Protozoa

Protozoa adalah organisme yang bersel tunggal, dimana beberapa spesies mempunyai lebih dari satu nukleus (inti sel) pada bagian atau seluruh daur hidupnya. Seperti halnya sel pada tubuh makhluk hidup lainnya, sel protozoa dilapisi oleh tiga lapisan uni membran yang didalamnya terdapat ektoplasma, endoplasma dan nukleus. Dalam endoplasma ditemukan nukleus, mitokondria, badan golgi dan sebagainya, sedangkan ektoplasma ditemukan flagela , cilia dan sebagainya. Protozoa pada dasarnya bergerak menggunakan 4 tipe organela yang merupakan bagian dari ektoplasma yaitu:
Flagela, cilia, pseudopodia dan undulata bergerigi.

- Flagella: bentuk langsing seperti rambut tunggal yang panjang
- Cilia: Bentuk flagela yang kecil dan lebih pendek
- Pseudopodia: Organela sementara yang menonjol biasanya digunakan untuk bergerak/menangkap makanan.
- Gerigi undulata: Pergerakan dengan menggunakan bentuk gelombang dari sel dengan pergerakan dari belakang kedepan dan sebaliknya.
Biasanya protozoa mempunyai dua stadium yang selalu dialaminya yaitu stadium trophozoit yaitu bentuk aktif dan bentuk cyste merupakan bentuk inaktif.

Genus: Entamuba

Klasifikasi:
Class : Rhizopoda
Ordo: Amoebida
Genus: Entamoeba
Spesies: Entamoeba histolytica
E. coli
E. ginggivalis
Diantara 3 spesies entamoeba, E. histolytica adalah paling patogen pada manusia. Organisme ini adalah salah satu agen penyakit penyebab dysentri. Selama beberapa tahun belakangan diketahui bahwa ada dua jenis entamoeba yang dibedakan menurut ukuran trophozoit dan cystenya. yaitu:
Ukuran besar : Trophozoit: 20-30 m
Cyste: 10-20 m
Ukuran kecil: Trophozoit : 12-15 m
Cyste: 5-9 m
E. histolytica ukuran besar ada dua strain yaitu patogenik dan non-patogenik. Ukuran kecil biasanya non-patogenik. Strain E. histolytica yang patogen adalah merupakan parasit protozoa yang paling penting pada orang dan banyak diteliti.
Daur hidup
Parasit ini mengalami fase pre dan meta dalam daur hidupnya yaitu:
Trophozoit---precyste---Cyste---metacyste-----metacyste trophozoit.
Trophozoit yang mengandung beberapa nukleus (uni nucleate trophozoit) kadang tinggal dibagian bawah usus halus, tetapi lebih sering berada di colon dan rectum dari orang atau monyet serta melekat pada mukosa. Hewan mamalia lain seperti anjing dan kucing juga dapat terinfeksi. Trophozoit yang motil berukuran 18-30 um bersifat monopodial (satu pseudopodia besar). Cytoplasma yang terdiri dari endoplasma dan ektoplasma, berisi vakuola makanan termasuk erytrocyt, leucocyte, sel epithel dari hospes dan bakteria. Didalam usus trophozoit membelah diri secara asexual.
Trophozoit menyusup masuk kedalam mukosa usus besar diantara sel epithel sambil mensekresi enzim proteolytik. Didalam dinding usus tersebut trophozoit terbawa aliran darah menuju hati, paru, otak dan organ lain. Hati adalah organ yang paling sering diserang selain usus. Di dalam hati trophozoit memakan sel parenchym hati sehingga menyebabkan kerusakan hati. Invasi amoeba selain dalam jaringan usus disebut amoebiasis sekunder atau ekstra intestinal.
Trophozoit dalam intestinal akan berubah bentuk menjadi precystic. Bentuknya akan mengecil dan bebentuk spheric dengan ukuran 3,5-20 um. Bentuk cyste yang matang mengandung chromatoid untuk menyimpan unsur nutrisi glycogen yang digunakan sebagai sumber energi. Cyste ini adalah bentuk inaktif yang akan keluar melalui feses.
Cyste sangat tahan terhadap bahan kimia tertentu. Cyste dalam air akan bertahan sampai 1 bulan, sedangkan dalam feses yang mengering dapat bertahan sampai 12 hari. Bila air minum atau makanan terkontaminasi oleh cyste E. histolytica, cyste akan masuk melalui saluran pencernaan menuju ileum dan terjadi excystasi, dinding cyste robek dan keluar amoeba “multinucleus metacystic” yang langsung membelah diri menjadi 8 uninucleat trophozoit muda disebut “amoebulae”. Amoebulae bergerak ke usus besar, makan dan tumbuh dan membelah diri asexual.
Multiplikasi (perbanyakan diri) dari spesies ini terjadi dua kali dalam masa hidupnya yaitu: membelah diri dengan “binary fission” dalam usus pada fase trophozoit dan pembelahan nukleus yang diikuti dengan cytokinesis dalam cyste pada fase metacystic.
Patologi
E. histolytica adalah spesies amoeba yang paling unik dan berbahaya diantara spesies amoeba lainnya yang menginfeksi orang. Hal tersebut karena protozoa ini mempunyai kemampuan untuk menghydrolysis jaringan hospes (histo=jaringan, lytic=lysis). Sekali amoeba ini berkontak dengan mukosa, parasit ini mensekresi enzim proteolytic, sehingga organisme ini dapat berpenetrasi kedalam epithelium kemudian kejaringan yang lebih dalam.
Lesi intestinal
Terjadi pertama didaerah caecum, appendix, colon ascenden dan berkembang ke colon lainnya. Bila sejumlah parasit ini menyerang mukosa akan menimbulkan ulcus(borok), yang mempercepat kerusakan mukosa. Lapisan muskularis usus biasanya lebih tahan. Biasanya lesi akan terhenti didaerah membran basal dari muskularis mukosa dan kemudian terjadi erosi lateral dan berkembang menjadi nekrosis. Jaringan tersebut akan cepat sembuh bila parasit tersebut dihancurkan (mati). Pada lesi awal biasanya tidak terjadi komplikasi dengan bakteri. Pada lesi yang lama (kronis) akan diikuti infeksi sekunder oleh bakteri dan dapat merusak muskularis mukosa, infiltrasi ke sub-mukosa dan bahkan berpenetrasi ke lapisan muskularis dan serosa.
Terjadinya kasus trophozoit terbawa aliran darah dan limfe ke lokasi lain dari tubuh, menyebabkan terjadinya lesi pada organ lain. Tingginya angka kematian karena penyakit ini disebabkan oleh robeknya colon bersamaan dengan terjadinya peritonitis. Lesi sekunder pada organ lain dapat pula ditemukan tetapi lebih sering dijumpai lesi pada hati (sekitar 5% dari kasus amebiasis).
Lesi pada hati
Hal ini terjadi bila trophozoit masuk kedalam venula mesenterika dan bergerak ke hati melalui sistem vena porta hepatis, kemudian masuk melalui kapiler darah portal menuju sinusoid hati dan akhirnya membentuk absces. Besarnya absces cukup bervariasi dari bentuk titik yang kemudian membesar sampai seperti buah anggur. Ditengah absces akan terlihat adanya cairan nekrosis, ditengahnya ada sel stroma hati dan bagian luarnya terlihat jaringan hati yang ditempeli oleh ameba. Bilamana absces pecah serpihan absces akan tersebar dan menginfeksi jaringan lainnya.
Lesi jaringan lainnya
Lesi pada jaringan lainnya seperti lesi pulmonaris (paru), otak, kulit dan penis, terjadi karena metastasis dari jaringan hati. Dimana semua kasus terjadi berasal dari absces jaringan hati.
Diagnosis
Diagnosis terutama dilihat dari gejala klinis dan reaksi tes imunologi. Pemeriksaan dengan sinar x dapat mendiagnosis adanya absces dalam hati. Pemeriksaan sampel feses cukup baik dilakukan untuk mendiagnosis infeksi dalam usus. Pemeriksaan beberapa kali terhadap feses pasien untuk menemukan trophozoit cukup baik dilakukan. Diagnosis secara imunologik cukup baik hasilnya. Penggunaan teknik fluoerscens antibodi cukup baik tetapi tidak dpat membedakan antara E. histolytica dengan E. hartmanni.
Pengobatan
Beberapa obat cukup baik untuk membunuh koloni amebiasis yaitu:
- Asam arsanilik dan derivatnya
- iodichlor hydroxyquinolines
Bererapa antibiotik terutama:
- Tetracycline, cukup baik, tetapi kurang baik untuk infeksi ectopic.
- Chloroquine phosphat dan niridazole, cukup efisien
- Metronidazole, merupakan pilihan tepat karena efektif terhadap amebiasis extra intestinal dan infeksi koloni (dosis 2g/hari, selama 3 hari).

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Cacar Air

Cacar Air



Cacar air (chicken pox) disebabkan oleh virus yang bernama varisela zoster. Virus ini menyerang kulit dengan membentuk luka yang berisi cairan. Cacar biasanya mengenai anak yang berusia 9 tahun ke atas. Orang dewasa jarang terkena cacar air, namun jika terkena umumnya lebih berat dibandingkan anak kecil.

Cacar air merupakan penyakit yang mudah sekali penularannya. Dapat melalui kontak langsung dengan luka penderita atau benda yang dipergunakan penderita. Dapat juga melalui udara, misalnya melalui batuk, bersin, bahkan nafas penderita. Masuknya virus ke dalam tubuh / masa inkubasi hingga munculnya gejala awal penyakit

Cacar Air



Cacar air (chicken pox) disebabkan oleh virus yang bernama varisela zoster. Virus ini menyerang kulit dengan membentuk luka yang berisi cairan. Cacar biasanya mengenai anak yang berusia 9 tahun ke atas. Orang dewasa jarang terkena cacar air, namun jika terkena umumnya lebih berat dibandingkan anak kecil.

Cacar air merupakan penyakit yang mudah sekali penularannya. Dapat melalui kontak langsung dengan luka penderita atau benda yang dipergunakan penderita. Dapat juga melalui udara, misalnya melalui batuk, bersin, bahkan nafas penderita. Masuknya virus ke dalam tubuh / masa inkubasi hingga munculnya gejala awal penyakit terjadi antara 14 – 16 hari. Gejala cacar air adalah nyeri kepala dan demam yang berlangsung sekitar 7 – 7 hari, kadang-kadang disertai pilek atau hidung tersumbat, bersin, dan batuk. Setelah demam reda, muncul bintik-bintik merah yang dimulai dari daerah sekitar wajah dan dada yang lalu menyebar ke seluruh tubuh disertai rasa gatal. Kondisi yang demikian diakhiri dengan munculnya vesikel (bintil yang berisi cairan berwarna jernih). Jumlah yang didapat setiap penderita bervariasi. Masa aktif penularan cacar air adalah 1 – 2 hari sebelum bintil pertama muncul. 6 – 7 hari setelah bintil terakhir muncul. Melewati masa tersebut, secara klinis, penderita tidak akan menularkan penyakitnya lagi.

