H Panji Irawan

Hari Kiamat dan Hisab

2010-04-29T17:48:00.000+07:00

- Seorang Arab Badui bertanya, "Kapankah tibanya kiamat?"
Nabi Muhammad SAW menjawab, "Apabila amanah diabaikan, maka tunggulah kiamat."
Orang itu bertanya lagi, "Bagaimana hilangnya amanat itu ya Rasulullah?"
Nabi Muhammad SAW menjawab, "Apabila perkara (urusan) diserahkan kepada orang yang bukan ahlinya, maka tunggulah kiamat." (HR. Bukhari)

- Belum terjadi kiamat sebelum seorang yang melewati kuburan berkata, "Alangkah baiknya sekiranya aku di tempat orang ini." (Maksudnya, dia ingin mati saja dan tidak ingin hidup karena beban berat yang selalu dihadapinya). (HR. Bukhari)

- Belum akan kiamat sehingga tidak ada lagi di muka bumi orang yang menyebut, "Allah.. Allah.." (HR. Muslim)

- Belum akan terjadi kiamat sehingga seorang membunuh tetangganya, saudaranya dan ayahnya. (HR. Muslim)

- Diantara tanda-tanda kiamat ialah ilmu terangkat, kebodohan menjadi dominan, arak menjadi minuman biasa, zina dilakukan terang-terangan, wanita berlipat banyak, dan laki-laki berkurang sehingga 50 orang wanita berbanding 1 pria. (HR. Bukhari)

- Belum akan datang kiamat sehingga manusia berlomba-lomba dengan bangunan-bangunan yang megah. (HR. Bukhari)

- Belum akan tiba kiamat melainkan matahari akan terbit dari Barat. Jika terbit dar Barat maka seluruh umat manusia akan beriman. Pada saat itu tidak bermanfaat lagi iman seseorang kepada dirinya sendiri yang belum beriman sebelum itu, atau dia belum mengusahakan kebaikan dalam masa imannya. (HR. Bukhari dan Muslim)

- Belum akan tiba kiamat sehingga harta banyak dan melimpah, dan orang keluar membawa zakat hartanya tetapi tidak ada yang mau menerimanya, dan negeri-negeri Arab kembali menjadi rerumputan hijau dengan sungai-sungai mengalir. (HR. Muslim)

- Tibanya kimat atas makhluk-makhluk yang jahat. (HR. Muslim). Penjelasan : artinya saat kiamat tiba, tidak ada lagi orang yang beriman. Jadi yang ditimpa azab kiamat ialah orang-orang yang jahat.

- Kamu akan dibangkitkan pada hari kiamat tanpa sandal, telanjang bulat dan tidak dikhitan.
Aisyah bertanya, "Ya Rasulullah, laki-laki dan perempuan saling melihat (aurat) yang lain?"
Nabi Muhammad SAW menjawab, "Pada saat itu segala urusan sangat dahsyat sehingga orang tidak memperhatikan (mengindahkan) hal itu." (Mustafaq'alaih).

- Didatangkan kebaikan-kebaikan (pahala) dan kejahatan-kejahatan (dosa) seorang hamba, lalu saling mengikis dan bila masih tersisa kebaikan (pahala) itu, Allah akan melapangkannya masuk surga. (HR. Bukhari)

- Amal seseorang tidak dapat menyelamatkannya.
Seorang sahabat lantas bertanya tentangg sabda tersebut, "Termasuk engkau juga, ya Rasulullah?"
Rasulullah SAW lalu menjawab, "Ya, aku juga, kecuali dikarunia Allah dengan rahmatNya. Walaupun demikian kamu harus berbuat yang benar (baik)." (HR. Bukhari dan Muslim)

- Yang pertama diadili antara manusia pada hari kiamat ialah kasus pembunuhan. (HR. Muslim)

Keutamaan Mempelajari Fikih dan Ilmu Agama

2010-04-29T17:43:00.000+07:00

Apabila Allah menginginkan kebaikan bagi seseorang maka, dia diberi pendalaman dalam ilmu agama. Sesungguhnya memperoleh ilmu hanya dengan belajar. (HR. Bukhari)

Keistimewaan Muslimin dan Mukminin

2010-04-22T08:14:00.001+07:00

- Sesungguhnya di kalangan hamba-hamba Allah ada orang yang apabila memohonkan sesuatu maka Allah akan menerimanya (mengabulkannya). (HR. Bukhari dan Muslim)

- Mencaci-maki seorang mukmin adalah suatu kejahatan, dan memeranginya adalah suatu kekufuran. (HR. Muslim)

- Seorang mukmin yang kuat lebih baik dan lebih disukai Allah daripada seorang mukmin yang lemah dalam segala kebaikan. Peliharalah apa-apa yang menguntungkan kamu dan mohonlah pertolongan Allah, dan jangan lemah semangat (patah hati). Jika ditimpa suatu musibah janganlah berkata, "Oh andaikata aku tadinya melakukan itu tentu berakibat begini dan begitu", tetapi katakanlah, "Ini takdir Allah dan apa yang dikehendaki Allah pasti dikerjakanNya." Ketahuilah, sesungguhnya ucapan : "Andaikata" dan "Jikalau" membuka peluang bagi karya setan. (HR. Muslim)

- Seorang mukmin bukanlah pengumpat dan suka mengutuk, yang keji dan yang ucapannya kotor (HR. Bukhari)

Islam - Iman - Ihsan

2010-04-22T07:27:00.000+07:00

- Pada suatu hari kami (Umar Ra dan para sahabat Ra) duduk-duduk bersama Rasulullah SAW. Lalu muncul dihadapan kami seorang yang berpakaian putih. Rambutnya hitam sekali dan tidak tampak tanda-tanda perjalanan. Tidak seorangpun dari kami yang mengenalnya. Dia langsung duduk menghadap Rasulullah SAW. Kedua kakinya menghempit kedua kaki Rasulullah. Dan kedua telapak tangannya diletakkan di atas paha Rasulullah SAW, seraya berkata,
"Ya Muhammad beritahu aku tentang Islam."
Lalu Rasulullah SAW menjawab, "Islam adalah bersyahadat bahwa tiada tuhan selain Allah dan Muhammad adalah Rasulullah, mendirikan Sholat, menunaikan zakat, puasa Ramadhan dan beribadah Haji bila mampu."
Kemudian dia bertanya lagi, "Kini beritahu aku tentang iman"
Rasulullah SAW menjawab, "Beriman kepada Allah, malaikat-malaikatNya, kitab-kitabNya, rasul-rasulNya, hari akhir dan beriman kepada Qodar baik dan buruknya."
Orang itu lantas berkata, "Benar. Kini beritahu Aku tentang ihsan."
Rasulullah berkata, "Beribadah kepada Allah seolah-olah anda melihatNya walaupun anda tidak melihatNya, karena sesungguhnya Allah melihat anda."
Dia bertanya lagi, "Beritahu aku tentang Assa'ah (azab kiamat)."
Rasulullah menjawab, "Yang ditanya tidak lebih tahu dari yang bertanya."
Kemudian dia bertanya lagi, "Beritahu aku tentang tanda-tandanya"
Rasulullah menjawab, "Seorang budak wanita melahirkan nyonya besarnya. Orang-orang tanpa sandal, setengah telanjang, melarat dan penggembala unta masing-masing berlomba membangun gedung-gedung bertingkat."
Kemudian orang itu pergi menghilang dari pandangan mata.
Lalu Rasulullah SAW bertanya kepada Umar, "Hai Umar, tahukah kamu siapa orang yang bertanya tadi?"
Lalu Aku (Umar) menjawab, "Allah dan rasulNya lebih mengetahui."
Rasulullah SAW lantas berkata, "Itulah Jibril datang untuk mengajarkan agama kalian." (HR. Muslim)

- Sufyan bin Abdullah berkata, "Ya Rasulullah, terangkan kepadaku tentang Islam. Aku tidak akan bertanya lagi kepada orang lain." Lalu Rasulullah SAW menjawab, "Ikrarkanlah (katakan): Aku beriman kepada Allah, kemudian berlakulah jujur (istiqomah)." (HR. Muslim)

- Sesungguhnya bermula datangnya Islam dianggap asing (aneh) dan akan datang kembali asing. Namun berbahagialah orang-orang asing itu. Para sahabat bertanya kepada Rasulullah SAW, "Ya Rasulullah, apa yang dimaksud orang asing (aneh) itu?" Lalu Rasulullah menjawab, "Orang yang melakukan kebaikan-kebaikan disaat orang-orang melakukan pengerusakan." (HR. Muslim)

Ketinggian Al-Qur'an

2010-04-22T07:16:00.000+07:00

- Aku tinggalkan untuk kalian dua perkara. Kalian tidak akan sesat selama berpegangan dengannya, yaitu Kitabullah (Al-Qur'an) dan sunnah Rasulullah SAW. (HR. Muslim)

- Sesungguhnya Allah dengan kitab ini (Al-Qur'an) meninggikan derajat kaum-kaum dan menjatuhkan derajat kaum yang lain. (HR. Muslim). Penjelasan : maksudnya Barangsiapa yang berpedoman dan mengamalkan isi Al-Qur'an maka Allah akan meninggikan derajatnya, tapi barangsiapa yang tidak beriman kepada Al-Quran maka Allah akan menghinakannya dan merendahkan derajatnya.

- Orang yang pandai membaca Al-Qur'an akan bersama malaikat yang mulia lagi berbakti, dan yang membaca tetapi sulit dan terbata-bata maka dia mendapat dua pahala. (HR. Bukhari dan Muslim)

- Sebaik-baik kamu ialah yang mempelajari Al-Qur'an dan mengajarkannya. (HR. Bukhari)

Muhammad Rasulullah SAW

2010-04-22T07:03:00.000+07:00

- Kepada Rasulullah SAW disarankan agar mengutuk orang-orang musyrik. Tetapi beliau menjawab : "Aku tidak diutus untuk (melontarkan) kutukan, tetapi sesungguhnya aku diutus sebagai (pembawa) rahmat." (HR. Bukhari dan Muslim)

- Rasulullah SAW melakukan shalat malam sehingga kedua kakinya bengkak. Beliau juga tidak senang bila ada orang berjalan di belakangnya." (Artinya, tidak sejajar dan berjalan dibelakangnya dengan maksud untuk menghormati beliau. (HR. Bukhari dan Muslim)

- Tiada seorang beriman hingga aku lebih dicintai dari ayahnya, anaknya, dan seluruh manusia. (HR. Bukhari)

- Aku Muhammad dan Ahmad (terpuji), yang dihormati, yang menghimpun manusia, nabi (penyeru) taubat, dan nabi (penyebar) rahmat. (HR. Muslim)

Perihal Nabi-Nabi dan Rasul-Rasul

2010-04-22T06:54:00.000+07:00

- Tiada Allah mengutus seorang Nabi kecuali pasti dia penggembala domba (HR. Bukhari dan Muslim)

- Kami (para Nabi) tidak diwarisi (meninggalkan warisan). Apa yang kami tinggalkan adalah sodaqoh (untuk umat). (HR. Bukhari)

- "Isa bin Maryam melihat sendiri seorang yang mencuri, lalu Isa' Alaihissalam berkata kepada orang itu, "Kamu mencuri." Tapi pencuri itu menjawab, "Tidak, demi Allah yang tiada Tuhan kecuali Dia." Isa lalu berkata lagi, "Aku beriman kepada Allah dan mendustakan mataku sendiri. (HR. Bukhari dan Muslim)"

Seruan dan Peringatan Allah SWT

2010-04-22T06:40:00.000+07:00

- Rasulullah SAW bersabda bahwa Allah SWT berfirman : "Anak Adam mendustakan Aku padahal tidak seharusnya dia berbuat demikian. Dia mencaci Aku padahal tidak seharusnya demikian. Adapun mendustakan Aku adalah dengan ucapannya bahwa Allah tidak akan menghidupkan aku kembali sebagaimana menciptakan aku pada permulaan." Ketahuilah bahwa tiada ciptaan (makhluk) pertama lebih mudah bagiku daripada mengulangi ciptaan. Adapun caci-makinya terhadap Aku ialah dengan berkata, "Allah mempunyai anak." Padahal Aku Maha Esa yang bergantung kepada-Ku segala sesuatu. Aku tiada beranak dan tiada pula diperanakkan dan tidak ada seorangpun setara dengan Aku." (HR. Bukhari)

- Anak Adam mengganggu Aku, mencaci-maki jaman (masa), dan Akulah jaman. Aku yang menggilirkan malam dan siang. (HR. Bukhari dan Muslim)

- Allah memiliki sembilan puluh sembilan nama, seratus kurang satu. Barangsiapa memperhitungkannya dia masuk surga. (Artinya, mengenalnya dan melaksanakan hak-hak nama-nama itu). (HR. Bukhari)

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2010-04-20T21:08:00.009+07:00

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Risiko Janin Jika Hamil Gangguan Jantung

2010-04-04T07:14:00.000+07:00

Kesehatan ibu hamil sangat berpengaruh pada janin yang sedang di kandungnya. Berikut ini risiko yang kemungkinan dialami bayi dari ibu yang pada saat hamil menderita gangguan jantung.

Bayi lahir dengan berat badan rendah. Hal ini terjadi karena pada umumnya aliran darah ke janin kurang, sehingga proses perkembangan janin dalam kandungan pun mungkin agak terhambat.

Bayi lahir prematur. Kondisi seperti ini biasanya terjadi karena kondisi ibu yang memburuk, sehingga bayi perlu segera dikeluarkan melalui operasi.

Agar risiko pada janin tersebut bisa diantisipasi, waspadai gejala gangguan jantung pada ibu hamil. Asosiasi Jantung di Amerika membagi gangguan jantung dalam 4 tingkatan.

Tingkat I: Ringan. Gejala: tanpa gejala, dapat melakukan kegiatan sehari-hari tanpa batas.

Tingkat II: Ringan. Gejala: ada sedikit gejala, yaitu kadang-kadang jika terlalu lelah terjadi bengkak di beberapa bagian tubuh. Selain itu, ada keterbatasan dalam melakukan latihan-latihan tertentu yang agak berat.

Tingkat III: Sedang. Gejala: dapat dikenali dari keterbatasan saat melakukan aktivitas yang berat. Selain itu, orang yang bersangkutan hanya merasa nyaman dalam keadaan istirahat.

Tingkat IV: Berat. Gejala: sukar melakukan kegiatan fisik. Bergerak sedikit saja sudah terengah-engah. Bahkan, gejala gangguan ini juga terasa di saat istirahat.

http://www.ayahbunda.co.id/mobile/article/mobArticleDetail.aspx?mc=001&smc=001&ar=852

Mengatasi Napas Pendek Ibu Hamil

2010-04-04T07:12:00.000+07:00

Salah satu masalah yang biasa dialami ibu hamil adalah napas pendek. Pada saat hamil, Anda bernapas untuk dua orang, Anda dan janin Anda. Kerja jantung dan paru-paru pun semakin berat. Ini yang menyebabkan napas ibu hamil pendek.

Untuk mengatasinya, coba lakukan hal-hal ini :

Segera tarik napas dalam, tahan sebentar, lalu hembuskan perlahan-lahan. Atau, fokuskan perhatian pada hembusan napas keluar dan tarikan napas ke dalam sampai tubuh Anda terasa relaks.

Lakukan latihan olah napas dengan cara berjalan santai atau berenang.

Biasakan melakukan segala sesuatu dengan tenang, tidak tergesa-gesa termasuk membiasakan jalan dengan santai, tubuh tegak dan bahu tidak tegang.

Hindari membawa beban berat. Bila membawa barang, bagi secara seimbang antara tangan kanan dengan kiri.

Tidurlah dengan posisi miring dan jangan posisi telentang. Atau, tidurlah dengan posisi setengah duduk dan gunakan beberapa bantal sebagai pengganjal bahu.

http://www.ayahbunda.co.id/mobile/article/mobArticleDetail.aspx?mc=001&smc=005&ar=449

Jalan kaki, Olah Raga Pas Ibu hamil

2010-04-04T07:10:00.000+07:00

Olahraga jalan kaki yang baik bagi jantung dan pembuluh darah adalah pilihan paling tepat bagi ibu hamil. Mudah, murah dan dapat dilakukan di mana saja.

Selama kehamilan Anda sehat, jalan kaki bisa dilakukan di usia kehamilan berapa pun. Olahraga jalan kaki juga tidak membebani tubuh, terutama persendian. Bonus lain adalah pemandangan indah dan udara segar.

Teknik berjalan kaki perlu lebih diperhatikan saat usia kehamilan masuk trimester kedua. Perut yang semakin besar akan menyebabkan pergeseran titik berat tubuh. Selain mempengaruhi keseimbangan tubuh yang membuat risiko jatuh semakin besar, peningkatan beban pada daerah pinggang akan mempermudah terjadinya nyeri pinggang.

Walau jalan kaki dianggap aman bagi ibu hamil, ada baiknya Anda tetap berkonsultasi lebih dulu dengan dokter. Setelah mendapat lampu hijau dari dokter, Anda bisa memulai olahraga ini dengan persiapan benar dan mencermati hal-hal penting berikut:

Cermati kondisi lingkungan.

Pilih lokasi yang aman, jalanan yang rata, tidak berbatu-batu dan tidak licin. Semakin dekat ke tanggal perkiraan bayi lahir, pilih lokasi yang dekat rumah, semisal jogging track di kompleks perumahan Anda

Suhu tidak terlalu dingin atau panas serta tidak banyak anginnya

Udaranya relatif bersih

Lalu lintas tidak terlalu ramai

Tidak terlalu tinggi dari permukaan laut. Makin tinggi dataran, kadar oksigen di udara makin tipis

Cegah dehidrasi. Selain bisa memicu kontraksi rahim, dehidrasi (kekurangan cairan) bisa meningkatkan suhu tubuh Anda. Kondisi yang tak bisa diabaikan, karena suhu tubuh janin lebih tinggi 0,5 derajat C dari suhu tubuh ibu. Minum air secukupnya 15 menit sekali, sebelum, selama dan setelah jalan kaki.

