DAFTAR ISI
BAB I PENDAHULUAN LATAR BELAKANG TUJUAN RUANG LINGKUP
BAB II TINJAUAN TEORI DEFINISI PATOFISIOLOGI PEMERIKSAAN PENUNJANG PENATALAKSANAAN PENATALAKSANAAN MEDIK DIAGNOSA KEPERAWATAN
BAB III TINJAUAN KASUS PENGKAJIAN DIAGNOSA KEPERAWATAN INTERVENSI IMPLEMENTASI EVALUASI
BAB IV PENUTUP KESIMPULAN SARAN DAFTAR PUSTAKA
1
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BAB I PENDAHULUAN
A.
Latar Belakang Sepsis adalah suatu sindroma radang sistemik yang ditandai dengan gejalagejala demam atau hipotermi, mengigil, takipnoe, takikardi, hipotensi, nadi cepat dan lemah serta gangguan mental yang disebabkan oleh infeksi mikroorganisme (Rasional 2002). Sepsis dapat disebabkan oleh infeksi bakteri gram negatif 70% (Pseudomas auriginosa, klebsiella, Enterobacter, echoli, proteus, neiseria). Infeksi bakteri gram positif 20-40% (stafilococus aureus, stretococus, pneumococus), infeksi jamur dan virus 2-3% (dengue hemoragic fever, herpes viruses), protozoa (malaria palcifarum). (Japardi,2002). Sepsis adalah suatu keadaan ketika mikroorganisme menginvasi tubuh menyebabkan penurunan perfusi organ dan disfungsi organ. Jika disertai hipotensi maka dinamakan syok sepsis (Linda D.U 2006). Sepsis adalah sindrom yang dikarakteristikkan oleh tanda-tanda klinis dan gejala-gejala yang parah yang dapat berkembang kearah septisema dan syok sepsis (Doenges, Maylyn 2000). Sepsis merupakan respon sistemik pejamu terhadap infeksi dimana patogen atau toksin dilepaskan ke dalam sirkulasi darah sehingga terjadi aktivasi proses inflamasi. Berbagai definisi sepsis telah diajukan, namun definisi yang saat ini digunakan di klinik adalah definisi yang ditetapkan dalam consensus American College of Chest Physician dan Society of Critical Care Medicine pada tahun 1992 yang mendefinisikan sepsis, sindroma respon inflamasi sistemik (systemic inflammatory response syndrome / SIRS), sepsis berat, dan syok/renjatan septik (Chen et.al,2009) .
B. Tujuan Presentasi 1. Tujuan Umum Agar dapat memberikan pemahaman tentang sepsis dan penanganannya. 2. Tujuan Khusus
Untuk memenuhi tugas pelatihan ICU Dewasa Diharapkan kita lebih memahami apa itu sepsis dan pemberian Asuhan Keperawatannya.
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C.
Ruang Lingkup Masalah
Makalah ini berisikan tentang Definisi, Fisiologi, Patofisiologi, Etiologi masalah, Pemeriksaan penunjang, Penatalaksanaan Medik, Pengkajian, Masalah Keperawatan, Rencana Tindakan, dan Evaluasi juga kesimpulan. Dari uraian diatas dan banyaknya kasus pasien dengan Sepsis yang sering dirawat diruang ICU, maka kami membahas masalah dengan kasus Sepsis dan penatalaksanaan asuhan keperawatan pada pasien Sepsis.
