Pengukuan Tekanan Darah.docx

8/17/2019 Pengukuan Tekanan Darah.docx

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Pengukuan Tekanan Darah

Sumber : Bate’s Guide to Physical Examination

Pemilihan Manset Tekanan Darah yang Tepat :

- Lebar kantong manset yang dapat dikembungkan harus berukuran kira-kira 4! lingkar

lengan atas "sekitar #$-#4 cm pada indi%idu de&asa rata-rata- Pan'ang kantong balon harus sekitar (! lingkar lengan atas "dengan pan'ang yang

mencukupi untuk melingkari lengan)- aneroid dikalibrasi secara berkala sebelum digunakan

Mempersiapkan Pengukuran Tekanan Darah :

- *dealnya+ meminta pasien untuk menghindari merokok atau minum minuman berka,ein

selama menit sebelum tekanan darah diukur dan untuk beristirahat selama

setidaknya . menit/- Pastikan ruang pemeriksaan tenang+ nyaman dan hangat/- Pastikan lengan yang dipilih tidak tertutup pakaian/ tidak boleh ada ,istula arterio%enous

untuk dialisis+ 'aringan parut karena pemotongan arteri brakialis+ atau tanda-tanda

lymphedema "terlihat setelah diseksi aksila atau terapi radiasi)/- Palpasi arteri brakialis untuk memastikan denyut nadi masih akti,/- Posisikan lengan sehingga arteri brakialis berada pada lipatan antecubital+ setinggi

'antung-kira-kira se'a'ar dengan interkostae 4 pada sambungannya dengan sternum/- 0ika pasien duduk+ istirahatkan lengan di atas me'a sedikit di atas pinggang pasien1 'ika

berdiri+ usahakan untuk menopang lengan pasien se'a'ar tinggi dada tengah/

Mengukur Tekanan Darah :

- 2empatkan kantong balon di tengah arteri brakialis/ Bagian tepi ba&ah manset harus

sekitar $+. cm di atas lipatan antecubital/ Lingkarkan manset dengan tepat/ Posisikan

lengan pasien sehingga sedikit ,leksi di bagian siku/- 3ntuk menentukan seberapa tinggi menaikkan tekanan manset+ pertama tentukan

tekanan sistolik dengan palpasi/ etika 5nda merasa arteri radial dengan 'ari satu

tangan+ segera pompa manset sampai denyut nadi radialis menghilang/ Baca nilaitekanan ini pada manometer dan tambahkan mm6g dari nilai yang didapatkan/

Gunakan penghitunag ini sebgai sasaran nilai untuk pemompaan selan'utnya sehingga

mencegah ketidak namanan karena tekanan tingguii maset yang tidak perlu/ 6al ini 'uga

menghindari kesalahan tertentu yang disebabkan oleh kesen'angan auskultasi- suatu

inter%al diam antara tekanan sistolik dan tekanan diastolik/- empiskan segera manset dan tunggu #. sampai detik/


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- Sekarang tempat bagian bel stetoskop dengan hati-hati diatas arteri brakialis+ pastikan

bah&a anda telah mengunci bagian u'ung pengeluaran udara dengan memutar penuh

penutup udara/ arena suara yang didengar "bunyi orotko,,) relati, ber,rekuensi

rendah+ terdengar lebih baik dengan bel stetoskop/- embangkan manset segera sekali lagi ke le%el hanya ditentukan+ dan kemudian

kempiskan perlahan-lahan dengan la'u penurunant sekitar $ sampai mm6g per detik/7atatat tekanan ini 'ika anda mendengar suara setidaknya dua ketukan berturut-turut/

2ekanan ini merupakan tekanan sistolik- 2erus menurunkan tekanan perlahan sampai suara men'adi teredam dan kemudian

menghilang/ 3ntuk mengkon,irmasi hilangnya suara+ dengarkan sampai tekanan turun

sekitar # sampai $ mm 6g/ emudian kempiskan manset secara cepat sampai ke nol/- 2itikmenghilangnya suara detak 'antung+ biasanya hanya beberapa mm6g diba&ah titik

munculnya suara+ memungkinkan penentuan terbaik tekanan diastolik yang sebenarnya

pada indi%idu de&asa

- Baca le%el tekanan sistolik dan diastolik samapi yang terdekat dengan $ mm6g/ 2unggu

$ menit atau lebih dan ulangi/ 8ata-ratakan hasil pembacaan 5nda/ 0ika dua bacaan

pertama memiliki perbedaan lebih dari . mm 6g+ lakukan pembacaan tambahan/- Bila menggunakan sphygmomanometer merkuri+ pastikan manometer %ertical "ecuali