Pemanasan dan peregangan

Warming up agar terhindar dari risiko cidera otot. Caranya, jalan kaki perlahan selama 5 menit sampai Anda merasa cukup hangat.

Setelah pemanasan, lakukan peregangan otot kurang lebih 5 menit. Meliputi leher, tangan, pinggul, otot bagian atas dan bawah kaki, termasuk otot hamstring (otot di sisi belakang paha dan pergelangan kaki). Peregangan juga sebaiknya dilakukan setelah selesai jalan kaki

Ajak suami atau teman. Selain lebih memotivasi agar berlatih rutin, Anda juga bisa mendapat pertolongan jika sewaktu-waktu dibutuhkan

Porsi harus pas. Bila Anda sebelumnya jarang berolahraga, cara terbaik untuk memulai olahraga jalan kaki adalah berjalan sejauh Anda mampu dan dengan kecepatan yang dirasa paling nyaman. Semisal 5-10 menit setiap pagi dan 5-10 meniti di sore hari di minggu pertama. Secara bertahap, tambah 1-2 menit setiap minggu sampai mencapai 30 menit, termasuk pemanasan dan pendinginan dengan frekuensi lima hari seminggu.

Bila sudah biasa berjalan kaki, lanjutkan dengan mulai olahraga ini selama 20-30 menit per hari selama 3 kali seminggu. Selanjutnya tingkatkan perlahan menjadi 30-60 menit lebih dari 3 kali seminggu. Namun, tetap diperhatikan jangan sampai berlebihan.

Hentikan dan segera ke dokter bila:
Terjadi pendarahan dari vagina
Keluar cairan ketuban dari vagina
Pusing atau merasa mau pingsan
Pandangan kabur
Jantung berdebar-debar
Kontraksi

http://www.ayahbunda.co.id/mobile/article/mobArticleDetail.aspx?mc=001&smc=001&ar=578

Hamil: Waspada Mioma Uteri dan Kelainan Jantung

2010-04-04T07:05:00.000+07:00

Mioma uteri. Miom atau tumor di dalam rahim adalah sel otot dinding rahim yang berubah menjadi tumor. Sebagian besar tidak berbahaya atau jarang berubah menjadi kanker. Keberadaannya dideteksi lewat pemeriksaan ultrasonografi (USG).
Gejala: Miom kecil tidak bergejala, tapi bila besar dapat menimbulkan nyeri di perut atau pinggul, perut terasa penuh, nyeri saat sanggama, gejala anemia karena banyak kehilangan darah (bila perdarahan), sering berkemih karena miom menekan kandung kemih, sembelit dan tekanan pada panggul.

Yang bisa dilakukan:

Bila timbul gejala, dokter akan memberi obat analgesik untuk meredakan nyeri dan Anda diminta istirahat.

Periksa rutin ke dokter karena miom dapat membesar dan mengancam kehamilan selama trimester pertama lantaran ia mendorong embrio sehingga tidak menempel dengan baik di dinding rahim.

Bila kehamilan berlanjut, miom dapat mendesak janin sehingga letaknya sungsang atau melintang. Risiko plasenta previa (plasenta yang tumbuh di bagian bawah rahim) serta perdarahan persalinan meningkat.

Kelainan Jantung. Ketika hamil. volume darah meningkat 30% - 50% membuat jantung bekerja ekstra keras untuk memompa darah agar mengalir ke seluruh tubuh. Jika kondisi jantung yang sudah terganggu, itu akan membahayakan kesehatan jantung dan ibu secara keseluruhan.
Gejala: sulit bernapas, pingsan, pembengkakan sendi, pertambahan bobot tubuh cepat, jantung berdebar lebih cepat, pusing, nyeri dada, sering lelah dan lemas.

Yang dapat dilakukan:

Pantau kehamilan oleh dokter kandungan dan dokter ahli jantung. Jika perlu, periksa jantung dengan alat pemantau jantung, echocardiogram dan electrocardiogram, pada setiap pemeriksaan rutin kehamilan.

Konsumsi obat-obatan untuk mengatur debar jantung dalam dosis yang aman bagi janin.

http://www.ayahbunda.co.id/mobile/article/mobArticleDetail.aspx?mc=001&smc=001&ar=1162

Cermati Degup Jantung Ibu Hamil

2010-04-04T06:48:00.000+07:00

Dalam kondisi normal pun, jantung ibu hamil bekerja lebih berat. Bagaimana pula kalau mengalami gangguan?

Kerja keras jantung. Di Amerika Serikat, diketahui bahwa gangguan jantung dialami oleh 1-4% ibu hamil, yang sebelumnya tidak pernah diketahui sama sekali oleh penderitanya. Di Indonesia, angka ini belum tercatat.

Munculnya gangguan jantung yang serius pada seorang ibu hamil, yang sebenarnya sudah menyandang gangguan jantung, memang bukan suatu kebetulan. Mengapa?

Kehamilan itu sendiri merupakan suatu proses yang membuat seluruh tubuh berubah. Pada saat hamil, volume darah akan bertambah sekitar 40%. Ini merupakan akibat dari meningkatnya kadar hormon estrogen, terutama pada usia kehamilan 30 minggu. Akibatnya, jantung harus bekerja lebih berat dan lebih cepat untuk memompa darah.

Selain itu, perlu Anda tahu, meningkatnya volume darah ini lebih besar dari peningkatan massa sel darah merah. Akibatnya, sering timbul anemia (kekurangan sel darah merah dalam darah) pada ibu hamil.

Jadi, tanpa adanya gangguan jantung pun, kerja jantung sebenarnya sudah berat ketika hamil. Tak heran, kalau seorang ibu hamil kadang-kadang juga akan merasakan napasnya terengah-engah dan mudah lelah, sekalipun kondisi jantungnya baik-baik saja.

Nah, apalagi mereka yang sebelumnya sudah menyandang gangguan jantung. Jantungnya tentu akan memikul beban yang lebih berat lagi.

Risikonya berat. Lalu, apa risiko yang ada di depan ibu hamil? Risiko itu bisa berupa serangan jantung, stroke, sampai membanjirnya aliran darah ke paru-paru. Jika sudah ada kelainan gagal jantung, biasanya suplai darah, baik yang ke otak atau ke ginjal, akan terganggu. Untuk memenuhi kebutuhan akan darah yang kaya oksigen, paru-paru harus bekerja keras, dan membengkak.

Prof. Michael Gatzoulis dari Bagian Kardiologi Rumah Sakit Royal Brompton, Inggris, menyebutkan, jika kondisi seperti itu tak diatasi, bukan tak mungkin dapat menyebabkan kematian pada ibu hamil. Jalan keluarnya?

Kehamilannya itu harus diawasi secara intensif oleh dokter spesialis kandungan dan dokter spesialis jantung. Jika perlu, si ibu hamil diberi obat-obatan untuk mengatasi gangguan jantungnya, yang tentu saja aman bagi janinnya

Bila kondisinya stabil, maka si ibu dapat melahirkan bayi pada usia kandungan yang mencukupi (38-40 minggu). Tapi adakalanya janin harus dikeluarkan lebih awal, misalnya di usia 32 minggu.

Proses persalinan pada ibu hamil yang menyandang gangguan jantung perlu perhatian lebih. Sebab, peningkatan aliran darah di pembuluh darah balik ke jantung yang terjadi ketika rahim berkontraksi, dapat membahayakan jantung. Pada proses persalinan itu, pengeluaran darah dari jantung meningkat 20% pada setiap kontraksi.

Jelaslah mengapa proses persalinan bayi dari ibu yang menyandang gangguan jantung, bukan hanya perlu ditunggui dokter ahli kandungan, tetapi juga dokter anestesi yang berpengalaman menangani pasien dengan gangguan jantung. Bahkan jika perlu, juga ditunggui dokter spesialis jantung dan dokter spesialis anak yang menangani bayi baru lahir. Sebab, pada kondisi tertentu ada pasien yang ketika melahirkan memang harus menjalani pembiusan agar tidak membahayakan jantungnya.

Pentingnya memeriksakan diri. Untuk mencegah kemungkinan yang tak diinginkan, dokter biasanya menganjurkan wanita, terutama yang sudah tahu bahwa ia sudah menyandang gangguan jantung, untuk berkonsultasi lebih dulu ke dokter sebelum hamil. Konsultasinya bukan hanya dengan dokter spesialis kandungan, tetapi juga dengan dokter ahli jantung.

"Repotnya, 85-90% dari mereka yang ketika masih anak-anak sudah dikoreksi ganguan jantungnya, seringkali tidak menghubungi lagi rumah sakit tempat mereka dirawat", ujar Prof. Philip Steer, ahli kandungan dari Chelsea, Inggris. Akibatnya, banyak wanita yang sudah terlanjur hamil, tanpa tahu risiko yang mungkin akan dialaminya.

Jadi, sekali lagi, konsultasikan kondisi kesehatan Anda sebelum hamil. Kalau Anda memang mengalami gangguan jantung tergolong ringan, tak perlu terlalu khawatir dengan keadaan Anda. Anda bisa kok, menjalani kehamilan dan persalinan normal selama dalam pantauan dokter.

http://www.ayahbunda.co.id/mobile/article/mobArticleDetail.aspx?mc=001&smc=001&ar=851

Ferguson Sadari MU Kini Tertekan

2010-04-04T05:27:00.000+07:00

VIVAnews - Banyak yang menempatkan laga Manchester United kontra Chelsea sebagai laga penentu jawara Liga Inggris musim ini. Dan kekalahan 2-1 MU dari The Blues kini disadari Sir Alex Ferguson sebagai sebuah kerugian Iblis Merah.

"Chelsea saat ini menjadi favorit. Itu tidak diragukan lagi," ujar Ferguson kepada Guardian.co.uk, Minggu 4 April 2010.

Ucapan Ferguson ini tentu bukan hanya untuk membuat kubu The Blues lengah. Pasalnya, kemenangan itu juga membuat skuad The Blues kini mengangkangi MU di klasemen sementara. The Blues kini berbalik unggul dua poin dari MU.

Tak hanya itu, di lima partai tersisa, Iblis Merah juga akan melawan tim-tim kuat macam Manchester City dan Tottenham Hotspur. Alasan itu pula yang membuat MU kini dalam kondisi tertekan.

Namun bukan Ferguson jika menyerah begitu saja. Pelatih tersukses di Liga Inggris ini tetap yakin timnya berpeluang mengejar Chelsea dan tampil sebagai juara untuk keempat kalinya secara beruntun.

Pasalnya Chelsea juga akan mendapat dua tantangan besar di lima laga terakhir. John Terrry cs akan mendapat lawan berat dari Liverpool dan Tottenham Hotspur.

"Kami akan merespon. Kami harus memenangkan lima pertandingan kami selanjutnya dan juara belum ditentukan," tegas Ferguson.
http://wap.vivanews.com/news/read/141298-ferguson_sadari_mu_kini_tertekan

Taklukkan MU, Chelsea Rebut Singgasana

VIVAnews - Manchester United harus rela kehilangan puncak klasemen setelah menelan kekalahan dari rival terberatnya Chelsea. Tuan rumah MU berhasil ditaklukkan Chelsea 1-2 di Old Trafford, Sabtu 3 April 2010.

Gol Chelsea dicetak Joe Cole di menit ke-20 di babak pertama dan Didier Drobga di menit ke-79. Sedangkan satu-satunya gol Iblis Merah dicetak Federico Macheda di menit ke-81.

Dengan kekalahan ini MU harus rela puncak klasemen Premeier League (Liga Inggris) direbut pasukan Carlo Ancelotti. Chelsea kini mengoleksi 74 poin sekaligus berhak memuncaki klasemen atau unggul dua poin dari MU di posisi kedua.

Setan Merah sebenarnya langsung menekan sejak peluit ditiup wasit Mike Dean di awal babak pertama. Peluang pertama Iblis Merah lahir lewat aksi Dimitar Berbatov saat pertandingan baru berjalan delapan menit. Sayang tandukan Berba tidak menemui sasaran.

MU kembali mengancam lewat aksi Patrice Evra di menit ke-11. Sayang tusukan Evra yang diakhiri tembakan masih mampu diantisiipasi Petr Cech.

Justru MU yang harus menelan pil pahit saat gawangnya jebol. Joe Cole berhasil memanfaatkan aksi Florent Malouda yang lolos dari jebakan off side. Dari sudut sempit, Malouda memberi bola pada Cole untuk mencetak gol backheel. Skor 1-0 buat keunggulan Chelsea ini bertahan hingga turun minum.

Di babak kedua, MU sempat mengurung pertahanan Chelsea. Namun lagi-lagi peluang demi peluang lewat MU lewat Berbatov tak mampu membuahkan hasil. Bahkan Chelsea kembali mengejutkan MU lewat gol Didier Drogba di menit ke-79.

Striker Pantai Gading yang masuk menggantikan Nicolas Anelka ini berhasil melapaskan tembakan keras yang gagal dihentikan Edwin van der Sar. Chelsea sementara unggul 0-2.

Keputusan Ferguson memasukan dua darah segar, Federico Macheda yang menggantikan Park Ji-sung dan Luis Nani menggantikan Paul Scholes sempat membuahkan hasil di menit ke-81.

Macheda berhasil memperkecil ketinggalan menjadi 1-2 setelah mampu memanfaatkan umpan terukur Nani. Macheda mencetak gol setelah bola sempat membentur tangannya. MU mencoba mengejar ketinggalan. Namun usaha itu tak membuahkan hasil hingga pertandingan usai.

Susunan Pemain:

MU: Edwin van der Sar, Nemanja Vidic, Rio Ferdinand, Patrice Evra, Gary Neville, Paul Scholes (Nani, 72'), Darren Fletcher (Darron Gibson, 86'), Ji-Sung Park (Federico Macheda, 72'), Ryan Giggs, Antonio Valencia, Dimitar Berbatov

Chelsea: Petr Cech, John Terry, Alex, Yuri Zhirkov, Paulo Ferreira, John Mikel Obi, Frank Lampard, Joe Cole (Salomon Kalou, 74'), Florent Malouda, Deco (Michael Ballack, 82'), Nicolas Anelka (Didier Drogba, 70')
http://wap.vivanews.com/news/read/141263-chelsea_taklukkan_mu_guna_rebut_singgasana

Babak 1 : MU Tertinggal Lewat Gol Joe Cole

VIVAnews - Manchester United sementara harus rela tertinggal 1-0 dari tamunya Chelsea. Gol semata wayang Chelsea di 45 menit babak pertama lahir lewat aksi gol Joe Cole di Old Trafford, Sabtu 3 April 2010.

Setan Merah sebenarnya langsung menekan sejak peluit ditiup wasit Mike Dean di awal babak pertama. Peluang pertama Iblis Merah lahir lewat aksi Dimitar Berbatov saat pertandingan baru berjalan delapan menit. Sayang tandukan Berba tidak menemui sasaran.

MU kembali mengancam lewat aksi Patrice Evra di menit ke-11. Sayang tusukan Evra yang diakhiri tembakan masih mampu diantisiipasi Petr Cech.

Justru MU yang harus menelan pil pahit saat gawangnya jebol. Joe Cole berhasil memanfaatkan aksi Florent Malouda yang lolos dari jebakan off side. Dari sudut sempit, Malouda memberi bola pada Cole.

Skor 1-0 buat keunggulan Chelsea ini bertahan hingga turun minum. Chelsea berpeluang mengkudet tampuk pimpinan Liga Inggris jika berhasil meraup tiga poin di lawatannya kali ini.
http://wap.vivanews.com/news/read/141255-mu_tertinggal_lewat_gol_joe_cole

Babak 2 : Macheda Balas Gol Drogba, Chelsea Unggul

VIVAnews - Setelah tertinggal 0-1 lewat gol Joe Cole di babak pertama, Manchester United kini tertinggal 1-2 dari tamunya Chelsea.

Bertanding di Old Trafford, Sabtu 3 April 2010, pada babak kedua sebenarnya MU kembali mengurung pertahanan Chelsea. Namun peluang demi peluang yang diciptakan Dimitar Berbatov tak membuahkan hasil.

Bahkan Chelsea kembali menambah gol lewat striker Didier Drogba yang berstatus sebagai pemain pengganti. Pada menit ke-79, Drobga berhasil melepaskan tembakan keras di sisi kiri kotak penalti MU. 2-0 buat Chelsea.

Ferguson mulai panik. Federico Macheda dimasukkan. Dan status sebagai super sub sempat dibuktikan striker muda Italia ini. Macheda mencetak gol di menit ke-81 meski gol itu berbau kontroversi setelah bola membentur tangan Macheda. Skor sementara 1-2.
http://wap.vivanews.com/news/read/141261-macheda_balas_gol_drogba__chelsea_unggul

Sebuah Lubang di Jantung si Mungil

2010-04-03T09:45:00.000+07:00

RIFQI Ibra Saputro seorang anak biasa. Usianya baru 1 tahun 7 bulan. Tapi ia lahir ke bumi dengan kondisi tak lazim. Jantung, organ penting yang tersimpan di dada kirinya, memang berdegup. Tapi darah yang terpompa tidak mencapai paru-paru.

Orang tua Rifqi, Saputro Eko Rahardjo dan Atika Rona, tak menangkap sesuatu yang aneh kecuali warna kebiruan di sekujur tubuhnya. Tapi kalangan kedokteran menyebutnya complete affect ventricular septal defect (CAVSD), satu dari sekian banyak kelainan jantung sejak lahir. Pertumbuhan Rifqi tidak sempurna.

Hingga pekan lalu, berat badannya sekitar 8 kilogram-jauh di bawah berat normal anak seusianya. Sesudah operasi, keadaannya membaik, tapi ia belum mampu jalan. Alkisah, dalam jantung si kecil terdapat sebuah keanehan: lubang besar di antara dua bagian jantung yang semestinya terpisah-antara bilik kanan (bagian pemompa darah ke luar jantung) dan bilik kiri; antara serambi (penerima darah) kanan dan serambi kiri.

