Decompensated Liver Cirrhosis by Dr.doaa

7/17/2019 Decompensated Liver Cirrhosis by Dr.doaa

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Decompensated

Liver CirrhosisM. Dzikrul haq, MD

Emergency Medicine Kediri General Hospital



Defnition:irrhosis is defnedhistologically as a di!usehepatic process characterized"y f"rosis and the con#ersion

o$ normal li#er architectureinto structurally a"normalnodules.



auses o$ li#er cirrhosis:

%& 'iral Hepatitis (, .)& *lcoholic li#er disease.+& on-alcoholic $atty

li#er disease */0D&.1& *utoimmune hepatitis.2& 3rimary "iliary

cirrhosis.4& 5econdary "iliary

cirrhosis associated6ith chronice7trahepatic "ile ducto"struction&.

8& 3rimary sclerosingcholangitis.

9& Hemochromatosis

& ;ilson disease.%<& *lpha-% antitrypsin

defciency.%%& Granulomatous disease

eg, sarcoidosis&.%)& =ype >' glycogen storagedisease.

%+& Drug-induced li#er diseaseeg, methotre7ate, alphamethyldopa, amiodarone&.

%1& 'enous out?o6 o"structioneg, (udd-hiari syndrome,#eno-occlusi#e disease&.

%2& ardiac cirrhosis: chronicright-sided heart $ailure,tricuspid regurgitation.



Causes of hepatic decompensation:*lkalosis.

Hypokalemia.G>= "leeding.Hypotension.Hepatoto7ic drugs.

>n$ection.Diuretic therapy.General anesthesia.5urgery and general anesthesia place the

cirrhotic li#er at risk $or decompensation.;hy@ *nesthesia reduces cardiac output,induces splanchnic #asodilation and causesa +<-2<A in hepatic "lood ?o6.



3athophysiology and clinical picture

o$ li#er cell $ailure:

1) Liver:

Hyper-"iliru"inemia d.t B secretory $unctiono$ the li#er&.

Hypo-al"uminemia d.t B synthetic $unction&C tissue edema, ascites, pleural e!usion.

Ele#ated li#er enzymes as a result o$hepatocellular damage.



2) GIT: Portal hypertension: defned as a

pressure gradient o$ > 1 mm!" "et6eenthe portal vein and I#C. >t is a maorcontri"utory $actor $or ascites andesophageal #arices.

#ariceal $leedin"

%scites: as a result o$ portal H=. >t is atransudate in nature 6ith proteinconcentration less than ).2 mgd0.

&$P: appears to "e caused "y the

translocation o$ G> tract "acteria across thegut 6all and also "y the hematogenousspread o$ "acteria. =he most commoncausati#e organisms are Escherichia coli,5treptococcus pneumoniae, Kle"siella, and

other gram-negati#e enteric organisms.3: a"dominal ain, $e#er, leukoc tosis,



') (enal: !epatorenal &yndrome>t is the occurrence o$ acute renal dys$unction in

patients 6ith pree7isitng li#er $ailure in the

a"sence o$ primary renal disease.May "e caused "y an im"alance "et6een renal

vasoconstrictors eg. *ngiontensin, *DH, E&and vasodilators eg. 3GE), 3G>), */&. 3lasmale#els o$ #asoconstrictors are ele#ated resulting indecreased renal per$usion. 5*>D5 inhi"it 3Gsynthesis and hence potentiate renal#asoconstriction 6ith a resulting drop inglomerular fltration. =hus the use o$ 5*>D5 iscontra indicated in patients 6ith decompensatedcirrhosis.

>t is diagnosed "y:reatinine clearance F 1< mlmin5erum creatinine %.2 mgd0

liguria urine #olume F 2<< mldayIrine a F %< mlEq0



*) Pulmonary:

+%) !epatopulmonary &yndrome

+!P&) =his is the presence o$ a"normal

intrapulmonary vascular dilatation that cancause pro$ound hypo,emia and can "e #erydiJcult to treat. >t may "e e7plained "y

decreased hepatic clearance o$ endogenous#asodilators eg. &.

H35 is marked "y the symptom o$ platypnea shortness o$ "reath occurring more in theupright position& and othrodeo,ia ) desaturation occurring more in the uprightposition&.

>t can "e diagnosed "y echocardio"raphy. 3tsare diagnosed 6hen their 3a) is less than 8<

mmHg. 5ome cases may "e corrected "y li#ertransplantation and pts may recei#e a speedy



+$) Portopulmonary hypertension 33H=&

33H= is defned as the presence o$ a meanP%P "reater than 2- mm!" in the presenceo$ normal 3;3.

>t results $rom e,cessive pulmonary

vasoconstriction and #ascular remodellingthat e#entually leads to right-heart $ailure.

>t is also diagnosed "y Dopplerechocardio"raphy.

Many liver transplantation programs rule outthe presence o$ 33H= in pts on the transplant6aiting list. 3ts 6ho de#elop 33H= requireaggressi#e medical therapy in e!ort to sta"ilize3*3 and decrease perioperati#e mortality



-) C.& chan"es: !epatic encephalopathyHepatic encephalopathy is a syndrome marked "y

personality changes, intellectual impairment, and adepressed le#el o$ consciousness occurring as a result o$di#ersion o$ portal "lood into the systemic circulationporto-systemic shunting&.

