BAB I PENDAHULUAN A. Latar Belakang
Stroke merupakan penyakit atau gangguan fungsional otak berupa kelumpuhan saraf (deficit neurologic) akibat terhambatnya aliran darah ke otak. Stroke adalah sindrom yang terdiri dari tanda dan/atau gejala hilangnya fungsi sistem saraf pusat fokal (atau global) yang berkembang cepat (dalam detik atau menit). Gejala-gejala ini berlangsung lebih dari 24 jam atau menyebabkan kematian, selain menyebabkan kematian stroke juga akan mengakibatkan dampak untuk kehidupan. Dampak stroke diantaranya, ingatan jadi terganggu dan terjadi penurunan daya ingat, menurunkan kualitas hidup penderita juga kehidupan keluarga dan orang-orang di sekelilingnya, mengalami penurunan kualitas hidup yang lebih drastis, kecacatan fisik maupun mental pada usia produktif dan usia lanjut dan kematian dalam waktu singkat (Junaidi, 2011). Penyakit stroke juga menjadi penyebab kematian utama hampir seluruh Rumah Sakit di Indonesia dengan angka kematian sekitar 15,4%. Tahun 2007 prevalensinya berkisar pada angka 8,3% sementara pada tahun 2013 meningkat menjadi 12,1%. Jadi, sebanyak 57,9% penyakit stroke telah terdiagnosis oleh tenaga kesehatan (nakes). Berbagai hasil penelitian diatas, faktor risiko stroke pada usia muda itu tidak jauh berbeda, seperti riwayat stroke pada keluarga, merokok, hipertensi, diabetes melitus dan aktivitas fisik serta tingkat stres hampir ada di setiap peneliti Dalam penelitian ini peneliti ingin melihat faktor risiko jenis kelamin, riwayat stroke pada keluarga, obesitas, merokok, hipertensi, diabetes melitus, aktivitas fisik dan tingkat stress. Selama ini masyarakat sering mengobati penyakit ini dengan obat-obatan medis yang diberikan oleh dokter, akan tetapi stroke juga bisa di sembuhkan dan menghilangkan gejala stroke dengan bekam.
B. Rumusan Masalah
Berdasarkan uraian masalah latar belakang diatas dapat dirumuskan masalah sebagai berikut : 1. Anatomi fisiologi organ stroke ? 2. Apa definisi stroke ? 3. Apa penyebab stroke ? 1
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4. Apa saja macam-macam stroke? 5. Bagaimana proses terjadinya stroke? 6. Apa saja tanda gejala stroke? 7. Bagaimana cara penatalaksaan stroke ? 8. Bagaimana Asuhan keperawatan pada stroke?
C. Tujuan 1. Tujuan umum
Untuk memenuhi tugas keperawatan kompelmenter 2. Tujuan khusus
Untuk mengetahui konsep stroke dan therapy bekam pada stroke D. Manfaat 1. Bagi mahasiswa
Manfaat makalah ini bagi siswa,baik penyusun maupun pembaca adalah untuk menambah wawasan terhadap seluk beluk tentang stroke 2. Bagi institusi
Makalah ini bagi institusi pendidikan kesehatan adalah sebagai tambahan referensi untuk menguji mahasiswa atau mahasiswinya tentang stroke 3. Bagimasyarakat
Makalah ini bagi masyarakat adalah sebagai penambah wawasan tentang stroke
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BAB II PEMBAHASAN
A. ANATOMI FISIOLOGI
Otak adalah alat tubuh yang sangat penting karena merupakan pusat computer dari semua alat tubuh. Bagia dari saraf sentral yang yang terletak didalam rongga tengkorak (cranium) dibungkus oleh selaput otak yang kuat. Otak terletak dalam rongga cranium berkembang darisebuah tabung yang mulanya memperlihatkan tiga gejala pembesaran otak awal (Pearce, 2013). a. Otak depan menjadi hemifer serebri, korpus striatum, thalamus, serta hipotalamus. b. Otak tengah, trigeminus, korpus callosum, korpus kuadrigeminus. c. Otak belakang, menjadi pons varoli, medulla oblongata, dan serebellum. Fisura dan sulkus membagi hemifer otak menjadi beberapa daerah. Korteks serebri terlibat secara tidur teratur. Lekukan diantara gulungan serebri disebut sulkus. Sulkus yang paling dalam membentuk fisura longitudinal dan lateralis. Daerah atau lobus letaknya
sesuai
dengan
tulang
yang
berada
di
atasnya
(lobus
frontalis,
