Loading ...


Fulminant Hepatic Failure

Q.509.. Define “subfulminant” hepatic failure?


 Fulminant Hepatic Failure

fulminant hepatic failure treatment fulminant hepatic failure procedure fulminant hepatic failure definition fulminant hepatic failure causes fulminant hepatic failure diagnosis fulminant hepatic failure criteria fulminant hepatic failure uptodate fulminant hepatic failure adults what causes fulminant hepatic failure

Revise please the abbreviation list on:


Q.508. Define FHF.?        

A. Hepatic failure: [acute, frequently fatal process é severe metabolic abnormalities, neurologic complications & MODS  Liver Dialysis].: Ac. hepatocyte dysfunction Dcr. protein level, clotting f. & global odema.

FHF: [Severe Ac. liver failure in a ptn. without pre-existing liver dis.,   ence-phalopathy dev. é two w., fr. 1st manifestation of liver dis. (us Jaundice)].

Q.509.. Define “subfulminant” hepatic failure?        

A. Subfulminant” hepatic failure: occ. > 2-3 w. fr. Jaundice.

Q.510.. What is the most common cause of hepatic encephalopathy (H.E.)?        

A. Acetaminophen overdose, is the most common cause of H.E.

- Aceta.: matabolite8 to NAD QI (N-acetyl-P-benzoquinone imine), wch. normally neutralized by Glutathione, but if the amount of aceta. overwhelm GlutaHepatic Encephalopathy” occ. by this (NAD QI) toxic metabolite.

Q.511.Which cause has the best prognosis?        

A. HAV. hs the best prognosis (No progression to ch. hepatitis, Dgx. by HAV anti-Ig M A.B.), 2nd best Drug-induced, Acetaminophen, é rate of onset indicative of dis. prognosis, with the most rapid onset  the best prognosis.

Q.512.Which patient is more susceptible?        

A. Glutathione”-depleted ptn. are more susceptible, us. due to:

1)   Alcoholism.

2)   Malnourishment.

3)   P450-inducing drugs, e.g. Rimactane.

- A single dose of 10 g. aceta. F.H.F., but a therapeutic dose of same drug F.H.F in alcoholics.

Q.513.What about anesthetic agents?

A. HalothaneF.H.F., but not used now,..[Enflurane, Isoflurane, Methoxy Flurane much less hepatotoxic.

Q.514.Mention the other causes?        

A. Other causes:

1)   Sulfonamides, NSAID, Phenacetin,  amiodarone, Valproic a., propyl thiouracil & ecstasy= MDMA (3,4-methylenedioxymethamphetamine).

2)   Mushroom: [Amnita Phalleides]rare, but recognized as a cause of FHF 8 Hepatic, renal, pancreatic, cerebral damage can occur due to [Toxin a-amantin] 8 Profuse watery Drr. & abdominal pain last 1-6 d. prior to liver failure.

3)   Wilson’s Syndrome: hemolytic anemia 2ndry to massive copper release fr. liver,  Kayser-Fleischer ring é slit lamp, low ceruloplasmin, unless liver T.X.,100% Fatal.

Q.515.What is the clinical picture?        

A.{N. & V., jaundice, Encephalopathy, Hypo.(Na, K, Gluc.), Metabolic acidosis, cerebral edema, uncal or cerebral herniation}… Rapid rise in brain water occ. due to incr. permeability of blood-brain barrier brain water in face of solid cranium I.C.T. &  cerebral perfusion. Decerbrate pattern, brain stem pattern cn be also observed.

Q.516. What is the clue of cerebral edema?        

A. Cerebral edema is manifested by:

1)   Bradycardia.

2)   Systolic Hypertension.

3)   Abnormal pupillary reflexes.

- I.C.P. cn be measured by [subdural transducer]  risk of bleeding & infc., so, only used é ventilated & sedated ptn.s. I.C.P. monitoring is advised in G. III/IV. Encephalopathy, as recovery cn occ.,  but permanent dge cn occ.

Q.517. Describe the full picture of other systemic organs & metabolic status?        

A. All ptn.s. hv. circulatory compromise & hypotension is common due to:

*      Circulating endotoxin.

*      TNF. effect.

- Microthrombi 🠟 vital organ perfusion, both Hpt. & microthrombi + Defective delivery & uptake of O2 Anaerobic metabolisma Lactc acidosis & MODS.

