edema sucitra

7/25/2019 EDEMA Sucitra

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EDEMA

SUCITRA.SETIAWAN

10.2015.002


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Pendahuluan

Edema adalah penimbunan cairan

berlebihan diantara sel sel tubuh atau

didalam bebagai rongga tubuh

Efusi

Ascites


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Pendahuluan lanj.

Sebab edema

Gagal jantung kongestif

Sirosis Hepatis

Sindroma efrotik

Penanganan ! Pen"akit Dasar


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Distribusi Cairan Tubuh

#airan tubuh $%& '(

Ekstraselular $)& '(*ntraselular $+& '(

*ntra,askular $- '( *nterstisial$- '(


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Pathogenesis

Hukum starling /erusakan /apiler 0olume Darah Arteri Efektif $0DAE(

#urah 1antung 2aktor Ginjal Sistem 3enin Angitensin AldosteronArginin 0asopresin Endhotelin Peptida atriuretik


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Hukum starling pada kapilerARTERI VENA

INTERSTITIAL

LIMFATIK


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Hukum Starling

Fm = KF(P-)

2m 4 /ecepatan perpindahan #airan/2 4 Permeabilitas /apiler

5P 4 Perbedaan 6ekanan Hidrostatik

57 4 Perbedaan 6ekanan 8smotik


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Mekanisme fisiologis dan pen"ebab edema$sumber 9uku Ajar *lmu Pen"akit Dalam(

Klinis Faktor yan

!"r#"nar$%

M"kanis&"

E'"&a lo(alIn)la&asiTro&!osis *"na 'ala&

+"ninkatan K)+"ninkatan ,+

-i#"rantarai ol"% sitokin!str$ksi *"na!str$ksi li&)"

E'"&a /"n"ralisataSin'ro&a N")rotik

//A oli$ria

/aal ant$nkon"sti)

Sirosis "#atis

Kasiokor

E'"&a i'io#atik

+"ninkatan K)

+"ninkatan ,++"n$r$nan ,3+"ninkatan ,+

+"ninkatan ,+

+"ninkatan ,++"n$r$nan ,3+"ninkatan K)+"n$r$nan ,3+"ninkatan ,+

-i#"rantarai ol"% sitokin

+"l"#asan al'ost"ron+"n$r$nan ka'ar al!$&in+"ninkatan *ol$&" 'ara%

+"n$r$nan ($ra% ant$n'i#"rantarai ol"% R"nin4aniot"nsin4 al'ost"ron

i#"rt"nsi #ortal ol"% al'ost"ron+"n$r$nan al!$&in ol"%#rostalan'in4 N+"n$r$nan ka'ar al!$&inl"% r"nin4 aniot"nsin 'anal'ost"ron


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Patofsiologi Edema$sumber Harrison(


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Sebab Edema

8bstruksi Aliran :imfe

Sindroma efrotik

Gagal 1antung /ongestif

Sirosis Hepatis

8bat;obatan

Edema *diopatik


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/erusakan /apiler

/apiler rusak < permeabilitas kapiler =< protein pindah ke interstisial

Etio ! 8bat

,irus bakteri pemanasan Mekanik

3> Hipersensitifitas *nflamasi ! edema non pitting? lokal? tanda

radang $@( merah dan panas


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Penurunan 0DAE

0ol darah arteri "ang adekuat mengisi

kapasitas pemb darah arteri

/eseimbangan rasio curah jantung thd

resistensi pemb darah

0DAE $;( !

; P$;( ,ol drh arteri!

perdrhan?dehidrasi

; #urah jtg $;( ! gagal jtg

; 6ahanan pemb drh arteri meningkat


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2aktor Ginjal 0DAE $;( < aliran darah ginjal $;( < sin"al bg sel

ju>tagomerular m= pelepasan renin. Mekanisme !

; 3espon baroreseptor mengurangi perfusi

ginjal men"ebabkan inkomplit filling arteriol

ginjal dan regangan sel ju>taglomerular b$;(

; 2iltrasi glomerulus $;( menurunkan beban acl

mencapai tubulus distal? dirasa oleh macula

densa? signal sel ju>taglomerular melpskan renin ; Akti,asi reseptor adrenergik di ju>taglomerular

oleh s" simpatis dan katekolamin untuk

menstimulasi pelepasan renin


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Arginin 0asopressin

3espon peningkatan osmolalitas non

osmotik

Menstimulasi reseptor 0) < me=

reabsorbsi air tub distal B duktus collect (Phosphodiesterase inhibitorJ!theoph"lline

Sodium;potassiumchloride

inhibitors!bumetanide$9ume>(?ethacr"nic acid$Edecrin(?furosemide$:asi>(

Sodium chlorideinhibitors!chlorthalidone

$H"groton(?h"drochlorothiaIide $Esidri>(?metolaIone$Diulo(

Aldosteroneantagonist!spironolactone

$Aldactone(Sodium channelblockers!amiloride$Midamor(?triamterene$D"renium(

D#6 4 distal con,oluted tubuleK ##6 4 cortical collecting tubule.J;6he mechanism b" Lhich phosphodiesterase inhibitors increase sodiumchloride e>cretion is not knoLn Lith certaint" and ma" in,ol,ehemod"namic and tubular effects $perhaps mediated b" c"clic adenosinemonophosphate(.Adapted Lith permission from Ellison DH. Diuretic drugs and the treatmentof edema! from clinic to bench and back again. Am 1 /idne" Dis +K)!%)N.