Cacar air yang terjadi pada anak-anak cenderung ringan, sehingga umumnya tidak perlu dirawat di rumah sakit. Cukup dengan rawat jalan. Jika daya tahan tubuh anak tinggi, maka penyakitnya dapat sembuh dalam waktu 2 minggu. Dalam masa itu, jangan biarkan anak terinfeksi penyakit lain. Jangan biarkan anak bermain ke luar dengan teman-temannya. Hindarkan anak dari apapun yang dapat membuat bintil-bintil yang dimilikinya pecah. Jika bintil pecah, kemungkinan besar akan terjadi infeksi bakteri. Dan kalau sudah begitu, anak harus diberi antibiotik, bahakan harus dirawat di rumah sakit.

Jika di rumah ada anggota keluarga yang belum pernah terjangkit cacar, dewasa maupun anak-anak usahakan untuk tidak melakukan kontak langsung. Langkah yang paling efektif dan aman adalah dengan melakukan vaksinasi cacar air. Vaksinasi ini diberikan 36 jam setelah kontak.

Hal-hal yang derlu dilakukan bila anak terkena cacar air :

1. Lebih baik jika perawatan anak dilakukan oleh orang yang sudah pernah terjangkit cacar. Karena biasanya orang yang sudah pernah terkena penyakit ini akan kebal.

2. Untuk anggota keluarga yang belum terkena cacar, sebaiknya jangan terlalu dekat dengan anak, agar tidak menghirup nafasnya.

3. Pisahkan barang-barang yang digunakan, seperti baju, handuk, peralatan makan, dan lain-lain. Bersihkan peralatan tersebut secara terpisah. Tempatkan pula anak dalam tempat tidur terpisah, dang anti seprai setiap hari.

4. Jaga kualitas dan kuantitas makanan anak. Berikan makanan yang mengandung banyak zat yang diperlukan tubuh.

5. Istirahat yang cukup. Jangan biarkan anak keluar bermain sementara bintil cacar masih terus tumbuh.

6. Minta kepada anak untuk tidak menggaruk bintil yang gatal. Potong kukunya atau pakaikan sarung tangan untuk mengurangi akibat garukan. Cairan yang terdapat di dalam bintil bersifat menular. Dan jika terjadi infeksi luka maka penyembuhannya akan lebih sulit, juga meninggalkan bekas (kropeng).

7. Oleskan obat gatal, seperti bedak calamine untuk mengurangi gatal dan mempercepat proses pengeringan luka.

8. Mandikan anak dengan antiseptik, dan pergunakan baju yang berbeda setiap harinya.

9. Perhatikan kondisi dan suhu tubuh anak setiap hari. Bila perlu, berikan anak obat untuk meredakan demam yang dideritanya.

10. Waspada akan keadaan darurat. Segeralah ke dokter bila bintil / vesikel terinfeksi kuman, misalnya berwarna merah, bengkak, dan bernanah. Dan juga bila anak menderita demam tinggi, sakit kepala, muntah, gatal yang tidak hilang-hilang, saat bintil-bintil telah menyebar ke seluruh tubuh dan keadaan anak sudah membaik.

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ACQUIRED IMMUNO DEFICIENCY SYNDROME

APAKAH AIDS ?

* Penyakit menular yang disebabkan oleh virus yang merusak sistem kekebalan tubuh.
* Virus penyebab AIDS adalah HIV (Human Immunodeficiency Virus)
* Penderita AIDS yang meninggal, bukan semata-mata disebabkan oleh virus AIDS, tetapi juga oleh penyakit lain yang sebenarnya bisa ditolak, seandainya sistem kekebalan tubuh tidak rusak oleh virus AIDS.
BAGAIMANA AIDS MENULAR ?

APAKAH AIDS ?

* Penyakit menular yang disebabkan oleh virus yang merusak sistem kekebalan tubuh.
* Virus penyebab AIDS adalah HIV (Human Immunodeficiency Virus)
* Penderita AIDS yang meninggal, bukan semata-mata disebabkan oleh virus AIDS, tetapi juga oleh penyakit lain yang sebenarnya bisa ditolak, seandainya sistem kekebalan tubuh tidak rusak oleh virus AIDS.


BAGAIMANA AIDS MENULAR ?

* 75-85 % Penularan terjadi melalui hubungan seks (5-10 % diantaranya melalui hubungan homoseksual)
* 5-10 % akibat alat suntik yang tercemar (terutama pada pemakai narkotika suntik)
* 3-5 % melalui transfusi darah yang tercemar
* 90 % infeksi pada bayi dan anak terjadi dari Ibu yang mengidap HIV
* 25-35 % bayi yang dilahirkan oleh Ibu pengidap HIV akan menjadi pengidap HIV
GEJALA AIDS

* Rasa lelah berkepanjangan
* Sesak nafas dan batuk berkepanjangan
* Berat badan turun secara menyolok
* Pembesaran kelenjar (di leher, ketiak, lipatan paha) tanpa sebab yang jelas
* Bercak merah kebiruan pada kulit (kanker kulit)
* Sering demam (lebih dari 38 °C) disertai keringat malam tanpa sebab yang jelas
* Diare lebih dari satu bulan tanpa sebab yang jelas
SIAPA KELOMPOK RESIKO TINGGI ?

* Siapa saja yang memiliki perilaku seksual berganti-ganti pasangan

BAGAIMANA MENCEGAH AIDS

* Tidak berganti-ganti pasangan seksual
* Pencegahan kontak darah, misalnya pencegahan terhadap penggunaan jarum suntik yang diulang
* Dengan formula A-B-C
o ABSTINENSIA artinya tidak melakukan hubungan seks sebelum menikah
o BE FAITHFUL artinya jika sudah menikah hanya berhubungan seks dengan pasangannya saja
o CONDOM artinya pencegahan dengan menggunakan kondom


PENELITIAN, ARTIKEL AIDS

* Adi Sasongko, Acquired Immuno Deficiency Syndrome, Yayasan Kusuma Buana, Jakarta, 1996.

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Radang Tenggorokan (Faringitis Akut)

Beberapa dari kita tentu pernah mengalami nyeri tenggorokan yang super hebat sehingga menelan sesuap nasi rasanya susah banget. Nyeri seperti ini tentu sangat sangat menjengkelkan, apalagi di depan kita tersedia makanan kesukaan kita yang lezat dan harum. Alangkah tersiksa rasanya, beberapa obat telah dicoba tetapi tidak juga mempan, begitu pula dengan obat obatan tradisional dari nenek tercinta.

Yap, faringitis atau radang tenggorokan memang merupakan penyakit yang sering diderita oleh pasien yang berobat ke tempat saya. Terkadang pasien dengan faringitis juga disertai dengan gejala flu yang lain seperti demam, sakit kepala, pilek dan batuk. Namun penyakit yang disebabkan oleh infeksi virus EBV atau kuman Strep. pyogenes ini dengan mudah

Beberapa dari kita tentu pernah mengalami nyeri tenggorokan yang super hebat sehingga menelan sesuap nasi rasanya susah banget. Nyeri seperti ini tentu sangat sangat menjengkelkan, apalagi di depan kita tersedia makanan kesukaan kita yang lezat dan harum. Alangkah tersiksa rasanya, beberapa obat telah dicoba tetapi tidak juga mempan, begitu pula dengan obat obatan tradisional dari nenek tercinta.

Yap, faringitis atau radang tenggorokan memang merupakan penyakit yang sering diderita oleh pasien yang berobat ke tempat saya. Terkadang pasien dengan faringitis juga disertai dengan gejala flu yang lain seperti demam, sakit kepala, pilek dan batuk. Namun penyakit yang disebabkan oleh infeksi virus EBV atau kuman Strep. pyogenes ini dengan mudah dapat dikenali dengan pemeriksaan tenggorokan pasien. Pada pemeriksaan ini ditemukan peradangan pada daerah faring dengan tanda berupa kemerahan serta ditemukannya pembesaran pada kelenjar limfe regional disekitarnya. Pada kasus yang berat bisa ditemukan nanah atau eksudat.

Permasalahan faringitis diperparah dengan keadaan pasien yang sulit menelan, bahkan tidak bisa makan. Keadaan ini tentu akan mengurangi asupan makanan yang bergizi ke tubuhnya yang pada gilirannya akan menganggu proses penyembuhan.

Namun tidak perlu khawatir, pada penderita faringitis yang disebabkan oleh virus, akan sembuh sendiri dalam beberapa hari. Pasien hanya diberikan obat symptomatis untuk mengurangi penderitaannya karena kesakitan menelan dan gejala flu yang lain. Sebaliknya bila faringitis disebabkan oleh bakteri, baru diperlukan antibiotika yang adekuat untuk membunuh bakteri jahat tersebut.

Komplikasi terjadi biasanya pada faringitis yang disebabkan oleh infeksi bakteri, dimana sering terjadi abses peritonsilar dan abses parafaring, yang penanganannya memerlukan tindakan pembedahan.

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Demam berdarah dengue(DBD)

Apakah demam dengue?

Demam dengue umumnya menyerang orang yang kekebalan tubuhnya sedang menurun. Sebenarnya saat kita terkena infeksi dengue, tubuh akan memproduksi kekebalan terhadap tipe virus dengue tersebut, kekebalan ini akan berlangsung seumur hidup. Sayangnya, demam dengue disebabkan oleh banyak strain atau tipe virus sehingga walaupun kita kebal terhadap salah satu tipe namun kita masih dapat menderita demam dengue dari tipe virus yang lain.

Demam berdarah dengue atau DBD merupakan demam dengue dengan derajat yang lebih berat. Perbedaan yang paling utama adalah pada demam dengue tidak ditemukan manifestasi perdarahan pada pasien. Pada kulit pasien dengan demam dengue hanya tampak ruam kemerahan saja sementara

Apakah demam dengue?

Demam dengue umumnya menyerang orang yang kekebalan tubuhnya sedang menurun. Sebenarnya saat kita terkena infeksi dengue, tubuh akan memproduksi kekebalan terhadap tipe virus dengue tersebut, kekebalan ini akan berlangsung seumur hidup. Sayangnya, demam dengue disebabkan oleh banyak strain atau tipe virus sehingga walaupun kita kebal terhadap salah satu tipe namun kita masih dapat menderita demam dengue dari tipe virus yang lain.

Demam berdarah dengue atau DBD merupakan demam dengue dengan derajat yang lebih berat. Perbedaan yang paling utama adalah pada demam dengue tidak ditemukan manifestasi perdarahan pada pasien. Pada kulit pasien dengan demam dengue hanya tampak ruam kemerahan saja sementara pada pasien demam berdarah dengue akan tampak bintik bintik perdarahan. Selain perdarahan pada kulit, penderita demam berdarah dengue juga dapat mengalami perdarahan dari gusi, hidung, usus dan lain lain. Bila tidak ditangani segera, demam berdarah dengue dapat menyebabkan kematian.