'ika 5nda menggunakan model lantai miring) dan membuat semua garis bacaan di

tingkat mata dengan meniskus/ 6indari in,lasi lambat atau berulang pada manset+

karena dapat mengakibatkan kongesti %ena yang menyebabkan pembacaan palsu/

- 2ekanan darah harus diambil pada kedua lengan setidaknya sekali/ Biasanya+ terdapatperbedaan tekanan . mm6g dan kadang-kadang sampai # mm 6g/

- Pada pasien yang memakai obat antihipertensi atau pasien dengan ri&ayat pingsan+

pusing postural+ atau deplesi %olume darah+ ukur tekanan darah pada tiga posisi-

terlentang+ duduk+ dan berdiri "kecuali kontraindikasi)/ 23runnya tekana sistolik $

mm6g atau lebih+ khususnya ketikadisertai ge'ala+ menun'ukka hipotensi ortotstatik

"postural)/


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Komplikasi/Kelainan Hati Akibat Diabetes Melitus

Sumber : 9Li%er isease and iabetes ;ellitus< Ga%in =/ Le%inthal+ ;+ and 5nthony S/ 2a%ill+ ;+>87P+ >57P "http:??'ournal/diabetes/org?clinicaldiabetes?%#@n$#AAA?Pg@/htm)

1. Deposito glikogen

Sintesis glikogen di hati terganggu pada diabetes karena kegagalan akti%asi sintesis

glikogen/ Pada pasien dengan diabetes kronis+ terdapat akumulasi glikogen+ yang menun'ukkan

bah&a pasien lama kekurangan insulin/ ;ekanisme deposisi glikogen sitoplasma tidak pasti

tapi mungkin terkait dengan %ariasi yang besar dalam konsentrasi glukosa dan ,rekuensi dosis

insulin/

;ekanisme untuk deposisi glikogen nuklir 'uga tidak 'elas+ dengan glikogen yang

disimpan menyerupai glikogen otot lebih dari glycogen hati/ Pasien dengan deposisi glikogendapat menun'ukkan kelainan hepatomegali+ kealinan enim hati dan mungkin memiliki sakit

perut dan bahkan mual dan muntah dan 'arang ascites/ Semua kelainan ini dapat menurun

dengan memperbaiki control glukosa darah/

2. Fatty i!er" #teatohepatitis

akumulasi lemak hati merupakan komplikasi diabetes/ Lemak disimpan dalam bentuk

trigliserida dan dapat merupakan mani,estasi dari peningkatan transportasi lemak ke hati+

sintesis lemak hati meningkat+ dan penurunan oksidasi atau penghilangan lemak dari hati/

Steatosis mungkin micro%esicular atau macro%esicular dan dapat berkembang men'adi ,ibrosis

dan sirosis/ 2ingkat kontrol gula darah tidak berhubungan dengan ada atau tidaknya lemak/

klinis yang paling umum adalah hepatomegali+ dan kebanyakan pasien memiliki atau hanya

transaminase sedikit tidak normal normal dan bilirubin normal/

Pola mor,ologi steatohepatitis diabetes menyerupai yang terlihat pada hepatitis alkoholik/

=amun+ perubahan histopatologi pada diabetes cenderung periportal "terletak di ona *)+

sedangkan pada hepatitis alkoholik didominasi pericentral "di ona ***)/ Penurunan berat badan

secara bertahap dan kontrol kadar glukosa darah direkomendasikan untuk pasien dengan

steatohepatitis+ penurunan berat badanC #! terbukti mampu menormalkan kadar enim hati/

$. #irosis

5da peningkatan insiden sirosis pada pasien diabetes/ iabetes meningkatkan risiko

steatohepatitis+ yang dapat berkembang men'adi sirosis/

%. Komplikasi Terapi Diabetes

http://gateway.cgstatic.info/code/r.php?r=yahoo%7CDiabetes%2520Mellitus&t=51&did=51&uid=0&type=bl&subid=1374_20668&rkw=Diabetes+Mellitus&rurl=http%3A%2F%2Fjournal.diabetes.org%2Fclinicaldiabetes%2Fv17n21999%2FPg73.htm&domain=diabetes.org&lnktype=10&v=0.129&lang=eng&browser=Chrome_44&country=ID&_=1460583254209http://journal.diabetes.org/clinicaldiabetes/v17n21999/Pg73.htmhttp://journal.diabetes.org/clinicaldiabetes/v17n21999/Pg73.htmhttp://journal.diabetes.org/clinicaldiabetes/v17n21999/Pg73.htmhttp://gateway.cgstatic.info/code/r.php?r=yahoo%7CDiabetes%2520Mellitus&t=51&did=51&uid=0&type=bl&subid=1374_20668&rkw=Diabetes+Mellitus&rurl=http%3A%2F%2Fjournal.diabetes.org%2Fclinicaldiabetes%2Fv17n21999%2FPg73.htm&domain=diabetes.org&lnktype=10&v=0.129&lang=eng&browser=Chrome_44&country=ID&_=1460583254209


