady et al - encephalopathy occurs after 4 weeks of jaundice Bernau et al – term Sub fulminant hepatic failure -encephalopathy 2wk-3 month after onset of jaundice
  5. 5. REVISED CRITERIA FOR SAHF (INT.SYMPOSIUM-’93)  INCLUSION CRITERIA - jaundice persisting > 8 weeks after its onset with ascites with/without encephalopathy - SGPT level TWICE upper limit of normal
  6. 6.  EXCLUSION CRITERIA- - presence of dilated biliary radicals on USG - evidence of varices larger than grade 1 on endoscopy - alcoholism - chronic renal failure - KF ring or low ceruloplasmin level - liver biopsy- established histology evidence of cirrhosis
  7. 7. SAHF- A CLINICAL ENTITY OR NOT?  After 8 weeks  Protracted course  Ascites- cardinal  Cerbral edema – unusual  Enceph- preterminal and gradual  Renal failure & SBP  Infections- 10-15%  Renal failure- mc.death  Within 8 weeks  Rapid & explosive  Cerberal edema & encephalopathy- determinent  Infection -80% cases  Cerebral edema ,septicemia –mc death SAHF FULMINANT HEPATIC FAILURE
  8. 8. AETIOLOGY  Most common cause is viral hepatitis  Herbal medicines
  9. 9. DIST. OF VIRUSES IN CASES OF SAHF Name of virus Shah et al Amarapurkar et al Zachariah et al HEP A virus 00 % 04% 03% HEP B virus 18 % 34% 19% HEP C virus 17% 58% 00% HEP D virus 00% 04% 00% HEP E virus 00% 00% 16%
  10. 10. PATHOLOGY  Sub massive or bridging necrosis  Portal- portal,central – central,portal –central  Ballooning degeneration of hepatocytes  Lobular inflammation  Proliferation of bile duct
  11. 11. CLINICAL PROFILE  Age – 4th – 5 th decade  Jaundice & ascites – cardinal  Encephalopathy – terminal event  Cerebral edema uncommon  Hepatomegaly – 40- 60%  Splenomegaly – 10- 30%  Renal failure & SBP –common  Renal failure- 50% death  GI bleed & infection- 30% death  Medically treated cases 70% -90% mortality  Survivors- c/c.liver disease within 1 to 2 yr
  12. 12. DISTRIBUTION OF CLINICAL FEATURES IN SAHF IN VARIOUS STUDIES Shah et al Tandon et al Gimson et al Zachariah et al Pruti H S et al JAUNDICE 100% 100% 100 100 100 ASCITES 80% 80% 60% 100% 100% ENCEPHAL OPATHY 40 % 60% 80% 30% 27%
  13. 13. COMPLICATION OF SAHF IN VARIOUS STUDIES Shah et al Tandon et al Gimson et al GI bleed 10% 20% 30% Renal failure 30% 40% 50% Infections 10% 10% 15%
  14. 14. LAB INVESTIGATIONS  Serum. Bilirubin –elevated  SGPT- elevated ( not more than 6 times normal)  S.Albumin-mildly decreased  Ascitic fluid- transudative  Coag .factors-2,5,7,9.10-decreased 50% -diagnostic,prognostic,therapeutic  serum fibronectin - decreased  Liver biopsy-sub massive or bridging fibrosis
  15. 15. COMPLICATIONS  Spontaneous bacterial peritonitis - infection of ascitic fluid - bacterial translocation - E.coli, S.viridans,S.aureus, Enterococcus  Diagnosis - PMN>250 cells /cu.mm in ascitic fluid - ascitic fluid culture /sensitivity Rx : INJ. Cefotaxime 1 gm 8 th hrly or 10-14 d Tab. Ofloxacin 400mg bd
  16. 16. HEPATO RENAL SYNDROME  Major cause of mortality (50%) in SAHF  Functional renal failure without renal pathology  Arterial renal circulation disturbances  Diagnosis – ascitis with step wise increase in s.creatinine  Type 1 HRS- prog. impairment in renal failure - s.creatinine > 2.5 mg% - 24hr creat.clearance <20ml/mt in 2weeks  Type 2 HRS-fairly stable dec. GFR& incr. creat.  Prognosis of HRS- poor  Defn.Rx liver transplantation
  17. 17. CRITERIA FOR HRS  Major criteria  Low GFR- s.creat >1.5mg/dl or 24 hr creat.clearance <40ml/mt  Absence of shock,ongoing infection,fluid loss,nephrotoxic drugs  No sustained improvement in renal function on diuretic withdrawl or plasma expansion 0f 1.5L  proteinuria,< 500 mg/dl  No usg evidence of obstructive uropathy or renal parenchymal disease