Daerah mana saja yang mudah terjangkit demam dengue?

Demam dengue banyak terjangkit di daerah tropis dan subtropis. Asia menempati urutan pertama dalam jumlah penderita demam dengue tiap tahun. Hal ini mungkin disebabkan oleh karena curah hujan di Asia yang sangat tinggi terutama di Asia timur dan selatan ditambah dengan sanitasi lingkungan yang tidak bagus.

WHO memperkirakan lebih dari 500.000 dari 50 juta kasus demam dengue memerlukan perawatan di rumah sakit. Lebih dari 40% penduduk dunia hidup di daerah endemis demam dengue.

Bagaimana penularan demam dengue?

Virus dengue ditularkan melalui gigitan nyamuk Aedes aegypti yang sebelumnya sudah menggigit orang yang terinfeksi dengue. Populasi nyamuk ini akan meningkat pesat saat musim hujan namun nyamuk Aedes aegypti juga dapat hidup dan berkembang biak pada bak bak penampungan air sepanjang tahun. Satu gigitan nyamuk yang telah terinfeksi sudah mampu untuk menimbulkan penyakit dengue pada orang yang sehat.

Penularan demam dengue tidak bisa langsung dari manusia ke manusia tetapi harus melalui perantara nyamuk sehingga kita tidak perlu khawatir kontak langsung dengan penderita demam dengue.

Apa saja gejala dan tanda demam dengue?

Setelah tergigit nyamuk pembawa virus, masa inkubasi akan berlangsung antara 3 sampai 15 hari sampai gejala demam dengue muncul. Gejala demam dengue akan diawali oleh perasaan menggigil, nyeri kepala, nyeri saat menggerakan bola mata dan nyeri punggung. Kesakitan pada tungkai dan sendi akan terjadi beberapa jam sejak gejala demam dengue mulai dirasakan. Suhu tubuh akan meningkat dengan cepat mencapai 40 derajat celcius dengan detak nadi yang normal serta tekanan darah yang cenderung turun. Bola mata akan tampak kemerahan. Kemerahan juga tampak pada wajah yang dengan cepat akan menghilang. Kelenjar pada leher dan tenggorokan terkadang ikut membesar.

Demam dan gejala lain dari demam dengue akan berlangsung selama 2 hari yang kemudian diikuti oleh penurunan suhu yang cepat dengan diiringi oleh produksi keringat yang meningkat. Periode penurunan suhu ini biasanya berlangsung sehari, selanjutnya suhu tubuh akan meningkat lagi dengan cepat. Saat ini seluruh tubuh pasien akan kemerahan kecuali pada wajah.

Bagaimana penanganan pasien demam dengue?

Karena demam dengue disebabkan oleh virus maka tidak ada pengobatan spesifik untuk penyakit ini termasuk penggunaan antibiotika. Umumnya pengobatan demam dengue hanya ditujukan untuk mengatasi gejala yang terjadi (simptomatis). Istirahat dan asupan cairan yang cukup merupakan dua hal yang sangat penting pada pasien demam dengue. Penggunaan aspirin dan NSAID harus dihindari. Penggunaan paracetamol terutama untuk mengatasi gejala demam dan sakit kepala yang terjadi.

Bagaimana kelanjutan pasien dengue?

Demam dengue tidak akan menyebabkan kematian. Pengalaman selama ini, kematian akibat demam dengue kurang dari 1% dari seluruh kasus yang terjadi. Perbaikan kondisi pasien akan berlangsung beberapa minggu.

Bagaimana dengan demam berdarah dengue?

Demam berdarah dengue atau DBD umumnya terjadi pada anak dibawah 10 tahun. Gejalanya antara lain nyeri pada perut, perdarahan, dan syok. Bila terjadi syok maka DBD sering disebut Dengue Syok Syndrome atau DSS. Pasien dengan DSS biasanya agak sulit untuk dipulihkan.

DBD dimulai dengan demam tinggi serta sakit kepala yang hebat. Terdapat gejala pada saluran nafas dan saluran pencernaan berupa nyeri menelan, batuk, mual, muntah dan nyeri perut. Syok dapat terjadi setelah 2 sampai 6 hari semenjak gejala DBD timbul. Gejala syok dimulai dengan penurunan suhu tubuh tiba tiba, akral dingin, nadi lemah, dan kebiruan pada bibir.

Pada DBD, terdapat perdarahan pada jaringan lunak, bintik perdarahan pada kulit, muntah darah, darah pada kotoran, gusi berdarah dan mimisan. Pada beberapa kasus dapat terjadi radang paru paru dan radang pada otot jantung atau miokarditis.

Pasien dengan DBD harus di monitor dengan ketat terutama pada hari ke empat sejak timbulnya gejala. Bila terjadi kebiruan atau sianosis maka pasien harus diberikan oksigen dan apabila terdapat kegagalan vaskuler maka pasien harus diinfus. Transfusi darah diperlukan untuk mengendalikan perdarahan.

Angka kematian pasien DBD sangat tinggi antara 3 sampai 30%. Sebagian besar kematian terjadi pada anak anak.

Bagaimana mencegah demam dengue?

Transmisi virus melalui nyamuk harus dihentikan untuk mencegah timbulnya demam dengue. Untuk melakukan ini maka pasien demam dengue harus dikelilingi oleh kawat nyamuk/kelambu sampai demam mereda.

Pencegahan demam dengue membutuhkan pengendalian atau eradikasi dari nyamuk pembawa virus. Lakukan 3 M (Menguras, Menutup dan Menimbun) tempat tempat yang disukai nyamuk untuk berkembang biak. Peranan pemerintah sangat diperlukan sebagai motivator disamping peranan masyarakat sebagai pelaksana.

Sampai saat ini belum ada vaksin yang pas untuk demam dengue, sehingga hanya pencegahan terpadulah yang bisa dilakukan.

Silakan berdiskusi disini : http://medisiana.com/viewtopic.php?p=433#433

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PENANGGULANGAN MASALAH GIZI BURUK

I. Latar belakang masalah

1. Terjadi ledakan kasus gizi buruk di beberapa daerah (NTB, NTT, Lampung, Banten)
2. Prevalensi gizi kurang dan gizi buruk tinggi dan selama beberapa tahun terakhir penurunannya sangat lambat
3. Penyebab kejadian gizi buruk :
a. Kemiskinan
b. Karena pola asuh yang tidak baik
c. Adanya penyakit kronis
4. Kejadian gizi buruk tidak terjadi secara akut tetapi ditandai dengan kenaikan berat badan anak yang tidak cukup selama beberapa bulan sebelumnya yang bisa diukur dengan melakukan penimbangan secara bulanan
5. Sebagian besar kasus gizi kurang dan gizi buruk dengan tatalaksana gizi buruk dapat dipulihkan di Puskesmas/RS

II. Tujuan
Umum : menurunkan angka gizi buruk dari 8,5% menjadi 5% pada akhir 2009 (target RPJM 2005-2009)
Khusus :
1. Meningkatkan cakupan deteksi dini gizi buruk melalui penimbangan bulanan balita di posyandu
2. Meningkatkan cakupan dan kualitas tatalaksana kasus gizi buruk di puskesmas/RS dan rumah tangga
3. Menyediakan Pemberian Makanan Tambahan Pemulihan (PMT-P) kepada balita kurang gizi dari keluarga miskin
4. Meningkatkan pengetahuan dan ketrampilan ibu dalam memberikan asuhan gizi kepada anak (ASI/MP-ASI)
5. Memberikan suplementasi gizi (kapsul Vit.A) kepada semua balita


PENANGGULANGAN MASALAH GIZI BURUK

I. Latar belakang masalah

1. Terjadi ledakan kasus gizi buruk di beberapa daerah (NTB, NTT, Lampung, Banten)
2. Prevalensi gizi kurang dan gizi buruk tinggi dan selama beberapa tahun terakhir penurunannya sangat lambat
3. Penyebab kejadian gizi buruk :
a. Kemiskinan
b. Karena pola asuh yang tidak baik
c. Adanya penyakit kronis
4. Kejadian gizi buruk tidak terjadi secara akut tetapi ditandai dengan kenaikan berat badan anak yang tidak cukup selama beberapa bulan sebelumnya yang bisa diukur dengan melakukan penimbangan secara bulanan
5. Sebagian besar kasus gizi kurang dan gizi buruk dengan tatalaksana gizi buruk dapat dipulihkan di Puskesmas/RS

II. Tujuan
Umum : menurunkan angka gizi buruk dari 8,5% menjadi 5% pada akhir 2009 (target RPJM 2005-2009)
Khusus :
1. Meningkatkan cakupan deteksi dini gizi buruk melalui penimbangan bulanan balita di posyandu
2. Meningkatkan cakupan dan kualitas tatalaksana kasus gizi buruk di puskesmas/RS dan rumah tangga
3. Menyediakan Pemberian Makanan Tambahan Pemulihan (PMT-P) kepada balita kurang gizi dari keluarga miskin
4. Meningkatkan pengetahuan dan ketrampilan ibu dalam memberikan asuhan gizi kepada anak (ASI/MP-ASI)
5. Memberikan suplementasi gizi (kapsul Vit.A) kepada semua balita

III. Strategi
1. Revitalisasi posyandu untuk mendukung pemantauan pertumbuhan
2. Melibatkan peran aktif tokoh masyarakat, tokoh agama, pemuka adat dan kelompok potensial lainnya.
3. Meningkatkan cakupan dan kualitas melalui peningkatan keterampilan tatalaksana gizi buruk
4. Menyediakan sarana pendukung (sarana dan prasarana)
5. Menyediakan dan melakukan KIE
6. Meningkatkan kewaspadaan dini KLB gizi buruk


IV. Kegiatan
1. Deteksi dini gizi buruk melalui bulan penimbangan balita di posyandu
 Melengkapi kebutuhan sarana di posyandu (dacin, KMS/Buku KIA, RR)
 Orientasi kader
 Menyediakan biaya operasional
 Menyediakan materi KIE
 Menyediakan suplementasi kapsul Vit. A
2. Tatalaksana kasus gizi buruk
 Menyediakan biaya rujukan khusus untuk gizi buruk gakin baik di puskesmas/RS (biaya perawatan dibebankan pada PKPS BBM)
 Kunjungan rumah tindak lanjut setelah perawatan di puskesmas/RS
 Menyediakan paket PMT (modisko, MP-ASI) bagi pasien paska perawatan
 Meningkatkan ketrampilan petugas puskesmas/RS dalam tatalaksana gizi buruk
3. Pencegahan gizi buruk
 Pemberian makanan tambahan pemulihan (MP-ASI) kepada balita gakin yang berat badannya tidak naik atau gizi kurang
 Penyelenggaraan PMT penyuluhan setiap bulan di posyandu
 Konseling kepada ibu-ibu yang anaknya mempunyai gangguan pertumbuhan
4. Surveilen gizi buruk
 Pelaksanaan pemantauan wilayah setempat gizi (PWS-Gizi)
 Pelaksanaan sistem kewaspadaan dini kejadian luar biasa gizi buruk
 Pemantauan status gizi (PSG)
5. Advokasi, sosialisasi dan kampanye penanggulangan gizi buruk
 Advokasi kepada pengambil keputusan (DPR, DPRD, pemda, LSM, dunia usaha dan masyarakat)
 Kampanye penanggulangan gizi buruk melalui media efektif

