ascites secondary to kidney disease

8/9/2019 Ascites Secondary to Kidney Disease

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ASCITES

SECONDARY TOKIDNEY DISEASE

Submitted to: Ms. Jesusa L. Capispisan

Submitted By: Marianne Claire P. Bartolome

Year/ Section: 3A-BS Nursing

Group !


2/13

DE"INITION:

A#cite# is an accumulation of serous fluid in the peritoneal cavit .

Causes include cirrhosis of the liver! tumour! tu"erculous peritonitis! and interference in venous

circulation! cardiac or renal failure. MAL#$NAN% A..! A condition sometimes occurring in theend stage of cancer &ith metastasis to the peritoneum' treatment ma consist of peritoneovenousshunt.-S(N. ) droperitoneum! a"dominal drops .

Ascites is the accumulation of fluid in the peritoneal cavit ! causing a"dominal s&elling. Causesinclude infection *such as tu"erculosis+! heart failure! portal h pertension! cirrhosis! and variouscancers *particularl of the ovar and liver+. ,"struction to the drainage of l mph from thea"domen results in ch lous ascites. *Ch le+

Ch le is an al aline mil li uid found &ithin the lacteal after a period of a"sorption. #t consists

of l mph &ith a suspension of minute droplets of digested fats! &hich have "een a"sor"ed fromthe small intestine. #t is transported in the l mphatic s stem to the thoracic duct.

$AT%O$%YSIO&OGY:

%he mechanism responsi"le for the development of ascites is not completel understood. Portalh pertension and the resulting increase in capillar pressure and o"struction of venous "loodflo& through the damaged liver are contri"uting factors. %he vasodilation that occurs in thesplanchnic circulation is also suspected causative factor. %he failure of the liver to meta"oli/ealdosterone increases sodium and &ater retention " the idne . Sodium and &ater retention!

increased intravascular fluid volume! increased l mphatic flo& and decreased s nthesis ofal"umin " the damaged liver all contri"ute to the movement of fluid from the vascular s steminto the peritoneal space. %he process "ecomes self-perpetuating as loss of fluid into the

peritoneal space causes further sodium and &ater retention " the idne in an effort to maintainthe vascular fluid volume.

As a result of liver damage! large amount of al"umin rich fluid! 01L or more! ma accumulate inthe peritoneal cavit as ascites. 2ith the movement of al"umin from the serum to the peritonealcavit ! the osmotic pressure of the serum decreases. %his! com"ined &ith increased portal

pressure! results in movement of fluid into the peritoneal cavit .

C&INICA& 'ANI"ESTATION:

#ncreased a"dominal girth and rapid &eight gain are common presenting s mptoms of ascites.%he patient ma "e short of "reath and uncomforta"le from the enlarged a"domen! and striae anddistended veins ma "e visi"le over the a"dominal &all. m"ilical hernias also occur fre uentlin those patients &ith cirrhosis. 4luid and electrol te im"alances are common.


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STRIAE AND DISTENDED (EINS (ISIB&E O(ER T%E ABDO'INA& )A&&

S%ORT O" BREAT%E AND *NCO'"ORTAB&E "RO' EN&ARGE ABDO'EN

DISTENDED (EIN IN T%E ABDO'EN


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INCREASED ABDO'INA& GIRT% AND RA$ID )EIG%T GAIN

*'BI&ICA& %ERNIAS

"&*ID AND E&ECTRO&YTE I'BA&ANCE


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ASSESS'ENT AND DIAGNOSTIC E(A&*ATION:

%he presence and e5tent of ascites are assessed " percussion of the a"domen. 2hen fluid has

accumulated in the peritoneal cavit ! the flan s "ulge &hen patient assumes a supine position.%he presence of fluid can "e confirmed either " percussing for shifting dullness or " detectinga fluid &ave. A fluid &ave is li el to "e found onl if a large amount of fluid is present. 6ailmeasurement and recording of a"dominal girth and "od &eight are essential to assess the

progression of ascites and its response to treatment.