Sembarut biru pada tubuh Rifqi adalah tanda bercampurnya darah bersih yang mengangkut oksigen (O2) dan darah kotor yang mengandung banyak karbon dioksida (CO2). Pasangan Saputro-Atika tidak pernah menaruh curiga pada jantung sang anak. Malah, ketika Rifqi menginjak usia 5 bulan, mereka sempat membawanya ke dokter gizi.

Waktu itu, bayi Rifqi ngambek: mogok makan, menolak air susu ibu. Dokter gizi tak menangkap keanehan dalam tubuh mungil Rifqi. Tapi, demi keamanan pasien, ia merekomendasikan Rifqi ke dokter jantung. Mereka terkejut bukan buatan setelah melihat hasil ekokardiografi. Rifqi menderita CAVSD.

Lebih terkejut mereka tatkala mendengar biaya operasi yang harus ditanggung kemudian: Rp 50 juta. Keluarga Saputro bukan orang berada. Rumah mereka kecil, di permukiman yang padat di kawasan Utan Kayu, Jakarta Timur-tepatnya di dekat kolong jembatan layang Cawang-Tanjung Priok.

Saputro, tulang punggung keluarga kecil tersebut, dalam keadaan menganggur kala dokter menyebut besarnya ongkos pengobatan. Penyakit jantung bawaan-sebagaimana yang diderita Rifqi-tentu tidak cuma terjadi di negeri ini. Dari seribu kelahiran normal di dunia, terdapat 10 bayi yang lahir dengan cacat jantung bawaan.

Indonesia patut mendapat perhatian khusus karena, menurut Dr. Jusuf Rahmat, Kepala Unit Bedah Jantung Anak Rumah Sakit Harapan Kita, Jakarta, pasien sulit mendapatkan terapi yang pantas. Ada 40 ribu bayi lahir dengan kelainan jantung, tapi hanya 600 kasus yang tertangani setiap tahun-artinya 2,4 persen. Sisanya meninggal atau sementara waktu harus bertahan dengan jantung tak sempurna.

Uang bisa memperbaiki katup jantung yang bocor, sekat bilik ataupun serambi yang berlubang, detak jantung yang tak teratur, atau kelainan pembuluh aorta. Tapi mayoritas (60 persen) penderita jantung bawaan di sini berasal dari kalangan menengah bawah. Dr. Fathema Djan S.P., ahli bedah jantung Rumah Sakit Cipto Mangunkusumo, Jakarta, mengakui hal itu. "Terlihat dari kartu sehat (dibagikan pemerintah) dan askes yang mereka bawa," kata Fathema. "Karena faktor gizi," kata Jusuf Rahmat dalam kesempatan lain.

Rifqi sendiri, sejak divonis menderita CAVSD, harus menunggu sekitar 8 bulan untuk mendapatkan operasi yang membebaskan itu. Saputro dan Atika sempat menyerah pasrah, sampai akhirnya sebuah yayasan justru mengulurkan tangan untuk menanggung ongkos operasi.

Ada sejumlah yayasan-sebutlah Children's Heart Correction Fund (CHCF) atau Yayasan Jantung Indonesia-yang punya perhatian ekstra terhadap penanganan kasus jantung bawaan. Mereka mendapat dana dari kalangan perorangan dan perusahaan yang peduli.

Tapi, Jusuf menggarisbawahi, kalangan penyandang dana amat selektif mengucurkan dana. "Prioritas diberikan kepada anak yang memiliki harapan hidup dan tingkat keberhasilan operasi tinggi," katanya. Uang sangat menentukan, tapi bukan segala-galanya dalam terapi kelainan jantung bawaan ini.

Atika, ibu Rifqi, menyayangkan pengetahuannya yang sempit tentang perkembangan janin. Sewaktu kandungannya berumur tiga bulan, ia punya kebiasaan buruk. "Saya memang tanpa sengaja minum puyer sakit kepala saat kandungan delapan minggu," katanya jujur. Pada saat itu, jantung terbentuk perlahan.

Proses pembentukan ini bisa berlangsung sempurna, mulus, tapi bisa pula terganggu, terputus, di tengah jalan. Dan kedokteran modern dapat mendeteksi perkembangan bayi di saat awal pembentukan hingga menjelang kelahiran. Atika mungkin bisa berhenti minum puyer antisakit kepala saat itu, tapi apa yang akan dilakukannya jika janinnya tetap mengidap kelainan? Indonesia negara dengan sejuta masalah kesehatan: kurang dana, kurang perlengkapan medis, dan kurang tenaga terampil pada bidang ini.

Dr. Fathema mengeluhkan tingginya pajak impor alat-alat operasi jantung. Pemerintah memasukkan bahan medis ke golongan barang mewah. Bahan dan alat operasi jantung hanya bersifat sekali pakai (disposable) dan itu masih harus diimpor dari Jepang, katanya. Dr. Jusuf bercerita tentang kebutuhan tenaga. Empat puluh ribu bayi yang lahir dengan kelainan jantung bawaan seharusnya mendapat penanganan dari 500 orang dokter ahli.

Namun Indonesia, yang padat penduduk, saat ini hanya memiliki dua dokter ahli bedah jantung anak dan 24 ahli bedah jantung. Mereka hanya tersebar di kota besar: Jakarta, Bandung, Surabaya, dan Medan. Tentu tidak semua penyakit jantung bawaan harus dioperasi. Jantung berlubang (ventricular septal defect) kecil, misalnya, tidak perlu dioperasi.

Tapi kasus seperti Rifqi tidak sesederhana itu dan harus segera diintervensi dengan pembedahan. Rifqi anak yang beruntung. Di dada kirinya masih tertoreh luka bekas jahitan operasi. Tapi, sejak operasi dua bulan lalu itu, bobot tubuhnya telah bertambah 1 kilogram. Tubuhnya tak lagi kebiruan. Banyak bayi dengan gangguan jantung bawaan yang bernasib malang. Tapi kini Rifqi mulai sering ngoceh, tumbuh ceria seperti anak normal umumnya. Ia punya jantung yang berdegup normal, dan punya masa depan.

Endah W.S.
http://majalah.tempointeraktif.com/id/arsip/2003/05/12/KSH/mbm.20030512.KSH87456.id.html

Sayangi Jantung, Awasi Kolesterol

2010-04-03T09:44:00.000+07:00

Meskipun kerap menjadi penyebab penyakit-penyakit menahun, bukan berarti tubuh tidak membutuhkan kolesterol sama sekali.

Penyakit jantung koroner masih menjadi penyebab utama kematian di seluruh dunia. Data Badan Kesehatan Dunia (WHO) tahun 2008 menyebutkan, penyakit jantung koroner telah membunuh 7,2 juta orang di seluruh dunia.

Di Indonesia, berdasarkan data Yayasan Jantung Indonesia, penyakit jantung juga masih menjadi pembunuh nomor satu, baik bagi pria maupun wanita. Bila sebelumnya pria lebih berisiko menderita sakit jantung, kini wanita berisiko sama besarnya dengan pria.

Jumlah penderita jantung pada wanita lebih banyak daripada laki-laki, dengan persentase satu banding setengah. Diperkirakan, perbandingan ini akan meningkat menjadi dua banding satu.Tingkat stres yang tinggi pada wanita bekerja, banyaknya wanita merokok, dan kesibukan yang tinggi sehingga kekurangan waktu untuk berolahraga, diperkirakan menjadi faktor semakin banyaknya wanita yang menderita penyakit jantung.Penyakit jantung, khususnya jantung koroner, masih menjadi ancaman bagi kelangsungan hidup manusia.

WHO memperkirakan angka kematian akibat penyakit ini akan terus meningkat hingga 2020, terlebih di negara berkembang seperti Indonesia. WHO juga memprediksi, pada 2020 pasien kardiovaskular yang meninggal dunia akan mencapai 18 juta orang, khusus di negara berkembang saja.

Sedangkan di negara-negara maju, angka kematian akibat penyakit jantung 'hanya' sembilan juta orang.`'Salah satu penyebab seseorang menderita penyakit jantung adalah terlalu banyak mengonsumsi kolesterol yang dapat menyumbat pembuluh darah di jantung,'' ujar dr M Ikhsan Mokoagow M Med Sci, dari FKUI.

http://koran.republika.co.id/koran/61/91322/Sayangi_Jantung_Awasi_Kolesterol

Pre-eklampsia Berhubungan dengan Penyakit Jantung

2010-04-03T09:41:00.000+07:00

LONDON -- Salah satu tabir tentang penyakit pre-eklampsia akhirnya terbuka sudah. Penyakit yang menyerang ibu hamil ini ternyata berkaitan erat dengan penyakit jantung. Para peneliti dari London's Institute for Women's Health akhirnya berhasil menemukan bukti-bukti baru yang mengaitkan kedua penyakit tersebut.

Penelitian yang dipublikasikan dalam British Medical Journal ini menyebutkan bahwa perempuan dengan sejarah pre-eklampsia memiliki risiko yang jauh lebih besar untuk menderita penyakit jantung.

http://www.arsip.net/id/link.php?lh=AVMFVgNXA14M

Menu Seimbang bagi Jantung

2010-04-03T09:39:00.000+07:00

JANGAN salah sangka, penyakit jantung koroner bukanlah penyakit masa kini. Sekelompok tim peneliti Inggris Januari lalu melaporkan temuannya di jurnal kedokteran terkemuka, Lancet: penyakit itu pun telah ada pada zaman Mesir kuno.

Pada sesosok mumi yang berumur lebih dari 3.500 tahun, mereka menemukan beberapa jejak penyakit jantung koroner, antara lain pengapuran (aterosklerosis) pada pembuluh darah. Memang tak jelas apakah sang mumi-tentu datang dari kalangan bangsawan-di masa hidupnya menganut gaya hidup modern, misalnya sedikit gerak, stres tinggi, dan makanan berlimpah lemak. Yang jelas, para ahli telah sepakat bahwa gaya hidup modernlah yang membuat jantung tak lagi tokcer, dan rawan penyakit.

Sejalan dengan makin besarnya penganut gaya hidup modern, penyakit jantung koroner kini menjadi momok kesehatan yang utama. Organisasi Kesehatan Dunia (WHO) memperkirakan, 7,2 juta jiwa di seluruh dunia melayang setiap tahun akibat penyakit sepanjang zaman itu. Meskipun tak ada data rinci, Departemen Kesehatan memastikan bahwa penyakit jantung juga merupakan penyebab kematian utama di Indonesia.

Menyimak laju agresif penyakit jantung, agaknya tak ada cara yang lebih ampuh daripada upaya pencegahan. Hal itu diingatkan kembali dalam peringatan Hari Jantung Se-dunia, yang diperingati setiap 30 September. Resep menjaga kesehatan jantung itu sendiri sebenarnya klasik: giat berolahraga, mengendalikan stres, menyingkirkan rokok, dan menjaga menu seimbang.

Kali ini, Yayasan Jantung Indonesia memberi tekanan yang lebih penting pada soal menjaga menu seimbang. Menjaga menu seimbang, menurut Harmani Kalim, dokter ahli jantung Rumah Sakit Harapan Kita, Jakarta, jauh lebih berguna ketimbang mengonsumsi suplemen makanan, semahal apa pun. Memang, sekarang ini perusahaan farmasi membanjiri pasar dengan ratusan suplemen makanan untuk jantung, misalnya penurun kolesterol, penurun tekanan darah, dan pelancar sirkulasi darah.

Tak hanya itu, makanan tradisional seperti jamur kombu pun turut meramaikan pasar. Masalahnya, seperti apa sebetulnya menu seimbang bagi penderita jantung, terutama yang pas buat orang Indonesia? Jawaban yang mendetail memang belum tersedia karena panduan nutrisi umumnya berdasar kondisi masyarakat Barat. Padahal orang Barat lebih banyak menyantap lemak dan protein hewani, yang kalorinya pas bagi iklim, aktivitas, dan postur tubuh mereka.

Nah, bila orang Indonesia sekadar mengekor pola konsumsi masyarakat Barat, yang terjadi justru penumpukan lemak yang tak diperlukan tubuh. Akibatnya, kadar kolesterol meningkat, dinding pembuluh darah menebal, dan muncul aterosklerosis yang rawan terhadap penyakit jantung koroner. Untuk itulah, "Kita butuh panduan pola makan ideal yang khas Indonesia," kata Harmani.

Yayasan Jantung Indonesia pun sadar akan perlunya panduan nutrisi khas negeri ini. Menurut Sekretaris Jenderal Yayasan Jantung Indonesia, Masino, panduan itu kini tengah dirancang oleh sebuah tim yang terdiri dari ahli kardiologi dan pakar gizi. Dalam panduan ini, para ahli akan mengukur kadar gizi beragam makanan khas Indonesia, seperti tahu, tempe, oncom, dan emping.

Namun, lepas dari pola makan, pembuluh darah memang menebal seiring bertambahnya usia. Setiap tahun, pembuluh darah menebal tiga persen saat kita memasuki usia 20 tahun. Karena itu, Harmani menyarankan check-up rutin agar laju penebalan pembuluh darah bisa dihambat, baik melalui diet ketat maupun dengan obat-obatan. Langkah ini terutama berguna bagi mereka yang berusia di atas 45 tahun, yang irama metabolismenya sudah mulai mengendur.

Suara senada muncul dari Winarto, ahli tanaman obat yang mengelola Klinik Herbal Karyasari, Jakarta. "Jantung orang berusia di atas 45 tahun butuh perhatian yang lebih khusus," katanya. Caranya cukup gampang, makanlah (seperti lalapan) tiga lembar daun dewa (Gynura segetum) setiap sore. Tanaman yang sepintas seperti semak liar ini dikenal berkhasiat sebagai antipenggumpalan darah dan melancarkan sirkulasi darah. Dengan daun dewa, menurut Winarto, timbunan lemak pada dinding pembuluh darah akan tergusur dan darah kembali mengalir lancar.

Tapi, sekali lagi, tanaman obat saja tak berguna bagi jantung bila si pengguna mengabaikan gaya hidup sehat. Resep klasik rajin berolahraga, makan dengan menu seimbang, dan pintar mengendalikan stres tetap berlaku. Mardiyah Chamim

http://majalah.tempointeraktif.com/id/arsip/2001/10/01/KSH/mbm.20011001.KSH83864.id.html

Katup Jantung nan Ramah

2010-04-03T09:36:00.000+07:00

TEMPO Interaktif, Jakarta: Lili, 42 tahun, meski berlabel guru olahraga, tak banyak bergerak. Ia lebih banyak mengeluarkan suara nyaring memerintahkan murid-muridnya melakukan gerakan yang benar saat kelompok remaja yang duduk di sekolah menengah itu tengah bersenam, bermain basket, memukul bola softball, ataupun berlari. Para murid sudah mafhum karena guru perempuan itu dikabarkan menderita kelainan pada katup jantungnya sehingga sering cepat lelah. Ini kejadian puluhan tahun lalu dan ternyata hingga sekarang jumlah penderitanya tak kunjung surut.

Tak satu pun murid itu paham pemicu derita sang guru. Selain tak berani bertanya, penyebab penyakit ini memang beragam. Mulai kebiasaan merokok, penggunaan obat terlarang (narkoba), hingga faktor usia (degeneratif). Namun, ahli bedah jantung Pusat Jantung Nasional Harapan Kita, dr Maizul Anwar, SpBTKV, menyatakan 60 persen kasus kelainan katup jantung disebabkan oleh demam rematik. Demam ini, kata Maizul, akibat infeksi bakteri streptokokus hemolitikus tipe A, yang terjadi pada masa pertumbuhan dan menyebabkan kerusakan pada katup jantung setelah 10 tahun terinfeksi. "Demam ini bisa menyebabkan penyempitan katup," ujarnya. Umumnya, demam rematik yang melanda anak ini kerap tidak ditangani lebih lanjut.

Menurut Dr Nur Haryono, SpJP (K), ahli bedah jantung Pusat Jantung Nasional Harapan Kita, pasien yang mengalami kelainan atau kerusakan katup jantung lazimnya mengalami gejala sesak napas, cepat lelah, disertai jantung berdebar-debar.

Gejala-gejala tersebut akan mengganggu kinerja empat katup di dalam jantung, yakni trikuspid, mitral, aortik, dan pulmonary, yang fungsinya mengkoordinasi sirkulasi darah ke seluruh tubuh. Secara medis, pada kebanyakan kasus, bedah jantung diperlukan untuk perbaikan dan penggantian salah satu katup yang rusak itu. Penggantinya dapat diambil dari katup buatan yang terbuat dari logam titanium atau jaringan biologis dari hewan.

Operasi katup jantung pertama tercatat pada 1913. Namun, baru pada 1960-an tersedia katup buatan mekanik untuk mengganti yang rusak. Di Indonesia, penggantian jantung mekanik menjadi masalah krusial akibat kondisi ekonomi yang rendah. Pasien banyak yang tidak mampu membeli obat pengencer darah (antikoagulan) buat sepanjang hidupnya. Risiko pemakaian antikoagulan juga tidak main-main. Sebut saja stroke, kecacatan bayi, dan perdarahan.

Didasari situasi itu, perbaikan atau penggantian dengan katup jantung biologis menjadi pilihan yang sesuai. Selain tidak perlu mengkonsumsi pengencer darah seumur hidup, banyak penelitian menunjukkan katup jaringan biologis lebih baik dalam hal angka kematian operasi, durabilitas jangka panjang, fungsi jantung, dan daya tahan.

Belum lagi, menurut dr Tri Wisesa, SpBTKV, spesialis jantung Pusat Jantung Nasional Harapan Kita, jaringan biologis ramah untuk pasien perempuan. Sebab, pemakaian antikoagulannya disyaratkan hanya tiga bulan. "Apalagi yang mau melahirkan," katanya. Ditambah performa katup jantung bio juga tidak mendapat penolakan dari tubuh, terutama katup generasi terakhir yang diberi antimineralisasi dan teknik preservasi terbaru.

