JURNAL READING STASE INTERNA

8/9/2019 JURNAL READING STASE INTERNA

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ح ر ل ن ا م ح ر ل س ا ا ب


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THE MANAGEMENT OF ASCITES

AND HYPONATREMIA CIRRHOSIS

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THE LIVER

-The liver is the largest organ in thebody, occupying the entire upper rightquadrant of the abdomen. !erforms over "## vital function.

It processes all nutrients the bodyrequiresold red blood cells are removed from

the blood by the liver and spleen

occmnmpati


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HEPAR


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6ASTALT

Gambar Sel Hati


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LIVER FUNCTIONS: Metabolism – Carbohydrate, Fat & Protein Secretory – bile, Bile acids, salts & pigments Excretory – Bilirubin, drugs, toxins Sy t!esis – lbumin, coagulation !actors Stora"e – "itamins, carbohydrates etc# #etoxi$icatio – toxins, ammonia, etc#

$


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FUN%SI HATIMetabolisme karbohidrat, lemak dan protein- Glukosa glikogen- Asam amino Protein- Lemak lipoprotein

Mengontrol pembekuan darah denganmenghasilkan faktor-faktor pembekuan darah.Metabolisme hormon, misalnya estrogen,testosteron, vitamin D, aldosteron dll.

Membantu penyerapan makanan denganmenghasilkan garamPusat detoksi kasi !at-!at beracun dalamtubuh.

%


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CIRRHOSIS OF THE LIVER


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MECHANISMS OF ASCITES IN CIRRHOSIS

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FLAPPIN% TREMOR

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cirrhosis complication

Caput medusae


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COMPLICATIONS OF CIRRHOSIS

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• Portal hypertension with portal to systemic shunting

• Loss of hepatocytes

• Other complications


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OR%AN #EFICITS IN CIRRHOSIS

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ASCITES


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PATHOPH&SIOLO%& OF ASCITES


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EVALUATION OF PATIENTS (ITHASCITES

.nclude standart hematology, electrolyte,renal/serum creatinin&B0 1,coagulation&li+ertest, usg abdomen, endos*opi#

dx paracentesis /3( ml o! !luid1 is re uired in allpatients presenting -ith their !irst episode o!ascites&e+idence o! clinical such as !e+er,abdominal pain, . bleeding, hepaticensephalopathy, hypotension or renal !ailure

est in the ascitic !luid should include cell count,albumin, total protein&culture blood


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%ENERAL MEASURES

lo- sodium diet o! 2(((mg5day# Patient

-ith serum sodium concentration '3(&'3)m 57 should be cautious about !luid inta*eto pre+ent !luid retention&de+elopment 89


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SPESIFIC MEASURES he current classi!ication o! ascites de!ined by

the .nternational scites Club : '# sites yang terdete*si hny dg usg, os td*

memerlu*an tx *husus,tp mere*a hrsmnghindari m*nan ber*adar garam tinggi 2# sites menyebab*an distensi sedang

bera*ibat discom!ort ringan5sedang,

3#Pasien dengan asites +olum besarmenyebab*an distensi abdomen dg signi!icantdiscom!ort# Pasien dg asites re!ra*ter yangtida* respon terhadap diureti* dosis tinggi


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MO#ERATE)VOLUM ASCITES Usually accumulated fluid slowly&do not develop large ascites unless

their sodium intake is very high/do not seek medical attention for long periode of time

Serum sodium&kreatinin concentration usually normal limits,os can be

managed as outpatients&do not require hospitalization unless othercomplication of cirrhosis

Effect low dose diuretic cause balance natrium negative

Spironolactone !"#$""mg/day%, amiloride !#$"mg/day%, furosemide"#'"mg/day% useful during the first few days to increase natriuresis

especially when marked peripher edema( )aution it can causeoverdiuresis hypokalemia&pre renal failure


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MO#ERATE)VOLUM ASCITES *he goal of treatment is to produce an average weight loss +""#

!""g/day in patient without edema perifer and ""#$"""g/daywith edema perifer until asites

-n the uncommon case of no response to low dose of diuretic,spironolactone may be increased up to a dose of'""mg/day&furosemide up to $."mg/day

Spironolactone may cause gynekomastia&dose needs to bereduced or stopped

*amo ifen " mg 0$ mll oral, useful in reducing pain


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Table 1 Management Practice Points in Patients with Ascites and Cirrhosis

Treatment strategy for patients with cirrhosis and moderate volume (grade 2) ascites