ASSESSING "OR "&*ID )A(E DAI&Y 'EAS*RE'ENT AND

RECORDING O" )EIG%T

DAI&Y 'EAS*RE'ENT AND RECORDING O" ABDO'INA& GIRT%


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'EDICA& 'ANAGE'ENT:

DIETARY 'ODI"ICATION:

%he goal of treatment for the patient &ith ascites is a negative sodium "alance to reduce fluidretention. %a"le salt! salt foods! salted "utter and margarine! and all ordinar canned and fro/enfoods that are not specificall prepared for lo&-sodium *7-g sodium+ diets should "e avoided. #tma ta e 7-3 months for the patient8s taste "uds to ad9ust to unsalted foods. #n the meantime! thetaste of unsalted foods can "e improved " using salt su"stitutes such as lemons 9uice! oregano!and th me. Commercial salt su"stitutes need to "e approved " the ph sician! "ecause those thatcontain ammonia could precipitate hepatic coma. Most salt su"stitutes contain potassium andshould "e avoided if the patient has impaired renal function. %he patient should ma e li"eral useof po&dered! lo&-sodium mil and mil products. #f fluid accumulation is not controlled &iththis regimen! dail sodium allo&ance ma "e reduced further to 1:: mg! and diuretics ma "eadministered.

6ietar control of ascites via strict sodium restriction is difficult to achieve at home. %heli elihood that the patient &ill follo& even a 7-g sodium diet increases if the patient and the

person preparing the meals understand the rationale for the diet and receive periodic guidancea"out selecting and preparing appropriate foods. Appro5imatel 0:; of patient &ith ascitesrespond to these measures alone. Nonresponders and those &ho finds sodium restriction difficultre uire diuretic therap .

DI*RETICS:

se of diuretics along sodium restriction is successful in 1 g *0.0 to 0.?1 l"s+ in patients &ithoutedema. 4luid restriction is not attempted unless the serum sodium concentration is ver lo&.

Possi"le complications of diuretic therap include fluid and electrol te distur"ances *includingh povolemia! h po alemia! and h ponatremia and h pochloremic al alosis+ andencephalopath . @ncephalopath ma "e precipitated " deh dration and h povolemia. #naddition! &hen potassium stores are depleted! the amount of ammonia in the s stemic circulationincreases! &hich ma cause impaired cere"ral functioning and encephalopath .

BED REST:

#n patients &ith ascites! an upright posture is associated &ith activation of the renin- angiotensin-aldosterone s stem and s mpathetic nervous s stem. %his causes reduced renal glomerularfiltration and sodium e5cretion and a decreased response to loop diuretics. %herefore! "ed restma "e useful therap ! especiall to the patients &hose condition is refractor to diuretics.


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$ARACENTESIS:

Paracentesis is the removal of fluid *ascites+ from the peritoneal cavit through a puncture orsmall surgical incision through a"dominal &all under sterile conditions. ltrasound guidancema "e indicated in some patients &ho are at high ris for "leeding "ecause of an a"normal

coagulation profile and in those &ho have had previous a"dominal surger and ma haveadhesion. Paracentesis once considered a routine form of treatment for ascites. )o&ever! it isno& performed primaril for diagnostic e5amination of a ascetic fluid! for treatment of massiveascites that is resistant to nutritional and diuretic therap and that is causing severe pro"lems tothe patients! and as prelude to diagnostic imaging studies! peritoneal dial sis! or surger . Asample of ascetic fluid ma "e send to the la"orator for cell count! al"umin and total proteinlevels! culture! and other tests.

Large-volume *1-? L+ paracentesis has "een sho&n to "e a safe method for treating patients &ithsevere ascites. %his techni ue! in com"ination &ith the # infusion of salt-poor al"umin or other

colloid! has "ecome a standard management strateg ielding an immediate effect. efractive!massive ascites is unresponsive to multiple diuretics and sodium restriction for 7 &ee s or moreand can result in se uelae such as respirator distress! &hich re uires rapid intervention.Al"umin infusions help to correct decreases in effective arterial "lood volume that lead tosodium retention. se of this colloid reduces the incidence of h ponatremia and renald sfunction associated &ith decreased effective arterial volume. %he "eneficial effects ofal"umin administration on hemod namic-sta"ilit and renal functional status ma "e related toan improvement in cardiac function as &ell as a decrease in the degree of arterial vasodilation.Although the patient &ith cirrhosis has greatl increased e5tracellular "lood volume! the idneincorrectl senses that the effective volume has decreased. %he renin-amgiotensin- aldosteronea5is is stimulated! and sodium is rea"sor"ed. #n addition! antidiuretic hormone *A6)+ secretionincreases! &hich leads to increased retention of free &ater and sometimes to the development ofdilutional h ponatremia. %herapeutic paracentesis provides onl temporar removal of fluids'ascites rapidl recurs! necessitating repeated fluid removal.