Secara statistik, Tri menyebutkan daya tahan jaringan biologis yang banyak diambil dari sapi dan babi itu lebih panjang. "Maksimal 20 tahun," ia menjelaskan. Keuntungan lain, pasien tidak perlu jauh dari asupan sayuran hijau dan makanan yang mengandung vitamin K. "Berseberangan dengan antikoagulan karena dapat membuat darah membeku," ujarnya.

Lebih jauh pemilihan jenis katup tetap didasarkan pada umur dan jenis kelamin. Maizul mengatakan, apabila jantung itu hanya bocor dan menyempit, bisa ditangani dengan perbaikan. Namun, jika sudah faktor degeneratif, ia patut diganti. Pemasangan katup buatan, baik mekanik maupun biologis, tergolong operasi besar, bisa memakan waktu 3-5 jam. Biayanya berkisar Rp 100 juta. "Mayoritas 90 persen operasi berhasil," ujarnya.

Adapun harga katup bio di pasar, menurut Direktur Operasional PT Reka (agen perusahaan Edwards Lifesciences, Amerika Serikat) Roberts Roby, mencapai Rp 17,6 juta, sedangkan untuk mekaniknya Rp 14,8 juta. Lantas ring untuk perbaikan katup jantung berkisar Rp 6,6 juta. Di Indonesia, kata Roby, orang cenderung memilih katup jantung sapi ketimbang babi.

- Pemakaian obat antikoagulan hanya 3 bulan (tidak seumur hidup).
- Daya tahan katup dari jaringan biologis lebih lama.
- Pilihan yang lebih pas untuk perempuan.
- Asupan sayuran hijau dan vitamin K tetap dibolehkan.
- Hitungannya lebih ekonomis.

Heru Triyono
http://www.tempointeraktif.com/hg/kesehatan/2008/11/18/brk,20081118-146604,id.html

Baru 5 Persen Penderita Jantung Bawaan Tertangani

2010-04-03T09:29:00.000+07:00

YOGYAKARTA - Sampai saat ini fasilitas untuk menangani pasien anak yang menderita penyakit jantung bawaan, terutama yang perlu operasi masih sangat kurang. Padahal setiap tahun di Indonesia ada sekitar 45 ribu anak yang menderita jantung bawaan dan 50 persennya perlu operasi.

Hal itu dikemukakan Guru Besar Departemen Ilmu Kesehatan Anak, Fakultas Kedokteran Universitas Indonesia dan Konsultan Jantung Anak, Prof Sudigdo Sastroasmoro, Selasa (8/5).

http://www.arsip.net/id/link.php?lh=BFlZXAwFUVNX

Perhatian !!!

2010-04-02T00:14:00.001+07:00

Informasi yang tersedia di situs ini dimaksudkan hanya untuk pengetahuan umum saja, bukan untuk menggantikan saran dokter Anda, juga bukan
untuk pengobatan kondisi medis khusus. Informasi ini juga bukan untuk menegakkan diagnosis penyakit atau mengobati penyakit tanpa berkonsultasi
dulu dengan dokter Anda. Anda dapat menanyakan kondisi medis anda ke dokter Anda secara langsung.

Waspadai Gejala Komplikasi Diabetes pada Retina

2010-04-01T10:46:00.000+07:00

DIABETIC RETINOPATHY adalah sebuah kondisi komplikasi diabetes akibat rusaknya pembuluh darah pada jaringan sensitif mata bagian belakang (retina). Penyakit diabetes yang memengaruhi retina dapat berakibat hingga menyebabkan kebutaan.

Dr Ian Yeo Yew San, dokter mata yang menjabat sebagai konsultan di Singapore National Eye Centre yang tergabung dalam layanan wisata sehat, FlyFreeForHealth, mengatakan, "Ketika terkena diabetes, tubuh tidak memanfaatkan gula (glukosa) dengan tepat. Jika kadar gula darah terlalu tinggi, maka lensa alami mata akan membengkak—sehingga pandangan menjadi kabur. Nantinya, jumlah gula yang terlalu banyak tersebut dapat merusak pembuluh darah kecil yang memberi nutrisi pada retina (capillary). Maka muncullah diabetic retinopathy.”

Pertanda dan Gejala
Pada tahap awal, diabetic retinopathy tidak memiliki gejala atau hanya menyebabkan gangguan mata ringan. Namun lama-kelamaan, bisa berujung pada kebutaan. Diabetic retinopathy biasanya memengaruhi kedua mata.

Gejala diabetic retinopathy meliputi :
• Bintik-bintik mengambang pada penglihatan
• Penglihatan kabur atau tidak fokus
• Garis-garis gelap atau merah yang menghalangi penglihatan
• Sulit melihat pada malam hari
• Penglihatan hilang sama sekali / buta

Pemeriksaan / Screening untuk Diabetic Retinopathy
Sebagai bagian dari tes mata, dokter Anda akan melakukan foto terhadap retina yang disebut dengan fluorescein angiography. Pertama-tama, dokter akan memperbesar pupil lalu memfoto bagian dalam mata. Lalu cairan warna khusus akan disuntikkan ke dalam urat nadi di lengan. Foto-foto lain akan diambil seiring dengan cairan warna yang mengalir dan mulai bersirkulasi pada mata. Dokter akan menggunakan foto-foto tersebut untuk melihat pembuluh darah mana yang tertutup, rusak ataupun bocor.

Dokter biasanya juga akan meminta Anda menjalani tes optical coherence tomography (OCT). Tes ini menghasilkan gambar-gambar pemeriksaan silang terhadap retina yang dapat menunjukkan ketebalan retina dan untuk mengetahui apakah cairan tersebut telah bocor ke dalam jaringan retina.

Dr Yeo menyarankan kepada pasien untuk mengendalikan diabetes dengan diet dan pengobatan untuk memperlambat atau mencegah pengembangan diabetic retinopathy atau komplikasi lainnya. Ada baiknya lakukan pemeriksaan mata setahun sekali.

http://m.kompas.com/news/read/data/2009.02.20.16503716

Tinggi, Biaya Kesehatan akibat Diabetes

2010-04-01T10:45:00.000+07:00

KOMPAS.com — Diabetes, yang selama ini menjadi masalah kesehatan negara maju, kini juga menjadi persoalan kesehatan negara berkembang. Diabetes dan komplikasinya, seperti stroke dan penyakit jantung, akan menjadi beban ekonomi terbesar bagi negara-negara berkembang.

"Diabetes telah bergeser dari persoalan kesehatan negara maju menjadi penyakit negara berkembang, seperti India dan China, dan ini akan menjadi beban pembiayaan kesehatan yang besar," kata Philip Clarke, peneliti dari University of Sydney School of Public Health.

Komplikasi diabetes antara lain penyakit jantung koroner, stroke, neuropati diabetik (gangguan pada pembuluh saraf), amputasi, gagal ginjal, dan kebutaan. Bila terjadi komplikasi, bisa terjadi kecacatan, menurunnya usia harapan hidup, dan tingginya pembiayaan kesehatan untuk semua golongan masyarakat.

Dalam penelitiannya, Clarke dan timnya menguji data 11.140 pasien diabetes di 20 negara, meliputi komplikasi yang diderita pasien, biaya perawatan, dan lamanya tinggal di rumah sakit. Hasilnya diketahui bahwa biaya kesehatan akibat penyakit diabetes meningkat tajam, terutama di negara-negara miskin.

Saat ini diperkirakan 250 juta orang di dunia menderita diabetes, angka ini akan terus bertambah dengan jumlah terbanyak, sekitar tiga perempatnya berada di negara berkembang. Indonesia saat ini menduduki urutan keempat setelah Amerika Serikat, China, dan India.

"Pasien di Asia dan Eropa Timur memiliki angka insiden stroke paling tinggi dibanding pasien dari negara maju. Pasien di negara berkembang juga lebih sedikit yang mendapat layanan kesehatan untuk penyakitnya dan lebih lama tinggal di rumah sakit," menurut laporan penelitian Clarke.

Pengeluaran per kapita China untuk biaya kesehatan diabetes diperkirakan 216 dollar AS (sekitar Rp 205.000) per tahun. Angka tersebut akan meningkat 10 kali lipat bila pasien mengalami komplikasi, misalnya stroke.

"Cara paling efisien untuk mengurangi tingginya biaya kesehatan adalah dengan mencegah terjadinya komplikasi. Bila pasien secara rutin mengontrol tekanan darahnya, biaya kesehatan bisa dipangkas," kata Clarke.

Dalam risetnya, Clarke melakukan survei di China, India, Malaysia, Filipina, Republik Ceko, Estonia, Hongaria, Lituania, Polandia, Rusia, Slowakia, Australia, Kanada, Perancis, Jerman, Irlandia, Italia, Belanda, Selandia Baru, dan Inggris.

⁠Penulis: AN ⁠ ⁠Editor: Anna ⁠ ⁠Sumber : Reuters⁠

http://m.kompas.com/news/read/data/2010.02.23.10380147

"Screening" Diabetes Sebaiknya Lebih Dini

2010-04-01T10:44:00.000+07:00

NEW YORK, KOMPAS.com - Saat ini disarankan agar pemeriksaan atau screening diabetes tipe 2 dilakukan mulai usia 45 tahun, terutama bagi mereka yang kelebihan berat badan. Namun studi terbaru menganjurkan, pemeriksaan diabetes tipe 2 sebaiknya dilakukan lebih dini yakni antara usia 30-45 tahun.

Pemeriksaan bertahap diabetes tipe 2 dinilai lebih efektif dan hemat biaya jika dilakukan pada usia 30 hingga 45 dan diulang setiap tiga sampai lima tahun, demikian laporan yang dimuat jurnal kesehatan Lancet.

Dr. Richard Kahn dari American Diabetes Association, Alexandria, Virginia, dan timnya menggunakan model matematika untuk membandingkan tujuh strategi pemeriksaan (rentang waktu dari usia 30 sampai usia 60 tahun atau berdasarkan diagnosis tekanan darah tinggi, dan diulangi setiap tiga sampai lima tahun sampai usia 75 tahun) dengan tanpa model pemeriksaan atau pemeriksaan maksimal (setiap enam bulan sejak usia 30 tahun).

Dalam studi tersebut, para peneliti mensimulasikan 325.000 responden yang tidak mengidap diabetes berusia 30 tahun. Model tersebut menunjukkan bahwa pemeriksaan diabetes tipe 2 sejak usia 30 atau 45 lebih hemat dari segi biaya dan dapat mencegah terjadinya serangan jantung, kematian dan komplikasi berkaitan dengan diabetes. Dibandingkan strategi tanpa pemeriksaan sama sekali, screening yang dimulai saat terdeteksinya tekanan darah tinggi ternyata kurang efektif.

Secara umum, Kahn merekomendasikan pemeriksaan sebaiknya dimulai orang memasuki rentang usia antara 30 dan 45 tahun, lalu dilanjutkan setiap tiga hingga lima tahun. Sebaliknya, bagi mereka yang obesitas atau memiliki sejarah keluarga diabetes, pemeriksaan sebaiknya dimulai lebih dini, tapi tidak pada usia 25 tahun.

⁠Penulis: AC ⁠ ⁠Editor: acandra ⁠ ⁠Sumber : Reuters⁠

http://m.kompas.com/news/read/data/2010.03.31.17360945

Periksa Kaki, Selamatkan Diabetesi dari Amputasi

2010-04-01T10:42:00.000+07:00

KOMPAS.com — Diabetes yang tidak terkontrol lama-lama bisa menyebabkan kaki penderita bermasalah. Mulai dari aliran darah yang tidak mencapai ke ujung-ujung kaki hingga kurangnya nutrisi.

Akibatnya, luka makin sulit sembuh dan kerusakan saraf permanen hingga tidak bisa lagi merasakan nyeri, panas maupun dingin pun bakal muncul. Diabetesi (penderita diabetes) pun akan makin rentan mengalami luka atau infeksi tanpa disadari karena sudah tak bisa merasakannya.

Jika diabetesi tidak menyadari dan luka terus berkembang maka infeksi berkepanjangan sampai harus amputasi bakal dialami. Risiko ini 10 kali lipat lebih sering dialami diabetesi dibanding bukan diabetesi.

Gangguan saraf tepi yang sering disebut neuropati diabetik perifer ini juga bisa menyebabkan nyeri hebat meski penyebabnya hanya sentuhan ringan. Untuk itu, periksalah kaki Anda setiap hari dengan saksama.

dr. Intan Airlina Febiliawanti
⁠Editor: Abd

http://m.kompas.com/news/read/data/2009.10.12.19261693

Pengguna Insulin, Waspadalah Risiko Hipoglikemia!

2010-04-01T10:41:00.000+07:00

KOMPAS.com — Gula (glukosa) yang berlebihan di dalam darah bisa merusak berbagai organ tubuh utama, termasuk jantung, saraf, mata, dan ginjal. Memang akibat tersebut tidak segera dirasakan. Tapi, jika Anda tidak mengontrol gula darah, kondisi itu pada akhirnya pasti akan dirasakan.

Karena itu, penderita diabetes disarankan untuk tetap mempertahankan kadar gula darah agar senantiasa mendekati normal. Akan tetapi, terkadang tindakan pengobatan yang berlebihan terhadap diabetes bisa menimbulkan gula darah rendah (hipoglikemia).

Hipoglikemia ternyata sama buruknya dengan kadar gula darah terlalu tinggi. Penelitian yang digelar para ahli dari Cardiff University terhadap 50.000 pasien diabetes tipe 2 menemukan, kadar gula darah yang terlalu rendah meningkatkan risiko kematian, khususnya pada pemakai insulin.

Perbedaan risiko kematian secara signifikan terlihat antara pasien yang memakai insulin dan mereka yang minum obat untuk meningkatkan pelepasan insulin. Ada beberapa hipotesis mengenai hal ini.

Dalam penelitian ini, pasien yang memakai insulin diminta untuk tidak menghentikan penggunaannya. Selain itu, faktor usia serta periode pasien mengidap penyakit diabetes juga ikut berpengaruh.

"Masih belum jelas benar apakah penggunaan insulin yang intensif meningkatkan risiko kematian atau faktor lain. Masih diperlukan pengujian dan penelitian lebih lanjut," kata ketua peneliti, Dr Craig Currie.

Menanggapi hasil studi ini, Dr Iain Frame, Kepala Riset Diabetes UK, mengatakan, selain faktor insulin, kita juga harus mempertimbangkan faktor lain yang lebih berpengaruh terhadap risiko kematian, yakni usia dan jangka waktu menderita diabetes.

"Makin tua usia pasien, makin banyak penyakit yang mudah menyerang. Faktor gaya hidup pasien dalam mengontrol kadar gula darahnya juga sangat penting," kata Frame.

Oleh sebab itu, ia menyarankan agar pasien diabetes selalu mengontrol kadar gula darahnya dengan cara mengatur pola makan dan rajin berolahraga serta mengonsumsi obat.

⁠Penulis: AN ⁠ ⁠Editor: acandra ⁠ ⁠Sumber : BBC⁠

http://m.kompas.com/news/read/data/2010.01.28.10051220

Penderita Diabetes Teledor, 5 Organ Taruhannya

2010-04-01T10:40:00.000+07:00

KOMPAS.com — Sekitar tahun 2000, International Diabetes Federation (IDF) menyebutkan bahwa diabetes merupakan penyakit keempat penyebab utama kematian di banyak negara maju.

Secara umum, sekitar 40 persen pasien diabetesi, entah tipe I (yang dialami sejak masa kanak-kanak atau yang tergantung insulin) dan atau tipe II (yang mulai dialami saat dewasa dan tidak tergantung insulin) akan mengalami komplikasi dalam perjalanan hidupnya.

Bila gula darah tidak terkendali karena pola makan yang tidak tepat, kebiasaan hidup tidak sehat, seperti merokok dan kurang kegiatan fisik, tetap dipertahankan, komplikasi bakal menyerang ke mana dia suka.

Berikut ini adalah organ-organ yang menjadi sasaran komplikasi akibat keteledoran para diabetesi:

1. Jantung - penyakit jantung koroner (PJK)
Keadaan ini muncul akibat glukosa darah yang tinggi dan terus-menerus atau persisten. Akibatnya, terjadinya penebalan dan pengerasan pembuluh darah arteri atau sering disebut aterosklerosis. Diabetesi berisiko dua sampai empat kali lebih tinggi terkena penyakit kardiovaskular dibandingkan yang tidak mengalami DM.

2. Otak - stroke
Aterosklerosis dapat terjadi di pembuluh darah otak. Akibatnya bisa ditebak, terjadi stroke. Risiko terserang stroke pada diabetesi yang juga mengalami hipertensi adalah dua kali lebih tinggi dibanding orang yang hanya menderita hipertensi saja.

3. Kaki - luka
Ulser atau luka pada kaki merupakan penyebab paling umum yang mengantar diabetesi masuk rumah sakit. Komplikasi ini terjadi akibat kerusakan saraf (neuropati) dan kurangnya aliran darah ke kaki.

Jika luka terinfeksi dan berkembang menjadi gangren, biasanya amputasi dilakukan. Diabetes merupakan penyebab amputasi yang paling sering di luar kecelakaan. Setidaknya 15-40 persen diabetesi lebih berisiko mengalami hal ini dibanding yang tidak.

4. Mata - retinopati
Retinopati diabetik merupakan komplikasi DM pada mata. Penglihatan mendadak akan buram atau berkabut. Ini terjadi akibat kadar gula darah yang tinggi sehingga terjadi sembab pada lensa mata. Bila pengobatan cukup dan kadar gula terkontrol, penglihatan pun akan normal lagi.

5. Ginjal - nefropati
Nefropati diabetes adalah komplikasi yang terjadi pada ginjal. Ini komplikasi yang menyebabkan terjadinya gagal ginjal dan kematian. Penyebabnya, kadar glukosa darah yang tinggi sehingga merusak pembuluh darah kapiler ginjal dan menyebabkan terjadinya tekanan darah tinggi.