>t is "elie#ed to "e caused "y the passage o$ neuroto7ins6hich "ypass hepatic deto7ifcation and reach the "rain#ia porto-systemic shunting. euroto7ins include short-chain $atty acids, mercaptans, $alse neurotransmitterseg, tyramine, octopamine&, ammonia H+&, andgamma-amino"utyric acid G%$%&. 3atients may ha#ealtered "rain energy meta"olism and increasedpermea"ility o$ the "lood-"rain "arrier.

=oday it is "elie#ed that neurosteroids may play a keyrole in hepatic encephalopathy. =hey are ele#ated in

patients 6ith encephalopathy and are capa"le o$ "indingto their receptor 6ithin the neuronal G*(* receptorcomple7 and can increase inhi"itory neurotransmission.

*cute encephalopathy occurs in $ulminating hepatic$ailure. =here is cere/ral edema and increased ICP.



5ymptoms are graded on the $ollo6ing scale:Grade - 5u"clinical normal mental status, "ut

minimal changes in memory, concentration,intellectual $unction, coordination.

Grade 1 - Mild con$usion, euphoria or depression,decreased attention, slo6ing o$ a"ility to per$ormmental tasks, irrita"ility, disorders o$ sleep pattern ie.in#erted sleep cycle&.

Grade 2 - Dro6siness, lethargy, gross defcits in a"ility

to per$orm mental tasks, o"#ious personality changes,inappropriate "eha#iour, intermittent disorientationusually $or time&. Diminished short term memory andconcentration. *steri7is on physical e7amination.

Grade ' - 5omnolent "ut arousa"le, una"le to per$ormmental tasks, disorientation to time and place, marked

con$usion, amnesia, occasional fts o$ rage, speech ispresent "ut incomprehensi"le.Grade * - Coma, 6ith or 6ithout response to pain$ul

stimuli.



Dia"nosis of hepatic encephalopathy:

a& Ele#ated $ree serum ammonia le#el./) 00G: sho6s non-specifc high amplitude lo6 $requency

6a#es and triphasic 6a#es.c& = scan and ML> o$ the "rain may "e necessary inruling out intracranial lesions. >n acute encephalopathy"rain edema may "e seen.

Common precipitatin" factors:Lenal $ailure, G>= "leeding, in$ection, constipation,

increased dietary protein intake. piates,"enzodiazepines, anti-depressants and anti-psychoticsmay also 6orsen encephalopathy. Hypokalemia andalkalosis due to #omiting or e7cessi#e use o$ K-losingdiuretics& increase solu"ility o$ H' thus increase itspassage across the "lood "rain "arrier.

Dierential dia"nosis of encephalopathy othercauses o$ coma&:

>ntracranial lesions intracranial hge, tumour, a"cess&,in$ections meningitis, encephalitis&, meta"olicencephalopathy hypoglycaemia, uremia, electrolyteim"alance&, alcoholic encephalopathy, post-seizure

encephalopathy.



) $lood:

*nemia: may result $rom $olic acid

defciency, hemolysis, hypersplenism, orG>= "leeding. =hrom"ocytopenia: usually is

secondary to hypersplenism and

decreased le#els o$ throm"opoietin.oagulopathy: results $rom decreased

hepatic production o$ coagulation$actors. Decreased #itamin K a"sorption

results in reduction o$ 'it-K-dependent$actors: >>, '>>, >, and . 3atients 6ithcirrhosis also may e7periencef"rinolysis and D>.



3) 4eta/olic chan"es:

/asting hypoglycemia: due to reduced glycogen

stores.

Electrolytes:.a and 5ater retention: occurs )ry to relati#e

hypo#olemia and )ry hyperaldosteronism.

Dilutional hyponatremia: occurs due to increased

*DH, )ry hyperaldosteronism, impaired renal handlingo$ $ree 6ater and decreased dietary a.

!ypo6alemia: due to diuresis and )ry

hyperaldosteronism.

!yper6alemia: may occure due to the use o$ K-

sparing diuretics, renal $ailure and meta"olic acidosis.

!ypoma"nesemia: due to poor dietary intake,

intestinal mala"sorption hyperaldosteronism anddiuretic therapy.



*cid "ase disorders: (espiratory al6alosis: due to

hyper#entilation )ry to ascites andhepatopulmonary N most common&.

4eta/olic al6alosis: due to K-losingdiuretics, hyperaldosteronism, or #omiting.

4eta/olic acidosis: in renal $ailure.

7) C#& chan"es:Hyperdynamic circulatory state due to:

3eripheral #asodilation "y endogenous#asodilators that "ypass hepatic meta"olism and glucagon&.

3ortal and systemic shunts.



ChildTurcottePu"h classi8cation:

hild-=urcotte-3ugh 5coring 5ystem $or irrhosis

Child Class %O2-4 points, Child Class $ O8-points, Child Class CO%<-%2 points&.