6. Manajemen program:
 Pelatihan petugas
 Bimbingan teknis

Selanjutnya »»

kasus gizi buruk pada anak balita yang meningkat akhir-akhir ini telah membangunkan pemegang kebijakan
untuk melihat lebih jelas bahwa anak balita sebagai sumber daya untuk masa depan ternyata mempunyai
masalah yang sangat besar. Berdasarkan angka human development index (HDI), Indonesia menduduki
peringkat ke 112 di dunia. Tidak tertutup kemungkinan peringkat ini akan bergeser ke posisi lebih rendah
(memburuk) apabila kondisi ini tidak ditangani secara cepat dan tepat.
Gizi Buruk Tidak Terjadi Tiba -tiba.
Kasus gizi buruk yang meningkat dan sangat ramai
dibicarakan sejak ditemukan di NTB, telah
membuka mata kita tentang masalah gizi anak
balita. Kenyataan di lapangan, setelah NTB, hampir
seluruh daerah di Indonesia segera melaporkan
adanya kasus gizi buruk di wilayahnya. Fenomena
ini kemungkinan berkaitan dengan pengalokasian
dana yang digulirkan oleh pemerintah (Pusat) untuk
penanggulangan kasus gizi buruk. Ironis memang.


Kontroversi seputar gizi buruk :
Apakah Ketidakberhasilan Departemen Kesehatan?
kasus gizi buruk pada anak balita yang meningkat akhir-akhir ini telah membangunkan pemegang kebijakan
untuk melihat lebih jelas bahwa anak balita sebagai sumber daya untuk masa depan ternyata mempunyai
masalah yang sangat besar. Berdasarkan angka human development index (HDI), Indonesia menduduki
peringkat ke 112 di dunia. Tidak tertutup kemungkinan peringkat ini akan bergeser ke posisi lebih rendah
(memburuk) apabila kondisi ini tidak ditangani secara cepat dan tepat.
Gizi Buruk Tidak Terjadi Tiba -tiba.
Kasus gizi buruk yang meningkat dan sangat ramai
dibicarakan sejak ditemukan di NTB, telah
membuka mata kita tentang masalah gizi anak
balita. Kenyataan di lapangan, setelah NTB, hampir
seluruh daerah di Indonesia segera melaporkan
adanya kasus gizi buruk di wilayahnya. Fenomena
ini kemungkinan berkaitan dengan pengalokasian
dana yang digulirkan oleh pemerintah (Pusat) untuk
penanggulangan kasus gizi buruk. Ironis memang.
Gizi buruk merupakan kejadian kronis dan bukan
kejadian yang tiba-tiba. Pertanyaan yang timbul
adalah di mana laporan hasil pemantauan status gizi
berada dan ke mana laporan tersebut dikirimkan
selama ini? Secara teknis, mestinya laporan tersebut
berada di Dinas Kesehatan (untuk Daerah) dan
Departemen Kesehatan (untuk Pusat). Secara teknis
pula, lembaga-lembaga tersebut bertanggungjawab
atas kajian data hasil pemantauan yang dilakukan
secara berkala mulai dari tingkat Puskesmas,
dengan Posyandu sebagai ujung tombak sumber
informasi. Demikian pula institusi rumah sakit,
merupakan unit pelayanan yang juga turut
berkontribusi atas tersedianya informasi kasus
tersebut karena berkaitan dengan fungsinya sebagai
pusat rujukan kasus.
Departemen Kesehatan telah menyelenggarakan
suatu pertemuan sosialisasi pencegahan dan
penanggulangan gizi buruk bagi pemegang
kebijakan di Batam 6-8 Oktober 2005 (Regional I)
dan di Yogyakarta 11-13 Oktober 2005 (Regional
II). Pada pertemuan yang dihadiri oleh para Kepala
Dinas Kesehatan Provinsi dan Direktur Rumah
Sakit Propinsi se-Indonesia tersebut telah dibahas
Rencana Aksi Nasional (RAN) Pencegahan dan
Penanggulangan Gizi Buruk 2005-2009, yang
menginformasikan 70% dari anggaran yang tersedia
akan di fokuskan pada promosi kesehatan (dalam
hal ini upaya promotif dan preventif), sementara
30% sisanya ditujukan untuk pelaksanaan kegiatan
operasional. Diantara agenda kegiatan dalam RAN
tersebut adalah pemberian makanan tambahan
berbasis makanan lokal, dan pelatihan kader.
Peran Posyandu
Lalu, bagaimana peran posyandu sesungguhnya? Jika
kita tanyakan kepada masyarakat tentang siapa yang
bertanggung jawab dalam pelaksanaan posyandu,
maka jawaban yang akan kita peroleh adalah Tenaga
Kesehatan.
Sejak awal, posyandu berperan sebagai pos terdepan
perpanjangan tangan Depkes dalam pemberikan
pelayanan kesehatan. Posyandu tidak membutuhkan
fasilitas dan biaya yang besar, bahkan dapat
dilakukan di rumah penduduk maupun tempat-tempat
pertemuan desa. Ini merupakan suatu modal dasar
yang sangat baik, yang sebaiknya disosialisasikan
kepada khalayak dan digunakan untuk mengubah
persepsi bahwa posyandu itu bukan milik kesehatan
melainkan milik masyarakat.
Kader adalah anggota masyarakat yang diberi
ketrampilan untuk menjalankan posyandu. Untuk
mencapai hasil yang optimal, pengetahuan kader
selalu harus diperbaharui dengan melakukan
penyegaran (refreshing), agar tercipta rasa percaya
diri dalam memberikan pelayanan. Dalam hal ini
peran masyarakat sangat penting, dengan melibatkan
organisasi yang ada termasuk Karang Taruna,
LKMD, dan PKK, dengan pertimbangan mempunyai
jaringan luas, untuk keberhasilan posyandu.
Penelitian yang dilakukan oleh Pusat Studi Gizi
Pangan dan Kesehatan Universitas Hasanuddin,
Makassar, yang berkaitan dengan posyandu
menemukan kegiatan posyandu umumnya hanya
dilakukan oleh 2-3 orang kader. Kader tersebut pada
umumnya adalah ibu rumah tangga dan tidak bekerja.
Tentu saja, pada situasi ekonomi seperti saat ini,
angan-angan agar mereka datang secara sukarela
sangat sulit untuk dipertahankan. Dengan status
otonomi daerah, sudah saatnya pemda setempat
mulai memberikan perhatian pada bidang kesehatan
dengan menyediakan anggaran khusus agar
posyandu dapat berjalan baik.
Data lain berkaitan dengan posyandu pada
penelitian tersebut adalah :
Ø Penyuluhan yang diberikan sekitar 22%,
Ø Balita yang mempunyai Kartu Menuju Sehat
(KMS) 56%,
Ø Ibu balita yang mengerti pembacaan KMS
13%.
Hasil studi tersebut juga menunjukkan sebuah ironi,
yaitu masyarakat datang ke posyandu bila ada
PMT, sesudah itu menganggap tidak perlu datang
menimbang balitanya untuk melihat
pertumbuhannya. Sementara itu, kebanyakan para
pemegang kebijakan selalu mengatakan anak yang
baik pertumbuhannya adalah anak yang naik berat
badannya. Nah, bagaimana bisa diketahui kenaikan
berat badan anak bila mereka tidak datang ke
posyandu, apalagi tidak mengerti arti KMS?
Siapa yang Bertanggungjawab?
Penanganan balita gizi buruk di rumah sakit bukan
merupakan satu-satunya jalan keluar dalam
mencegah dan menangani kejadian gizi buruk ini.
Apakah ada jaminan anak yang sudah keluar dari
perawatan rumah sakit, tidak akan jatuh ke kondisi
gizi buruk lagi? Tentu saja tidak ada jaminan,
kecuali ketersediaan pangan di rumah tangga
cukup, dan pengetahuan orang tua tentang masalah
gizi memadai. Untuk adanya jaminan tersebut
sudah jelas ada sektor non-kesehatan yang
bertanggungjawab.
Sekarang sudah saatnya masalah gizi anak balita ini
ditangani dengan lebih terintegrasi, melibatkan
unsur masyarakat dan organisasi setempat, dengan
meningkatkan kesadaran pentingnya penimbangan
bulanan untuk mendeteksi kemungkinan adanya
gangguan pertumbuhan yang akan menjadi tanda
awal terjadinya masalah gizi. Bila hal ini dapat
dilasanakan dengan baik, maka gangguan
pertumbuhan dapat diatasi lebih dini dan masalah gizi
buruk tidak akan muncul. Harus disadari bahwa anak
balita merupakan calon generasi penerus bangsa,
yang akan menjadi pemimpin-pemimpin bangsa di
masa depan.
Bila kita kaji dari hasil temuan kas us lalu dikaitkan
dengan sebab-akibat timbulnya masalah gizi buruk,
kejadian masalah gizi buruk bukan semata-mata
tanggung jawab Departemen Kesehatan atau Dinas
Kesehatan di daerah. Masalah ini jelas disebabkan
oleh berbagai faktor yang pada akhirnya mengerucut
sehingga si anak tidak mendapat asupan gizi yang
cukup selama kurun waktu yang lama. Mungkin
karena ketiadaan pangan di rumah tangga, yang
apabila dikaji penyebabnya akan sangat banyak dan
tidak berkaitan dengan sektor kesehatan. Atau
mungkin karena kelalaian orangtua dalam
pengasuhan bayi dan anak balita, sehingga asupan
gizi untuk anak tidak terawasi dengan baik, sehingga
timbul masalah gizi buruk.
Oleh karenanya, penanggulangan masalah gizi pada
umumnya dan masalah gizi buruk khususnya,
merupakan tanggung jawab bersama yang melibatkan
banyak sektor yang terkait dengan segi pelayanan
kesehatan, pendidikan, ekonomi, sosial, budaya,
maupun pertanian yang menyangkut ketersediaan
pangan di tingkat rumah tangga. Sudah tentu
pemerintah (Pusat maupun Daerah) bertanggung
jawab secara keseluruhan dalam upaya menyiapkan
seluruh sumberdaya yang ada, baik berupa
sumberdaya alam, manusia, maupun biaya yang
dapat menanggulangi masalah tersebut lebih dini.
Pengerahan sumberdaya sektor kesehatan saja, hanya
akan menjadikan upaya penanggulangan masalah
seperti pemadam kebakaran, bukan mempersiapkan
agar tidak terjadi kebakaran. (emanz/gizi.net)
–— –— –— –— –— –—

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Balita Dengan Gizi Buruk di Indonesia 175 Ribu
Senin, 06 Juni 2005 | 19:45 WIB

TEMPO Interaktif, Mataram:Sebanyak 175 ribu balita (bayi usia lima tahun) di Indonesia mengalami gizi buruk (Marasmus Kwashiorkor), dan lima juta balita lainnya mengalami gizi kurang.