temporalis,oarientalisdan oksipitalis)(Pearce, 2013). Fisura longitudinalis merupakan celah dalam pada bidang media laterali memisahkan lobus temparalis dari lobus frontalis sebelah anterior dan lobus parientalis sebelah posterior. Sulkus sentralis juga memisahkan lobus frontalis juga memisahkan lobus frontalis dan lobus parientalis. Adapun bagian-bagian otak meluputi(Pearce, 2013). : a. Cerebrum Cerebrum (otak besar) merupakan bagian terbesar dan terluas dari otak,
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lapisan kelabu (zat kelabu) yaitu pada bagian korteks serebral dan zat putig terdapat pada bagian dalam yang mengndung mengndung serabut syaraf(Pearce, 2013). Pada otak besar ditemukan beberapa lobus yaitu(Pearce, 2013) : a) Lobus frontalis adalah bagian dari serebrum yang terletak dibagian sulkus sentralis. b) Lobus parientalis terdapat didepan sulkus sentralis dan dibelakang oleh korako oksipitalis. c) Lobus temporalis terdapat dibawah lateral dan fisura serebralis dan didepan lobus oksipitalis. d) Oksipitalisyang mengisi bagian belakang dari serebrum. Korteks
serebri
terdiri
dari
atas
banyak
lapisan
sel
saraf
yang
merupakan.ubstansi kelabu serebrum. Korteks serebri ini tersusun dalam banyak gulungan-gulungan dan lipatan yang tidak teratur, dan dengan demikian menambah daerah permukaan korteks serebri, persis sama seperti melipat sebuah benda yang justru memperpanjang jarak sampai titik ujung yang sebenarnya. Korteks serebri selain dibagi dalam lobus juga dibagi menurut fungsi dan banyaknya area. Secara umum korteks dibagi menjadi empat bagian (Pearce, 2013) : a) Korteks sensori, pusat sensasi umum primer suatu hemisfer serebri yang mengurus bagian badan, luas daerah korteks yang menangani suatu alat atau bagian tubuh tergantung ada fungsi alat yang bersangkutan. Korteks sensori bagian fisura lateralis menangani bagian tubuh bilateral lebih dominan. b) Korteks asosiasi. Tiap indra manusia, korteks asosiasi sendiri merupakan kemampuan otak manusia dalam bidang intelektual, ingatan, berpikir, rangsangan yang diterima diolah dan disimpan serta dihubungkan dengan data yang lain. Bagian anterior lobus temporalis mmpunyai hubungan dengan fungsi luhur dan disebut psikokortek. c) Kortekes motorik menerima impuls dari korteks sensoris, fungsi utamanya adalah kontribusi pada taktus piramidalis yang mengatur bagian tubuh kontralateral. d) Korteks pre-frontal terletak pada lobus frontalis berhubungan dengan sikap mental dan kepribadian.
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b. Batang Otak
Batang otak terdiri dari 3 bagian yaitu (Pearce, 2013) : a) Diensephalon Diensephalon merupakan bagian atas batang otak. yang terdapat diantara serebelum dengan mesensefalon. Kumpulan dari sel saraf yang terdapat di bagian depan lobus temporalis terdapat kapsul interna dengan sudut menghadap kesamping. Fungsi dari diensephalon yaitu (Pearce, 2013) : 1) Vasokonstriktor, mengeclkan pembuluh darah 2) Respirator, membantu proses pernafasan 3) Mengontrol kegiatan refleks 4) Membantu kerja jantung Mesensefalon, atap dari mesensefalon terdiri dari empat bagian yang menonjol keatas. Dua disebelah atas disebut korpus kuadrigeminus superior dan dua sebelah bawah selaput korpus kuadrigeminus inferior. Serat nervus toklearis berjalan ke arah dorsal menyilang garis tengah ke sisi lain. Fungsi dari mesenphalon yaitu(Pearce, 2013) : 1) Membantu pergerakan mata dan mengangkat kelopak mata. 2) Memutar mata dan pusat pergerakan mata. b) Pons Varolli Pons varoli barikum pantis yang menghubungkan mesensefalon dengan pons varoli dan dengan serebelum, terletak didepan serebelum diantara otak tengah dan medulla oblongata. Disini terdapat premoktosid yang mengatur gerakan