MoPemen Modifed lassifcation o$ 0i#er Disease:

#aria/les

&corin" Points

1 +Class %)

2 +Class $) ' +Class C)

1)0ncephalopathy

I9 II III9 I#

2) %scites 4ild

4oderate9severe

') &erum

/iliru/in+m"dL)

; *< *<-< > -<

*) &erumal/umin +"L)

> '<- '<-2<7 ; 2<7

-) Prothrom/inTime prolon"ed+seconds)

1* > *

) &erum&odium+mmolL)

> 1' 1'12 ; 12

3) &erumcreatinine+m"dL)

; 1<- 1<-2<- > 2<-

7) Leucocyticcount

' '

; 1 112 > 12

The sur"ical ris6 is classi8ed accordin" to the scorin" point

mild +=1 points)9 moderate +111* points) and severe +1-



=reatment+1) ttt of GIT /leedin" +variceal /leedin"):

Ipper G>= endoscopy to e7clude other causes o$hematemesis as peptic ulcer and gastritis.

Gastric lava"e through a G tu"e using cold saline.Leplacement o$ "lood loss "y >' ?uids and "lood products

antishoc6 measures&.#asopressin infusion or its analogue =erlispressin&: >' in$usion: <.+-<.9 unitsmin 0ocalised in$usion into 5uperior mesenteric artery

identifed "y selecti#e arteriography&: <.%2-<.)untismin

$alloon tamponade "y 5engstaken-(lakemoore,Minnesota tu"es.

0mer"ency sclerotherapy.>' nitro"lycerin and propranolol can decrease portal

pressure.ctreotide:somatostatin analogue that acts as intestinal

#asocontrictor.!2 $loc6ers: eg. Lanitidine



+2) ttt of 0ncephalopathy: =reatment o$ the precipitanting $actors o$ hepatic

encephalopathy eg. meta"olic distur"ances, G>"leeding, in$ection, constipation&.

Lactulose is a nona"sor"a"le disaccharide thatstimulates the passage o$ ammonia $rom tissues intothe gut lumen and inhi"its intestinal ammoniaproduction.

ther cathartics, including colonic lava"e also may"e e!ecti#e in patients 6ith se#ere encephalopathy.

.eomycin and other anti"iotics eg. metronida?ole,oral #ancomycin& ser#e as second-line agents. =hey6ork "y decreasing the colonic concentration o$ammoniagenic "acteria. eomycin dosing is )2<-%<<< mg orally )-1 times daily.

(ifa,imin is a nona"sor"a"le anti"iotic that candecrease colonic le#els o$ ammoniagenic "acteria,6ith resulting impro#ement in symptoms o$ hepaticencephalopathy.

@luma?enil: a "enzodiazepine receptor antagonistthat has "een tried success$ully in hepaticencephalopathy.



+') ttt of !epatorenal A:

E7pansion o$ intra#ascular #olume 6ith

al"umin Q //3. Proper hydration. *#oid nephroto7ic drugs as: aminoglycosides,

cyclosporine and contrast dyes.

4annitol to pre#ent renal $ailure.

!emodialysis. Liver transplantation: kidney $unction

usually reco#ers 6hen patients 6ith cirrhosisand hepatorenal syndrome undergo li#er

transplantation. >$ end stage renal $ailure de#elops com/ined

liver6idney transplantation is needed.



+*) .utrition of hepatic patient:

Caloric reBuirements:

)2-+< KcalKgday o$ normo#olemic (;. Protein reBuirements:

3tn restriction is contro#ersial "ut still routinely

implemented esp. in pts 6ith =>355&. *mount: 1<-4< gday or <.9gkgday o$

normo#olemic (;&.

=ype: rich in "ranched chain non-aromatic&amino acids.

5ome studies support that parentral ptn carriesless risk o$ encephalopathy since not con#erted "ycolonic "acteria into H'<

4icronutrients: =hiamine, $olic acid, Mg,

Rn.



+-) %voidance of heaptoto,icmedications:

Medications associated 6ith drug-induced li#er disease include: .&%IDs

Isonia?ide

valproic acid 0rythromycin

amo,icillinclavulanate

etocona?ole

chlorproma?ine

%mino"lycosides are consideredo"ligate nephroto7ins in patients 6ith

cirrhosis and should "e a#oided.



+) %nal"esia in patients 5ith hepaticfailure:

*lthough high-dose acetaminophen is a 6ell-kno6n hepatoto7in, most hepatologists permitthe use o$ acetaminophen in patients 6ithcirrhosis at doses up to ) gd.

.&%ID use may predispose patients 6ith

cirrhosis to de#elop G> "leeding. 3atients 6ithdecompensated cirrhosis are at risk $or 5*>D-induced renal insuJciency, "ecause o$prostaglandin inhi"ition and 6orsening o$ renal

"lood ?o6. piate analgesics are not contraindicated

"ut must "e used 6ith caution in patients 6ithpree7isting hepatic encephalopathy.



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Decompensated Liver Cirrhosis by Dr.doaa