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2erapi insulin dapat meningkatkan risiko patien tertular hepatitis %irus karena paparan

'arum/ Pengendalian in,eksi yang baik secara signi,ikan mengurangi risiko ini/

Golongan biguanide yaitu met,ormin "Glucophage) tidak mengalami metabolismehepatik dan+ seperti klorpropamid "iabinese)+ tidak berubah setelah diekskresikan dalam urine/

Sebaliknya+ glyburide sul,onylurea ";icronase+ Glynase+ iabeta) diekskresikan dalam empedu

dan urin dalam . ? . rasio/ Sul,onylurea glipiide "Glucotrol+ Glucotrol DL) dimetabolisme

terutama oleh hati+ dan pada penyakit hati dapat mengakibatkan meningkatnya kadar obat

dalam darah/

Sul,onilurea dapat menyebabkan hepatitis kronis dengan perubahan necroin,lammatory

dan perubahan granulomatosa/ lorpropamid merupakan yang paling hepatotoksik+

menyebabkan hepatitis kolestasis/ ;eskipun sangat 'arang+ acetohexamide dan glyburide

dapat menyebabkan nekrosis hepatoseluler akut/ Biguanides+ seperti met,ormin hidroklorida+

tidak dikaitkan dengan kerusakan hati/


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Terapi DM pa&a Pasien &engan 'angguan 'in(al

)nsulin

*nsulin eksogen normal akan dimetabolisme di gin'al+ sehingga pada gangguan ,ungsi

gin'al &aktu paruh insulin akan meman'ang karena turunnya kecepatan degradasi+ oleh

karenanya pada pasien diabetes tipe # dengan gangguan ,ungsi gin'al episode hipoglikemia

meningkat . kali dibandingkan pasien dengan ,ungsi gin'al normal/

Belum ada rekomendasi 'enis insulin yang harus dihindari atau dapat digunakan1

beberapa peneliti menyarankan agar menghindari penggunaan insulin dengan lama ker'a

pan'ang+ satu penelitian kecil membandingkan pasien diabetes dengan atau tanpa (Diabetic Kidney Disease) menun'ukkan baik insulin regular dan insulin lispro mengalami

penurunan eliminasi+ meskipun e,ekti%itas insulin regular 'uga terganggu sehingga diperlukan

dosis yang lebih tinggi/ *nsulin lispro tidak menyebabkan perbedaan metabolisme glukosa pada

pasien dengan atau tanpa + sehingga meskipun belum ada rekomendasi yang 'elas+ pasien

diabetes dengan penurunan ,ungsi gin'al yang mendapatkan insulin harus lebih diperhatikan

baik dalam penyusuaian dosis untuk mengkontrol glukosa darah maupun menghindari ke'adian

hipoglikemia/

Terapi *ral Diabetes

Seperti halnya insulin+ eliminasi beberapa obat 'uga menurun pada pasien dengangangguan ,ungsi gin'al yang 'uga akan memperpan'ang paparan obat maupun metabolitnya

yang berpotensi meningkatkan e,ek samping/ Eliminasi sul,onylurea dan metabolitnya sangat

dipengaruhi oleh ,ungsi gin'al+ sehingga pada pasien PG stadium -. generasi pertama

sul,onylurea harus dihindari+ tetapi generasi kedua yaitu glipiide dapat direkomendasikan oleh

karena metabolitnya tidak akti, dan risiko hipoglikemia 'auh lebih rendah/

;eskipun mekanisme belum cukup 'elas+ obat diabetes alpha glukosi&ase inhibitor

dan metabolitnya dapat menyebabkan kerusakan akibat akumulasi dosis+ sehingga tidak

diperbolehkan pada pasien dengan serum kreatinine C $ mg?dL/

Met+ormin" tidak memperlihatkan e,ek samping hipoglikemia tetapi perhatian khusus

harus dilakukan pada pasien diabetes PG karena risiko asidosis laktat+ bahkan pada pasiengangguan ,ungsi gin'al ringan+ hal itu 'uga disebabkan akumulasi obat dan metabolitnya

sehingga kontraindikasi pada pria dengan klirens kreatinin C #+. mg?dL dan pada &anita dengan

klirens kreatinin C #+4 mg?dL/

Thia,oli&ine&iones "2) diduga memperlihatkan e,ek proteksi bahkan mencegah atau

memperlambat progresi%itas yang dipengaruhi oleh kontrol gula darah+ beberapa

penelitian kecil memperlihatkan penurunan albuminuria pada pasien yang mendapatkan 2+