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BAB II TINJAUAN TEORI
A. Defisnisi Sepsis adalah suatu keadaan ketika mikroorganisme menginvasi tubuh dan menyebabkan penurunan perfusi organ dan disfungsi organ. Jika disertai hipotensi maka dinamakan syok sepsis (lindaa D.U 2006). Sepsis adalah sindroma yang dikarakteristikan oleh tanda-tanda klinis dan gejalagejala infeksi yang parah yang dapat berkembang kearah septisemia dan syok septik (Doenges,Marylyn E,2000) Sepsis adalah suatu sindroma radang sistemik yang ditandai dengan gejala- gejala demam atau hipotermi, menggigil,takipnea, takikardia,hipotensi, nadi cepat dan lemah serta gangguan mental yang disebabkan oleh infeksi mikroorganisme (rasional,2002). Sampai saat ini sepsis masih merupakan salah satu penyakit infeksi yang mortalitas dan morbilitas tinggi. Di amerika serikat, kurang lebih 750.000 orang menderita sepsis setiap tahunnya dan lebih dari 210.000 210.000 orang diantaranya meninggal dunia. Di indonesia, indonesia, penyakit ini juga banyak di jumpai pada penderita rawat inap di rumah sakit dan secara keseluruhan lebih dari 25% penderita sepsis meninggal (rasional,2002) Sepsis dapat di sebabkan oleh infeksi bakteri gram negatif 70% (pseudomonas, auriginosa, klebsiella, enterobakter, echoli, proteus, neiseria). Infeksi bakteri gram positif 20-40% (stafilokokus aureus, stretokokus, pnemokokus), infeksi jamur dan virus 2-3% (dengue hemorrhagic fever, herpes viruses) protozoa (malaria falsiparum) (japardi,2002). - Derajat sepsis: 1. Systemic inflamantory response syndrom (SIRS) Inflamasi yang meluas dengan indikasi disertai 2 ata u lebih dari gejala dibawah:
Temperature > 38’C 38’C atau < 36’C
HR > 90/menit
RR > 20/min atau PCO² low
WBC >12x 10 gram
2. Sepsis Hadirnya gejala sirs dan adanya definitif infeksi dari hasil kultur.
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3. Severe sepsis Jika muncul organ disfungsi, hipoperfusi atau hipotensi, laktat asidosis,oliguria dan gangguan alat status mental. Jika pasien hipotensi metabolisme anaerob terjadi karena kurangnya oksigen untuk menghasilkan energi, oliguria disebabkan karena perfusi kurang keginjal maka MAP kurang. 4. Septic shock Septic shock dengan hipotensi tidak mencukupinya fluid replacement seperti hipoperfusi,oliguria, lactat asidosis, gangguan alat status mental, pasi en membutuhkan inotropik atau vasopresure dan pemberian cairan. Gambaran khusus syock sepsis karena terdapat banyak jenis syok septik, maka sulit menggolongkan keadaan tersebut. Beberapa gejala antara lain:
Demam tinggi Seringkali vasodilatasi nyata diseluruh tubuh terutama pada jaringan yang terinfeksi Curah jantung yang tinggi pada sekitar separuh penderita, disebsbkan oleh adanya vasodilatasi jaringan yang terinfeksi dan oleh derajat metabolik yang tinggi dan vasodilatasi ditempat lain dalam tubuh, akibat dari rangsangan toksin bakteri terhadap metabolisme sel dan dari suhu s uhu tubuh yang tinggi. Melambatnya aliran darah, mungkin disebabkan oleh aglutinasi sel darah merah sebagai respon terhadap jaringan yang mengalami degenerasi. Pembentukan bekuan kecil di daerah yang luas dalam tubuh, keadaan yang disebut koagulasi intravaskular menyebar. Hal ini juga menyebabkan faktorfaktor pembekuan menjadi habis terpakai sehingga timbul perdarahan dibanyak jaringan, terutama dinding usus dan traktus intestinal.