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6abel -. /arakteristik Diuretik Oang 9iasa Dipakai

;"nis -i$r"tikT"atk"ra

+ot"nsi E)"k +ri&"r E)"ks"k$n'"r

-osis&%r

Kolikasi

Car!oni(an%i'ras"1in%i!itorA("ta7ola&i'Loo# 'i$r"ti(

F$ros"&i'Eta(ryni( a(i'Tia7i'Klorotia7i'i'roklorotia7i'M"to7alon+otasssi$&S#arrinTria&t"r"n

A&ilori'S#ironolakton

T$!$l$s#roksi&al

Loo# o)"nl"

T$!$l$s-istalis

-$kt$s

Kontort$s

Ekskr"si< >Ekskr"si K>Ekskr"si :

>

Ekskr"si K

=Ekskr"si :=

250:500

?0:@0050:?00

500:100050:100245:10

100:900

5:10100:?00

i#okal"&iai#"rklor"&iaAsi'osis

i#okal"&iaAlkalosis

i#okal"&iaAlkalosis

i#"rkal"&ia

Asi'osis

Sumber ! #omprehensi,e #linical ephrolog"-


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Therapi

Gagal Jantung Kongestif 6ujuan ! M= /ualitas hidup

meC progresi,itas

meC mortalitas

Diuretik ! Spironolakton < me= sur,i,al? meCmortalitas dan morbiditas gagal jantung dg OHA *** dan *0 Sirosis! ; Diuretik Spironolakton

; 3estriksi atrium

Sindroma Nefrotik : ; 3estriksi atrium

; Diuretik :oop diuretik atau kombinasi

6iaIid? metoIalon atau aIetaIolamid

; Spironolakton ! Hipoaldosteronisme skdr


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6abel.% 3ekomendasi Penanganan edema

Strength of Recommendations

Key clinical recommendation Label References

reatment !ith an angiotensin-con"erting en#yme inhi$itor or angiotensin-rece%tor $loc&er should $e considered in %atients !ith calcium channel $loc&er-

induced %edal edema'

*+ ,

S%ironolactone (ldactone) should $e used to decrease mor$idity and mortalityrates in %atients !ith ./0 class 111 or 12 heart failure'

3 45

he use of a trans6ugular intrahe%atic %ortosystemic shunt may $e su%erior tolarge-"olume %aracentesis in relie"ing ascites and %rolonging sur"i"al'

3 + ,

ra"el stoc&ings (i'e'+ 7su%%ort hose8) should $e !orn during flights longer thanse"en hours to %re"ent edema and D2'

3 9

S%ironolactone should $e used in %atients !ith cirrhosis and grade or ,ascites to com$at hy%eraldosteronism'

C 4:

Paracentesis is the treatment of choice in %atients !ith grade , ascites andshould $e used in con6unction !ith sodium restriction and diuretic thera%y'

C 4:

;ong-term use of com%ression garments in con6unction !ith meticulous s&incare and a"oidance of $lood %ressure measurements and other constrictionsshould $e considered in %atients !ith lym%hedema'

C ,uality %atient-oriented e"idence C = consensus+disease-oriented e"idence+ usual %ractice+ o%inion+ or case series' See %age * for more information'

Sumber ! N


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Resistensi Diuretik

/egagalan tubuh membuat keseimbangan @

"gnegatif Lalaupun dengan diuretik dosis maks.

Etiologi ! tabel

Ada ) 1enis

; Longterm Tolerance : Hipertropi nefron distal

dan reassorsi natrium erlei!an

" Shortterm 6olerance: #espon diuretik me$

krn p$ %ol intra%ask Penanganan Penama!an diuretik tempat ker&a eda


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6A9:E %reatment Failure? Causes in Patients a&ing ;oo% Diuretics

.oncom%lianceonadherence to drug regimenonadherence to sodium restrictionrue diuretic resistanceAltered intestinal absorption of loop diureticsDecreased renal perfusion caused b" loL ,olume? arterial disease? or drug use$e.g.? A#E inhibitors? SA*Ds(Pharmacokinetic causes related to diuretic half;life3educed tubular secretion caused b" loL ,olume? kidne" disease? or drug use6olerance caused b" chronic use of loop diuretics

A#E 4 angiotensin;con,erting enI"meK SA*D 4 nonsteroidal anti;inflammator"drug.Adapted Lith permission from Dormans 6P? Gerlag PG? 3ussel 2G? Smits P.#ombination diuretic therap" in se,ere congesti,e heart failure. DrugsK--!%%.


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TERIMA ASI!

edema sucitra

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