Risiko terjadi serta berat atau ringannya komplikasi ginjal ini sejalan dengan lamanya DM diidap. Kebanyakan komplikasi muncul setelah 10-15 tahun penderita mengidap DM. @abd

⁠Editor: acandra ⁠ ⁠Sumber : Tabloid Gaya Hidup Sehat⁠

http://m.kompas.com/news/read/data/2010.01.08.10145017

Konsumsi "Softdrink" Picu Diabetes

2010-04-01T10:38:00.000+07:00

JAKARTA, KOMPAS.com — Diabetes mellitus atau kencing manis telah menjadi masalah kesehatan dunia. Bila tidak ditangani, diabetes akan membawa komplikasi pada berbagai penyakit lain, seperti penyakit jantung, stroke, gagal ginjal, hingga impotensi.

Dr Kristen Bibbins-Domingo, peneliti dari University of California, San Fransisco, Amerika Serikat, baru-baru ini memublikasikan hasil penelitiannya mengenai insiden penyakit jantung dengan konsumsi softdrink.

Ia mengatakan, meningkatkan konsumsi minuman bersoda yang umumnya mengandung gula tinggi berdampak pada terjadinya 130.000 kasus baru diabetes, 14.000 kasus baru penyakit jantung, dan 50.000 penderita gangguan jantung dalam satu dekade terakhir.

"Dari hasil penelitian ini bisa disimpulkan, semua kebijakan yang bisa mengurangi konsumsi softdrink mungkin akan berdampak positif bagi kesehatan masyarakat," kata Dr Kristen Bibbins-Domingo.

Dengan menggunakan simulasi komputer, penyakit jantung dikaitkan dengan berbagai faktor, seperti obesitas dan konsumsi makanan mengandung garam. "Selama ini kita kurang memperhitungkan insiden antara softdrink dengan penyakit jantung karena memang minuman ini lebih populer pada para remaja. Fokus penelitian penyakit ini lebih banyak orang dewasa berusia di atas 35 tahun," papar Domingo.

Ia menambahkan, kaitan antara insiden penyakit kardiovaskular dan diabetes sangat nyata. Meski demikian, faktor meningkatnya obesitas juga mungkin berpengaruh.

"Berbagai penelitian menunjukkan dampak konsumsi minuman manis. Selama beberapa dekade terjadi peningkatan konsumsi minuman manis," katanya.

Para ahli mengingatkan, untuk mencegah diabetes, kita harus mengurangi asupan minuman dengan tambahan gula. Jika didiagnosis diabetes maka gula darah, berat badan, tekanan darah, dan kadar lemak darah harus dikendalikan. Kalau dengan olahraga tidak terkontrol, harus dilakukan dengan obat.

⁠Penulis: AN ⁠ ⁠Editor: acandra ⁠ ⁠Sumber : Healthday News⁠

http://m.kompas.com/news/read/data/2010.03.11.1451064

Inilah Cara Diabetesi Memeriksa Kakinya

2010-04-01T10:37:00.000+07:00

KOMPAS.com - Neuropati diabetik perifer atau gangguan saraf tepi yang terjadi pada diabetesi (penderita diabetes) kerapkali menyebabkan masalah pada kaki hingga harus amputasi bila tidak terkontrol. Ini terjadi akibat diabetesi tidak bisa lagi merasakan nyeri meski ada iritasi atau infeksi di kaki. Karena itu, memeriksa kaki setiap hari menjadi kewajiban diabetesi. Bagaimana caranya?

1. Periksalah semua sela jari termasuk kuku karena luka bisa berasal dari daerah yang kecil sehingga tidak terlihat jelas.

2. Bila tidak memungkinkan memeriksa kaki sendiri, mintalah anggota keluarga lain untuk memeriksa keadaan kaki Anda.

3. Bersihkanlah kedua kaki dan cucilah setiap hari dengan air hangat tetapi tidak terlalu panas. Sebelumnya Anda bisa mengetes suhu air dengan tangan. Hindari merendam kaki terlalu lama karena jika ada luka terkena air dalam waktu lama dan berulang akibatnya sembuhnya pun lama. Setelah itu keringkan kaki Anda termasuk sela - sela jari dengan handuk kecil yang lembut.

4. Selalu pakai sandal atau sepatu. Kalau perlu pakailah kaus kaki karena mungkin ada sepatu dari bahan tertentu yang bisa menyebabkan kaki iritasi hingga menyebabkan infeksi.

Meski Anda suka memakai stoking, kaos kaki nilon atau yang berbahan tipis, namun kaus kaki berbahan tipis tidak melindungi kaki dengan baik. Jadi sebaiknya pakailah kaus kaki yang berbahan tebal sehingga kaki terlindung cukup baik.

dr. Intan Airlina Febiliawanti
⁠Editor: Abd ⁠

http://m.kompas.com/news/read/data/2009.10.12.19420346

Hipertensi Bisa Disertai Diabetes

2010-04-01T10:35:00.000+07:00

KOMPAS.com - Jika tekanan darah sering diatas 120/90 mmgHg, otomatis risiko diabetes meningkat dua kali lipat. Ini kalau dibandingkan dengan orang yang tekanan darahnya normal. Demikian menurut penelitian yang dilakukan ilmuwan dari Brigham and Woman Hospital dan Harvard Medical School selama 10 tahun.

Yang dimaksud dengan tekanan darah tinggi adalah ukuran tekanan darah di atas batas normal, baik saat kita sedang santai, terlebih saat kita sedang marah atau stres dalam jangka waktu tertentu.

Diabetes meningkatkan risiko darah tinggi sebab penumpukan gula dan kolesterol menyebabkan pengerasan pembuluh darah arteri. Ujung-ujungnya darah tidak mengalir lancar, sehingga tekanannya menjadi naik. Selain menjadi pemicu darah tinggi, penyakit diabetes juga bisa menjadi penyakit "bayangan" untuk gagal jantung dan gangguan fungsi ginjal.

Segera memeriksakan diri ke dokter, manakala kita curiga tekanan darah sudah di atas normal. Pemeriksaan ini dimaksudkan untuk mengetahui tingkat risiko diabetes. Untuk mencegah risiko penyakit berat lain seperti jantung dan ginjal, minta agar dokter melakukan tes rutin bagi penderita darah tinggi, yaitu:

- Tes urin untuk memeriksa kadar proten dalam air seni
- Tes darah untuk memeriksa apakah ginjal kita berfungsi dengan baik.
- Tes kadar kolesterol
- Tes EKG untuk memeriksa kesehatan jantung.

Perlu juga kita ketahui bahwa tekanan darah tinggi bukanlah suatu penyakit seperti flu yang bisa sembuh karena menelan obat. Tekanan darah tinggi harus diatasi dengan perubahan gaya hidup. Rutinlah berolahraga, cegah obesitas, batasi garam, dan hentikan kebiasaan merokok.

⁠Editor: Anna ⁠ ⁠Sumber : Prevention Indonesia⁠

http://m.kompas.com/news/read/data/2009.10.17.09284888

Gaya Hidup Buruk Picu Diabetes

2010-04-01T10:34:00.000+07:00

JAKARTA, KOMPAS.com- Sekitar 80 persen prevalensi diabetes melitus merupakan tipe dua. Hal ini menunjukkan gaya hidup yang tidak sehat menjadi pemicu utama meningkatnya penyakit tersebut. Diabetes merupakan penyebab kematian kedua terbesar di perkotaan. Hal itu terungkap dalam seminar sehari mengenai Diabetes yang diselenggarakan Departemen Kesehatan, Kamis (5/11).

Organisasi Kesehatan Dunia PBB menetapkan tanggal 14 November sebagai Hari Diabetes Sedunia. Tema peringatan tahun ini ialah Pahami Diabetes dan Kendalikan. Diabetes melitus merupakan penyakit kronis yang disebabkan ketidakmampuan tubuh memproduksi hormon insulin atau karena penggunaan yang tidak efektif dari produksi insulin. Hal ini ditandai dengan tingginya kadar gula dalam darah.

Diabetes tipe dua umumnya terkait genetis atau keturunan yang juga dipengaruhi dan dipicu faktor risiko seperti pola makan, kurang beraktivitas, merokok, minum beralkohol, obesitas, hipertensi hiperglikemia, hiperkolesterol.

Dalam sambutannya, Direktur Jenderal Pengendalian Penyakit dan Penyehatan Lingkungan Tjandra Yoga Aditama mengungkapkan, buruknya gaya hidup itu tercermin dalam Riset Kesehatan Dasar (Riskesdas) pada tahun 2007, prevalensi kurang makan buah dan sayur sebesar 93,6 persen, kurang aktivitas fisik pada penduduk berusia di atas 10 tahun sebesar 48,2 persen, prevalensi merokok setiap hari bagi penduduk di atas 10 tahun sebesar 23,7 persen, dan konsumsi alkohol dalam satu bulan terakhir 4,6 persen.

Hasil riset yang sama menunjukkan, diabetes melitus menduduki peringkat kedua sebagai penyebab kematian pada kelompok 45-54 tahun di perkotaan. Sedangkan, di pedesaan, diabetes melitus menduduki peringkat keenam deng an jumlah proporsi kematian sebesar 5,8 persen.

⁠Penulis: INE ⁠ ⁠Editor: made

http://m.kompas.com/news/read/data/2009.11.05.21154658

Diabetes Penyebab Utama Gagal Ginjal

2010-04-01T10:33:00.000+07:00

MEDAN, RABU - Penyebab utama seseorang mengalami gagal ginjal kronik hingga membutuhkan pelayanan Hemodialisa (cuci darah) adalah akibat penyakit diabetes dan darah tinggi.
"Jika kedua penyakit ini dikontrol dengan baik melalui pengobatan teratur maka penyakit ginjal akan dapat dicegah sedini mungkin atau diperlambat," kata Kepala Unit Dialisis RSU Pirngadi Medan, Prof. Dr. Harun, di Medan, Rabu.

Ia mengatakan, penyakit ginjal kronik juga dapat meningkatkan rIsiko terjadinya penyakit jantung dan pembuluh darah (kardiovaskuler) yang akhirnya juga merupakan penyebab kematian terbanyak penderita gagal ginjal.

Menurut dia, sebenarnya gagal ginjal dapat dicegah jika sejak dini sudah dideteksi melalui pemeriksaan darah dan air seni. Dan mayoritas mereka di negara berkembang yang berada pada tahap dini penyakit ini pada umumnya tidak mengetahui jika telah menderita gagal ginjal.

"Untuk itu deteksi dini dari ketidakberesan ginjal menjadi sangat penting dan memungkinkan pengobatan yang sesuai sebelum terjadi kerusakan ginjal atau terjadi manifes perparahan karena komplikasi yang lain.

Sementara itu kepala Staf Medis Fungsional Penyakit Dalam RSU Pirngadi Medan, dr Zulhelmi, mengatakan, pada umumnya masyarakat tidak waspada dengan ginjal mereka karena pada tingkat ringan, gangguan ginjal sering tidak dirasakan.

Gangguan dapat bertambah parah hingga pada akhirnya ginjal tidak berfungsi lagi.

"Periksalah ke dokter, karena melalui pemeriksaan laboratorium dengan sedikit contoh darah dan urine dapat diketahui apakah fungsi ginjal masih normal atau sudah terganggu, sehingga dapat dilakukan pengobatan sedini mungkin," katanya.

Ia menyebutkan, gejala awal gagal ginjal dapat diketahui saat terjadinya gangguan nyeri saat buang air kecil, berdarah, keluar batu, nyeri pinggang, pucat dan gampang capek.

Source : Antara
⁠Penulis: AC

http://m.kompas.com/news/read/data/2008.03.12.09084976

Diabetes, Mother of Disease

2010-04-01T10:31:00.000+07:00

KOMPAS.com - Para penderita diabetes alias kencing manis ini janganlah terlalu menganggap sepele penyakit yang satu ini, karena ternyata tanpa Anda sangka penyakit ini menyimpan sejuta kejutan! Tahukah Anda bahwa si "manis" ini merupakan "mother of disease"- ibu dari segala penyakit?

"Dengan adanya diabetes, Anda bisa menderita kelainan berbagai macam organ tubuh, dari mata, jantung, lambung, hati, ginjal, kulit sampai kaki," kata dr.Candra Wibowo, Sp.PD dari Mitra International Hospital Jatinegara, Jakarta.

Dokter Candra menuturkan, diabetes bisa menyebabkan aliran pembuluh darah menjadi kurang baik yang berakibat pada kerusakan organ dalam mata dari retina yang disebut retinopati diabetik dan menyebabkan kebutaan perlahan - lahan, hingga kerusakan pada lensa seperti katarak.

Perubahan metabolisme sel lapisan dalam pembuluh darah juga bisa menyebabkan aliran darah kurang baik dan menjadi kaku (tidak elastis). Akibatnya organ-organ yang harus dialiri darah menjadi kekurangan nutrisi dan oksigen. Hal ini bisa menyebabkan timbulnya serangan jantung koroner, stroke dan luka yang susah sembuh.

Masalah kesehatan lain yang kerap dialami pasien diabetes (diabetesi) adalah gastropati diabetik dengan gejala perasaan kembung, begah, dan cepat kenyang. Para diabetesi juga seringkali terlihat semakin kurus. Hal ini terjadi karena tubuh butuh lebih banyak insulin karena insulin yang ada dalam tubuh hanya digunakan separuh akibat ketidakefesieanan reseptor atau biasa disebut resitensi insulin.

Diabetes juga menyebabkan kebocoran protein di ginjal, yang berakibat gagal ginjal di mana seseorang memerlukan terapi pengganti ginjal, seperti cuci darah, cuci rongga perut, atau cangkok ginjal.

Komplikasi lain yang mungkin dihadapi diabetesi adalahkaki diabetik. Komplikasi ini terjadi karena terjadinya kerusakan saraf, pasien tidak dapat membedakan suhu panas dan dingin, rasa sakit pun berkurang.

"Saat diabetes sudah lama dan tidak terkontrol, aliran pembuluh darah kita jarang sampai ke ujung - ujung tubuh, termasuk jari kaki, tangan, ujung rambut hingga penis. Dari situ jika mengalami luka di kaki atau tangan akan sulit sembuh karena aliran darah yang memberi makanan tidak sampai ke ujung jari kaki atau tangan tersebut. Untuk rambut bahkan bisa menyebabkan alopesia atau kebotakan dan bagi laki – laki, bisa terjadi disfungsi ereksi ", papar dokter Candra.

Oleh karena itu kontrol secara teratur gula darah Anda dengan cara rutin berolahraga dan melakukan diet. Selain itu hindari semua kelainan yang mungkin mengancam anda di masa depan sehingga kualitas hidup Anda akan lebih baik meskipun Anda penderita diabetes.

dr. Intan Airlina Febiliawanti

http://m.kompas.com/news/read/data/2009.10.06.15341370

Diabetes Melitus Dapat Sembuh?

2010-04-01T10:26:00.000+07:00

KOMPAS.com - Saya (48) penderita diabetes melitus sejak 10 tahun ini. Sewaktu pertama didiagnosis, saya sempat terpukul. Hidup rasanya akan berubah. Setelah saya jalani, ternyata kehidupan saya sehari-hari dapat berjalan seperti biasa. Hanya saya harus menjaga makan, seperti menghindari makanan manis, teratur berolahraga, serta minum obat pengendali gula darah dan obat lain secara teratur.

Selain diabetes melitus, saya juga menderita kolesterol tinggi dan hipertensi. Untunglah sekarang semua umumnya terkendali. Selama 10 tahun, pernah beberapa kali gula saya di atas normal atau tekanan darah saya meningkat. Berkat kesadaran dan keinginan kuat untuk sehat, semua dapat diatasi dengan baik.

Dokter yang mengobati saya memberi informasi cukup lengkap. Selain informasi langsung, saya juga diberi informasi tertulis berupa buku atau kesepakatan pengendalian diabetes melitus.

Menurut pemahaman saya, diabetes melitus yang saya derita disebabkan produksi insulin oleh kelenjar pankreas saya tidak mencukupi. Karena insulin yang mengubah glukosa menjadi energi, kekurangan insulin akan mengakibatkan kadar glukosa saya meningkat. Untuk itu saya harus membatasi makanan yang banyak mengandung glukosa, berolahraga untuk membakar glukosa dalam tubuh, dan minum obat untuk merangsang pembentukan insulin.

Saya masih aktif bekerja di bagian keuangan perusahaan swasta. Saya menjaga makanan dengan membawa makanan dari rumah untuk makan siang. Adapun untuk makan pagi dan malam, saya makan di rumah. Sesekali saya makan di restoran atau pesta perkawinan, tetapi saya menjaga agar yang saya konsumsi tidak banyak berbeda dari yang saya makan sehari-hari.

Saya bersyukur keadaan jantung, mata, dan ginjal yang juga dapat mengalami komplikasi diabetes melitus dan hipertensi ternyata baik. Jadi, saya merasa pengendalian diabetes melitus dan hipertensi saya sudah merupakan bagian hidup. Prestasi saya di tempat kerja juga tidak terganggu. Saya cukup kontrol ke dokter satu atau dua bulan sekali.

Belum lama ini, saya membaca iklan tentang terapi yang dapat menyembuhkan diabetes melitus. Meski saya merasa cukup nyaman dengan keadaan kesehatan saya, jika memang diabetes melitus dapat disembuhkan saya tentu akan sangat bersyukur.

Pengetahuan saya tentang kesehatan terbatas. Dokter saya tidak merekomendasi mencoba pengobatan tertentu. Apakah memang diabetes melitus sampai saat ini belum dapat disembuhkan? Jika demikian, kenapa banyak iklan menjanjikan kesembuhan penyakit, termasuk diabetes mellitus? Mohon pendapat Dokter.

PL di J

Pemahaman Anda mengenai diabetes melitus sudah baik. Untunglah pemahaman tersebut juga diwujudkan dengan gaya hidup yang mendukung.

Diabetes melitus dapat disebabkan berbagai sebab. Salah satunya oleh obat. Nah, jika obat yang menjadi penyebab tersebut dihentikan, diabetes melitus juga akan hilang.