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obat ini di metabolisme di hati sehingga dapat diberikan bahkan pada pasien diabetes yang

men'alani dialisis tanpa perlu penyesuaian dosis/


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)nsulin

- Bila dengan kombinasi macam obat masih tidak mencapai target maka langkah

berikutnya adalah pengobatan insulin basal

- Bila pasien datang dengan keadaan a&al 6b5#c F #+! atau GS F g?dl dengan

ge'ala metabolic+ maka pengobatan langsung dengan :

a/ ;et,ormin insulin basal H insulin prandial

b/ ;et,ormin insulin basal GLP-# 85

)n&ikasi terapi insulin- 6b5#c CA! dengan kondisi dekompensasi metabolic- Penurunan berat badan yang cepat- 6iperglikemia yang berat disertai dengan ketosis- risis hiperglikemia- Gagal dengan kombinasi I6I dosis optimal


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- Stress berat "in,eksi sitemik+ operasi besar+ *;5+ stroke)- ehamilan dengan ;/; gestastional yang tidak terkendali dengan perencanaan

makan- Gangguan ,ungsi gin'al atau hati yang berat- ontraindikasi atau alergi terhadap I6I- ondisi perioperati, sesuai dengan indikasi

Dasar Pemberian Terapi )nsulin :- Sasaran utama terapi hiperglikemia adalah mengendalikan gula darah puasa "basal)/

*nsulin yang dapat digunakan adalah insulin basal- Penyesuaian dosis indulin basal untuk pasien ra&at 'alan dapat dilakukan dengan

menambah $-4 unit setiap -4 hari bila sasaran belum tercapai- 5pabila sasaran glukosa darah basal telah terapai sedangkan 6b5#c belum tercapai

maka dilakukan pengendalian glukoasa darah prandial/ *nsulin yang dipergunakanadalah insulin ker'a cepat yang disuntikkan .-# menit sebelum makan atau insulin ker'apencek yang disuntikkan menit sebelum makan


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28E52;E=2 J 5s in the non-7 population+ the treatment o, nondialysis 7 and dialysis patients &ith diabetes

in%ol%es both nonpharmacologic and pharmacologic therapies K/

2he nonpharmacologic therapies include dietary modi,ication+ exercise+ and &eight reduction/ 2he additional burden

o, 7 dietary reMuirements ",or example salt+ protein+ and %olume restrictions) may ,urther complicate diets in

patients &ith diabetes/ "See N*nitial management o, blood glucose in adults &ith type $ diabetes mellitusN+ section on

Oiabetes educationO/)

Pharmacologic therapies include insulin and oral agents/ Iur approach %aries depending upon &hether patients are

on dialysis or not/

=ondialysis 7 patients J >or nondialysis 7 patients &ith type $ diabetes+ the choice o, initial agent depends

upon glycemic goals "see OGoals o, therapyO abo%e)1 the risk o, medication-associated ad%erse e%ents "hypoglycemia+

lactic acidosis)1 and patient pre,erences and con%enience/ =ondialysis 7 patients &ith type $ diabetes may be

treated &ith an oral agent+ although many patients end up on insulin therapy because it is more e,,ecti%e/ 2he oralagents that are thought to be relati%ely sa,e in patients &ith nondialysis 7 include short-acting sul,onylureas "eg+

glipiide) and repaglinide/ *, an oral agent is used+ the short-acting sul,onylurea+ glipiide+ is the pre,erred agent

among nondialysis 7 patients &ho ha%e an estimated glomerular ,iltration rate "eG>8) mL?min?#/@/ 2he dose

,or glipiide is $/. to # mg?day/ Glyburide and other long-acting sul,onylureas are generally not recommended in any

7 patient &ith type $ diabetes+ because o, the risk o, hypoglycemia/ Some clinicians recommend the use o, the

meglitinide repaglinide "starting &ith a dose o, /. mg) ,or nondialysis 7 patients since these agents are not

renally cleared/ "See N*nitial management o, blood glucose in adults &ith type $ diabetes mellitusN+ section on O7hoice

o, therapyO and NSul,onylureas and meglitinides in the treatment o, diabetes mellitusN/)

;et,ormin+ &hich is a pre,erred agent in patients &ithout kidney disease+ should not be used among 7 patients

&ith eG>8 mL?min?#/@ because o, an increased risk o, lactic acidosis K/ 6o&e%er+ &e agree &ith the $#$

idney isease Iutcomes Quality *nitiati%e "?IQ*) guidelines that met,ormin may be used among patients &ith an

eG>8 C4. mL?min?#/@ K#(/ 2he use o, met,ormin among patients &ith eG>8 bet&een and 44 mL?min?#/@ is le,tup to the discretion o, the clinician+ although the ?IQ* guidelines suggest that its use among indi%idual patients be

re%ie&ed/ *n general+ &e recommend lea%ing patients &ith this le%el o, kidney ,unction on met,ormin gi%en the rarity o,

complications and the clinical utility o, met,ormin in maintaining glycemic control/ 5mong all patients &ith G>8 R

mL?min?#/@ m$+ met,ormin should be used &ith caution &hen the G>8 is &orsening at an unpredictable rate/ "See