Start with a low-sodium diet !" mmol#day$ and spironolactone %"&1"" mg#day$ to reach goal of weight loss' (""&%"" g#day) *f needed+ doses to be increased e,ery days up to ."" mg#day of spironolactone) /urosemide can be added at a starting dose of 0"&." mg#day and subse uently increased to 12" mg#day if needed) Treatment strategy for patients with cirrhosis and large-volume (grade 3) ascites Total paracentesis plus intra,enous albumin 3 g per liter of ascites remo,ed$ followed by a low-sodium diet !" mmol#day$ and diuretics if patient tolerated them

beforehand) Treatment strategy for refractory ascites Total paracentesis plus intra,enous albumin can be performed as needed) Consider use of T*PS in patients with ,ery fre uent recurrent ascites without se,erely impaired hepatic function+ aged 4 " years+ and no hepatic encephalopathy


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LAR%E)VOLUME ASCITES *he ma1ority of these patients have intense sodium retention urin sodium lower

than $"mEq/2%,so that ascites accumulate rapidly

Serum creatinine level are normal/only moderately increased, indicatingnormal/moderately reduced 345

6s can t with diuretik alone/parasentesis followed by diuretic( 7iuretic aloneare given at increasing dose maks( '""mg/day for spinorolakton ,$." mg/dayfor furosemide

)omplete removal of asites with paracentesis and give -8 albumin g/2% is afaster&more effective measure in controlling asites

)urrent guidelines support paracentesis followed by diuretik as the metode ofchoice to treat large volum asites

9aracentesis is faster, more effective&associated with fewer adverse event

compared with diuretic


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)irculatory dysfunction after large volum paracentesis is associated withhigh asites reccurance rate, development of :5S/7: in ";case

-f more than !2 are removed, albumin is recommended, although the useof albumin after paracentesis is controversial

)omplication paracentesis such as bleeding, infection, intestinal perforation

-n some cases, severe hemorrhage due to parasentesis may occur duetrauma of a(hipogastrik inferior

9atien trombositopenia


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2$

PUN%SI ASITES


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REFRACTOR& ASCITES 6ccur in nearly $"; of patients with cirrhosis&ascites

-n patient nonrefractory ascites sodium e creation increase,refrakter sodium e creation can=t be increase with diuretic no respon

with high dose diuretic

>dvanced liver disease high rekurensi after parasentesis large volum,increase risk type $ :5S& poor prognosis

6s can be treated with either repeated large volum parasentesis withekspansi plasma/*-9S( 9aracentesis v bsr?albumin initial t forrefrakter asites

@embandingkan v(bsr pasentesis ditambah albumin dibandingkan dg*-9S yg sedang dilakukan pd pasien asites refrakter


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FUTURE THERAPIES ;tudi aca* '%4 pasien sirosis dg asites

menerima 3 dosis )mg,'2,)mg,2)mg5hr orplacebo '4 hr# os diberi spinorolancton'((mg5hr&!urosemide 2(


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H&PONATREMIA IN CIRRHOSIS 6ccur due to e cessive losses of sodium&)ES,either the

kidney high dose of diuretic% or 3- diarrhea/e cessive vomit%(

:iponatremia ini dikenal hiponatremia hipervolemik atau 7:

7: in cirrhosis is defined as a reduction in serum sodiumconcentration below $+"mEq/2 in the setting of ascites and oredema

:yponatremia had more severe liver disease, worse control oftheir asites, a higher rate of hepatic enchepalophaty, SA9 and :5S


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3'

56A*7

L*896

To:ic 70 metabolites/rom *ntestines

9orta systemic

shunts

PATHO%ENESIS OF HEPATICENCEPHALOPATH&


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CERE'RAL A#APTATION TOH&PONATREMIA >hen serum sodium !alls, -ater mo+es into brain cells in

response to osmotic gradients to attain osmotic e uilibrium,producing brain edema

+idence in cirhosis, increase brain glutamin and reduceosmolite organi* other, especially myoinositol

;e+eral studi indicate lo- sodium increase ris* encephalopaty :

'1induced by amonia in!usion indicated that the presence o!hiponatremia increase brain edema compared -ith animal -ithnormal serum sodium le+el

21hyponatremi producing met#change in brain cell5hepaticense!allopati


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TERAPI FARMA*OLO%IS he management o! 89 in cirrhosis ha+e !ocused on inhibiting

"P# he aim o! therapy in 89 is to increase solute !ree -aterexcreation, blo*ing reseptor "2# he drug ha+e been e+aluated inthe tx o! 89, C9F and cirrhosis

?o@a+aptan,sata+aptan,tol+aptan menun=u**an agen ini e!e*ti!dlm mening*at*an natrium serum dan *eseimbangan cairanmenyb#pnurunan BB yg signi!i*an pd sirosis


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