TRANS+*G*&AR INTRA%E$ATIC $ORTOSYSTE'IC S%*NT ,TI$S-

%#PS is a method of treating ascites in &hich a cannula is threaded into the portal vein " thetrans9ugular route. %o reduce portal h pertension! an e5panda"le stent is inserted to serve as anintrahepatic shunt "et&een the portal circulation and the hepatic vein. %#PS is the treatment ofchoice for refractive ascites. #t is e5tremel effective in decreasing sodium retention! improvingthe renal response to diuretic therap and preventing recurrence of fluid accumulation.

Because of the development of ascites in patients &ith cirrhosis is associated &ith a 1:;mortalit rate! an patient &ho is considered a candidate for liver transplantation should "ereferred for %#PS.

OT%ER 'ET%ODS O" TREAT'ENT:

Ascites can also "e treated " the insertion of a peritoneovenous shunt to redirect ascitic fluid

from the peritoneal cavit into the s stemic circulation. )o&ever! this procedure is seldom used "ecause of the high complication rate and high incidence of shunt failure. #n fact! use of thisshunt has virtuall "een a"andoned! e5cept for patients &ho are not candidates for livertransplantation.


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$ARACENTESIS


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S*RGERY ON $ATIENTS )IT% ASCITES

Surger is prone to complications in patients &ith ascites. A"dominal surger is prone toinfection and there is a potential for poor &ound anastomotic healing. %he underl ing liverdisease ma cause a coagulopath . enal failure complicating liver disease *hepatorenals ndrome+ is a ma9or ris &hich can "e minimised " ensuring optimal renal perfusion. Patients&ho have o"structive 9aundice are often surgical candidates! at least for some form of " pass

procedure. %he presence of ascites in these patients increases the mortalit ! particularl fromhepatorenal s ndrome! and thus less invasive procedures such as "iliar stenting are preferred.

N*RSING 'ANAGE'ENT:


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#f a patient &ith ascites from liver d sfunction is hospitali/ed! nursing measures includeassessment and documentation of inta e and output! a"dominal girth! and dail &eight to assessfluid status. %he nurse monitors serum ammonia and electrol te levels to assess electrol te

"alance! response to therap ! and indicators of encephalopath .

$RO'OTING %O'E AND CO''*NITY.BASE CARE

TEAC%ING $ATIENTS SE&".CARE

%he patient treated for ascites is li el to "e discharged &ith some ascites still present. Beforehospital discharge! the nurse teaches the patient and famil a"out the treatment plan! includingthe need to avoid all alcohol inta es! adhere to a lo&-sodium diet! ta e medication as prescri"ed!and chec &ith ph sician "efore ta ing an ne& medications. Additional patient and famil

teaching addresses s in care and the need to &eigh the patient dail and to &atch for and reportthe signs and s mptoms of complications.

CONTIN*ING CARE:

A referral for home care ma "e &arranted! especiall if the patient lives alone or cannot provideself Dcare. %he home visits ena"le the nurse to assess the changes in the patient8s condition and&eight! a"dominal girth! s in and cognitive and emotional status. %he home care nurse assessesthe home environment and the availa"ilit of resources needed to adhere to the treatment plan*e.g. a scale to o"tain dail &eights! facilities to prepare and stores appropriate foods! resourcesto purchase needed medications+. #t is important to assess the patient8s adherence to the treatment

plan and the a"ilit to "u ! prepare! and eat appropriate foods. %he nurse reinforces previousteaching and emphasi/es the need for regular follo&-up and the importance of eeping scheduledhealth care appointments.

ascites secondary to kidney disease

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