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2) Pusat saraf nervus trigeminus. c) Medula Oblongata Medulla oblongata merupakan bagian dari batang otak yang paling bawah yang menghubungkan pons varoli dengan medula spinalis. Bagian bawah medulla oblongata merupakan persambungan medulla spinalis ke atas, bagian atas medulla oblongata yang melebar disebut kanalis sentralis di daerag tengah bagian ventral medulla oblongata(Pearce, 2013). Medulla oblongata mengandung nukleus atau badan sel dari berbagai saraf otak yang penting. Selain itu medulla mengandung “pusat - pusat pusat vital” yang berfungsimengendalikan pernafasan dan sistem kardiovaskuler. Karena K arena itu, suatu cedera yang terjadi pada bagian ini dalam batang otak dapat membawa akibat yang sangat serius (Pearce, 2013). c. Cerebellum Otak kecil di bagian bawah dan belakang tengkorak dipisahkan dengan cerebrum oleh fisura transversalis dibelakangi oleh pons varoli dan diatas medulla oblongata. Organ ini banyak menerima serabut aferen sensoris, merupakan pusat koordinasi dan integrasi. Bentuknya oval, bagian yang kecil pada sentral disebut vermis dan bagian yang melebar pada lateral disebut hemisfer. Serebelum berhubungan dengan batang otak melalui pundunkulus serebri inferior. Permukaan luar serebelum berlipat-lipat menyerupai serebellum tetapi lipatannya lebih kecil dan lebih teratur. Permukaan serebellum ini mengandung zat kelabu. Korteks serebellum dibentuk oleh substansia grisia, terdiri dari tiga lapisan yaitu granular luar, lapisan purkinye dan lapisan granular dalam. Serabut saraf yang masuk dan yang keluar dari serebrum harus melewati serebellum(Pearce, 2013). B. DEFINISI
Stroke adalah adanya tanda-tanda klinik yang berkembang cepat akibat gangguan fungsi otak fokal (global) dengan gejala-gejala yang berlangsung selama 24 jam atau lebih yang menyebabkan kematian tanpa adanya penyebab lain yang jelas selain vaskular (Muttaqin, 2011). Menurut WHO (2012) stroke infark merupakan suatu kondisi penyakit yang disebabkan oleh terhentinya aliran darah yang mensuplai otak secara tiba-tiba, baik karena adanya sumbatan maupun rupturnya pembuluh darah, kondisi ini menyebabkan jaringan
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Stroke iskemik atau “brain attack”adalah kehilangan fungsi yang tiba-tiba tiba -tiba sebagai akibat dari gangguan suplai darah ke bagian-bagian otak, akibat sumbatan baik sebagian atau total pada arteri. Tipe stroke ini terjadi hampir 80% dari kejadian stroke (Goldszmidt & Caplan, 2011).
Berdasarkan penjelasan beberapa ahli diatas maka dapat disimpulkan bahwa Stroke infark tersebut ialah stroke yang disebabkan oleh sumbatan pada pembuluh darah servikokranial atau hipoperfusi jaringan otak oleh berbagai faktor seperti aterotrombosis, emboli, atau ketidakstabilan hemodinamik yang menimbulkan gejala serebral fokal, terjadi mendadak, dan tidak menghilang dalam waktu 24 jam atau lebih. Kurangnya aliran darah didalam jaringan otak menyebabkan serangkaian reaksi biokimia, yang dapat merusak atau mematikan sel-sel saraf di otak. Kematian jaringan otak juga dapat menyebabkan hilangnya fungsi yang dikendalikan oleh jaringan itu. Aliran darah yang berhenti juga dapat membuat suplai oksigen dan zat makanan ke otak juga berhenti. Stroke merupakan penyakit neurogenik yang menyebabkan gangguan fungsi otak baik fokal maupun global dan penyebab kecacatan paling banyak. C. ETIOLOGI
Aliran darah ke otak bisa menurun dengan beberapa cara. Iskemia terjadi ketika suplai darah ke bagian otak terganggu atau tersumbat. Iskemia biasanya terjadi karena trombosis