5. MODS Terjadi akibat danya fungsi organ secara akut seperti hemeostasis yang harus di intervensi
B. Patofisiologi Pasien dengan sepsis mengalami imunosupresi, termasuk kehilangan atau terhambatnya hipersensitifitas, kemampuan membersihkan infeksi, dan sebagai predosposisi terhadap infeksi nosokomial. Satu alasan kegagalan dari strategianti inflamasi pada pasien sepsis adalah perubahan sindroma dari waktu ke waktu. Awalnya sepsis mempunyai karakteristik dengan meningkatnya mediator inflamasi, tetapi bila sepsis menetap, terjadi pergeseran pada keadaan imonosepresif. Terdapat bukti bahwa imonosupresi pada sepsis memperlihatkan bahwa darah yang distimulasi oleh
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mengurangi kadar sel B, T sel CD4 dan sel-sel dendriticfolicular. Kehilangan limfosit dan sel-sel dendrit sangat penting karena hal ini dapat mengancam jiwa. Sistem komplemen yang sudah diaktifkan akan merangsang netrofil untuk saling mengikat dan menempel ke endotel vaskuler, akhirnya dilepaskan derivat asam arakhidonat, enzim lisosom superoksida radikal, sehingga memberikan efek vasoaktif lokal pada mikrovaskuler yang mengakibatkan terjadi kebocoran vaskuler. Disamping itu sistem komplemen yang sudah aktif dapat secara langsung menimbulkan meningkatnya efek kemotaksis, superoksida radikal, enzim lisosom. LBP-LPS monosit kompleks dapat mengaktifkan cytokines, kemudian cytokines akan merangsang neotrofil atau sel endotel, sel endotel akan mengaktifkan faktor jaringan PARASIT-INH-I. Sehingga dapat mengakibatkan vasodilatasi pembuluh darah dan DIC. Cytokines dapat secara langsung dapat menimbulkan demam, perubahan- perubahan metabolik dan perubahan hormonal. Faktor XII (hageman faktor) akan diaktivasi oleh peptidoglikan dan asam teikot yang terdapat pada dinding bakteri gram positif. Faktor XII yang sudah aktif akan meningkatkan pemakaian faktor koagulasi sehingga terjadi disseminated intravaskular coagulation (DIC). Faktor XII yang yang sudah aktif akan merubah prekallikrein hipotensive agent yang potensial bradikinin, bradikinin akan menyebabkan vasodilatasi pembuluh darah. Terjadinya kebocoran kapiler, akumulasi netrofil dan perubahan-perubahan metabolik, perubahan hormonal, vasodilatasi, DIC akan menimbulkan sindroma sepsis. Hipotensi respiratory distress syndrome, multiple organ failure akhirnya kematian (japardi,2002).
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C. Patoflow
Invasi Mikroorganisme
Melepaskan Toksin
Penumpukan Sekret Ketidakefektifan jalan nafas
Pelepasan Mediator (Prostaglandin, Kinin, Histamin, dan Endorphine)
Efek Vaskuler Peripheal
Vasodilatasi/ Vasokontriksi
Tekanan Sirkulasi darah
Efek Miokardial
Permeabilitas Kapiler meningkat
Penurunan Kontraktilitas Jantung
Maldistribusi Sirkulasi Darah
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D. Etiologi Masalah Mayoritas dari kasus-kasus sepsis disebabkan oleh infeksi-infeksi bakteri gram negatif(-) dengan presentase60-70% kasus, beberapa disebabkan oleh infeksi-infeksi jamur, dan sangat jarang disebabkan oleh penyebeb-penyebeb lain dari infeksi atau agenagen yang mungkin menyebabkan SIRS. Agen-agen infeksius, biasanya bakteri-bakteri, mulai menginfeksi hampir segala lokasi organ atau alat-alat yang ditanam (contohnya: kulit, paru, saluran pencernaan, tempat operasi, kateter intravena,dll.). Agen-agen yang menginfeksi atau racun-racun mereka ( atau kedua-duanya) kemudian menyebar secara langsung atau tidak langsung kedalam aliran darah. Ini mengizinkan mereka untuk menyebar kehampir segala sistem organ lain. Kriteria SIRS berakibat ketika tubuh mencoba untuk melawan kerusakan yang dilakukan oleh agen-agen yang dialirkan darah ini. Sepsis sampai syok septik secara klasik telah diakui penyebabnya adalah bakteri gram negatif, tetapi mungkin juga disebabkan oleh mikroorganisme lain,gram positif, jamur, virus bahkan parasit. Timbulnya syok septik dan acute respiratoty distress syndrome (ARDS) sangat penting pada bakterimia gram negatif. Syok terjadi pada 20-35% penderita bakteriagram negatif (john,1994).