”Gizi buruk dialami balita di semua daerah se Indonesia. Bukan hanya di Nusa Tenggara Barat saja,” kata Pejabat Direktorat Gizi Departemen Kesehatan Rita dalam
rapat penanggulangan gizi buruk di NTB, Senin (6/6).

Ia juga mengemukakan bahwa di NTB, wanita dewasa yang tidak memiliki ijazah atau tidak berpendidikan mencapai 60 persen. Kalau dikaitkan dengan pemeliharaan anak, maka anaknya mempunyai masalah dua kali lipat dari ibu yang memiliki pendidikan lebih tinggi. “Penyuluhan yang diberikan susah dicerna ibu yang tidak berpendidikan,” ucapnya.

Indikasinya, angka penurunan penderita gizi kurang di NTB pada 1989-2003 hanya delapan persen. Dari semula 45 persen, kata Rita, kini masih diatas 35 persen. Sedangkan gizi buruk 10 persen, di atas itu masih ada 25 persen anak gizi kurang yang sangat riskan mengalami gizi buruk apabila tidak ditanggulangi.

Dalam rapat yang dipimpin Sekretaris Daerah NTB, Nanang Samodra terungkap The Habibie Center (THC) akan ikut membantu menanggulangi gizi buruk yang menyebabkan busung lapar di NTB.

Ketua Umum Ikatan Dokter Indonesia Farid A. Muluk bersama Umar Juoro dari THC sudah bertemu pejabat Dinas Kesehatan dan IDI NTB di Mataram, Ahad (5/6) siang.

Proposal yang akan diajukan untuk menanggulangi gizi buruk tersebut direncanakan kebutuhan biayanya mencapai Rp 10 miliar untuk pemberian susu setiap bulan atau Rp 300 per gelas kepada setiap balita di 1.000 desa se NTB.
“Kebutuhan ini berat kalau ditanggulangi daerah," ujar Ketua IDI Nusa Tenggara Barat SDA Soesbandoro kepada Tempo, Senin (6/6). Supriyantho Khafid

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icterus dan colostomy

download disini yach?
http://www.ziddu.com/download.php?uid=aa%2BhlZ2saKuelJmlsqyZlJyiZLCWlpmn4


kalo masih kurang coba pake searching yang da diatas tulisin
"ikterus+obstruktif" (pake tanda petik yach..)

"colostomy" (pake tanda petik juga_)

kalo masih susah juga, just callme

Selanjutnya »»

Efektifitas Kartu Menuju Sehat (KMS) Anak Balita sebagai Sarana Penyuluhan Gizi di Posyandu

Keywords: Kartu Menuju Sehat (KMS); penyuluhan gizi; Posyandu; anak balita; Abstrak Penelitian Kesehatan
Subject: COMMUNITY HEALTH CENTERS; INFANT NUTRITION; HEALTH PROMOTION

Kartu Menuju Sehat (KMS) selama ini hanya digunakan sebagai alat pemantau keadaan berat badan anak balita dan belum dimanfaatkan secara optimal sebagai alat penyuluhan gizi bagi ibu anak balita. Tujuan penelitian adalah untuk mendapatkan informasi tentang faktor-faktor yang mempengaruhi efektivitas KMS anak balita sebagai sarana pemantauan pertumbuhan anak balita dan penyuluhan gizi di Posyandu.

Disain yang digunakan dalam penelitian ini adalah cross-sectional survey. Penelitian dilaksanakan di 16 Posyandu di Kabupaten Kempar dan Belawan di Propinsi Riau, 5 orang petugas gizi tingkat Puskesmas, 9 orang bidan di desa, 58 orang kader Posyandu dan 328 ibu balita pengguna Posyandu menjadi responden penelitian. Data dikumpulkan dengan cara wawancara.

Dari penelitian tersebut didapat hasil bahwa petugas gizi tingkat Puskesmas tidak seluruhnya berlatar belakang pendidikan SPAG tetapi ada pula yang berpendidikan SMU, SMEA, dan SPK serta ada bidan desa yang berpendidikan SPK. Sebagian besar (50%) petugas gizi dan bidan di desa belum pernah mengikuti pelatihan KMS. Seluruh petugas gizi dan bidan di desa pernah melakukan kunjungan ke Posyandu untuk kegiatan imunisasi, penyuluhan, pemantauan status gizi dan memberikan pelayanan kesehatan.

Tidak semua petugas gizi memahami dengan baik grafik pertumbuhan, pesan diare, imunisasi, pedoman makanan balita dan tindakan pelayanan gizi di Posyandu. Motivasi menjadi kader sebagian besar (41.4%) karena ingin membantu masyarakat untuk kemajuan desa. 51.7% kader tidak pernah melakukan penyuluhan arena tidak tahun materi apa yang harus diberikan dalam penyuluhan, dan hanya 46.6% kader pernah mendapat pelatihan mengenai KMS. Guna KMS menurut kader adalah untuk memantau pertumbuhan balita (58.6%), yang menyebutkan sarana penyuluhan hanya 3.4%. Tingkat pengetahuan kader tentang grafik pertumbuhan dalam KMS masih rendah hanya 8.6% yang tahu, pesan diare diketahui oleh hampir 60.0% kader, dan pesan imunisasi diketahui oleh hampir 90.0% untuk mengetahui perkembangan berat badan anak. KMS lebih dari 90% disimpan sendiri oleh ibu balita. Ibu balita yang tahu tentang arti grafik dalam KMS sebanyak 18.0%, yang tahu tentang pesan imunisasi sebanyak 29.0% dan tahu tentang pesan diare sebanyak 58.0%, sedangkan yang tahu tentang jenis makanan yang harus diberikan sesuai umur anak sebanyak 61.3%. KMS sebagai sumber informasi pemberian makanan balita, imunisasi dan diare hanya dilakukan oleh 16.0% ibu balita. Panduan penggunaan KMS balita bagi petugas kesehatan (th 2000) baru sampai di tingkat provinsi.

Dari penelitian ini dapat disimpulkan bahwa KMS anak balita sudah efektif sebagai alat pemantau pertumbuhan anak balita tetapi belum efektif sebagai sarana penyuluhan gizi di Posyandu karena masih rendahnya pemahaman kader dan ibu balita terhadap arti grafik pertumbuhan anak. Di samping itu sedikit sekali kader yang tahu nasehat gizi yang harus diberikan pada ibu balita.

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Drugs and Narcotics

These days, drugs can be found everywhere, and it may seem like everyone's doing them. Many teens are tempted by the excitement or escape that drugs seem to offer. But learning the facts about drugs can help you see the risks of chasing this excitement or escape. Read on to learn more.

The Deal on Substances

Thanks to medical and drug research, there are thousands of drugs that help people. Antibiotics and vaccines have revolutionized the treatment of infections. There are medicines to lower blood pressure, treat diabetes, and reduce the body's rejection of new organs. Medicines can cure, slow, or prevent disease, helping us to lead healthier and happier lives. But there are also lots of illegal, harmful drugs that people take to help them feel good or have a good time.

How do drugs work? Drugs are chemicals or substances that change the way our bodies work. When you put them into your body (often by swallowing, inhaling, or injecting them), drugs find their way into your bloodstream and are transported to parts of your body, such as your brain. In the brain, drugs may either intensify or dull your senses, alter your sense of alertness, and sometimes decrease physical pain. A drug may be helpful or harmful. The effects of drugs can vary depending upon the kind of drug taken, how much is taken, how often it is used, how quickly it gets to the brain, and what other drugs, food, or substances are taken at the same time. Effects can also vary based on the differences in body size, shape, and chemistry.

Although substances can feel good at first, they can ultimately do a lot of harm to the body and brain. Drinking alcohol, smoking tobacco, taking illegal drugs, and sniffing glue can all cause serious damage to the human body. Some drugs severely impair a person's ability to make healthy choices and decisions. Teens who drink, for example, are more likely to get involved in dangerous situations, such as driving under the influence or having unprotected sex.

And just as there are many kinds of drugs available, there are as many reasons for trying drugs or starting to use drugs regularly. People take drugs just for the pleasure they believe they can bring. Often it's because someone tried to convince them that drugs would make them feel good or that they'd have a better time if they took them.

Some teens believe drugs will help them think better, be more popular, stay more active, or become better athletes. Others are simply curious and figure one try won't hurt. Others want to fit in. A few use drugs to gain attention from their parents. Many teens use drugs because they are depressed or think drugs will help them escape their problems. The truth is, drugs don't solve problems. Drugs simply hide feelings and problems. When a drug wears off, the feelings and problems remain - or become worse. Drugs can ruin every aspect of a person's life.

What are some of the more common drugs?

Alcohol

The oldest and most widely used drug in the world, alcohol is a depressant that alters perceptions, emotions, and senses.

How It's Used: Alcohol is a liquid that is drunk.

Effects & Dangers:

• Alcohol first acts as a stimulant, and then it makes people feel relaxed and a bit sleepy.
• High doses of alcohol seriously affect a person's judgment and coordination. Drinkers may have slurred speech, confusion, depression, short-term memory loss, and slow reaction times.
• Large volumes of alcohol drunk in a short period of time may cause alcohol poisoning.

Addictiveness: Teens who use alcohol can become psychologically dependent upon it to feel good, deal with life, or handle stress. In addition, their bodies may demand more and more to achieve the same kind of high experienced in the beginning. Some teens are also at risk of becoming physically addicted to alcohol. Withdrawal from alcohol can be painful and even life threatening. Symptoms range from shaking, sweating, nausea, anxiety, and depression to hallucinations, fever, and convulsions.

Amphetamines

Amphetamines are stimulants that accelerate functions in the brain and body. They come in pills or tablets. Prescription diet pills also fall into this category of drugs.

Street Names: speed, uppers, dexies, bennies

How They're Used: Amphetamines are swallowed, inhaled, or injected.

Effects & Dangers:

• Swallowed or snorted, these drugs hit users with a fast high, making them feel powerful, alert, and energized.
• Uppers pump up heart rate, breathing, and blood pressure, and they can also cause sweating, shaking, headaches, sleeplessness, and blurred vision.
• Prolonged use may cause hallucinations and intense paranoia.

Addictiveness: Amphetamines are psychologically addictive. Users who stop report that they experience various mood problems such as aggression and anxiety and intense cravings for the drugs.

Cocaine and Crack

Cocaine is a white crystalline powder made from the dried leaves of the coca plant. Crack, named for its crackle when heated, is made from cocaine. It looks like white or tan pellets.

Street Names for Cocaine: coke, snow, blow, nose candy, white, big C

Street Names for Crack: freebase, rock

How They're Used: Cocaine is inhaled through the nose or injected. Crack is smoked.