Q.518.What is effect on blood picture?        

A. Thrombocytopenia occur due to:

1)   Consumption.

2)   Splenomegaly.

3)   Low production by B.M.

Q.519.What is the effects on coagulation profile?        

A. Liver compromise  production of:  factor I, II,..V, VII, IX, X. P.T.& P.T.T.

- . reduced rapidly, as it has short ½ life, So, the {level of f.V.} often used as a measure of dis. progression & considered independent prognostic factor.

- Hge. is not common, but if occur G.I. is the most common.

Q.520.What coagulopathy is candidate to occur?        

A. DIC occur due to:

1)   Release of thromboblastic material fr. necrotic hepatocyte.

2)   Platelet activating F. & circulating bacterial non-hepatic endotoxin.

3)   Expression of tissue factor on active endothelial cells Coagulation cascade.   

Q.521.What about immunological status & liability for infection?        

A. Immunocompromised status arise  Bacterial & fungus (Candida, aspergilla) infection is expected due to: 

1.    Complement deficiency.

2.    Diminished Opsonin activity.

3.    Impaired leucocytic function. 

Q.522.What about kidney function?     

A. Renal dysfunction occur é 55% of cases due to:

1.    H.R.S.

2.    Circulation: compromised R.B.F.

3.    Direct toxin of : 

                                                                                               I.        Aceta overdose.

                                                                                             II.        A.B. use.

                                                                                           III.        Radiocontrast.

Q.523. Which modality of dialysis is suitable for those patients?        

A. CRRT is the 1st choice, even é hemodynamically stable ptn., do NOT use IRRT (Intermittent Renal Replacement Therapy ICT , but no rise in CRRT.

Q.524. How to evaluate those patients?        

A. Full biochemistry, coagulation profile, ceruloplasmin level, P.T., F.V.

- Swan Ganz catheter, i.v. H2 blocker’s  gastric bleeding, liver biopsy é minority of cases, transjugular approach in case of coagulopathy, due to less risk of bleeding é percutaneous approach.

Q.525. How to manage?        

A. Management:

1)   Few cases respond, to [NAC, N-acetyl Cysteine] It enhances availability of [Glutathione], if given within 36 h.  improved outcome :

*      [NAC] mg/kg., oral , foll. by 70 mg/kg./4 h./17 dose.

*      [NAC] i.v. 150 mg bolus, foll. by 70 mg. i.v./4h./12 doses.

2)   Acyclovir, for herpes Simplex.

3)   Lamivudine for HBV.

4)   Acute fatty liver & HEELP (Hemolysis, Elevated Liver Enzymes, Low Platelet)  Immediate delivery of the fetus.

5)   Amantia toxin  High-dose Penicillin (300,000-one million U/kg/d.) anta-gonizes muchroom toxin(Amatoxin & Sylibin) 20-48  mg/kg/d.Block hepatocyte toxin uptake.

Q.526. How to do supportive hepatic care?        

A. Supportive hepatic care:

1)   Fluid resuscitation for hypotension, occ. due:

*      Dcr. systolic vascular resistance.

*      Incr. endothelial permeability.

2)   [Albumin& F.F.P.] 1st line of fluid resuscitation, once it occ., maintain é:

3)   Dextrose 5% & ½ N.S. 0.45%, if B.P. still low. (Wedge= 12-14).

4)   Noradrenaline, due to its preferential effect on a receptor.

5)   Bacteria ammonia, So give lactulose ammonia absorption.

6)   Avoid use of “ Neomycin” in H. encephalopathy  Oto/Nephrotoxic.

7)   [Flagyl infusion] Bacterial flora & ammonia production.

8)   Antipyretics for fever: as fever  I.C.P.

9)   Vit. K+ for coagulopathy, FFP Only if bleeding occurs.

Q.527. How to deal with brain odema?        

A. A common cause of death, So, ICP. monitoring + [Romazicon]  to keep cerebral brain perfusion pressure (C.P.P.)>50, If I.C.P>30 & C.P.P< 40 Permanent Neural dge.

Q.528.Which type of sedation is valid for those patients?        

A. Flu ma zenil  (Romazicon)رومازيكون a benzodiazepine antagonist improve short outcome. 

Q.529. Explain, how can kidney function affect the lines of therapy?        