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Stenosis menghambat aliran darah yang biasanya lancar pada arteri. Darah akan berputar di permukaan yang terdapat plak, menyebabkan penggumpalan yang akan melekat pada plak tersebut. Akhirnya rongga pembuluh darah tersumbat. Selain itu, penyumbatan dapat terjadi karena inflamasi pada arteri atau disebut arteritis. Trombus bisa terjadi di semua bagian sepanjang arteri karotis. Bagian yang biasa terjadi penyumbatan adalah di bagian yang mengarah pada percabangan dari karotid utama ke bagian dalam dan luar dari arteri karotid (Muttaqin, 2011 : 235). Trombosis terjadi karena penurunan aktivitas simpatis dan penurunan tekanan darah. Trombosis serebri ini disebabkan karena adanya (Muttaqin, 2011 : 235). a) Aterosklerostis yaitu mengerasnya atau berkurangnya kelenturan dan elastisitas dinding pembuluh darah. b) Hiperkoagulasi yaitu darah yang bertambah kental yang akan menyebabkan viskositas hematokrit meningkat sehingga dapat melambatkan aliran darah cerebral c) Arteritis atau radang pada arteri b. Emboli Emboli serebral merupakan penyumbatan pembuluh darah otak oleh bekuan darah, lemak dan udara. Pada umumnya emboli berasal dari trombus di jantung yang terlepas dan menyumbat sistem arteri serebral. Emboli tersebut berlangsung cepat dan gejala timbul kurang dari 10 – 10 – 30 30 detik (Muttaqin, 2011 : 235). D. KLASIFIKASI
Beberapa klasifikasi stroke non-haemorragic dapat dibedakan menjadi 2 yaitu: a) Berdasarkan etiologi Stroke
non-hemoragikdapat
dibagi
menjadi
empat
jenis
berdasarkan
penyebabnya, yaitu (Pudiastuti, 2012) 2012) : 1. Stroke trombotik arteri besar disebabkan oleh aterosklerosis plak di pembuluh
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Emboli berasal dari jantung dan beredar ke pembuluh darah otak, lokasi yang paling sering terkena adalah arteri serebri media, serebelum dan daerah arteri serebral posterior (Goldszmidt & Caplan, 2011). 4. Stroke kriptogenik sebagian pasien mengalami oklusi mendadak pembuluh intrakranium besar tanpa penyebab yang jelas (Goldszmidt & Caplan, 2011). b) Berdasarkan perjalanan penyakit Berdasarkan perjalanan klinis, dikelompokkan menjadi(Muttaqin, 2011) : 1. Trancient Iskemik Attack (TIA) (TIA) atau serangan iskemik sepintas Merupakan gangguan neurologis fokal akibat gangguan peredaran darah di otak yang timbul mendadak dan hilang dalam beberapa menit (durasi rata-rata 10 menit) sampai beberapa jam (24 jam). Disebabkan oleh gangguan akut fungsi fokal serebral, emboli maupun trombosis. Satu sampai dua jam biasanya TIA dapat ditangani, namun apabila sampai tiga jam juga belum bisa teratasi sekitar 50 % pasien sudah terkena infark(Muttaqin, 2011). 2. Reversible Ischemic Neurological Deficit (RIND) atau Defisit Neurologik Iskemik Sepintas Adalah gejala neurologik yang timbul akan menghilang dalam waktu lebih lama dari 24 jam, tapi tidak lebih dari seminggu (Muttaqin, 2011). 3. Stroke Progresif ( Progessive Stroke atau Stroke in Evolution) Evolution) Pada keadaan ini gejala atau tanda neurologis fokal terus berkembang dimana terlihat semakin berat dan memburuk setelah 48 jam. Defisit neurologis yang timbul berlangsung bertahap dari ringan sampai menjadi berat. 4. Stroke Complete Gangguan neurologis yang timbul sudah menetap atau permanen, maksimal sejak awal serangan dan sedikit memperlihatkan parbaikan dapat didahului dengan Trancient Iskemik Attack berulang. Kelainan ini tidak t idak berkembang lagi bergantung
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Perdarahan otak dapat disebabkan oleh pecahnya dindingpembuluh darah oleh emboli (Smeltzer, 2013). Menurut Hudak & Gallo (2011) alairan darah disetiap otak terhambat karena trombus atau embolus, maka terjadi kekurangan oksigen ke jaringan otot, kekurangan oksigen pada awalanya mungkin akibat iskemia imun (karena berhentinya jantung atau hipotrnsi) hipoxia karena proses kesukaran bernafas suatu sumbatan pada arteri koroner dapat mengakibatkan kematian jaringan atau infark. Perdarahan intraksional biasanya disebabkan oleh ruptura arteri cerebri ekstravasasi darah terjadi didaerah otak atau subarachnoid, sehingga jaringan yang terletakk didekatnya akan tertekan. Darah ini sangat mengiritasi jaringan otak, sehingga mengakibatkan vasospasme pada