Effects & Dangers:

• Cocaine is a stimulant that rocks the central nervous system, giving users a quick, intense feeling of power and energy. Snorting highs last between 15 and 30 minutes; smoking highs last between 5 and 10 minutes.
• Cocaine also elevates heart rate, breathing rate, blood pressure, and body temperature.
• Injecting cocaine can give you hepatitis or AIDS if you share needles with other users. Snorting can also put a hole inside the lining of your nose.
• First-time users - even teens - of both cocaine and crack can stop breathing or have fatal heart attacks. Using either of these drugs even one time can kill you.

Addictiveness: These drugs are highly addictive, and as a result, the drug, not the user, calls the shots. Even after one use, cocaine and crack can create both physical and psychological cravings that make it very, very difficult for users to stop.

Cough and Cold Medicines (DXM)

Several over-the-counter cough and cold medicines contain the ingredient dextromethorphan (also called DXM). If taken in large quantities, these over-the-counter medicines can cause hallucinations, loss of motor control, and "out-of-body" (or disassociative) sensations.

Street Names: triple C, candy, C-C-C, dex, DM, drex, red devils, robo, rojo, skittles, tussin, velvet, vitamin D

How They're Used: Cough and cold medicines, which come in tablets, capsules, gel caps, and lozenges as well as syrups, are swallowed. DXM is often extracted from cough and cold medicines, put into powder form, and snorted.

Effects & Dangers:

• Small doses help suppress coughing, but larger doses can cause fever, confusion, impaired judgment, blurred vision, dizziness, paranoia, excessive sweating, slurred speech, nausea, vomiting, abdominal pain, irregular heartbeat, high blood pressure, headache, lethargy, numbness of fingers and toes, redness of face, dry and itchy skin, loss of consciousness, seizures, brain damage, and even death.
• Sometimes users mistakenly take cough syrups that contain other medications in addition to dextromethorphan. High doses of these other medications can cause serious injury or death.

Addictiveness: People who use cough and cold medicines and DXM regularly to get high can become psychologically dependent upon them (meaning they like the feeling so much they can't stop, even though they aren't physically addicted).

Depressants

Depressants, such as tranquilizers and barbiturates, calm nerves and relax muscles. Many are legally available by prescription (such as Valium and Xanax) and are bright-colored capsules or tablets.

Street Names: downers, goof balls, barbs, ludes

How They're Used: Depressants are swallowed.

Effects & Dangers:

• When used as prescribed by a doctor and taken at the correct dosage, depressants can help people feel calm and reduce angry feelings.
• Larger doses can cause confusion, slurred speech, lack of coordination, and tremors.
• Very large doses can cause a person to stop breathing and result in death.
• Depressants and alcohol should never be mixed - this combination greatly increases the risk of overdose and death.

Addictiveness: Depressants can cause both psychological and physical dependence.

Ecstasy (MDMA)

This is a designer drug created by underground chemists. It comes in powder, tablet, or capsule form. Ecstasy is a popular club drug among teens because it is widely available at raves, dance clubs, and concerts.

Street Names: XTC, X, Adam, E, Roll

How It's Used: Ecstasy is swallowed or sometimes snorted.

Effects & Dangers:

• This drug combines a hallucinogenic with a stimulant effect, making all emotions, both negative and positive, much more intense.
• Users feel a tingly skin sensation and an increased heart rate.
• Ecstasy can also cause dry mouth, cramps, blurred vision, chills, sweating, and nausea.
• Sometimes users clench their jaws while using. They may chew on something (like a pacifier) to relieve this symptom.
• Many users also experience depression, paranoia, anxiety, and confusion. There is some concern that these effects on the brain and emotion can become permanent with chronic use of ecstasy.
• Ecstasy also raises the temperature of the body. This increase can sometimes cause organ damage or even death.

Addictiveness: Although the physical addictiveness of Ecstasy is unknown, teens who use it can become psychologically dependent upon it to feel good, deal with life, or handle stress.

GHB

GHB, which stands for gamma hydroxybutyrate, is often made in home basement labs, usually in the form of a liquid with no odor or color. It has gained popularity at dance clubs and raves and is a popular alternative to Ecstasy for some teens and young adults. The number of people brought to emergency departments because of GHB side effects is quickly rising in the United States. And according to the U.S. Drug Enforcement Agency (DEA), since 1995 GHB has killed more users than Ecstasy.

Street Names: Liquid Ecstasy, G, Georgia Home Boy

How It's Used: When in liquid or powder form (mixed in water), GHB is drunk; in tablet form it is swallowed.

Effects & Dangers:

• GHB is a depressant drug that can cause both euphoric (high) and hallucinogenic effects.
• The drug has several dangerous side effects, including severe nausea, breathing problems, decreased heart rate, and seizures.
• GHB has been used for date rape because it is colorless and odorless and easy to slip into drinks.
• At high doses, users can lose consciousness within minutes. It's also easy to overdose: There is only a small difference between the dose used to get high and the amount that can cause an overdose.
• Overdosing GHB requires emergency care in a hospital right away. Within an hour GHB overdose can cause coma and stop someone's breathing, resulting in death.
• GHB (even at lower doses) mixed with alcohol is very dangerous - using it even once can kill you.

Addictiveness: When users come off GHB they may have withdrawal symptoms such as insomnia and anxiety. Teens may also become dependent upon it to feel good, deal with life, or handle stress.

Heroin

Heroin comes from the dried milk of the opium poppy, which is also used to create the class of painkillers called narcotics - medicines like codeine and morphine. Heroin can range from a white to dark brown powder to a sticky, tar-like substance.

Street Names: horse, smack, Big H, junk

How It's Used: Heroin is injected, smoked, or inhaled (if it is pure).

Effects & Dangers:

• Heroin gives you a burst of euphoric (high) feelings, especially if it's injected. This high is often followed by drowsiness, nausea, stomach cramps, and vomiting.
• Users feel the need to take more heroin as soon as possible just to feel good again.
• With long-term use, heroin ravages the body. It is associated with chronic constipation, dry skin, scarred veins, and breathing problems.
• Users who inject heroin often have collapsed veins and put themselves at risk of getting deadly infections such as HIV, hepatitis B or C, and bacterial endocarditis (inflammation of the lining of the heart) if they share needles with other users.

Addictiveness: Heroin is extremely addictive and easy to overdose on (which can cause death). Withdrawal is intense and symptoms include insomnia, vomiting, and muscle pain.

Inhalants

Inhalants are substances that are sniffed or "huffed" to give the user an immediate rush or high. They include household products like glues, paint thinners, dry cleaning fluids, gasoline, felt-tip marker fluid, correction fluid, hair spray, aerosol deodorants, and spray paint.

How It's Used: Inhalants are breathed in directly from the original container (sniffing or snorting), from a plastic bag (bagging), or by holding an inhalant-soaked rag in the mouth (huffing).

Effects & Dangers:

• Inhalants make you feel giddy and confused, as if you were drunk. Long-time users get headaches, nosebleeds, and may suffer loss of hearing and sense of smell.
• Inhalants are the most likely of abused substances to cause severe toxic reaction and death. Using inhalants, even one time, can kill you.

Addictiveness: Inhalants can be very addictive. Teens who use inhalants can become psychologically dependent upon them to feel good, deal with life, or handle stress.

Ketamine

Ketamine hydrochloride is a quick-acting anesthetic that is legally used in both humans (as a sedative for minor surgery) and animals (as a tranquilizer). At high doses, it causes intoxication and hallucinations similar to LSD.

Street Names: K, Special K, vitamin K, bump, cat Valium

How It's Used: Ketamine usually comes in powder that users snort. Users often do it along with other drugs such as Ecstasy (called kitty flipping) or cocaine or sprinkle it on marijuana blunts.

Effects & Dangers:

• Users may become delirious, hallucinate, and lose their sense of time and reality. The trip - also called K-hole - that results from ketamine use lasts up to 2 hours.
• Users may become nauseated or vomit, become delirious, and have problems with thinking or memory.
• At higher doses, ketamine causes movement problems, body numbness, and slowed breathing.
• Overdosing on ketamine can stop you from breathing - and kill you.

Addictiveness: Teens who use it can become psychologically dependent upon it to feel good, deal with life, or handle stress.

LSD

LSD (which stands for lysergic acid diethylamide) is a lab-brewed hallucinogen and mood-changing chemical. LSD is odorless, colorless, and tasteless.

Street Names: acid, blotter, doses, microdots

How It's Used: LSD is licked or sucked off small squares of blotting paper. Capsules and liquid forms are swallowed. Paper squares containing acid may be decorated with cute cartoon characters or colorful designs.

Effects & Dangers:

• Hallucinations occur within 30 to 90 minutes of dropping acid. People say their senses are intensified and distorted - they see colors or hear sounds with other delusions such as melting walls and a loss of any sense of time. But effects are unpredictable, depending on how much LSD is taken and the user.
• Once you go on an acid trip, you can't get off until the drug is finished with you - at times up to about 12 hours or even longer!
• Bad trips may cause panic attacks, confusion, depression, and frightening delusions.
• Physical risks include sleeplessness, mangled speech, convulsions, increased heart rate, and coma.
• Users often have flashbacks in which they feel some of the effects of LSD at a later time without having used the drug again.

Addictiveness: Teens who use it can become psychologically dependent upon it to feel good, deal with life, or handle stress.

Marijuana

The most widely used illegal drug in the United States, marijuana resembles green, brown, or gray dried parsley with stems or seeds. A stronger form of marijuana called hashish (hash) looks like brown or black cakes or balls. Marijuana is often called a gateway drug because frequent use often leads to the use of stronger drugs.

Street Names: pot, weed, blunts, chronic, grass, reefer, herb, ganja

How It's Used: Marijuana is typically smoked in cigarette (joints), hollowed-out cigars (blunts), pipes (bowls), or water pipes (bongs). Some people mix it into foods or brew it as a tea.

Effects & Dangers:

• Marijuana can affect mood and coordination. Users may experience mood swings that range from stimulated or happy to drowsy or depressed.
• Marijuana also elevates heart rate and blood pressure. Some people get red eyes and feel very sleepy or hungry. The drug can also make some people paranoid or cause them to hallucinate.
• Marijuana is as tough on the lungs as cigarettes - steady smokers suffer coughs, wheezing, and frequent colds.

Addictiveness: Teens who use marijuana can become psychologically dependent upon it to feel good, deal with life, or handle stress. In addition, their bodies may demand more and more marijuana to achieve the same kind of high experienced in the beginning.

Methamphetamine

Methamphetamine is a powerful stimulant.

Street Names: crank, meth, speed, crystal, chalk, fire, glass, crypto, ice

How It's Used: It can be swallowed, snorted, injected, or smoked.

Effects & Dangers:

• Users feel a euphoric rush from methamphetamine, particularly if it is smoked or shot up. But they can develop tolerance quickly - and will use more meth for longer periods of time, resulting in sleeplessness, paranoia, and hallucinations.
• Users sometimes have intense delusions such as believing that there are insects crawling under their skin.
• Prolonged use may result in violent, aggressive behavior, psychosis, and brain damage.
• The chemicals used to make methamphetamine can also be dangerous to both people and the environment.