Bakteri gram negatif yang sering menyebabkan sepsis adalah E.coli, klebsiella Sp. Pseudomonas Sp, Bakterides Sp, dan proteus Sp. Bakteri gram negative mengandung liposakarida pada dinding selnya yang disebut endotoksin. Apabila dilepaskan dan masuk kedalam aliran darah, endotoksin dapat menyebabkan berbagai perubahan biokimia yang merugikan dan mengaktivasi imun dan mediator biologis lainnya yang menunjang timbulnya syock sepsis. Organisme gran positif yang sering menyebabkan sepsis adalah staphilococus, stretococcus dan pnemococcus. Organisme gram positif melepaskan endotoksin yang berkemampuan menggerakkan mediator imun dengan cara yang sama dengan endotoksin.
E. Pemeriksaan Penunjang
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7. Fibrinogen ↑ 8. Platelet ↑ 9. CRP ↑ (C ↑ (C reaktive protein ) TNF dan interleukin stimulasi hepar melepas CRP. 10. PCT ↑ (procalsitonin) biomarker cascade cytokines 11. Kultur (lika, sputum,urine, darah ) yaitu untuk mengidentifikasi organisme penyebab sepsis. Sensitifitas menentukan pilihan obat yang paling efektif. 12. SDR : Ht mungkin meningkat pada kasus hopovolemik karena hemokonsentrasi. Leucopenia ( penurunan SDB) terjadi sebelumnya, diikuti oleh pengulangan leukositosis (1500-30000) dengan peningkatan pita (berpindah kekiri) yang mengindikasikan produksi SDP tidak matur dalam jumlah besar. 13. Elektrolit serum : berbagai ketidak seimbangan mungkin terjadi dan menyebabkan asidosis, perpindahan cairan dan perubahan fungsi ginjal. 14. Trombosit : penurunan kadar dapat terjadi karena agregasi trombosit 15. PT/APTT : mungkin memanjang mengidentifikasikan koagulopati yang diasosiasikan dengan hati/ sirkulasi toksin/ status syok. 16. Laktat serum > 2 meq : meningkat dalam asidosis metabolik, disfungsi hati, syok 17. Glukosa serum : hiperglikemi yang terjadi menunjukkan glikoneogenesis dan glikonolisis didalam hati sebagai respon dari puasa/ perubahan seluler dalam metabolisme 18. BUN/Kreatinin : peningkatan kadar diasosiasikan dengan dehidrasi, ketidakseimbangan atau kegagalan ginjal, dan disfungsi atau kegagalan hati. 19. GDA : alkalosis respiratorik dan hipoksemia dapat terjadi sebelumnya dalam tahap lanjut hipoksemia, asidosis respiratorik dan asidosis metabolik terjadi karena kegagalan metabolisme kompensasi. 20. EKG : dapat menunjukkan segmen ST dan gelombang T dan distritmia menyerupai infark miokard
F. Penatalaksanaan medik Penatalaksanaan sepsis yang optimal mencakup eliminasi petogen penyebab infeksi, mengontrol sumber infeksi dengan tindakan drainase atau bedah bila diperlukan, terapi antimikroba yang sesuai, resusitasi bila terjadi kegagalan organ atau renjatan.vasopresor
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3. Steroid Kortokosteroid intravena ( hydrocortisone 200-300 mg/hari, selama & hari dalam 3-4 kali pemberian atau dengan drip infus direkomendasikan untuk pasien syok sepsis. 4. Recombinant human acticuted protein (rhAPC) rhAPC direkomendasikan pada pasien dengan resiko kematian ( multiple organ failure, septik syok, ARDS). rhAPC suatu anti koagulan endogen dengan sifat anti inflamasi memperlihatkan perbaikan suvival pada pasien sepsis dengan disfungsi organ. Antibiotik- antibiotik yang tepat untuk merawat sepsis adalah kombinasi-kombinasi dari dua atau tiga antibiotik-antibiotik yang diberikan pada saat yang sama kebanyakan kombinasi-kombinasi biasanya termasuk vancomycin untuk merawat banyak infeksi-infeksi MARS. Bagaimanapun, sekali organisme yang menginfeksi diisolir, laboratorium-laboratorium dapat menentukan antibiotik-anttibiotik mana paling efektif melawan organisme-organisme, dan antibiotik-antibiotik itu harus digunakan untuk merawat pasien sebagai tambahan pada antibiotik-antibiotik, dua intervens-intervensi therapeutik utama lain, dukungan sistem organ dan operasi, mungkin diperlukan. 