arteri disekitar perdarahan, spasme sp asme ini dapat menyebar keseluruh hemisfer otak, bekuan yang semuanya lunak akhirnya akan larut dan mengecil, otak yang terletak disekitar tempat bekuan dapat membengkan dan mengalami nekrosis. Stroke non Hemoragik terjadi akibat penyumbatan aliran darah arteri yang lama ke bagian otak. Stroke non hemoragik dapat terjadi akibat thrombus (bekuan darah di arteri serebril) atau embolus(bekuan darah yang berjalan ke otak dari tempat lain di tubuh). Stroke trombotik terjadi akibat oklusi aliran darah, karena aterosklerosis berat. Individu mengalami satu atau lebih serangan iskemik sementara Transient Iskemik Attack (TIA) sebelum stroke trombotik yang sebenarnya terjadi. TIA adalah gangguan fungsi otak singkat yang reversibel akibat hipoksia serebral. TIA mungkin terjadi ketika pembuluh darah aterosklerotik mengalami spasme, atau saat kebutuhan oksigen otak meningkat dan kebutuhan ini tidak dapat dipenuhi karena aterosklerosis yang berat. Stroke embolik berkembang setelah oklusi arteri oleh embolus yang terbetuk di luar l uar otak. Sumber umum embolus yang menyebabkan stroke adalah jantung setelah miokardium atau fibrilasi atrium, dan embolus yang merusak arteri karotis komunis atau aorta (Corwin, 2009).
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F.
MANIFESTASI KLINIS
Manifestasi klinik klien yang terkena serangan stroke menurut (Black & Hawk, 2009), bervariasi tergantung pada penyebabnya, luas area neuron yang rusak, lokasi neuron yang terkena serangan, dan kondisi pembuluh darah kolateral di serebral (Smeltzer, 2013) yang dapat berupa : 1) Kehilangan Motorik. Stroke adalah penyakit motor neuron atas ata s dan mengakibatkan kehilangan kontrol volunter terhadap gerakan motorik. Disfungsi motor yang paling umum adalah Hemiparesis (kelemahan) dan hemiplegia (paralisis pada satu sisi tubuh) sering terjadi setelah stroke, yang biasanya desebabkan karena stroke pada bagian anterior atau bagian tengah arteri serebral, sehingga memicu terjadinya infark bagian motorik dari kortek frontal. 2) Aphasia, klien mengalami defisit dalam kemampuan berkomunikasi,termasuk berbicara, membaca, menulis dan memahami bahasa lisan.Terjadi jika pusat bahasa primer yang terletak di hemisfer yang terletak di hemisfer kiri serebelum tidak mendapatkan aliran darah dari arteri serebral tengah karena mengalami stroke, ini terkait erat dengan area wernick dan brocca. 3) Disatria,
dimana
klien
mampu
memahami
percakapan
tetapi
sulit
untuk
mengucapkannya, sehingga bicara sulit dimengerti. Hal ini disebabkan oleh terjadinya paralisis otot yang bertanggung jawab untuk untuk menghasilkan bicara. 4) Apraksia
yaitu
ketidakmampuan
untuk
melakukan
tindakan
yang
dipelajarisebelumnya, seperti terlihat ketika klien mengambil sisir dan berusaha untuk menyisir rambutnya. 5) Disfagia, dimana klien mengalami kesulitan dalam menelan karena stroke pada arteri vertebrobasiler yang mepengaruhi saraf yang mengatur proses menelan, yaitu N V (trigeminus), N VII (facialis), N IX (glossofarengeus) dan N XII (hipoglosus).
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10) Perubahan perilaku, terjadi jika arteri yang terkena stroke bagian otak yang mengatur perilaku dan emosi mempunyai porsi yang bervariasi, yaitu bagian kortek serebral, area temporal, limbik, hipotalamus, kelenjar pituitari yang mempengarui korteks motorik dan area bahasa. 11) Inkontinensia baik bowel ataupun kandung kemih merupakan salah satu bentuk neurogenic blader atau ketidakmampuan kandung kemih, yang kadang terjadi setelah stroke. Saraf mengirimkan pesan ke otak tentang pengisian kandung kemih tetapi otak tidak dapat enginterpretasikan secara benar pesan tersebut dan tidak mentransmisikan pesan ke kandung kemih untuk tidak mengeluarkan urin. Ini yang menyebabkan terjadinya frekuensi urgensi dan inkontinensia.