(A) Normal Renal f.Ø [mannitol] ½ -1 g./kg.  I.C.T. a diuresis = twice  volume of mannitol shd be expected within one h., the dose cn be repeated, but Stop mannitol if Osmolality reaches :*320* mosmol/kg.

- “Mannitol” cn cause intravascular vol. depletion & AKI.

(B) In R.F., mannitol cn be coupled é hemofiltration, to keep osmotic effect:  twice vol. of mannitol given shd be removed by U.F., to ensure this effect.

Q.530.What are other lines to reduce I.C.P.?       

A. Hyperventilation to dcr. PCO2 to “30 used to reduce I.C.P., but some studies showed: PCO2 <24

cerebral V.C.  !!

- If the prev. measures fail to keep CPP.>50

use Phenobarbital to induce coma.

Q.531. What is the role of transplantation in treatment?        

A. (1) Liver transplantation: should be tried EXCEPT in:

*      ARDS.

*      Sc vo 2 level.?

*      Uncontrolled intracranial H.T.

     (2) Hepatocyte T.x. on Splenic bed, hs bn tried é some success.

Q.532. How can Liver dialysis help those patients?        

A. Liver dialysis uses hemoadsorption = H.DX. é thick suspension of Pulvirized Sorbent, replacing Dzt solution in the Dzr to remove potential toxins fr. bld.

- The small size of charcoal particles provide 300,000 m2 of S.A., much more S.A. of ordinary charcoal column (few thousands).

- Q.B.: 200-250 ml/min., toxins pass directly across Cellulose membrane, where they bind the small particles of charcoal or cation exchange in sorbent solution,…ttt. of 6 h./d/5 d.

Q.533.What other sorbent system can help in management in hepatic failure?        

v  M.A.R.S.: (Molecule AdsoRbent Circulatory System)=non-albumin permeable polysulphone DX membrane, used é bld perfused in one side & 20 % albumin on Dzt side, another sorbent system, dev. for managing hepatic failure.

v  Albumin-bound substances:[bilirubin- bile salts- tryptophane & F.A.] cleared across the membrane to the (Dzt albumin), wch’s regenerated by passing thr. (charcoal column), foll. by (anion exchange resin column) & finally (Bic-arbonate buffer Dzt) to remove small toxins e.g. [ammonium & aromatic a.a.]

- MARS  improves survival & impair encephalopathy . Outcome is improved in Ac.  on ch. Liver failure  but not in FHF.

Q.534. What is the Bioartficial Liver?        

A. BAL (Bioartficial Liver) a device in wch Hepatocytes are inoculated into one side of a semipermeable membrane. Blood passed into Plasma separator. Plasma  warmed, oxygenated, then passed thr. the device that houses the hepatocytes. The membrane acts to prevent A.B. fr. entering the cell compartment fr. the plasma, but allow hepatocyte to extract O2, nutrients  & toxins from plasma & allow metabolites to pass to hepatocytes from the plasma.

- Current BAL use Procine hepatocyte or human immortalized hepatocytes.

- The Heat assisst device hs bn also evaluated, for further studies.


Revise please the abbreviation list on:



الحَمدُ للّهِ حَمداً كما ينبغي لجلالِ وَجههِ وعظيمِ سُلطانهِ }



Hemodialysis,21,My Publications,2,Peritoneal dialysis,14,Prevention of renal failure,61,Renal face,43,Renal Transplantation,49,TOP RECENT,37,
fedo: Fulminant Hepatic Failure
Fulminant Hepatic Failure
Q.509.. Define “subfulminant” hepatic failure?
Loaded All Posts Not found any posts VIEW ALL Readmore Reply Cancel reply Delete By Home PAGES POSTS View All RECOMMENDED FOR YOU LABEL ARCHIVE SEARCH ALL POSTS Not found any post match with your request Back Home Sunday Monday Tuesday Wednesday Thursday Friday Saturday Sun Mon Tue Wed Thu Fri Sat January February March April May June July August September October November December Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov Dec just now 1 minute ago $$1$$ minutes ago 1 hour ago $$1$$ hours ago Yesterday $$1$$ days ago $$1$$ weeks ago more than 5 weeks ago Followers Follow THIS PREMIUM CONTENT IS LOCKED STEP 1: Share to a social network STEP 2: Click the link on your social network Copy All Code Select All Code All codes were copied to your clipboard Can not copy the codes / texts, please press [CTRL]+[C] (or CMD+C with Mac) to copy Table of Content