N;et,ormin in the treatment o, adults &ith type $ diabetes mellitusN+ section on O7ontraindicationsO and N;et,ormin in

the treatment o, adults &ith type $ diabetes mellitusN+ section on OLactic acidosisO/)

Ither agents including thiaolidinediones+ alpha-glucosidase inhibitors+ and dipeptidyl peptidase-4 "PP-4) inhibitors

are generally not considered ,irst-line agents among 7 patients+ because o, limited data regarding long-term sa,ety

and e,,icacy/ Sitagliptin and saxagliptin reMuire dose ad'ustment in the setting o, reduced G>8/

Patients &ho ,ail therapy &ith oral agents are treated &ith insulin/ 2he indications ,or initiating insulin therapy and the

principles underlying insulin therapy are the same ,or nondialysis 7 patients as ,or the general diabetic population/

"See NGeneral principles o, insulin therapy in diabetes mellitusN and N*nsulin therapy in type $ diabetes mellitusN/)

5mong patients &ho are treated &ith insulin+ the starting dose o, insulin may need to be lo&er than &ould ordinarily

be used ,or patients &ith normal kidney ,unction/ 7 is associated &ith decreased renal and ultimately hepatic

metabolism o, insulin "see N7arbohydrate and insulin metabolism in chronic kidney diseaseN)/ 5s a result+ the

,ollo&ing dose recommendations ha%e been made ,or insulin dosing in this setting K#-:


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=o dose ad'ustment is reMuired i, the G>8 is C. mL?min

2he insulin dose should be reduced to approximately @. percent o, baseline &hen the G>8 is bet&een # and .

mL?min

2he dose should be reduced by as much as . percent &hen the G>8 is # mL?min

2he initial dose o, intermediate- or long-acting insulin in patients &ithout 7 is approximately # units or /$ units?kg

"algorithm #)/ 2hus+ in a patient &ith an eG>8 bet&een # and . mL?min+ the initial dose &ould be approximately @

units "@. percent o, # units)/ 2he balance bet&een altered insulin resistance and insulin clearance as renal

dys,unction progresses is di,,icult to predict in any indi%idual patient+ so insulin ad'ustment is o,ten largely empiric/

2here,ore+ it is important that blood glucose le%els be monitored closely and that indi%idually appropriate dose

ad'ustments in insulin therapy be made/

6emodialysis patients J >or most hemodialysis patients+ &e use insulin rather than oral agents/ 2his is consistent

&ith the $. ?IQ* guidelines+ &hich suggest that+ among dialysis patients+ ne&er insulin regimens and insulin

preparations should be used rather than oral agents ,or glycemic control K4/ 2his is due to the lack o, adeMuate data

concerning the use o, oral agents in dialysis patients and their inability to adeMuately excrete many such agents/

2he principles o, insulin therapy are the same ,or dialysis patients as ,or the general diabetic population/ Se%eral

di,,erent insulin regimens can be used to achie%e glycemic control/ Examples include t&ice-daily intermediate-acting

insulin+ &ith regular insulin gi%en be,ore break,ast and be,ore supper+ or long-acting insulin+ &ith t&o or three times

daily supplemental regular insulin+ gi%en t&o or three times per day be,ore meals K.+R/ >or hemodialysis patients+

the initial dose o, insulin should be decreased by approximately . percent+ as described abo%e ,or nondialysis 7

patients &ith G>8 # mL?min/ 2he dose should be titrated up&ard+ as indicated by blood glucose monitoring/ ;ost

patients &ill reMuire more insulin than this initial dose/ "See NGeneral principles o, insulin therapy in diabetes mellitusN

and N*nsulin therapy in type $ diabetes mellitusN/)

5 consensus approach does not exist to the choice o, insulin in patients &ith diabetes and ES8 K$/ Some suggest

that long-acting insulin preparations should be a%oided+ &hile others ,eel that such agents should be used/

Some clinicians pre,er to use oral agents rather than insulin+ especially among patients &ho are already on these

agents and ha%e achie%ed acceptable glycemic control/ 2he pre,erred agents are glipiide or repaglinide since they

are primarily metabolied by the li%er+ since inacti%e or only %ery &eakly acti%e metabolites are excreted in the urine+

and since the risk o, hypoglycemia is lo&er than &ith other oral agents K@/ 5lthough repaglinide drug concentration

and elimination hal,-li,e are increased marginally in patients &ith reduced G>8+ dose reductions are not necessary+

and this agent may be an appropriate therapy ,or patients &ith ES8 K(/

Peritoneal dialysis patients

2reatment regimens J >or patients &ho &ere already on an oral agent &ith good glycemic control prior to starting

dialysis+ &e typically continue the oral agent/ >or patients &ho de%elop diabetes a,ter starting dialysis+ &e generally

treat ,irst &ith an oral agent/ 6o&e%er+ o%er time+ many peritoneal dialysis patients &ill reMuire insulin/