Diabetes yang Anda derita berbeda. Tampaknya Anda menderita diabetes melitus tipe dua. Kalangan kedokteran lebih banyak menggunakan istilah diabetes melitus seperti ini sebagai diabetes melitus terkendali, bukan sembuh. Jika Anda tidak lagi mengendalikan makan, tidak berolahraga, atau tidak minum obat pengendali gula darah, glukosa Anda akan kembali tinggi.

Mereka yang berhasil mengendalikan gula darah dengan gaya hidup sehat dan konsumsi obat penurun gula darah umumnya seperti Anda, dapat hidup produktif dan kualitas hidupnya cukup baik.

Penelitian dalam bidang kedokteran masih berjalan terus. Sudah tentu kita berharap suatu waktu akan ada obat penyembuh diabetes melitus.

Berbagai cara telah dicoba, antara lain dengan membuat pankreas buatan yang mampu menghasilkan cukup insulin. Pankreas ini dikembangkan dari sel punca (stem cell), tetapi penelitiannya masih pada binatang. Diperlukan waktu untuk menilai penerapannya pada manusia.

Saya juga mengetahui cukup banyak terapi yang ditawarkan selain yang didasarkan pada ilmu kedokteran. Sebagian menawarkan terapi yang dapat menyembuhkan diabetes melitus. Saya mendukung pendapat dokter yang mengobati Anda agar tetap menjalani terapi seperti yang Anda jalani sekarang karena menurut penelitian, terapi seperti itulah yang terbukti bermanfaat.

Dunia kedokteran sangat terbuka dengan kemungkinan terapi baru, tetapi terapi tersebut harus dapat dibuktikan manfaatnya sebelum digunakan masyarakat.

Pada era informasi bebas sekarang ini, masyarakat perlu jeli membedakan informasi yang didukung bukti dari informasi yang belum didukung bukti nyata. Sudah tentu Anda tidak ingin kecewa jika diabetes melitus Anda nanti menjadi tidak lagi terkontrol.

Anda sudah memahami diabetes melitus yang tidak terkontrol dapat mengakibatkan komplikasi akut maupun kronik yang dapat membahayakan kesehatan Anda, bahkan menimbulkan komplikasi yang sulit diatasi.

Jadi, kembali ke pertanyaan Anda, para pakar kesehatan dewasa ini masih beranggapan diabetes melitus dapat dikendalikan, tetapi belum dapat disembuhkan. Sudah tentu kita berharap akan ada penemuan baru di bidang kedokteran. Sementara menunggu penemuan tersebut, saya berharap Anda tetap dapat melanjutkan gaya hidup Anda yang berhasil mengendalikan diabetes melitus dan hipertensi Anda. (dr Samsuridjal Djauzi)

⁠Editor: acandra ⁠ ⁠Sumber : Kompas Cetak

http://m.kompas.com/news/read/data/2009.12.07.07482339

Diabetes Dapat Berujung pada Cuci Darah

2010-04-01T10:25:00.000+07:00

Jakarta, Kompas - .Kadar gula darah yang tidak terkontrol pada pengidap diabetes dapat menyebabkan berbagai komplikasi. Salah satu kondisi buruk dan mahal ialah gagal ginjal yang menyebabkan pengidap terpaksa cuci darah.

”Pasien cuci darah terbanyak biasanya pengidap diabetes dan kemudian diikuti darah tinggi,” ujar Dante Saksono Harbuwono, spesialis penyakit dalam dari Divisi Metabolik dan Endokrin Universitas Indonesia dalam acara ajang wicara tentang diabetes pada Women Health Expo, Jumat (5/2).

Sekadar gambaran, pada studi di Amerika, dari 100 persen pasien cuci darah sekitar 43 persen di antaranya merupakan pengidap diabetes, 28 persen pengidap darah tinggi, dan selebihnya karena penyakit lain.

Penyakit kronis

Diabetes melitus (DM) merupakan penyakit kronis yang timbul akibat kadar gula darah yang tinggi. Kadar gula darah tinggi itu disebabkan

ketidakmampuan tubuh memproduksi hormon insulin atau penggunaan yang tidak efektif dari produksi insulin.

Gula darah dapat meningkat karena makanan, stres, sakit, dan obat-obatan tertentu.

Dante mengatakan, apabila gula darah tidak terkontrol, dapat terjadi komplikasi. Komplikasi berhubungan dengan perubahan metabolik. Di ginjal, misalnya, terjadi gangguan atau perubahan pada sirkulasi serta fungsi penyaringan.

Di dalam ginjal terdapat jutaan pembuluh darah kecil yang berfungsi sebagai penyaring guna mengeluarkan produk sisa dari darah. Kadar gula darah yang tinggi membuat ginjal menyaring terlalu banyak darah.

Setelah beberapa tahun, sistem penyaring akan bocor sehingga protein keluar di urine. Kerja ginjal yang berat tersebut menyebabkan ginjal kehilangan kemampuan menyaring darah sehingga terjadi gagal ginjal. Kontrol terhadap gula darah dan tekanan darah akan memperkecil kemungkinan kerusakan ginjal.

”Tekanan darah juga harus dijaga agar tidak tinggi karena ikut berpengaruh terhadap fungsi juga,” ujarnya. Cara menjaga kadar gula darah dan tekanan darah, antara lain, yaitu dengan diet yang tepat, olahraga teratur, dan konsumsi obat jika diperlukan.

Timbunan lemak

Komplikasi lainnya ialah gangguan terhadap jantung. Sekitar 75-80 persen kematian pada diabetes karena kelainan jantung dan pembuluh darah. Hal ini karena timbulnya timbunan lemak di pembuluh darah sehingga aliran darah terhambat. Jika itu terjadi di pembuluh darah jantung, dapat menimbulkan serangan jantung.

Selain itu, komplikasi juga dapat menimpa pembuluh darah lain di mata (kebutaan), kelamin, kaki, dan otak.

Faktor pencetus diabetes melitus, antara lain, adalah kurang gerak, makan berlebihan, kehamilan, dan kekurangan produksi hormon insulin. Diabetes tidak dapat disembuhkan, tetapi kadar gula darah dapat dikendalikan sehingga berbagai komplikasi dapat dicegah.

Dante mengatakan, masalah diabetes tipe II semakin serius. Jumlah pengidap terus bertambah. Di Jakarta, misalnya, tahun 1980, prevalensi diabetes sebesar 2,8 persen dan pada 2005 menjadi 12,1 persen.

Salah satu kendala penanganan diabetes adalah pasien tidak mencari informasi yang benar dan mencoba mengobati sendiri. Pengidap, misalnya, beranggapan, mengonsumsi yang pahit-pahit, seperti brotowali, pare, atau buah mengkudu, akan melawan diabetes.

Sering kali setelah mengonsumsi bahan-bahan itu pengidap lalu tidak melakukan kontrol lagi terhadap penyakitnya. Persoalan lain ialah kepatuhan pengidap yang rendah. Setelah tidak ada gejala kemudian pola hidup pengidap kembali buruk. (INE)

http://m.kompas.com/news/read/data/2010.02.06.03484463

Awasi Komplikasi Diabetes!

2010-04-01T10:24:00.000+07:00

JAKARTA, KOMPAS.com - Kadar gula darah yang tidak terkontrol pada penderita diabetes dapat menyebabkan berbagai komplikasi. Komplikasi berhubungan dengan perubahan-perubahan metabolik.

"Salah satu kondisi buruk dan mahal ialah gagal ginjal yang menyebabkan penderita terpaksa menjalani cuci darah. Pasien cuci darah terbanyak biasanya penderita diabetes dan kemudian diikuti darah tinggi," ujar Saksono Harbuwono Spesialis Penyakit Dalam dari Divisi Metabolik dan Endokrin Universitas Indonesia dalam acara talkshow tentang diabetes pada Women Health Expo, Jumat (5/2/2010).

Sekadar gambaran, studi di Amerika, dari 100 persen pasien cuci darah, sekitar 43 persen diantaranya merupakan penderita diabetes, 28 persen penderita darah tinggi, dan selebihnya karena penyakit lain.

Komplikasi lainnya ialah gangguan terhadap jantung. Sekitar 75-80 persen kematian pada diabetes karena kelainan jantung dan pembuluh darah. Hal ini disebabkan karena timbulnya timbunan lemak di pembuluh darah sehingga aliran darah terhambat. Jika itu terjadi di pembuluh darah jantung, dapat timbul serangan jantung. Selain itu, komplikasi dapat menimpa pembuluh darah lain di mata (kebutaan), kelamin, kaki, dan otak.

Tentang Diabetes

Diabetes Melitus (DM) merupakan penyakit kronis yang timbul akibat kadar gula darah yang tinggi. Kadar gula darah tinggi itu disebabkan ketidakmampuan tubuh memproduksi hormon insulin atau penggunaan yang tidak efektif dari produksi insulin. Gula darah dapat meningkat karena makanan, stres, sakit, dan abat-obatan tertentu.

Faktor pencetus diabetes melitus antara lain kurang gerak, makan berlebihan, kehamilan dan kekurangan produksi hormon insulin. Diabetes tidak dapat disembuhkan tetapi kadar gula darah dapat dikendalikan sehingga berbagai komplikasi dapat dicegah. Kunci penanganan diabetes ialah menjaga kadar gula darah. Cara menjaga kadar gula darah dan tekanan darah antara lain diet yang tepat, olah raga teratur, dan konsumsi obat jika diperlukan.

Dante mengatakan, diabetes tipe II semakin menjadi masalah serius. Jumlah penderitanya juga terus bertambah. Di Jakarta misalnya, pada tahun 1980 prevalensi diabetes sebesar 2,8 persen dan di tahun 2005 menjadi 12,1 persen.

⁠Penulis: KOMPAS Indira Permanasari S ⁠ ⁠Editor: Edj ⁠

http://m.kompas.com/news/read/data/2010.02.05.21370524

Apakah Saya Berisiko Diabetes?

2010-04-01T10:23:00.001+07:00

KOMPAS.com — Indonesia menempati urutan keempat di dunia setelah Amerika Serikat, India, dan China dalam angka penderita diabetes. Diperkirakan sedikitnya 14 juta orang di negeri ini menderita diabetes dan tiap tahun jumlahnya terus meningkat.

Ada sejumlah faktor yang dianggap bisa meningkatkan risiko, yakni:

Glukosa puasa terganggu
Jika pemeriksaan gula darah (glukosa) menunjukkan Anda mengalami pradiabetes (gula darah berkisar 111-125 mg/dL), berarti Anda berisiko tinggi terkena diabetes.

Adanya riwayat keluarga
Seseorang berisiko lebih tinggi terkena diabetes tipe 1 atau tipe 2 jika orangtua atau saudara laki-laki atau perempuannya menderita penyakit ini.

Kelebihan berat badan
Sebagian besar penderita diabetes tipe 2 memiliki kelebihan berat badan. Semakin banyak jaringan lemak, semakin resisten otot dan sel jaringan terhadap insulin, terutama jika kelebihan lemak berada di sekitar perut.

Kurang beraktivitas
Semakin kurang aktif, makin besar risiko Anda terkena diabetes.

Usia
Risiko terkena diabetes tipe 2 bertambah seiring dengan meningkatnya usia.

Riwayat diabetes gestasional
Lebih dari separuh wanita yang mengalami diabetes gestasional (diabetes pada kehamilan) kelak akan terkena diabetes tipe 2 dalam hidupnya. Wanita yang pernah melahirkan bayi dengan berat badan lebih dari 4,5 kg juga berisiko lebih tinggi.

Sindrom ovarium polikistik
Sindrom ovarium polikistik adalah bentuk umum akibat ketidakseimbangan hormon pada wanita. Sindrom ini terkait kuat dengan risiko diabetes tipe 2. Banyak wanita yang menderita sindrom ini memiliki kadar insulin darah yang tinggi dan kurang peka terhadap efek insulin dibandingkan orang lain.

Hipertensi atau lemak darah yang abnormal
Karena orang yang memiliki tekanan darah tinggi dan kadar lemak darah (lipid) abnormal berisiko terkena diabetes, semua pengidap kedua kondisi itu harus melakukan pemeriksaan diabetes.

⁠Penulis: AN ⁠ ⁠Editor: acandra ⁠ ⁠Sumber : Mayo Clinic⁠

http://m.kompas.com/news/read/data/2010.01.28.10271141

Agar Diabetesi Tidak Diamputasi

2010-04-01T10:21:00.000+07:00

KOMPAS.com — Salah satu hal yang dikhawatirkan terjadi pada orang dengan diabetes (diabetesi) adalah jika terjadi luka yang membusuk (gangren), lalu harus diamputasi. Secara medis diketahui, luka membusuk itu akan terus merembet ke bagian tubuh lain. Satu-satunya jalan untuk menghentikannya adalah dengan memotong bagian busuk itu.

Bagaimana caranya agar terhindar dari kejadian mengerikan itu? Ikuti saran berikut ini:

- Jaga gula darah tetap normal dengan cara-cara sesuai yang diajarkan dokter, yakni mengontrol makan, berolahraga, dan minum obat.

- Jaga berat badan ideal. Terlalu gemuk akan meningkatkan risiko lipatan-lipatan tubuh lembab, menjadi sarang kuman, dan mengalami lecet akibat gesekan.

- Hindari segala macam kemungkinan yang dapat menyebabkan tubuh mengalami luka. Perlu diingat, pada diabetesi, luka akan membawa risiko sulit sembuh dan membusuk.

- Hentikan kebiasaan berolahraga atau joging tanpa alas kaki karena akan meningkatkan risiko kaki mengalami perlukaan. Perlu diingat, bagian yang jauh dari jantung memiliki kemungkinan kebas karena aliran darah tidak cukup. Akibatnya, jika kaki tertusuk pasir, duri, paku, dan sebagainya, tidak akan terasa.

- Sebelum menggunakan sepatu, selalu pastikan bahwa di dalam sepatu benar-benar bersih dan aman, tidak terselip pasir atau sesuatu yang dapat menimbulkan luka.

- Perhatikan cara yang benar saat memotong kuku, baik kuku tangan, maupun kuku kaki supaya menghindari kemungkinan tertusuk.

- Jika terjadi perlukaan, segeralah berkonsultasi ke dokter ahli agar mendapatkan penanganan yang tepat.

⁠Sumber : Tabloid Gaya Hidup Sehat⁠
http://m.kompas.com/news/read/data/2009.06.18.0918092

650.000 Anak Mengidap Diabetes

2010-04-01T10:18:00.000+07:00

SURABAYA, KOMPAS.com - Sekitar 650.000 anak Indonesia mengidap diabetes mellitus tipe 2. Gaya hidup tidak sehat dan tidak seimbang memicu peningkatan jumlah diabetes mellitus di Indonesia.

Ketua Pusat Diabetes dan Nutrisi (PDN) RSU Dr Soetomo Surabaya Askandar Tjokroprawiro mengatakan, Departemen Kesehatan mencatat sedikitnya 13 juta penduduk Indonesia mengidap diabetes mellitus (DM). Lima persen di antaranya atau sekitar 650.000 orang masih anak-anak, yang umumnya mengidap DM tipe 2. ”DM tipe 2 disebabkan oleh gaya hidup yang tidak sehat sehingga menyebabkan resistensi insulin,” jelas Askandar, Selasa (3/11).

Saat ini, DM tipe 2 merupakan jenis diabetes yang paling banyak ditemukan. ”Jika dulu DM tipe 2 dihubungkan dengan usia lanjut, sekarang dapat menyerang sejak usia anak-anak, remaja, dan usia dewasa. Anak-anak sekarang yang banyak makan makanan tidak sehat dan kurang bergerak rawan mengidap DM tipe 2,” tuturnya.

Orangtua harus memerhatikan kebiasaan makan dan aktivitas fisik anaknya di rumah. Selain itu, orangtua juga harus memerhatikan perkembangan berat badan anaknya. Anak yang terindikasi menderita DM biasanya sering cepat lapar dan haus, buang air kecil banyak, dan berat badannya tidak pernah naik. ”Kalau melihat gejala-gejala itu harus hati-hati. Coba ajak anak untuk memeriksa kadar gula darahnya. Kadar gula darah yang normal pada anak sama dengan kadar gula yang normal bagi orang dewasa, yakni berkisar 100-140 mg/dl,” Askandar menjelaskan.

Peneliti pada PDN, Agung Pranoto, mengatakan, peningkatan jumlah pengidap DM cukup tinggi. Secara nasional, rata-rata pengidap naik 5,7 persen. Namun, di beberapa kota besar seperti Jakarta, peningkatan jumlah pengidap bisa mencapai 12 persen per tahun. ”Kondisi ini memprihatinkan karena angka kematian akibat diabetes cukup tinggi. Di seluruh dunia, rata-rata enam orang meninggal setiap menit akibat komplikasi diabetes,” kata Agung.

Bahkan, ada kemungkinan jumlah penderita DM di Indonesia lebih banyak dari yang terdata di Departemen Kesehatan.

Askandar juga mengungkapkan, pengidap DM rawan terkena osteoporosis. Kadar gula yang tinggi pada darah memacu hormon yang mengurangi tingkat kepadatan tulang. Jika dibiarkan, penderita DM akhirnya akan terkena osteoporosis dan mudah patah tulang. (RAZ)

⁠Editor: tof ⁠ ⁠Sumber : Kompas Cetak⁠
http://m.kompas.com/news/read/data/2009.11.04.06021036

10 Kebiasaan Kecil Pemicu Diabetes

2010-04-01T10:14:00.000+07:00

Dalam hidup ini berlaku hukum "tabungan". Apa yang kita lakukan menjadi tabungan di masa mendatang. Apa yang kita tabung sedikit demi sedikit akan terasa hasilnya bertahun-tahun kemudian. Begitu pun dengan penyakit. Mulai dari segelas minuman favorit hingga suka menonton TV hingga larut. Siapa nyana kalau itu bisa meningkatkan risiko diabetes?

