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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!