5. Resusitasi Mencakup tindakan airway (A), breathing (B), circulation (C) (C) dengan oksigenasi, terapi cairan (kristaloid dan/koloid), vasopresor/inotropik, dan tranfusi bila diperlukan tujuan resusitasi pasien dengan sepsis berat atau yang mengalami hipoperfusi dalam 6 jam pertama adalah CVP 8-12 8-12 mmHg, MAP ≥65 mmHg, urine ≥ 0.5 ml/kg/jam dan saturasi oksigen ≥70% ≥70% dengan resusitasi cairan dan CVP>8-12 mmHg, maka dilakukan tranfusi PRC untuk mencapai hematokrit ≥30% ≥ 30% dan atau pemberian dobutamin (sampai maksimal 20meq/kg/menit). 6. Eliminasi sumber infeksi Tujuan: menghilangkan patogen penyebab, oleh karena antibiotik pada umumnya tidak mencapai sumber infeksi seperti abses, viskus yang mengalami obstruksi dan implan prostesis yang terinfeksi. Tindakan ini dilakukan secepat mungkin mengikuti resusitasi yang adekuat. 7. Terapi antimikroba Merupakan modalitas yang sangat penting dalam pengobatan sepsis. Terapi antibiotik
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8. Terapi suportif Oksigenasi Pada keadaan hipoksemia berat dan gagal nafas bila disertai dengan penurunan kesadaran atau kerja ventilasi yang berat, ventilasi mekanik segera dilakukan. Terapi cairan a. Hipovolemia harus segera diatasi dengan cairan kristaloid (NaCL 0.9% atau ringer laktat) maupun koloid. b. Pada keadaan albumin rendah (<2 g/dL) disertai tekanan hidrostatik melebihi tekanan onkotik plasma, koreksi albumin perlu diberikan. c. Tranfusi PRC diperlukan pada keadaan perdarahan aktif atau bila kadar Hb rendah pada kondisi tertentu, sepsis pada iskemia miokard dan renjatan septik. Kadar Hb yang akan dicapai pada sepsis masih kontroversi antara 8-10 g/dL.
Vasopresor dan inoprotik Sebaiknya diberikan setelah keadaan hipovolemik teratasi dengan pemberian cairan adekuat, akan tetapi pasien masih hipotensi. Vasopresor diberikan mulai dosis rendah dan dinaikan (titrasi) untuk mencapai MAP 60 mmHg atau tekanan darah sistolik 90mmHg. dapat dipakai dopamin >8µg/menit,norepinefrin 0.031.5µg/kg/menit,phenylepherine 1.5µg/kg/menit,phenylepherine 0.5-8µg/kg/menit atau epinefrin 0.1-0.5µg/kg/menit atau fosfodieterase inhibitor (amrinone dan milrinone). 9. Bikarbonat Secara empirik bikarbonat diberikan bila pH <7.2 atau serum bikarbonat <9mEq/L dengan disertaiupaya untuk memperbaiki keadaan hemodinamik. 10. Disfungsi renal Akibat gangguan perfusi organ. Bila pasien hipovolemik/hipotensi, segera diperbaiki degan pemberian cairan adekuat,vasopresor dan inotropik bila diperlukan.dopamin dosis renal (1-3µg/kg/menit) seringkali diberikan untuk mengatasi gangguan fungsi ginjal pada sepsis, namun secara evidence based belum terbukti. Sebagai terapi pengganti gagal ginjal akut dapat dilakukan hemodialisis maupun hemofiltrasi kontinue. 11. Nutrisi
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sepsis berat dan renjatan, terjadi penurunan aktivitas antikoagulan dan spresi proses fibrinolisis sehingga mikrotrombus menumpuk di sirkulasi mengakibatkan kegagalan organ. Terapi antikoagulan, berupa heparin, antitrombin dan subsitusi faktor pembekuan bila diperlukan dapat diberikan, diberikan, terapi terbukti menurunkan mortalitas. 14. Kortikosteroid Hanya diberikan dengan indikasi insufisiensi adrenal. Hidrokortison dengan dosis 50 mg bolus IV 4x/hari selama 7 hari pada pasien renjatan septik menunjukan penurunan mortalitas dibandingkan kontrol. Keadaan tanpa syok, kortikosteroid sebaiknya tidak diberikan dalam terapi sepsis.