5s ,or nondialysis 7 patients+ the pre,erred oral agent is glipiide/ 2he dose ,or glipiide is $/. to # mg?day/

8epaglinide+ &hich has minimal kidney clearance+ is an alternati%e "starting &ith a dose o, /. mg?day)/ ;et,ormin

should not be used among peritoneal dialysis patients+ because o, an increased risk o, lactic acidosis K/

;ost peritoneal dialysis patients reMuire insulin to maintain good glycemic control/ Patients on continuous ambulatory

peritoneal dialysis "75P) or continuous cycler peritoneal dialysis "77P) &ho are being treated &ith insulin may be

treated &ith subcutaneous or intraperitoneal insulin/ Te pre,er subcutaneous insulin/ 2he principles underlying

subcutaneous insulin therapy are the same ,or nondialysis 7 patients as ,or the general diabetic population "see


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12/14

management o, blood glucose in adults &ith type $ diabetes mellitusN+ section on O*nitial pharmacologic therapyO and

N;anagement o, persistent hyperglycemia in type $ diabetes mellitusN+ section on O2reatment optionsO/)

Sul,onylureas J Glipiide is the sul,onylurea o, choice in patients &ith 7/ 2he dose ,or glipiide is $/. to #

mg?day/ "See NSul,onylureas and meglitinides in the treatment o, diabetes mellitusN/)

2he administration o, sul,onylureas in ES8 reMuires care,ul attention to dosing and routes o, eliminationK$++.$+./ 2he sul,onylureas are strongly protein bound+ particularly to albumin K.$/ 2hus+ ele%ated plasma drug

le%els cannot be e,,iciently re%ersed by hemodialysis/ >urthermore+ displacement o, these drugs ,rom albumin by beta

blockers+ salicylates+ and &ar,arin can lead to hypoglycemia due to increased plasma concentration o, the

physiologically important ,ree drug/ Ilder sul,onylureas "acetohexamide+ chlorpropamide+ tolaamide+ and

tolbutamide) ha%e been largely replaced by ne&er agents such as glyburide+ glipiide+ and glimepiride/

2he basic principles o, sul,onylurea metabolism can be summaried as ,ollo&s:

Glyburide has &eak acti%e metabolites that are excreted in the urine and accumulate in patients &ith impaired

kidney ,unction/

Glimepiride is primarily metabolied by the li%er+ &ith renal excretion o, acti%e metabolites K$/

Glipiide and tolbutamide are metabolied by the li%er and primarily excreted in the urine as inacti%e metabolites/

6o&e%er+ each has one metabolite that may ha%e &eak hypoglycemic acti%ity/

;eglitinides J ;eglitinides+ such as repaglinide or nateglinide+ are sul,onylurea-like agents that stimulate insulin

secretion K$/ "See NSul,onylureas and meglitinides in the treatment o, diabetes mellitusN/)

8epaglinide is principally metabolied by the li%er+ &ith less than # percent renally excreted K$/ 6ypoglycemia may

be more common among patients &ith ad%anced 7 &hen starting therapy &ith repaglinide than among sub'ects

&ith normal or less impaired kidney ,unction+ and maintenance doses tended to be lo&er in these patients in one

study K(/ *nitiation o, treatment should be &ith /. mg daily1 close+ care,ul monitoring o, blood glucose le%els is

essential as the dose is titrated/

=ateglinide is hepatically metabolied+ &ith renal excretion o, acti%e metabolites/ Tith decreased kidney ,unction+ the

accumulation o, acti%e metabolites and hypoglycemia has occurred K.4+../ 2his drug must there,ore be used

cautiously in this setting+ i, at all/

ipeptidyl peptidase 4 "PP-4) inhibitors J 5lthough some PP-4 inhibitors ha%e been studied in patients &ith

kidney dys,unction+ the data are limited+ and+ there,ore+ &e suggest not using PP-4 inhibitors among such patients/

6o&e%er+ limited data suggest that these agents are e,,ecti%e and relati%ely sa,e in 7 and ES8 patients K.R+.@/

ose ad'ustments are needed ,or some agents in this class/

PP-4 is an enyme expressed on the sur,ace o, most cell types that deacti%ates the incretin hormones glucagon-like

peptide-# "GLP-#) and glucose-dependent insulinotropic polypeptide "G*P)/ PP-4 inhibitors cause a glucose-

dependent increase in insulin release/ 2he use o, PP-4 inhibitors in patients &ithout ES8 is discussed else&here/"See Nipeptidyl peptidase 4 "PP-4) inhibitors ,or the treatment o, type $ diabetes mellitusN+ section on