Addictiveness: Methamphetamine is highly addictive.

Nicotine

Nicotine is a highly addictive stimulant found in tobacco. This drug is quickly absorbed into the bloodstream when smoked.

How It's Used: Nicotine is typically smoked in cigarettes or cigars. Some people put a pinch of tobacco (called chewing or smokeless tobacco) into their mouths and absorb nicotine through the lining of their mouths.

Effects & Dangers:

• Physical effects include rapid heartbeat, increased blood pressure, shortness of breath, and a greater likelihood of colds and flu.
• Nicotine users have an increased risk for lung and heart disease and stroke. Smokers also have bad breath and yellowed teeth. Chewing tobacco users may suffer from cancers of the mouth and neck.
• Withdrawal symptoms include anxiety, anger, restlessness, and insomnia.

Addictiveness: Nicotine is as addictive as heroin or cocaine, which makes it extremely difficult to quit. Those who start smoking before the age of 21 have the hardest time breaking the habit.

Rohypnol

Rohypnol (pronounced: ro-hip-nol) is a low-cost, increasingly popular drug. Because it often comes in presealed bubble packs, many teens think that the drug is safe.

Street Names: roofies, roach, forget-me pill, date rape drug

How It's Used: This drug is swallowed, sometimes with alcohol or other drugs.

Effects & Dangers:

• Rohypnol is a prescription antianxiety medication that is 10 times more powerful than Valium.
• It can cause the blood pressure to drop, as well as cause memory loss, drowsiness, dizziness, and an upset stomach.
• Though it's part of the depressant family of drugs, it causes some people to be overly excited or aggressive.
• Rohypnol has received a lot of attention because of its association with date rape. Many teen girls and women report having been raped after having rohypnol slipped into their drinks. The drug also causes "anterograde amnesia." This means it's hard to remember what happened while on the drug, like a blackout. Because of this it can be hard to give important details if a young woman wants to report the rape.

Addictiveness: Users can become physically addicted to rohypnol, so it can cause extreme withdrawal symptoms when users stop.

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DPR. target Hacker selanjutnya.....

JAKARTA - Setelah penjebolan yang terjadi di situs Depkominfo, Golkar, Postel, dan Depdiknas, diprediksi target hacker berikutnya adalah situs Dewan Perwakilan Rakyat (DPR).

Seorang pembaca Okezone yang tidak ingin disebutkan namanya menyatakan telah menemukan bug di situs resmi DPR. Bahkan dia mengaku, telah menemukan bug tersebut sekira empat bulan yang lalu dan telah memberitahukan kepada staf humas dan admin DPR. Sayangnya hingga sekarang, dia belum melihat adanya perbaikan.

"Permasalahannya, apakah harus dirusak terlebih dahulu webnya baru diperbaiki atau gaji admin di DPR sangat sedikit sehingga malas melakukan update security?" tulisnya kepada Okezone, di Jakarta, Selasa (22/4/2008).

Surat yang dikirimkannya kepada Okezone ini, secara bersamaan ternyata juga dikirim ke beberapa pihak terkait seperti Humas dan Admin DPR. Ia pun mengirimkan sebuah gambar sebagai bukti adanya bug tersebut.

Dia berharap, dengan notifikasi ini pihak DPR dapat segera men-debug ulang source code mereka dan di-patch sesegera mungkin sehingga tidak akan terjadi hal yang tidak diinginkan. (srn)

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Dompu di dunia maya

hi friend....!!!!, terutama kalian yang pada berasal dari Dompu, aku punya rancangan komunitas asyik di dunia maya nama kotanya Dompoe, kalo kalian mau gabung jadi warga negaranya, masuk aja ke http://dompoe.myminicity.com
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stroke means

Stroke

Also called: Brain attack

A stroke is a medical emergency. Strokes happen when blood flow to your brain stops. Within minutes, brain cells begin to die. There are two kinds of stroke. The more common kind, called ischemic stroke, is caused by a blood clot that blocks or plugs a blood vessel in the brain. The other kind, called hemorrhagic stroke, is caused by a blood vessel that breaks and bleeds into the brain. "Mini-strokes" or transient ischemic attacks (TIAs), occur when the blood supply to the brain is briefly interrupted.

Symptoms of stroke are

• Sudden numbness or weakness of the face, arm or leg (especially on one side of the body)
• Sudden confusion, trouble speaking or understanding speech
• Sudden trouble seeing in one or both eyes
• Sudden trouble walking, dizziness, loss of balance or coordination
• Sudden severe headache with no known cause

If you have any of these symptoms, you must get to a hospital quickly to begin treatment.

National Institute of Neurological Disorders and Stroke

Selanjutnya »»

Stroke

Stroke
From Wikipedia, the free encyclopedia
Jump to: navigation, search
For other uses, see Stroke (disambiguation).
Stroke
Classification and external resources
ICD-10 I61.-I64.
ICD-9 434
OMIM 601367
DiseasesDB 2247
MedlinePlus 000726
eMedicine neuro/9 emerg/558 emerg/557 pmr/187
MeSH D020521

Stroke or cerebrovascular accident (CVA) is the rapidly developing loss of brain functions due to a disturbance in the blood vessels supplying blood to the brain. This can be due to ischemia (lack of blood supply) caused by thrombosis or embolism, or due to a hemorrhage.[1] In medicine, a stroke, fit, or faint is sometimes referred to as an ictus [cerebri], from the Latin icere ("to strike"), especially prior to a definitive diagnosis.

Stroke is a medical emergency and can cause permanent neurological damage, complications and death if not promptly diagnosed and treated. It is the third leading cause of death and the leading cause of adult disability in the United States and Europe. It is predicted that stroke will soon become the leading cause of death worldwide.[2] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking, atrial fibrillation, migraine with aura, and thrombophilia (a tendency to thrombosis). Blood pressure is the most important modifiable risk factor of stroke.

The traditional definition of stroke, devised by the World Health Organisation in the 1970s,[3] is a "neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. It divides stroke from TIA, which is a related syndrome of stroke symptoms that resolve completely within 24 hours. With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly.[4]

Stroke is occasionally treated with thrombolysis ("clot-buster"), but usually with supportive care (physiotherapy and occupational therapy) and secondary prevention with antiplatelet drugs (aspirin and often dipyridamole), blood pressure control, statins and anticoagulation (in selected patients).[5]
Contents
[hide]

* 1 Classification
o 1.1 Ischemic stroke
o 1.2 Hemorrhagic stroke
* 2 Signs and symptoms
* 3 Pathophysiology
* 4 Diagnosis
o 4.1 Physical examination
o 4.2 Imaging
o 4.3 Underlying etiology
* 5 Prevention
* 6 Treatment
o 6.1 Early assessment
o 6.2 Ischemic stroke
+ 6.2.1 Thrombolysis
+ 6.2.2 Mechanical thrombectomy
o 6.3 Embolic stroke
o 6.4 Hemorrhagic stroke
o 6.5 Care and rehabilitation
* 7 Prognosis
* 8 Epidemiology
* 9 History
* 10 References
* 11 Further reading
* 12 External links

[edit] Classification
A slice of brain from the autopsy of a person who suffered an acute MCA stroke
A slice of brain from the autopsy of a person who suffered an acute MCA stroke

Strokes can be classified into two major categories: ischemic and hemorrhagic. Ischemia is due to interruption of the blood supply, while hemorrhage is due to rupture of a blood vessel or an abnormal vascular structure. 80% of strokes are due to ischemia; the remainder are due to hemorrhage.

[edit] Ischemic stroke

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction and necrosis of the brain tissue in that area. There are four reasons why this might happen: thrombosis (obstruction of a blood vessel by a blood clot forming locally), embolism (idem due to a embolus from elsewhere in the body, see below), systemic hypoperfusion (general decrease in blood supply, e.g. in shock) and venous thrombosis. Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin).

Thrombotic stroke

In thrombotic stroke, a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual, onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below) if the thrombus breaks off, at which point it is called an "embolus". Thrombotic stroke can be divided into two types depending on the type of vessel the thrombus is formed on:

* Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall (Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and fibromuscular dysplasia.
* Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery, stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and microatheroma (small atherosclerotic plaques).

Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[6]

Embolic stroke

Embolic stroke refers to the blockage of an artery by an embolus, a traveling particle or debris in the arterial bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious endocarditis).

Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolus is partially resorbed and moves to a different location or dissipates altogether.

Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree. In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain.

Cardiac causes can be distinguished between high- and low-risk:[7]

* High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and coronary artery bypass graft (CABG) surgery
* Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm, atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch

Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by the major cerebral arteries. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.

Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other types of ischemic stroke.

[edit] Hemorrhagic stroke

Main articles: Intracranial hemorrhage and intracerebral hemorrhage


CT scan showing an intracerebral hemorrhage.
CT scan showing an intracerebral hemorrhage.

Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury).

Intracerebral hemorrhage (ICH) is bleeding directly into the brain tissue, forming a gradually enlarging hematoma (pooling of blood). It generally occurs in small arteries or arterioles and is commonly due to hypertension, trauma, bleeding disorders, amyloid angiopathy, illicit drug use (e.g. amphetamines or cocaine), and vascular malformations. The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage.

[edit] Signs and symptoms

Stroke symptoms typically develop rapidly (seconds to minutes). The symptoms of a stroke are related to the anatomical location of the damage; nature and severity of the symptoms can therefore vary widely. Ischemic strokes usually only affect regional areas of the brain perfused by the blocked artery. Hemorrhagic strokes can affect local areas, but often can also cause more global symptoms due to bleeding and increased intracranial pressure. On the basis of the history and neurological examination, as well as the presence of risk factors, a doctor can rapidly diagnose the anatomical nature of the stroke (i.e. which part of the brain is affected), even if the exact cause is not yet known.

If the area of the brain affected contains one of the three prominent Central nervous system pathways—the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

* hemiplegia and muscle weakness of the face
* numbness
* reduction in sensory or vibratory sensation

In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is usually on the opposite side of the body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily suggest a stroke, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms.

In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brainstem therefore can produce symptoms relating to deficits in these cranial nerves:

* altered smell, taste, hearing, or vision (total or partial)
* drooping of eyelid (ptosis) and weakness of ocular muscles
* decreased reflexes: gag, swallow, pupil reactivity to light
* decreased sensation and muscle weakness of the face
* balance problems and nystagmus
* altered breathing and heart rate
* weakness in sternocleidomastoid muscle with inability to turn head to one side
* weakness in tongue (inability to protrude and/or move from side to side)

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

* aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
* apraxia (altered voluntary movements)
* visual field defect
* memory deficits (involvement of temporal lobe)
* hemineglect (involvement of parietal lobe)
* disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
* anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)

If the cerebellum is involved, the patient may have the following:

* trouble walking
* altered movement coordination
* vertigo and or disequilibrium

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing on the brain.