1. Teh manis

Penjelasannya sederhana. Tingginya asupan gula menyebabkan kadar gula darah melonjak tinggi. Belum risiko kelebihan kalori. Segelas teh manis kira-kira mengandung 250-300 kalori (tergantung kepekatan). Kebutuhan kalori wanita dewasa rata-rata adalah 1.900 kalori per hari (tergantung aktivitas). Dari teh manis saja kita sudah dapat 1.000-1.200 kalori. Belum ditambah tiga kali makan nasi beserta lauk pauk. Patut diduga kalau setiap hari kita kelebihan kalori. Ujungnya: obesitas dan diabetes.

Pengganti: Air putih, teh tanpa gula, atau batasi konsumsi gula tidak lebih dari dua sendok teh sehari.

2. Gorengan

Karena bentuknya kecil, satu gorengan tidak cukup buat kita. Padahal gorengan adalah salah satu faktor risiko tinggi pemicu penyakit degeneratif, seperti kardiovaskular, diabetes melitus, dan stroke. Penyebab utama penyakit kardiovaskular (PKV) adalah adanya penyumbatan pembuluh darah koroner, dengan salah satu faktor risiko utamanya adalah dislipidemia. Dislipidemia adalah kelainan metabolisme lipid yang ditandai dengan peningkatan kadar kolesterol total, LDL (kolesterol jahat) dan trigliserida, serta penurunan kadar HDL (kolesterol baik) dalam darah. Meningkatnya proporsi dislipidemia di masyarakat disebabkan kebiasaan mengonsumsi berbagai makanan rendah serat dan tinggi lemak, termasuk gorengan.

Pengganti: Kacang Jepang, atau pie buah.

3. Suka ngemil

Kita mengira dengan membatasi makan siang atau malam bisa menghindarkan diri dari obesitas dan diabetes. Karena belum kenyang, perut diisi dengan sepotong atau dua potong camilan seperti biskuit dan keripik kentang. Padahal, biskuit, keripik kentang, dan kue-kue manis lainnya mengandung hidrat arang tinggi tanpa kandungan serta pangan yang memadai. Semua makanan itu digolongkan dalam makanan dengan glikemik indeks tinggi. Sementara itu, gula dan tepung yang terkandung di dalamnya mempunyai peranan dalam menaikkan kadar gula dalam darah.

Pengganti: Buah potong segar.

4. Kurang tidur.

Jika kualitas tidur tidak didapat, metabolisme jadi terganggu. Hasil riset para ahli dari University of Chicago mengungkapkan, kurang tidur selama 3 hari mengakibatkan kemampuan tubuh memproses glukosa menurun drastis. Artinya, risiko diabetes meningkat. Kurang tidur juga dapat merangsang sejenis hormon dalam darah yang memicu nafsu makan. Didorong rasa lapar, penderita gangguan tidur terpicu menyantap makanan berkalori tinggi yang membuat kadar gula darah naik.

Solusi: Tidur tidak kurang dari 6 jam sehari, atau sebaiknya 8 jam sehari.

5. Malas beraktivitas fisik

Badan Kesehatan Dunia (WHO) mengatakan, kasus diabetes di negara-negara Asia akan naik hingga 90 persen dalam 20 tahun ke depan. "Dalam 10 tahun belakangan, jumlah penderita diabetes di Hanoi, Vietnam, berlipat ganda. Sebabnya? Di kota ini, masyarakatnya lebih memilih naik motor dibanding bersepeda," kata Dr Gauden Galea, Penasihat WHO untuk Penyakit Tidak Menular di Kawasan Pasifik Barat.

Kesimpulannya, mereka yang sedikit aktivitas fisik memiliki risiko obesitas lebih tinggi dibanding mereka yang rajin bersepeda, jalan kaki, atau aktivitas lainnya.

Solusi: Bersepeda ke kantor.

6. Sering stres

Stres sama seperti banjir, harus dialirkan agar tidak terjadi banjir besar. Saat stres datang, tubuh akan meningkatkan produksi hormon epinephrine dan kortisol supaya gula darah naik dan ada cadangan energi untuk beraktivitas. Tubuh kita memang dirancang sedemikian rupa untuk maksud yang baik. Namun, kalau gula darah terus dipicu tinggi karena stres berkepanjangan tanpa jalan keluar, sama saja dengan bunuh diri pelan-pelan.

Solusi: Bicaralah pada orang yang dianggap bermasalah, atau ceritakan pada sahabat terdekat.

7. Kecanduan rokok

Sebuah penelitian di Amerika yang melibatkan 4.572 relawan pria dan wanita menemukan bahwa risiko perokok aktif terhadap diabetes naik sebesar 22 persen. Disebutkan pula bahwa naiknya risiko tidak cuma disebabkan oleh rokok, tetapi kombinasi berbagai gaya hidup tidak sehat, seperti pola makan dan olahraga.

Pengganti: Permen bebas gula. Cara yang lebih progresif adalah mengikuti hipnoterapi. Pilihlah ahli hipnoterapi yang sudah berpengalaman dan bersertifikat resmi.

8. Menggunakan pil kontrasepsi

Kebanyakan pil kontrasepsi terbuat dari kombinasi hormon estrogen dan progestin, atau progestin saja. Pil kombinasi sering menyebabkan perubahan kadar gula darah. Menurut dr Dyah Purnamasari S, Sp PD, dari Divisi Metabolik Endokrinologi RSCM, kerja hormon pil kontrasepsi berlawanan dengan kerja insulin. Karena kerja insulin dilawan, pankreas dipaksa bekerja lebih keras untuk memproduksi insulin. Jika terlalu lama dibiarkan, pankreas menjadi letih dan tidak berfungsi dengan baik.

Solusi: Batasi waktu penggunaan pil-pil hormonal, jangan lebih dari 5 tahun.

9. Takut kulit jadi hitam

Menurut jurnal Diabetes Care, wanita dengan asupan tinggi vitamin D dan kalsium berisiko paling rendah terkena diabetes tipe 2. Selain dari makanan, sumber vitamin D terbaik ada di sinar matahari. Dua puluh menit paparan sinar matahari pagi sudah mencukupi kebutuhan vitamin D selama tiga hari. Beberapa penelitian terbaru, di antaranya yang diterbitkan oleh American Journal of Epidemiology, menyebutkan bahwa vitamin D juga membantu keteraturan metabolisme tubuh, termasuk gula darah.

Solusi: Gunakan krim tabir surya sebelum "berjemur" di bawah sinar matahari pagi selama 10-15 menit.

10. Keranjingan soda

Dari penelitian yang dilakukan oleh The Nurses' Health Study II terhadap 51.603 wanita usia 22-44 tahun, ditemukan bahwa peningkatan konsumsi minuman bersoda membuat berat badan dan risiko diabetes melambung tinggi. Para peneliti mengatakan, kenaikan risiko itu terjadi karena kandungan pemanis yang ada dalam minuman bersoda. Selain itu, asupan kalori cair tidak membuat kita kenyang sehingga terdorong untuk minum lebih banyak.

Pengganti: Jus dingin tanpa gula.*

⁠Sumber : Prevention⁠

http://m.kompas.com/news/read/data/2009.02.26.16105884

Penyakit Asma pada Anak

2010-03-31T18:10:00.001+07:00

Penyakit asma (asthma) menyebabkan pembengkakan dan peradangan di saluran udara yang mengarah ke paru-paru. Ketika penyakit asma kambuh, maka saluran udara menjadi sempit dan kencang. Sehingga udara bisa lewat dengan mudah dan membuat Anda sulit untuk bernafas. Hal ini juga disebut serangan asma atau exacerbations.

Penyakit Asma menjangkiti anak-anak dalam berbagai cara. Beberapa anak hanya mengalami serangan asma selama musim alergi, ketika mereka menghirup udara dingin, atau saat mereka latihan / olahraga. Lainny memiliki banyak serangan buruk yang sering membuat mereka ke dokter.

Bahkan jika anak Anda memiliki sedikit serangan asma, anda tetap harus merawat asmanya. Jika pembengkakan dan iritasi pada saluran udara anak tidak dikontrol, asma anak Anda dapat menurunkan kualitas hidup, mencegah anak Anda dari latihan, dan meningkatkan risiko anak pergi ke rumah sakit.

Meski penyakit asma merupakan penyakit seumur hidup, pengobatan dapat mengendalikan dan menjaga anak Anda sehat. Banyak anak-anak dengan penyakit asma bermain olah raga dan hidup sehat, hidup aktif.

Apa yang menyebabkan penyakit asma?

Para Ahli tidak tahu persis apa yang menyebabkan penyakit asma. Tetapi ada beberapa hal yang kami ketahui:

Penyakit asma merupakan keturunan.

penyakit asma jauh lebih umum pada orang dengan alergi, meskipun tidak semua orang dengan alergi mendapat penyakit asma. Dan tidak semua orang dengan alergi memiliki penyakit asma.

Pencemaran dapat menyebabkan penyakit asma atau membuatnya lebih buruk.

Gejalanya apa saja?

Gejala asma dapat ringan atau parah. Anda mungkin memiliki serangan ringan sekarang dan kemudian, atau mungkin gejala asma parah setiap hari, atau mungkin perpaduannya. Seberapa sering anda memiliki gejala-gejala juga dapat berubah. Bila Anda memiliki penyakit asma, Anda dapat:

Desahan, membuat keras atau lembut siulan kebisingan yang terjadi bila anda bernafas dalam dan keluar.

Batuk.

Merasa keketatan di dada.

Merasa kekurangan nafas.

Kesulitan tidur karena batuk atau sulit bernapas.

Cepat lelah saat latihan atau olahraga.

Gejala Anda mungkin parah pada malam hari.

Serangan asma parah dapat mengancam jiwa dan memerlukan perawatan darurat.

Bagaimana penyakit asmadidiagnosis?

Bersama dengan melakukan pemeriksaan fisik dan bertanya tentang kesehatan, dokter Anda mungkin akan melakukan tes fungsi paru-paru. Tes ini meliputi:

Spirometry. Dokter menggunakan tes ini untuk mendiagnosa dan memantau penyakit asma. Itu mengukur seberapa cepat Anda dapat memindahkan udara ke dalam dan ke luar paru-paru Anda dan berapa banyak udara yang bergerak.

Peak expiratory flow (PEF). Hal ini menunjukkan seberapa cepat Anda dapat bernafas saat Anda mencoba sekuat mungkin.

Sebuah latihan atau tantangan inhalasi. Tes ini mengukur seberapa cepat Anda bisa bernafas setelah latihan atau setelah meminum obat-obatan.

Ronsen dada, untuk melihat jika ada penyakit lain yang menyebabkan gejala Anda.

Tes alergi, jika dokter Anda berpikir gejala Anda dapat disebabkan oleh alergi.

Anda harus rutin checkups dengan dokter Anda untuk melacak penyakit asma Anda dan memutuskan pengobatan.

Obat Asma?

Ada dua bagian untuk pengobatan penyakit asma. Tujuannya adalah untuk:

Kontrol penyakit asma jangka panjang. Untuk melakukannya, gunakan rencana harian perawatan asma. Ini adalah rencana tertulis yang menginformasikan tentang obat yang diambil. Hal ini juga membantu Anda melacak gejala dan mengetahui dengan baik perawatan / pengobatan sedang bekerja. Banyak orang mengambil obat pengontrol yang biasanya merupakan inhaled corticosteroid setiap hari. Menggunakan obat pengontrol setiap hari membantu mengurangi pembengkakan di saluran udara dan mencegah serangan. Dokter akan menunjukkan cara menggunakan pengisap dengan benar. Hal ini penting agar Anda mendapatkan jumlah obat yang benar untuk membantu Anda bernafas lebih baik.

Perlakuan ketika serangan asma terjadi. Menggunakan rencana tindakan asma, yang memberitahu anda apa yang harus dilakukan bila Anda memiliki serangan asma. Membantu Anda mengidentifikasi memicu yang dapat menyebabkan serangan Anda. Anda menggunakan obat-obatan penyelamat, seperti albuterol, selama serangan penyakit asma.

Menggunakan pengisap (inhaler) dengan spacer adalah cara terbaik untuk mengobati untuk paru-paru anak Anda. Tetapi anak Anda harus menggunakan dengan benar pengisap (inhaler) itu agar bekerja dengan baik. Jika Anda tidak yakin bagaimana cara menggunakan pengisap (inhaler) yang benar, meminta dokter Anda untuk menunjukkan bagaimana caranya.

Jika anak Anda perlu menggunakan pengisap lebih sering dari biasanya, berbicara dengan dokter. Ini adalah tanda bahwa penyakit asma anak Anda tidak terkontrol dan dapat menimbulkan masalah.

Serangan asma dapat mengancam hidup, tapi Anda mungkin dapat mencegah mereka jika anda mengikuti rencana. Dokter Anda dapat mengajarkan keterampilan yang anda perlukan untuk pengobatan penyakit asma anak Anda dan rencana tindakan.

Bagaimana Anda mencegah serangan asma?

Anda dapat mencegah beberapa serangan asma oleh menghindari hal-hal yang menyebabkan mereka. Hal ini disebut pemicu. Pemicu bisa berupa:

Irritants di udara, seperti asap rokok atau polusi udara. Jangan merokok, dan coba untuk menghindari sekitar mereka yang merokok.

Hal-hal yang Anda alergi terhadapnya, seperti bulu binatang peliharaan (kucing, anjing), debu, kecoa, atau serbuk sari. Bila Anda dapat menghindari hal-hal yang Anda alergi terhadapnya. Hal itu dapat juga membantu memastikan untuk memilih jenis obat alergi.

Tanya tentang dokter menggunakan inhaler (pengisap) jika latihan ini dapat memicu Anda.

Hal-hal lain seperti panas, udara dingin, infeksi, atau obat-obatan, seperti aspirin dan nonsteroidal anti-inflammatory drugs (NSAIDs). Coba untuk tidak latihan di luar saat itu dingin dan panas. Berbicara dengan dokter tentang beberapa vaksin untuk mencegah infeksi, dan bertanya tentang obat-obatan apa yang harus Anda hindari.

Dapat menakutkan ketika anak Anda memiliki serangan asma. Anda mungkin merasa tidak tertolong, namun memiliki rencana perawatan harian dan rencana tindakan penyakit asma yang akan membantu Anda tahu apa yang harus dilakukan selama mengalami serangan. Serangan asma yang cukup parah mungkin akan untuk membutuhkan perawatan medis yang mendesak, tetapi pada kebanyakan kasus, Anda dapat menangani gejala di rumah jika Anda mempunyai rencana tindakan penyakit asma yang baik.

http://kesehatan.07x.net/index.php/asmacat/50-asma-anak.html

Leukemia

2010-03-31T17:59:00.000+07:00

Leukemia merupakan jenis kanker yang dimulai di sumsum tulang, yang merupakan jaringan lunak di tulang yang bertanggung jawab untuk memproduksi sel darah merah, sel darah putih, dan platelets. Beberapa sel dapat mengubah menjadi leukemia sel, yang selanjutnya membagi menjadi lebih sehat sel. Sebagai kanker tulang sumsum menciptakan lebih banyak sel-sel leukemia, sel-sel sehat mendorong mereka keluar dan menggantikan mereka, sehingga sulit untuk darah berfungsi dengan baik, dan yang mengarah ke masalah medis serius.

Terdapat empat jenis utama leukemia menjadi dua kategori tergantung bagaimana leukemia berlangsung dan perbedaan antara normal dan abnormal sel.

Leukemia Akut
1. Akut Myelogenous leukemia (AML) merupakan kanker yang menyebar dengan cepat di dalam darah dan sumsum tulang. Karena yang asli leukemic sel, sumsum tulang yang memproduksi berbagai blasts, atau belum, nonfunctional sel. Di bawah keadaan sehat, sel-sel ini akan berkembang menjadi sel-sel darah putih yang memerangi infeksi, sel darah merah membawa oksigen ke seluruh tubuh, atau platelets untuk membantu clotting. Namun, pada orang yang AML, blasts ini tidak mengalami perkembangan normal dan menghambat produksi sel-sel baru.

2. Akut Lymphocytic leukemia (ALL) adalah kanker yang mirip dengan leukemia akut myelogenous kecuali, daripada mempengaruhi semua jenis sel, dimulai di lymphocytes. Lymphocytes adalah sel darah putih yang mempertahankan tubuh terhadap infeksi. Sumsum tulang yang membuat sel belum banyak dikenal sebagai blasts, yang pada orang yang sehat akan menjadi lymphocytes. Dalam orang yang SEMUA Namun, ini tidak blasts mengembangkan biasanya menjadi sel darah putih. Sel-sel yang abnormal kemudian mengambil tempat di benak biasanya dikhususkan untuk sehat sel, dan menghambat penciptaan sel-sel baru. Proses ini dapat mengakibatkan pengurangan sel darah merah dan perkembangan anemia, serta pengurangan sel darah putih yang mengarah ke sistem kekebalan lemah.

Leukemia Kronis
3. Kronis Lymphocytic leukemia (CLL), seperti jenis leukemia, berkembang di dalam darah dan sumsum tulang. Leukemia kronis berlangsung pada lambat menilai dari akut leukemia, namun tetap mempengaruhi lymphocytes, yang biasanya memerangi infeksi. CLL membuat terlalu banyak nonfunctional lymphocytes yang mengambil tempat sel sehat. Sebagai sel kanker terus bertambah banyak, mereka menghambat efektivitas fungsional lymphocytes, yang mengarah ke sistem kekebalan lemah. Anemia penyembuhan lambat dan juga dapat terjadi dalam CLL pasien sebagai sel-sel darah merah dan platelets akan diganti dengan yang abnormal lymphocytes.

4. Kronis Myeloid leukemia (CML) adalah lambat tumbuh-jenis leukemia yang membuat sumsum hampir-fungsional-sel darah merah, putih, dan di disproporsional platelets-angka. Banyak sel darah putih dan platelets yang dibuat, sementara jumlah sel darah merah yang dibentuk. Aliran darah dimulai untuk memperlambat sebagai jumlah sel darah putih meningkat dan pasien mungkin mengalami anemia parah karena penurunan dalam sel-sel darah merah.