G. PENATALAKSANAAN
1) Secara Keperawatan Menurut Powers., et al (2018) rekomendasi AHA/ASA Guidline pada penatalaksanaan gawat darurat stroke infark adalah sebagai berikut : a) Primary survey (penilaian awal ) i.
Airway, Airway, lihat adanya sumbatan jalan nafas atau tidak o
Sumbatan partial jalan nafas: biasanya dada masih mengembang - Sadar, biasanya masih bernafas, batuk, dan berbicara minta tolong Tidak sadar, terdengar suara nafas tambahan stridor (benda padat),
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saturasi <94%, glukosa dan aliran darah yang adekuat dengan mengontrol atau memperbaiki disritmia (irama dan frekuensi) serta tekanan darah. iii.
Circulation Lihat sumber perdarahan, kaji status mental, lihat adanya hipotensi dan pembesaran vena jugularis, cek nadi, suhu, dan kelembaban. Berikan terapi cairan (misalnya koloid, produk darah, kristaloid) untuk meningkatkan volume intravaskuler dan mempertahankan parameter hemodinamik.
b) Secondary survey o
Mengendalikan hipertensi dan menurunkan TIK Dengan meninggikan kepala 0-45 o menghindari flexi dan rotasi kepala yang berlebihan
o
Selanjutnya, bebaskan jalan napas, beri oksigen
1-2 liter/menit sampai sampai
didapatkan hasil analisis gas darah. o
Menurunkan kerusakan iskemik cerebral Tujuannya adalah agar kerusakan jaringan otak tidak meluas. Tindakan awal difokuskan untuk menyelematkan sebanyak mungkin area iskemik dengan memberikan O2, untuk mempertahankan saturasi >94%, glukosa dan aliran darah yang adekuat dengan mengontrol / memperbaiki disritmia (irama dan frekuensi) serta tekanan darah.
2) Secara Medis
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puncak tercapai 2 jam sesudah diminum. Cepat diabsorpsi, konsentrasi di otak rendah. Hidrolise ke asam salisilat terjadi cepat, tetapi tetap aktif. Ikatan protein plasma: 50-80 persen. Waktu paruh (half time) plasma yaitu 4 jam. Pasien yang tidak tahan aspirin atau gagal dengan terapi aspirin, dapat menggunakan tiklopidin atau clopidogrel. Obat ini bereaksi dengan mencegah aktivasi platelet, agregasi, dan melepaskan granul platelet, mengganggu fungsi membran
platelet
dengan
penghambatan
ikatan
fibrinogen-platelet
yang
diperantarai oleh ADP dan antraksi platelet-platelet.Efek samping tiklopidin adalah diare (12,5 persen) dan netropenia (2,4 persen). Bila obat dihentikan akan reversibel. Pantau jumlah sel darah putih tiap 15 hari selama 3 bulan. Komplikas yang lebih serius, teyapi jarang, adalah pur-pura trombositopenia trombotik dan anemia aplastik. 2) Anti koagulan Warfarin dan heparin sering digunakan pada TIA dan stroke yang mengancam. Suatu fakta yang jelas adalah antikoagulan tidak banyak artinya bilamana stroke telah terjadi, baik apakah stroke itu berupa infark lakuner atau infark massif dengan hemiplegia. Keadaan yang memerlukan penggunaan heparin adalah trombosis arteri basilaris, trombosis arteri karotisdan infark serebral akibat kardioemboli. Pada keadaan yang terakhir ini perlu diwaspadai terjadinya perdarahan intraserebral karena pemberian heparin tersebut.