G. Pengkajian 1. Riwayat kesehatan
Riwayat masa lalu, riwayat penyakit kronik
Acute illness ( trauma burns)
Luka Riwayat kesehatan keluarga Riwayat sosial Medikasi Nutrisi Pengkajian fisik
2. 3. 4. 5. 6.
Inspeksi, palpasi, perkusi, auskultasi
Monitoring suhu, nadi, RR, TD
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Circulation
Kaji denyut jantung > 100 kali permenit merupakan tanda signifikan
Monitoring tekanan darah
Periksa waktu pengisisan kapiler
Pasang infus menggunakan kanul yang besar
Berikan cairan koloid atau haemacel
Lakukan pemeriksaan darah lengkap
Siapkan untuk pemeriksaan kultur
Catat temperature, kemungkinan pasien pyreksia atau temperature < 36ºC
Siapkan pemeriksaan urin dan sputum
Berikan antibiotic spectrum luas sesuai kebijakan dokter
Disability
Bingung merupakan sala satu tanda pertama pada pasien sepsis padahal sebelumnya tidak ada masalah. Kaji tingkat kesadaran menggunakan AVPU Exposure jika sumber s umber infeksi tidak diketahui, cari adanya cidera, luka dan tempat suntikan s untikan dan tempat infeksi lainnya. Tanda ancaman kehidupan Sepsis berat diidentifikasikan sebagai sepsis yang menyebabkan kegagalan fungsi organ, jika sudah menyebabkan ancaman kehidupan maka pasien harus dibawa keruang ICU,adapun indikasi sebagai berikut
Penurunan fungsi ginjal
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6. Gangguan kebersihan jalan nafas berhubungan peningkatan sekret akibat adanya penumpukan sekter 7. Pola nafas tidak efektif berhubungan dengan kelemahan otot bantu nafas 8. Ketidakseimbangan nutrisi, kurang dari kebutuhan tubuh berhubungan dengan peningkatan metabolisme 9. Kurang pengetahuan, mengenai penyakit, prognosis dan kebutuhan pengobatan dapat dihubungkan dengan kurangnya pemajanan/meningkat, kesalahan interprestasi informasi, keterbatasan kognitif.
I. Intervensi 1. Penurunan cardiac output berhubungan dengan penurunan afterlod, penurunan preload, ketidak efektifan kontraktilitas otot jantung. Hal yang diharapkan /kriteria evaluasi: penurunan cardiac output tidak terjadi yang dibuktikan dengan tanda-tanda vital stabi, nadi verifer jela, kulit hangat, tingkat kesadaran umum. Tindakan/intervensi: a. Observasi tanda-tanda vital Rasional Untuk mengetahui perubahan hemodinamik, ada atau tidaknya penurunan cardiac output. b. Pantau frekuensi dan irama jantung, perhatikan distritmia Rasional
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Penurunan pengeluaran urin dengan peningkatan berat jenis akan mengindikasikan penurunan perfungsi ginjal yang di hubungkan dengan perpindahan cairan dan vasokontriksi selektif, terdapat te rdapat kemungkinan munculnya poliuria sementara selama fase hiperdinamik ( dalam waktu curah jantung meningkat) tetapi dapat menyebabkan perkembanagan ke arah oliguri. f. Kolaborasi Berikan cairan parenteral. (rujuk pada DK: kekurangan volume cairan, resiko tinggi terhadap) Rasional Untuk mempertahankan perfusi jaringan, sejumlah besar cairan mungkin dibutuhkan untuk mendukung volume sirkulasi. Diuresis Rasional Untuk mengurangi kerja jantung akibat adanya penurunan fungsi ginjal. g. Pantau pemeriksaan laboratorium,misalnya AGD, kadar laktat Rasional Perkembangan asidosis respirstorik/metabolik merefleksikan kehilangan mekanisme kompensasi, misalnya misalnya penurunan perfusi ginjal/ekskresi ginjal/ekskresi hidrogen, dan akumulasi asam laktat. 2. Gangguan perfusi jaringan berhubungan dengan cardiac output yang tidak mencukupi. Hasil yang diharapkan/kriteria evaluasi: menunjukan perfusi jaringan nadi yang kuat yang dibuktikan dengan tanda-tanda vital stabil, nadi verifer jelas, kulit hangat dan kering, tingkat kesadran umum haluaran urin sesuai dan bising usus aktif.
