sub acute hepatic failure
Post on 28-Nov-2014
107 Views
Preview:
DESCRIPTION
TRANSCRIPT
SUB ACUTE HEPATIC FAILUREGUIDE- DR.ATUL SHENDE
CANDITATE-DR.SARATH MENON.R
DIVISION OF GASTROENTEROLOGY
MGM MEDICAL COLLEGE ,INDORE
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
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
DEFINITION & TERMINOLOGY
Gimson et al( King’s college )- term LOHF - evidence of hepatic
decompensation - 8 – 24 weeks from onset of icterusO’ Grady et al - encephalopathy occurs after 4
weeks of jaundiceBernau et al – term Sub fulminant hepatic
failure -encephalopathy 2wk-3 month
after onset of jaundice
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
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
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
AETIOLOGY
Most common cause is viral hepatitis
Herbal medicines
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%
PATHOLOGY
Sub massive or bridging necrosis Portal- portal,central – central,portal –central Ballooning degeneration of hepatocytes Lobular inflammation Proliferation of bile duct
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
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%
ENCEPHALOPATHY
40 % 60% 80% 30% 27%
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%
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
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 /sensitivityRx : INJ. Cefotaxime 1 gm 8 th hrly or 10-
14 d Tab. Ofloxacin 400mg bd
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
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
Minor criteria Urine volune <500ml/d Urine Na < 10 meq/l Urine osmolality greater than plasma
osmolaliy Serum Na < 130 meq/l
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
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
MANAGEMENT
Supportive therapy Specific therapy - control of liver cell necrosis - acceleration of liver cell
regeneration - replacement of necrosed liver
tissue
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
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
REPLACEMENT OF NECROSED LIVER CELLS
LIVER SUPPORT SYSTEM & BIO ARTIFICIAL LIVER
1.Hepatassist liver support system2 . Extra-corporeal liver assist device (ELAD)
Advantages: less cost - shortage of donor livers - avoid immunosupressent agents - bridging time to liver
transplantation
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
HEPATASSIST LIVER SUPPORT SYSTEM
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
EALD
ELAD
LIVER TRANSPLANTATION
Curative treatment in FHF with survival rate @ 50-70%
Useful in SAHF but limitation
Chance of viral replication in transplant
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
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
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
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
top related