O7andidatesO/)

Linagliptin is only minimally excreted in the urine "# percent) and does not reMuire dose ad'ustment in patients on

dialysis+ but its use in ES8 patients is limited K.(/ Sitagliptin is largely excreted in the urine+ &ith @ to ( percent o,

an oral dose appearing unchanged in the urine K.A/ *, sitagliptin is used among ES8 patients+ a dose reduction to

$. mg daily "usual dose # mg daily) is recommended/ 5lthough sitagliptin is partially cleared by hemodialysis+ it

may be gi%en &ithout regard to the timing o, dialysis KR/ *n,ormation on the use o, sitagliptin in ES8 patients is


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limited KR#+ but it appears to ha%e eMual e,,icacy to glipiide K.R+.@/ Saxagliptin and its primary acti%e metabolite are

excreted in the urine "total urinary excretion approximately R to @. percent)1 a daily dose o, $/. mg is the

recommended dose ,or patients &ith ES8/ Saxagliptin is remo%ed by hemodialysis and should be administered

a,ter dialysis KR$/ Saxagliptin &as reported to be &ell tolerated in a single small study KR/ Uildagliptin also appears

to be e,,ecti%e in this population in limited study KR4/

2hiaolidinediones J Gi%en the risk o, edema ,ormation and heart ,ailure+ as &ell as possible increased mortality &ithrosiglitaone+ thiaolidinediones should be a%oided in patients &ith ad%anced 7+ especially i, they ha%e pre-

existing heart ,ailure/

2hiaolidinediones enhance tissue sensiti%ity to insulin and suppress hepatic glucose production %ia binding to

peroxisome proli,erator-acti%ated receptor "PP58) gamma KR./ "See N2hiaolidinediones in the treatment o, diabetes

mellitusN/)

6emodialysis does not a,,ect the pharmacokinetics o, these drugs/

8osiglitaone+ &hich is in,reMuently used and has 3S >ood and rug 5dministration ">5) restrictions independent o,

kidney ,unction+ and pioglitaone are highly protein bound+ primarily to albumin+ and almost completely metabolied

by the li%er K$/ *n an obser%ational study+ the use o, rosiglitaone &as also associated &ith increased all-cause and

cardio%ascular mortality in hemodialysis patients KRR/ 8osiglitaone has inacti%e metabolites+ and # percent o, the

original compound is excreted in the urine1 pioglitaone is associated &ith three acti%e metabolites/ Tith both agents+

the accumulation o, the parent drug or the ma'or metabolites does not occur in the setting o, 7/

2hese agents are associated &ith heart ,ailure and the ,ormation o, edema+ &hich may be more ,reMuent in patients

also recei%ing insulin K$/ 2he mechanism o, edema ,ormation &ith these agents appears to be related to stimulation

o, PP58 gamma-mediated sodium reabsorption by renal epithelial sodium channels in the distal tubule KR@/

2hiaolidinedione-associated edema may not pose a problem ,or oliguric or anuric dialysis patients/ 5lthough

unpro%en clinically+ amiloride+ spironolactone+ or similar agents may there,ore be e,,ecti%e ,or managing this ,luid

retention/

5lpha-glucosidase inhibitors J 5lpha-glucosidase inhibitors+ such as acarbose or miglitol+ are not recommended in

patients &ith renal dys,unction K$/

2hese agents slo& carbohydrate absorption ,rom the gastrointestinal tract and reduce postprandial blood sugar

peaks/ "See N5lpha-glucosidase inhibitors and lipase inhibitors ,or treatment o, diabetes mellitusN/)

Tith acarbose+ increased le%els o, the parent drug and metabolites are obser%ed &ith 7+ although an increased

risk o, hypoglycemia has not been documented/ ;iglitol is absorbed to a greater extent than acarbose and is largely

renally excreted+ &ith increased accumulation in patients &ith decreased kidney ,unction/

;et,ormin J Biguanides+ such as met,ormin+ are primarily excreted unchanged in the urine/ 2hus+ patients &ith

kidney dys,unction are more susceptible to drug accumulation and lactic acidosis &ith these compounds/ 2hey should

there,ore be a%oided in patients &ith se%ere 7 K$/ "See N;et,ormin in the treatment o, adults &ith type $ diabetes

mellitusN/)

Sodium-glucose cotransporter-$ "SGL2-$) inhibitors J 2hese agents+ se%eral o, &hich ha%e been appro%ed ,or use

alone or in combination &ith others agents in the 3S+ including dapagli,loin+ canagli,loin+ and empagli,loin+ inhibit

glucose absorption in the proximal tubule+ causing glucosuria+ &eight loss+ and impro%ed glycemic control/ 3se o,

these medications is not recommended &ith an estimated glomerular ,iltration rate "eG>8) 4. to R mL?min?#/@

m$+ and they are contraindicated &ith eG>8 mL?min?#/@ m$+ including patients &ith ES8 &ho are on dialysis