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d. Perhatikan kualitas/kekuatan denyut perifer Rasional Pada awal nadi cepat/kuat karena peningkatan curah jantung. Nadi dapat menjadi lemah/lambat karena hipotensiterus menerus, penurunan curah jantung,dan vasokonstriksi perifer jika terjadi syok. e. Kaji frekuensi pernapasan, kedalaman, dan kualitasperhatiakan dispenea berat. Rasional Peningkatan pernapasan terjadi sebagai respons terhadap efek-efek langsung dari endotoksin pada pusat pernafasan di dalam otak, dan juga perkembangan hipoksia, stres dan demam. Pernafasan bisa jadi dangakal bila terjadi insufisiensi pernafasan, menimbulkan resiko kegagalan pernafasan akut. f. Catat haluan urine setiap jam dan berat jenisnya. jenisn ya. Rasional Penurunan haluan urine dengan peningkatan berat jenis akan mengindikasikan penurunan perfungsi ginjal yang di hubungan dengan perpindahan cairan dan vasokonstriksi selektif, terdapat kemungkinan munculnya poliuria sementara selama fase hiperdinamik (dalam waktu curah jantung meningkat) tetapi dapat menyebabkan perkembangan ke arah oliguri. g. Kolaborasi Berikan cairan parenteral. Rujuk pada DK: kekurangan kekurangan pada volume volume cairan, resiko tinggi terhadap) Rasional Untuk mempertahankan perfusi jaringan, sejumlah besar cairan mungkin di butuhkan untuk mendukung volume volume sirkulasi.
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Suhu ruangan / jumlah selimut harus di ubah untuk mempertahankan suhu mendekati normal c. Berikan kompres hangat hindari penggunaan alkohol. Rasional Dapat membantu mengurangi demam.catatan:penggunaan air es/alkohol mungkin menyebabkan kedinginan, peningkatan suhu secara aktual, selain itu alkohol dapat mengeringkan kulit. d. Kolaborasi i. Berikan anti piretik misalnya aspirin, asitaminofen ii. Rasional iii. Di gunakan untuk mengurangi demam dengan aksi sentralnya pada hipotalamus iv. Berikan selimut pendingin v. Rasional vi. Di gunaka gunaka untuk mengurangi mengurangi demam umumnya lebih besar dari 39-40 derajat selcius pada waktu terjadi kerusakan/gangguan pada otak. Kekurangan volume cairan, resiko tinggi terhadap permeabilitas kapiler/kebocoran
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d. Kaji membran mukosa kering, turgor kulit yang kurang baik, dan rasa haus. Rasional Hipovolemia/cairan runang ketiga akan memperkuat tanda-tanda dehidrasi e. Amati edema dependen/perifer pada sakrum,skrotum, pungggung kaki Rasional Kehilangan cairan dari kompartemen vaskuler kedalam ruang intertitial akan menyebabkan edema jaringan f. Kolaborasi Berikan cairan IV, misalnya kristaloid (D5W,NS) dan koloid (albumin, plasma beku segar) sesuai indikasi Rasional Sejumlah cairan mungkin dibutuhkan untuk mengatasi hipovolemia relatif (vasodilatasi perifer) : menggantikan kehilangan dengan meningkatkan permeabilitas kapiler ( misalnya mis alnya penumpukan cairan dalam rongga peritoneal) dan meningkatkan sumber-sumber tatalaksana (misalnya demam/diaforesis) g. Pantau nilai laboratorium, misalnya Ht/jumlah SDM, BUN,/Kr Rasional