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Golongan obat ini digunakan sebagai terapi reperfusi untuk mengembalikan perfusi darah yang terhambat pada serangan stroke akut. Jenis obat golongan ini adalah alteplase, tenecteplase dan reteplase, namun yang tersedia di Indonesia hingga saat ini hanya alteplase. Obat ini bekerja memecah trombus dengan mengaktivasi plasminogen yang terikat pada fibrin. Boleh dilakukan terapi ini jika tekanan darah sistol < 185 mmHg, dan diastole <110 mmHg Efek samping yang sering terjadi adalah risiko pendarahan seperti pada intrakranial atau saluran cerna; serta Angioedema Pada pasien yang menggunakan terapi ini usahakan untuk menghindari penggunaan bersama obat antikoagulan dan antiplatelet dalam 24 jam pertama setelah terapi untuk menghindari risiko perdarahan. 4) Diuretika digunakan untuk menurunkan edema serebral 5) Antipiretik dan analgetik digunakan untuk mengurangi mengurangi hipertermi (S>38 oC) dan nyeri kepala 6) Antihipertensi Menurut penelitian yang dilakukan Castillo J, dkk (2004) menunjukan bahwa setiap penurunan tekanan darah 10 mmHg pada pasien stroke yang masuk rumah sakit dengan tekanan darah sistolik ≤ 180 mmHg dan juga peningkatan tekanan darah 10 mmHg pada pasien stroke yang masuk dengan tekanan darah sistolik > 180 mmHg dalam 24 jam pertama setelah gejala stroke iskemik akut dapat berakibat pada perburukan fungsi neurologis (
1 poin pada Canadian
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Bagian tubuh yang sering mengalami memar akibat tekanan dari bagian tubuh lain yang paling sering adalah pinggul, pantat, sendi kaki dan tumit. Bila memar ini tidak dirawat dengan baik maka akan terjadi ulkus dekubitus dan infeksi. 3) Pneumonia Pasien stroke tidak bisa batuk dan menelan dengan sempurna, hal ini menyebabkan akumulasi sekret terkumpul di paru-paru dan selanjutnya menimbulkan pneumonia. 4) Atrofi otot Atrofi otot atau pengecilan otot serta kontraktur atau kekauan sendi dapat disebabkan karena kurang gerak dan immobilisasi. 5) Depresi dan Ansietas Gangguan perasaan sering terjadi pada stroke dan menyebabkan reaksi emosional dan fisik yang tidak diinginkan karena terjadi perubahan dan kehilangan fungsi tubuh.
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I.
ASUHAN KEPERAWATAN TEORI a) Pengkajian
i) Identitas klien Biasanya pada kasus cerebral infark karena usia di atas 55 tahun merupakan resiko tinggi terjadinya serangan stroke.Jenis kelamin laki-laki lebih tinggi 30% di banding wanita.Ras: kulit hitam lebih tinggi tinggi angka kejadiannya (Muttaqin, 2011). ii) Keluhan utama Biasanya klien datang ke rumah sakit dalam kondisi: penurunan kesadaran atau koma serta disertai kelumpuhan dan keluhan sakit kepala hebat bila masih sadar (Muttaqin, 2011). iii) Riwayat penyakit sekarang Serangan stroke seringkali
berlangsung sangat mendadak, mendadak, pada saat klien
melakukan aktivitas. Biasanya terjadi nyeri kepala, mual, muntah bahkan kejang sampai klien kehilangan sadar, disamping gejala kelumpuhan separuh badan atau
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dan kelumpuhan seisi otot-otot pterigoideus dan pada saraf IX dan X yaitu kemampuan menelan kurang baik, kesukaran membuka mulut. d. Leher, biasanya ditemukan kekakuan pada otot leher e. Paru, batuk peningkatan produksi sputum, sesak nafas, penggunaan otot bantu nafas, serta perubahan kecepatan dan kedalaman pernafasan. Adanya ronchi akibat peningkatan produksi sekret dan penurunan kemampuan untuk batuk akibat penurunan kesadaran klien. Pada klien yang sadar baik sering kali tidak didapati kelainan pada pemeriksaan sistem respirasi. f. Jantung, dapat terjadi hipotensi atau hipertensi, denyut jantung irreguler, adanya murmur g. Integumen, biasanya ditemukan suhu tubuh pasien meningkat ( >37,5°C) h. Genetalia, biasanya ditemukan hasil pasien mengalami penurunan sensasi keinginan untuk berkemih atau buang air besar, bisa terjadi distensi. i.
Ekskremitas,
kehilangan
kontrol
volenter
gerakan
motorik.
Terdapat
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ii.
Apatis, yaitu keadaan yang segan untuk berinteraksi dengan lingkungan sekitarnya, sikapnya acuh tak acuh
iii.
Delirium, yaitu keadaan yang gelisah, disorientasi (Orang, tempat dan waktu), memberontak, berteriak, berhalusinasi dan berhayal
iv.
Somnolen (Optundasi), yaitu keadaan kesadran menurun dan respon psikomotor yang lambat dan mudah tertidur, namun kesadarn dapat pulih bila diransang (mudah dibangunkan) tetapi jatuh tertidur lagi, mampu memberi jawaban verbal.
v.