KR(-@/ 2hese drugs ha%e also been implicated in causing diabetic ketoacidosis in indi%iduals &ith type # and type $


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diabetes K@#/ "See N;anagement o, persistent hyperglycemia in type $ diabetes mellitusN+ section on OSGL2$

inhibitorsO/)

5PP8I576 2I P8IBLE; P52*E=2S J Some diabetic patients ha%e persistent hyperglycemia+ se%ere

hyperglycemia+ diabetic ketoacidosis+ ,reMuent hypoglycemia+ or alternating episodes o, hyperglycemia and

hypoglycemia/

6yperglycemia J *nadeMuate insulin dose and noncompliance "&ith diet or the insulin regimen) are the most

common causes o, persistent hyperglycemia in diabetic dialysis patients "de,ined as an 6b5#c le%el CA percent) K@$/

5n additional problem is that micro%ascular disease can cause erratic absorption o, insulin ,rom the subcutaneous

tissue+ particularly i, the patient does not rotate in'ection sites K4#/ "See NGeneral principles o, insulin therapy in

diabetes mellitusN+ section on OSite o, in'ectionO/) 2he approach to these issues is the same ,or 7 patients as ,or

non-7 patients and is discussed else&here/ "See NGeneral principles o, insulin therapy in diabetes mellitusN+

section on Oeterminants o, insulin e,,icacyO and N;anagement o, persistent hyperglycemia in type $ diabetes

mellitusN+ section on O*ndications ,or a second agentO/)

Se%ere hyperglycemia and ketoacidosis J Se%ere hyperglycemia+ &ith serum glucose concentrations occasionally

C# mg?dL ".. mmol?L)+ may be obser%ed among dialysis patients &ith diabetes/ 3nlike those &ithout ES8+

ho&e%er+ hypo%olemia and marked hypernatremia do not occur+ since glucosuria is absent in anuric indi%iduals/ 2he

net e,,ect is minimal symptoms+ e%en among those &ith extreme hyperglycemia K@/

6o&e%er+ these patients may ha%e marked hyperkalemia due to potassium e,,lux ,rom cells in response to

extracellular ,luid hypertonicity+ as &ell as hyponatremia and acute intra%ascular %olume expansion K@4/ Patients &ith

type # diabetes may also de%elop diabetic ketoacidosis/

*nstead o, ,luid replacement+ management is principally dependent upon the administration o, lo& doses o,

intra%enous insulin "commonly beginning at a dose o, $ units?hour) K@/ 5s &ith nondialysis patients &ith se%ere

hyperglycemia and diabetic ketoacidosis+ serum glucose and potassium concentrations must be closely monitored/

"See Niabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: 2reatmentN+ section on O;onitoringO/)

6ypoglycemia J >reMuent or persistent hypoglycemia in diabetic dialysis patients is o,ten due to se%ere

underdialysis+ &ith poor calorie intake+ or occult disease+ such as in,ection or malignancy/ >reMuent ad'ustment o,insulin dose and e%aluation o, blood glucose diaries are essential in this setting+ as is pro%ision o, an adeMuate

dialysis dose "see NPrescribing and assessing adeMuate hemodialysisN and NPrescribing and assessing adeMuate

peritoneal dialysisN and NProtein intake in maintenance hemodialysis patientsN and N5ssessment o, nutritional status

in end-stage renal diseaseN)/ rugs that inter,ere &ith the counterregulatory response to hypoglycemia "such as beta

blockers) and long-acting insulin and oral agents should be discontinued+ i, possible+ until more stable glycemic

control &ithout hypoglycemia is achie%ed/

5lternating hypoglycemia and hyperglycemia J ES8 patients &ith diabetes o,ten ha%e gastroparesis K4#+ &hich

complicates the timing o, insulin in'ections/ Gastric-emptying studies &ill con,irm the diagnosis+ &hich can o,ten be

e,,ecti%ely treated &ith metoclopramide or bethanechol "urecholine) K4#/ *mpro%ement in glycemic control may also

impro%e gastric motility/ "See Niabetic autonomic neuropathy o, the gastrointestinal tractN+ section on

OGastroparesisO/)

Ither causes o, brittle blood glucose include patient misunderstanding o, the timing o, insulin in'ections+ poor

compliance &ith dietary restrictions and insulin therapy+ erratic eating habits+ and poor timing o, continuous

ambulatory peritoneal dialysis "75P) exchanges/ 2hese problems can o,ten be corrected &ith patient re-education/

=oncompliance+ impaired %ision+ and a depressi%e illness should also be sought/ "See N2he adult patient &ith brittle

diabetes mellitusN/)

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