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Menunjukan oksigen sistemik tidak adekuat/hipoksemia e. Catat batuk dan produksi sputum purule Rasional Pnemonia merupakan infeksi nosokomial umum yang dapat terjadi karena aspirasi organisme orofaringeal atau menyebar dari lokasi lain f. Kolaborasi Pantau AGD/nadi oksimetri Rasional Hipoksemia dihubungkan dengan penurunan ventilasi/perubahan pulmonal (misalnya edema intertisial, atelektasis, dan paru pulmonal) dan peningkatan kebutuhan (misalnya demam) Tinjau sinar X dada Rasional Perubahan menunjukan perkembangan/resolusi dari komplikasi pulmonal, misalnya infiltrasi/ edema. Gangguan bersihan jalan nafas berhubungan ber hubungan dengan penumpukan sekret
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Memulai perubahan gaya hidup yang di perlukan, ikut serta dalam program pengobatan. Tindakan/intervensi a. Tinjauan proses penyakit dan harapan masa depan Rasional Memberikan pengetahuan dasar dimana pasien dapat membuat pilihan. b. Tinjau faktor resiko individual dan bentuk penularan/tempat masuk infeksi. Rasional Terapi glukortikoid, disfungsi ginjal/hati, penyakit neoplastik, penyakit jantung rematik dan DM dapat mencetuskan septisemia. Menyadari terhadap bagaimana infeksi ditularkan akan memberikan informasi untuk merencanakan/melakukan tindakan protektif. c. Berikan informasi mengenai terapi obat-obatan,interaksi, efek samping, dan pentingnya ketaatan pada program
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BAB III TINJAUAN KASUS
A. PENGKAJIAN 1. IDENTITAS KLIEN Nama Umur No. MR Tgl masuk Tgl pengkajian Penanggung Jawab Status Pernikahan
: Tn. H : 58 tahun : 4144330 : 29/11/2016 : 30/11/2016 : BPJS : Menikah
2. RIWAYAT KESEHATAN KLIEN
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c. Circulation TD: 93/61 mmHg (dengan topangan norephineprin 0.07mcg/KgBB/Jam), Nadi: 105 x/menit, MAP 69, Suhu: 37 C, BB: 49 Kg, Terpasang CVC +7, DC terpasang, produksi urin 1.224/24 jam, BK : -254.6, Hb: 9.5 g/dl, Ht: Ht: 29.7%, Erit: 4.13, Leukosit: 20.600/ul, Trombosit: 504.000 ul, Na/K/CL: 125/3.54/91.1, Ur/Cr : 19/0.20, Laktat: 1.2, PCT :0.16, Albumin : 2.92, GDS : 135 g/dl d. Disability
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Data Penunjang - Hasil Laboratorium Tgl 30/11/2016 Hb 9.5 pH Ht 29.7 PCO2 Eritrosit 4.13 PaO2 Leukosit 20.600 BE Trombosit 504.000 HCO3 Ureum/ creatinin 19/0.20 SaO2 PT/APTT 0.9/1.07 SvO2
7.49 30.9 110.5 0.4 23.9 99.6
7.40 47.4 50.8 4.7 29.7 85.3
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3. Analisa Data No. Data Fokus Masalah Etiologi 1 DS :Ketidak efektifan Penumpukan DO : bersihan jalan nafas sekret K/u lemah, kesadaran DPO dengan midazolam 1mg/jam,
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3
DS : DO :
Gangguan jaringan TD 93/61mmHg (dengan Norephineprin 0.07
:
perfusi berhubungan dengan cardiac output yang tidak mencukupi
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C. INTERVENSI KEPERAWATAN
No.
Hari/ Tgl/ Jam
1
Rabu, 30/11/16
Diagnosa Keperawat an Ketidak efektifan bersihan
Rencana Tujuan dan Kriteria Hasil -Tujuan: Setelah diberikan
Rencana Tindakan
Rasional
Mandiri 1.Observasi
1.Untuk
Par af
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