If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

[edit] Pathophysiology

Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds and after a few hours will suffer irreversible injury possibly leading to death of the tissue, i.e., infarction. Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system, typically in the heart as a consequence of atria fibriliation, or in the carotid arteries. These break off, enter the cerebral circulation, then lodge in and occlude brain blood vessels.

Due to collateral circulation, within the region of brain tissue affected by ischemia there is a spectrum of severity. Thus, part of the tissue may immediately die while other parts may only be injured and could potentially recover. The ischemia area where tissue might recover is referred to as the ischemic penumbra.

As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails leading to failure of energy dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to apoptosis.

Ischaemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact, many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se. Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling .[6]

These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism, unlike most other organs.

Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge Reactive oxygen species, inhibit apoptosis, or inhibit excitotoxic neurotransmitters, for example, have been shown experimentally to reduce tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported be neuroprotective in stroke. This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results in one large-scale clinical trial, a second trial failed to show favorable results.[6]

In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.

As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.

Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[6]

[edit] Diagnosis

Stroke is diagnosed through several techniques: a neurological examination, CT scans (most often without contrast enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.[8]

[edit] Physical examination

A systematic review found that acute facial paresis, arm drift, or abnormal speech are the best findings.[9]

[edit] Imaging

For diagnosing ischemic stroke in the emergency setting:[10]

* CT scans (without contrast enhancements)

sensitivity= 16%
specificity= 96%

* MRI scan

sensitivity= 83%
specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

* CT scans (without contrast enhancements)

sensitivity= 89%
specificity= 100%

* MRI scan

sensitivity= 81%
specificity= 100%

For detecting chronic hemorrhages, MRI scan is more sensitive.[11]

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood flow and PET with FDG isotope the metabolic activity of the neurons.

[edit] Underlying etiology

When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli. Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used techniques include:

* an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral artieries
* an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may spread to the brain vessels through the bloodstream)
* a Holter monitor study to identify intermittent arrhythmias
* an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous malformation)
* blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria

[edit] Prevention

Given the disease burden of stroke, prevention is an important public health concern.[12] Primary prevention is a lot less effective than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[12] Recent guidelines detail the evidence for primary prevention in stroke.[13] Because stroke may indicate underlying atherosclerosis, it is important to determine the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke in patients who have suffered a myocardial infarction.[14]

The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation. Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking[15][16] (active and passive), heavy alcohol consumption[17] and illicit drug use,[18] lack of physical activity, obesity and unhealthy diet.[19] Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[20] The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-counter cough and cold drugs containing sympathomimetics.[21][22]

No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise, reducing alcohol consumption or smoking cessation.[23] Nonetheless, given the large body of circumstantial evidence, best medical management for stroke includes advise on diet, exercise, smoking and alcohol use.[24] Medication or drug therapy is the most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

Blood pressure

Hypertension accounts for 35-50% of stroke risk.[25] Epidemiological studies suggest that even a small blood pressure reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[26] Lowering blood pressure has been conclusively shown to prevent both ischemic and hemorrhagic strokes.[27][28] It is equally important in secondary prevention.[29] Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[30][31][32] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[33] The available evidence does not show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other forms of cardiovascular disease should be considered and cost.[33][34]

Atrial fibrillation

Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial fibrillation.[35] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke prevention.[36]

Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke.[37][28] Statins have been shown to reduce the risk of stroke by about 15%.[38] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[39] statins might exert there effect through mechanisms other than their lipid-lowering effects.[38] Most

Diabetes mellitus

Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and retinopathy but not macrovascular complications such as stroke.[40][41]

Anticoagulation drugs

Aspirin or other antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic attack. Low doses of aspirin (for example 75-150 mg) are as effective as high doses but have fewer side-effects; the lowest effective dose remains unknown.[42] Thienopyridines (clopidogrel, ticlopidine) are modestly more effective than aspirin and have a decreased risk of gastrointestinal bleeding, but they are more expensive.[43] Their exact role remains controversial. Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[43] Dipyridamole can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side-effect.[44] Low-dose aspirin is also effective for stroke prevention after sustaining a myocardial infarction.[14] Oral anticoagulants are not advised for stroke prevention —any benefit is offset by bleeding risk.[45]

In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.[46][47] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women.[48][49]

Surgery

Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases.[24] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention after a previous symptomatic stroke.[50] Carotid artery stenting has not been shown to be equally useful.[51][52] Patients are selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences.[24] Surgery is most efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5 years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery (within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.[53][54]

Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[55] Studies of surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke.[56][57] To be beneficial, the complication rate of the surgery should be kept > 4%. Even then, for 100 surgeries, 5 patients will benefit by avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-free but would also have done so without intervention.[24]

Nutritional and metabolic interventions

A meta-analysis concluded that lowering homocysteine with folic acid and other supplements may reduce stroke.[58] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. Lonn reported positve results;[59] whereas the trial by Toole was negative.[60]

[edit] Treatment

[edit] Early assessment

Early recognition of the signs of stroke is generally regarded as important. Only detailed physical examination and medical imaging provide information on the presence, type, and extent of stroke, and hence hospital attendance — even if the symptoms were brief — is advised.[citation needed]

Studies show that patients treated in hospitals with a dedicated Stroke Team or Stroke Unit and a specialized care program for stroke patients have improved odds of recovery.

[edit] Ischemic stroke

An ischemic stroke is due to a thrombus (blood clot) occluding a cerebral artery, a patient is given antiplatelet medication (aspirin, clopidogrel, dipyridamole), or anticoagulant medication (warfarin), dependent on the cause, when this type of stroke has been found. Hemorrhagic stroke must be ruled out with medical imaging, since this therapy would be harmful to patients with that type of stroke.

Whether thrombolysis is performed or not, the following investigations are required:

* Stroke symptoms are documented, often using scoring systems such as the National Institutes of Health Stroke Scale, the Cincinnati Stroke Scale, and the Los Angeles Prehospital Stroke Screen. The Cincinnati Stroke Scale is used by emergency medical technicians (EMTs) to determine whether a patient needs transport to a stroke center.
* A CT scan is performed to rule out hemorrhagic stroke
* Blood tests, such as a full blood count, coagulation studies (PT/INR and APTT), and tests of electrolytes, renal function, liver function tests and glucose levels are carried out.

Other immediate strategies to protect the brain during stroke include ensuring that blood sugar is as normal as possible (such as commencement of an insulin sliding scale in known diabetics), and that the stroke patient is receiving adequate oxygen and intravenous fluids. The patient may be positioned so that his or her head is flat on the stretcher, rather than sitting up, since studies have shown that this increases blood flow to the brain. Additional therapies for ischemic stroke include aspirin (50 to 325 mg daily), clopidogrel (75 mg daily), and combined aspirin and dipyridamole extended release (25/200 mg twice daily).

It is common for the blood pressure to be elevated immediately following a stroke. Studies indicated that while high blood pressure causes stroke, it is actually beneficial in the emergency period to allow better blood flow to the brain.

If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

If the stroke has been the result of cardiac arrhythmia with cardiogenic emboli, treatment of the arrhythmia and anticoagulation with warfarin or high-dose aspirin may decrease the risk of recurrence. Stroke prevention treatment for a common arrhythmia, atrial fibrillation, is determined according to the CHADS/CHADS2 system.

[edit] Thrombolysis

In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen activator, tPA, is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values, high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of investigators[61] which showed that tPA improves the chances for a good neurological outcome. When administered within the first three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled patients had a good functional outcome. However, in the NINDS trial 6.4% of patients with large strokes developed substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued as a "magic bullet" and it is important for patients to be aware that despite the study that supports its use, some of the data were flawed and the safety and efficacy of tPA is controversial. A recent study found the mortality to be higher among patients receiving tPA versus those who did not.[62] Additionally, it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[63] Until additional evidence clarifies such controversies, physicians are advised to use their discretion when considering its use. Given the cited absence of definitive evidence, AAEM believes it is inappropriate to claim that either use or non-use of intravenous thrombolytic therapy constitutes a standard of care issue in the treatment of stroke.

[edit] Mechanical thrombectomy
Merci Retriever L5.
Merci Retriever L5.

Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body. In August 2004, based on data from the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Trial, the FDA cleared several of these devices, called the Merci X5 and X6 Retrievers.[64][65] The newer generation Merci L5 Retriever was additionally used in the Multi MERCI trial.[66][67][68][69] Both the MERCI and Multi MERCI trials required the first pass with the Merci Retriever to be initiated within 8 hours of onset of symptoms.

[edit] Embolic stroke

Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by 60% while antiplatelet agents can reduce stroke by 20%.[70]. However, a recent meta-analysis suggests harm from anti-coagulation started early after an embolic stroke.[71]

[edit] Hemorrhagic stroke

Patients with bleeding into (intracerebral hemorrhage) or around the brain (subarachnoid hemorrhage), require neurosurgical evaluation to detect and treat the cause of the bleeding. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at optimum levels.

[edit] Care and rehabilitation

Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to difficulties, prevent secondary complications and educate family members to play a supporting role.

A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one third of the patients manifest post stroke depression.

Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.

For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process. Often, assistive technology such as a wheelchair, walkers, canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; PT involves re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written words, problems forming speech and problems with eating (swallowing).

Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.

Stroke rehabilitation should be started as immediately as possible and can last anywhere from a few days to several months. Most return of function is seen in the first few days and weeks, and then improvement falls off with the "window" considered officially by U.S. state rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and most patients will improve to some extent : a correct diet and exercise are known to help the brain to self-recover.

[edit] Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability.[72] Stroke can affect patients physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion.[73] Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.

Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy, and psychosis.

30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances, lowered self esteem, and withdrawal.[74] Depression can reduce motivation and worsen outcome, but can be treated with antidepressants.

Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to laugh and cry pathologically, without regard to context or emotion.[72] Some patients show the opposite of what they feel, for example crying when they are happy.[75] Emotional lability occurs in about 20% of stroke patients.

Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.

Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke increases the likelihood of a seizure.[76][77]

[edit] Epidemiology

Stroke could soon be the most common cause of death worldwide.[78] Stroke is the third leading cause of death in the Western world, after heart disease and cancer,[2] and causes 10% of deaths worldwide.[79]

The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[80] Advanced age is one of the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[74][6] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.

Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[81] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.

Men are 1.25 times more likely to suffer strokes than women,[6] yet 60% of deaths from stroke occur in women.[75] Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[6] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

[edit] History
Hippocrates first described the sudden paralysis that is often associated with stroke.
Hippocrates first described the sudden paralysis that is often associated with stroke.

Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis. Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this phenomenon.[82][83]

The word stroke was used as a synonym for apoplectic seizure as early as 1599,[84] and is a fairly literal translation of the Greek term.

In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that people who had died of apoplexy had bleeding in their brains.[82][6] Wepfer also identified the main arteries supplying the brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke when he suggested that apoplexy might be caused by a blockage to those vessels.[6]

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