Stupor (Sopor), yaitu keadaan letargi seperti tidur lelap, tetapi ada respon terhadap nyeri
vi.
Coma, yaitu keadaan yang tidak bisa dibangunkan, tidak ada respon terhadap rangsangan apapun, (respon kornea, maupun reflek muntah, mungkin juga tidak ada respon pupil terhadap cahaya)
b) Kuantitatif
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1. Reflek biceps (BPR), ketukan pada jari pemeriksa yang ditempatkan pada tendon muskulus biceps brachii, posisi lengan diketuk pada sendi siku.Respon, fleksi lengan pada sendi siku. 2. Reflek Triceps (TPR), ketukan pada tendon otot triceps, posisi lengan fleksi pada sendi siku dan sedikit pronasi.Respon, ekstensi lengan bawah pada sendi siku. 3. Reflek Periosto Radialis, ketukan pada periosteum ujung distal os. Symmetric posisi lengan setengah fleksi dan sediki pronasi.Respon, fleksi lengan bawah di sendi siku dan supinasi karena kontraksi muskulus brachiradialis. 4. Reflek Periostoulnaris, ketukan pada periosteum proseus styloid ilna, posisi lengan stengah fleksi dan antara pronasi dan supinasi.Respon, pronasi tangan akibat kontraksi muskulus pronator pronator quadrates Reflek Patela (KPR), ketukan pada tendon patella dengan hammer.
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2. Ekskremitas Inferior a. Babinski, gores telapak kaki dilateral dari bawah keatas. (+) bila dorsofleksi ibu jari dan abduksi kearah lateral empat jari lain. b. Chaddok, gores bagian bawah malleolus medial (+) bila dorsofleksi ibu jari dan abduksi kearah lateral empat jari lain. c. Oppenheim, gores dengan dua sendi interfalang jari tengah dan jari telunjuk di sepanjang os tibia atau cruris. d. (+) bila dorsofleksi ibu jari dan abduksi kearah lateral empat jari lain. e. Gordon, tekan atau remas muskulus gastrocnemeus atau betis dengan keras. f. Schaeffer, tekan atau remas tendon achilles. (+) bila dorsofleksi
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tembakau, kopi dan sebagainya. Bandingkan dengan hidung bagian kiri dan kanan. 2. Optikus Disfungsi persepsi visual karena gangguan jarak sensorik primer diantara sudut mata dan korteks visual. Gangguan hubungan visula-spasial sering terlihat pada klien dengan hemiplegia kiri. Klien mungkin tidak dapat memakai pakaian tanpa bantuan karena
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Fungsi sensasi, kaji sensasi rasa bagian anterior lidah, terhadap asam,manis, asin, pahit 6. Acustikus a. coclear ( mengkaji pendengaran ) tutup satu telinga klien, pemeriksa berbisik di satu telinga lain, atau menggesekkan jari bergantian kanan dan kiri b. vestibulator ( mengkaji keseimbangan ), klien diminta berjalan
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b. Sirkulasi Data Subyektif : 1. Riwayat penyakit jantung (penyakit katup jantung, disritmia, gagal jantung, endocarditis bacterial) dan polisitemia. Data Obyektif : 1. Hipertensi arterial 2. Diritmia, perubahan EKG
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3. Kelemahan,
kesemutan,/kebas,
sisi
yang
rekena
terlihat
seperti
lumpuh/mati 4. Penglihatan berkurang 5. Sentuhan 6. Gangguan rasa pengecapan Data objektif : 1. Status mental : koma biasanya menandai stadium pendarahan , gangguan
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2.
Hambatan mobilitas fisik berhubungan dengan gangguan neuromuskular ditandai dengan kesulitan membolak-balikkan posisi, keterbatasan rentang gerak dan penurunan kemampuan motorik kasar kasar dan motorik halus
3.
Hambatan komunikasi verbal berhubungan dengan gangguan fisiologis penurunan sirkulasi otak yang ditandai dengan gagap, pelo, sulit bicara, sulit mengungkapkan kata,
tidak
dapat
bicara,
kesulitan
memahami
komunikasi,
kesulitan
mempertahakan komunikasi, dan kesulitan mengekspresikan pikiran secara verbal
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b. NOC
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5. Tidak terganggu
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a. Batasan Karakteristik
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berdiri
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a. Dorong pasien untuk belajar duduk di tempat tidur atau sisi tempat tidur
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