  18. 18.  Minor criteria  Urine volune <500ml/d  Urine Na < 10 meq/l  Urine osmolality greater than plasma osmolaliy  Serum Na < 130 meq/l
  19. 19. COAGULOPATHY  GI bleed & IC bleed  GI bleeding causes death in 20-30%  Several causes - dec. factor II,V,VII,IX,X - dec. anti-thrombinIII & protein C - thrombocytopenia
  20. 20. HEPATIC ENCEPHALOPATHY  Gradual and terminal in contrary to FHF- rapid and determinant for diagnosis  Accumulation gut derived ammonia get to brain by vascular shunting  False neurotransmitters and mercaptans  Cerebral edema uncommon
  21. 21. MANAGEMENT  Supportive therapy  Specific therapy - control of liver cell necrosis - acceleration of liver cell regeneration - replacement of necrosed liver tissue
  22. 22. SUPPORTIVE THERAPY  Management in ICU  Adequate nutrition by oral or parentral route  Fluid and electolyte balance  Identify and treat the complications like infections, hepatorenal syndrome, GI bleed
  23. 23. SPECIFIC THERAPY  CONTROL OF LIVER CELL NECROSIS - no standard drug available today - corticosteroids not useful as in FHF - antiviral drugs are tried in various trials do not show good results  ACCELERATION OF LIVER CELLS - prostaglandlins (PGE-1) @ 0.2-0.6 micro gm/kg/hr. for 28 days (sinclair et al) hepatocyte growth factors – hepatotrophin - induces DNA synthesis in hepatocytes
  24. 24. REPLACEMENT OF NECROSED LIVER CELLS  LIVER SUPPORT SYSTEM & BIO ARTIFICIAL LIVER 1.Hepatassist liver support system 2 . Extra-corporeal liver assist device (ELAD) Advantages: less cost - shortage of donor livers - avoid immunosupressent agents - bridging time to liver transplantation
  25. 25. HEPATASSIST LIVER SUPPORT SYSTEM  Use of pig liver  Bioreactor- heart of system - hollow container with semipermeable membrane (0.2) micron porous fibres - allow hepatocytes to contact with plasma  Venous blood taken from superfecial femoral vein  Treatment last for 6 hrs
  26. 26. HEPATASSIST LIVER SUPPORT SYSTEM
  27. 27. ELAD  Early stages of development  Uses hepatoblastoma cells grown in hollow fibre cartridges  Blood passes through the porous channels in cell chamber = removal of bilirubin & synthesis of albumin and clotting factor  Uses 200gm hepatocytes  No kuppfer cells,bile duct epithelial cells
  28. 28. EALD
  29. 29. ELAD
  30. 30. LIVER TRANSPLANTATION  Curative treatment in FHF with survival rate @ 50- 70%  Useful in SAHF but limitation  Chance of viral replication in transplant
  31. 31. SELECTION CRITERIA Kings college criteria  PT > 100 sec or INR .6.5 or any 3 of follow. variables  Age <10 or >40 yr  Etiology non A ,non B hepatitis,idiosyncrytic drug reaction  PT> 50 sec  S.bilirubin >18 mg/dl
  32. 32. TYPES OF LIVER TRANSPLANTATION  Most common  Permanent  Native liver removed  New liver in same anatomic position  Long term immuno suppression  Split graft can be used  Temporary  Heterotopic position  Native liver in situ  Immunosuppresents weaned off  Donor graft can be removed orthotopic auxillary
  33. 33. HEPATOCYTE TRANSPLANTATION  New development in hepatology  Researches ongoing  Hepatocytes transplanted in spleen  Native liver in situ  Advantages: - replacement to complex liver transplantation - avoid surgical complications - avoid long term immuno-suppression
  34. 34. CONCLUSION  Condition seen in indian subcontinent  Viral etiology  Persistent jaundice > 8 weeks from onset  Ascitis cardinal symptom  Liver biopsy-sub massive or bridging fibrosis  Renal failure- bad prognosis  Mortality upto 70% in medically treated  Best available option- liver transplantation

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