Gejala-gejala untuk setiap jenis leukemia bervariasi, namun umum termasuk gejala demam dan panas dingin, kelelahan, sering infeksi, kehilangan nafsu makan dan berat, bengkak Kelenjar getah bening, mudah bruising atau pendarahan, sesak nafas, sakit tulang, malam sweats, dan perdarahan masuk ke kulit.

Hitung darah lengkap, atau CBC, adalah tes darah yang mengukur hitungan sel darah merah, sel darah putih dihitung, tingkat hemoglobin, dan platelet count, antara lain. Hal ini umumnya digunakan untuk mendiagnosa leukemia. Metode lain yang digunakan untuk diagnosing leukemia termasuk sumsum biopsies, cairan tulang belakang tes, ujian fisik, kromosom screenings, dan sinar-X dada.

Pengobatan untuk leukemia mungkin termasuk kemoterapi, radiasi, terapi biologi, terapi bertarget seperti kinase inhibitors, dan sumsum tulang dan sel batang-transplantations.

http://kesehatan.07x.net/index.php/leukemia/62-leukemia-kanker-darah.html

Kanker Prostat

2010-03-31T17:55:00.001+07:00

Kanker prostat adalah kanker ganas (cancerous) tumor yang dimulai dari sel yang prostata, biasanya kelenjar yang sel. Biasanya, kanker prostat tumbuh perlahan, tetapi telah mulai tumbuh dan menyebar dengan cepat dalam beberapa kasus.

Dengan mengukur tingkat kanker prostat antigen-spesifik, atau PSA, di dalam darah atau dengan melakukan digital dubur ujian (dre), kemungkinan untuk mendeteksi kanker prostat dalam tahap awal pembangunan. Selama dre kelenjar prostat yang diperiksa untuk gundukan atau solid massa, yang dapat diidentifikasi sebagai Tumors.

Umum gejala kanker prostat yang perlu sering kencing (terutama pada malam hari), kesulitan kencing, atau sakit dan kesulitan dengan seruan. Gejala lain mungkin termasuk darah dalam air seni atau semen. Jika dokter Anda mencurigai prostata kanker, ia akan cenderung melakukan biopsi untuk membuat diagnosis dan, jika memang kanker, untuk menentukan tahap penyakit dan seberapa cepat atau lambat mungkin tumbuh dan menyebar.

Yang paling umum untuk perawatan kanker prostat mungkin termasuk operasi, radiasi, dan terapi hormon. Kemoterapi dapat digunakan dalam kasus-kasus penyakit lebih maju. Yang paling umum untuk operasi kanker prostat adalah radikal prostatectomy yang cukup menghapus kanker prostat di dalam kasus penyakit yang tidak menular.

Pencegahan
tujuan strategi pencegahan kanker prostat adalah untuk mencegah manusia dari penyakit berkembang. Sayangnya, meskipun kemajuan yang signifikan dalam penelitian selama 16 tahun, tujuan ini belum tercapai. Kedua genetik dan lingkungan faktor risiko untuk kanker prostat telah diidentifikasi, tetapi bukti-bukti belum cukup kuat untuk membantu orang saat ini menghadapi risiko untuk kanker prostat.

Dengan kontras, beberapa keberhasilan telah terlihat dengan strategi yang dapat menunda perkembangan dan kemajuan dari kanker prostat. Studi dengan finasteride dan dutasteride, yang biasanya digunakan untuk laki-laki dengan noncancerous kondisi BPH, telah menunjukkan bahwa mereka dapat berperan dalam perlambatan perkembangan kanker prostat; berkelanjutan studi akan membantu untuk menentukan peran yang optimal dari agen ini.

Sementara itu, diet dan perubahan gaya hidup telah ditunjukkan untuk mengurangi resiko kanker prostata pembangunan dan kemajuan, dan dapat membantu orang dengan kanker prostat hidup lebih baik lagi dan kehidupan.

Gejala Kanker Prostat
Jika kanker tertangkap pada tahap awal, kebanyakan manusia tidak akan mengalami gejala. Beberapa laki-laki, namun, akan mengalami gejala yang mungkin menunjukkan adanya kanker prostat, termasuk:
* berat badan turun tanpa sebab yang jelas
     * perlu sering kencing, terutama pada malam hari;
     * Kesulitan mulai kembali memegang hajat atau urine;
     * Lemah atau gangguan aliran air seni;
     * Sakit di perkemihan;
     * Kesulitan dalam memiliki ereksi;
     * Darah di air kencing atau mani, atau
     * Sering mengakami kekakuan atau sakit pada bagian bawah belakang, hips, thighs atau atas.

Perawatan Kanker Prostat
Tidak ada "satu ukuran cocok semua" untuk pengobatan kanker prostata, sehingga setiap orang harus belajar sebanyak dia dapat tentang berbagai pilihan dan perawatan, dalam hubungannya dengan dokter, membuat keputusan sendiri tentang apa yang terbaik untuk dia.

Bagi kebanyakan orang, keputusan akan istirahat pada kombinasi klinis dan faktor psikologis. Laki-laki dengan diagnosis kanker prostata diterjemahkan hari ini mungkin akan hidup selama bertahun-tahun, sehingga setiap keputusan yang dibuat sekarang akan berbalas untuk waktu yang lama. Cermat dari berbagai pilihan yang penting adalah langkah pertama dalam memutuskan pada perawatan terbaik saja.

Berkonsultasi dengan semua tiga jenis kanker prostata pakar-a urologist, oncologist yang radiasi dan medis oncologist-akan memberikan penilaian yang paling komprehensif yang tersedia perawatan dan hasil yang diharapkan.

http://kesehatan.07x.net/index.php/kanker-prostat-prostate-cancer/64-kanker-prostat-prostate-cancer.html

Gameshark Membaca EKG

2010-03-30T20:19:00.002+07:00

1. Periksa skala dan kelayakan hasil rekaman
2. Tentukan irama dasar
3. Hitung QRS rate
4. Tentukan aksis
5. Periksa gelombang P
6. Hitung interval PR
7. Periksa komplek QRS
8. Periksa ST segmen
9. Periksa gelombang T

1. Periksa skala dan kelayakan hasil rekaman
Skala : Skala kecepatan kertas dan skala voltase
Kelayakan : artefak tidak mengganggu pemeriksaan, ada identitas, tanggal pemeriksaan, skala lengkap

2. Tentukan irama dasar
Normal : irama sinus / sinus rhytm, gelombang P positif di Lead II, III, aVF, dan gelombang P negatif di aVR
Kelainan :
- irama junctional : gelombang P negatif di lead II / hilang / di belakang kompleks QRS
- irama idioventrikular
- atrial fibrilasi : gelombang P kecil-kecil halus dan banyak / tidak terlihat, QRS rate sangat tidak teratur
- supraventrikular takikardi (SVT) : komplek QRS cepat teratur, gelombang P hilang / dibelakang komplek QRS
- atrial flutter : P rate 220-350x/menit, reguler, komplek QRS seringkali regular dengan AV blok

3. Hitung QRS rate
Normal : 60-100x/menit
Bila irama reguler : hitung jarak R ke R dalam kotak kecil / besar. QRS rate adalah 1500 dibagi jumlah kotak kecil atau 300 dibagi jumlah kotak besar
Bila irama irreguler : misalnya pada AF, hitung jumlah komplek QRS dalam 6 kali 5 kotak besar x 10

QRS rate kurang dari 60x/menit : bradikardi
QRS rate lebih dari 100x/menit : takikardia

4. Tentukan aksis
Yang minimal ditentukan adalah aksis dalam bidang frontal
Normal range untuk deviasi aksis -30' sampai +110'
Untuk memudahkan memakai komplek QRS di lead I dan aVF
- lead I dominan positif dan lead aVF dominan positif : normal aksis
- lead I dominan positif dan lead aVF dominan negatif : deviasi aksis kiri
- lead I dominan negatif dan lead aVF dominan positif : deviasi aksis kanan
- lead I dominan negatif dan lead aVF dominan negatif : aksis superior

Bila ada deviasi aksis dengan cara ini belum tentu suatu kelainan karena yang dijadikan patokan antara aksis 0-90'

5. Periksa gelombang P
Normal : durasi < 0,12 detik, voltase 0,3 mV. Positif di lead II dan negatif di lead aVR
Kelainan :
- pembesaran atrium kiri : P mitral, gelombang P lebar dan memiliki "Notched", mudah di lihat di lead I / II. Gelombang P lebar, bifasik, dengan komponen defleksi negatif yang dominan
- pembesaran atrium kanan : P pulmonal, gelombang P tinggi, ramping dan runcing, di lihat di lead II, III, aVF. Gelombang P di V1 bisa runcing, bifasik atau negatif

6. Hitung interval PR
Normal : durasi 0,12 - 0,20 detik, interpretasi terbaik mengikutsertakan heart rate pasien, pada heart rate yang tinggi PR interval akan memendek, dan sebaliknya heart rate rendah, interval PR akan memanjang. Teratur, dalam tiap siklus durasi interval PR sama
Kelainan :
- pemendekan interval PR : Wolff-Parkinson-White syndrome atau Lown-Ganong-Levine syndrome, junctional rhytm
- pemanjangan interval PR : AV blok derajat 1
- interval PR semakin memanjang : AV blok derajat 2 tipe 1
- AV blok derajat 2, Mobitz II : gelombang P diikuti QRS sampai pada satu saat gelombang P tidak diikuti QRS. Maka dalam 1 siklus gelombang P > komplek QRS, interval PR sama panjang
- blok konstan : gelombang P saja, tidak diikuti komplek QRS sebanyak 2-3 x, sampai pada satu saat baru muncul gelombang P diikuti komplek QRS
- AV blok derajat 3 : blok total / komplit : atrium dan ventrikel masing-masing berdenyut sendiri-sendiri. Kadang gelombang P hilang tertutup gelombang T atau komplek QRS

Sambil periksa interval PR, lihat juga segmen PR
Normal : isoelektrik
Kelainan : depresi segmen PR pada perikarditis

7. Periksa komplek QRS
Normal : durasi maksimal 0,10 detik, selalu mengikuti gelombang P. Pattern komplek QRS di precordial lead dominan negatif di V1 dan positif di V6. Voltase komplek QRS tidak melebihi batas-batas tertentu
Kelainan :
- durasi memanjang : LVH, dilatasi ventrikel, Bundle Branch Block, irama ventrikel
- kelainan voltase :
A. LVH :
R di aVL > 13 mm
R di V5-V6 > 27 mm
S di V1 ditambah R di V5 atau V6 > 35mm
Bisa disertai depresi ST segmen dan gelombang T terbalik di prekordial kiri (V5 / V6), deviasi aksis ke kiri, pemanjangan durasi QRS dan Ventrikular Activating Time (VAT)

B. RVH :
Gelombang R > gelombang S di V1 atau V3R
qR di V1 / V3R
Persisten S di V5 - V6
Depresi ST dan T terbalik di V1-V3
Deviasi aksis ke kanan
Bisa tampak R tinggi di aVF yang disertai depresi segmen ST dan gelombang T terbalik

RBBB : Durasi komplek QRS bisa normal / memanjang, jika durasi masih normal = RBBB inkomplit, jika durasi memanjang = RBBB komplit, R' (gelombang R ada 2 puncak seperti huruf M) di V1 dan aVR, gelombang S di lead I dan V6 lebar dan dalam

8. Periksa ST segmen
Diukur mulai dari akhir gelombang S hingga awal gelombang T
Normal : elevasi 2 kotak dari garis isoelektris, depresi 1/2 kotak dari garis isoelektris
Kelainan :
- ST elevasi : defleksi ke atas / positif = infark
- ST depresi : defleksi ke bawah / negatif = iskemia

Lokasinya
V1-V2 : septum LV
V3-V4 : dinding anterior LV
V5, V6, I, AVL : dinding lateral LV
II, III, aVF : dinding inferior LV

ST elevasi :
V1-V4 : anterior wall, dari arteri LAD
V5, V6, I, aVL : lateral wall, dari arteri distal LAD / sirkumfleksa
II, III, aVF : inferior wall, dari Right coronary
V3R, V4R : RV, dari Right coronary

9. Periksa gelombang T
normal T wave
causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left bundle branch block

causes of small, flattened or inverted T waves are numerous and include ischaemia, age, race, hyperventilation, anxiety, drinking iced water, LVH, drugs (e.g. digoxin), pericarditis, PE, intraventricular conduction delay (e.g. RBBB)and electrolyte disturbance.

Kumpulan gambar EKG = http://www.ecglibrary.com/ecghome.html

Mengatasi Tekanan Darah Tinggi-Hipertensi

2010-03-28T06:10:00.000+07:00

Tekanan Darah
Sebelum membahas mengenai tekanan darah tinggi atau hipertensi, ada baiknya Anda mengenal terlebih dahulu tentang tekanan darah. Saat Anda melakukan pemeriksaan fisik atau pemeriksaan klinis ke dokter, biasanya ada alat khusus yang digunakan oleh dokter untuk memeriksa tekanan darah. Alat untuk memeriksa tekanan darah disebut sphigmomanometer atau dikenal juga dengan tensimeter. Ada tensimeter digital dan ada juga tensimeter air raksa yang masih umum digunakan untuk pemeriksaan klinis.

Dokter akan melakukan pemeriksaan tekanan darah dengan menyuruh Anda duduk atau berbaring, karena itu posisi terbaik untuk mengukur tekanan darah. Lalu dokter biasanya akan mengikat kantung udara pada lengan kanan kecuali pada lengan tersebut terdapat cedera. Setelah itu, dilakukan pengukuran tekanan darah. Perbedaan antara tekanan sistolik dan diastolik disebut tekanan denyut.

Apa yang dimaksud dengan tekanan darah? Tekanan darah yaitu tekanan yang dialami darah pada pembuluh arteri ketika darah di pompa oleh jantung ke seluruh anggota tubuh manusia. Tekanan darah dibuat dengan mengambil dua ukuran dan biasanya terdapat dua angka yang akan disebut oleh dokter. Misalnya dokter menyebut 140-90, maka artinya adalah 140/90 mmHg. Angka pertama (140) menunjukkan tekanan ke atas pembuluh arteri akibat denyutan jantung atau pada saat jantung berdenyut atau berdetak, dan disebut tekanan sistolik atau sering disebut tekanan atas. Angka kedua (90) menunjukkan tekanan saat jantung beristirahat di antara pemompaan, dan disebut tekanan diastolik atau sering juga disebut tekanan bawah.

Setelah mengetahui tekanan darah, pasti Anda ingin mengetahui apakah tekanan darah Anda termasuk rendah, normal atau tinggi. Berikut ini penggolongan tekanan darah berdasarkan angka hasil pengukuran dengan tensimeter untuk tekanan sistolik dan diastolik:

Tekanan Darah
Sistolik (angka pertama)
Diastolik (angka kedua)
- Darah rendah atau hipotensi
Di bawah 90
Di bawah 60

- Normal
90 - 120
60 - 80

- Pre-hipertensi
120 - 140
80 - 90

- Darah tinggi atau hipertensi (stadium 1)
140 - 160
90 - 100

- Darah tinggi atau hipertensi (stadium 2 / berbahaya)
Di atas 160
Di atas 100

Mengapa Tekanan Darah Meningkat?
Apa yang menyebabkan tekanan darah bisa meningkat? Sebagai ilustrasi, jika Anda sedang menyiram kebun dengan selang. Jika Anda menekan ujung selang, maka air yang keluar akan semakin kencang. Hal itu karena tekanan air meningkat ketika selang ditekan. Selain itu, jika Anda memperbesar keran air, maka aliran air yang melalui selang akan semakin kencang karena debit air yang meningkat.

Hal yang sama juga terjadi dengan darah Anda. Jika pembuluh darah Anda menyempit, maka tekanan darah di dalam pembuluh darah akan meningkat. Selain itu, jika jumlah darah yang mengalir bertambah, tekanan darah juga akan meningkat.

Penyebab Darah Tinggi
Ada beberapa hal yang bisa menyebabkan seseorang memiliki tekanan darah tinggi. Ada faktor penyebab tekanan darah tinggi yang tidak dapat Anda kendalikan. Ada juga yang dapat Anda kendalikan sehingga bisa mengatasi penyakit darah tinggi. Beberapa faktor tersebut antara lain:
1. Keturunan
Faktor ini tidak bisa Anda kendalikan. Jika seseorang memiliki orang-tua atau saudara yang memiliki tekanan darah tinggi, maka kemungkinan ia menderita tekanan darah tinggi lebih besar. Statistik menunjukkan bahwa masalah tekanan darah tinggi lebih tinggi pada kembar identik daripada yang kembar tidak identik. Sebuah penelitian menunjukkan bahwa ada bukti gen yang diturunkan untuk masalah tekanan darah tinggi.

2. Usia
Faktor ini tidak bisa Anda kendalikan. Penelitian menunjukkan bahwa seraya usia seseorang bertambah, tekanan darah pun akan meningkat. Anda tidak dapat mengharapkan bahwa tekanan darah Anda saat muda akan sama ketika Anda bertambah tua. Namun Anda dapat mengendalikan agar jangan melewati batas atas yang normal.

3. Garam
Faktor ini bisa Anda kendalikan. Garam dapat meningkatkan tekanan darah dengan cepat pada beberapa orang, khususnya bagi penderita diabetes, penderita hipertensi ringan, orang dengan usia tua, dan mereka yang berkulit hitam.

4. Kolesterol
Faktor ini bisa Anda kendalikan. Kandungan lemak yang berlebih dalam darah Anda, dapat menyebabkan timbunan kolesterol pada dinding pembuluh darah. Hal ini dapat membuat pembuluh darah menyempit dan akibatnya tekanan darah akan meningkat. Kendalikan kolesterol Anda sedini mungkin.

5. Obesitas / Kegemukan
Faktor ini bisa Anda kendalikan. Orang yang memiliki berat badan di atas 30 persen berat badan ideal, memiliki kemungkinan lebih besar menderita tekanan darah tinggi.

6. Stres
Faktor ini bisa Anda kendalikan. Stres dan kondisi emosi yang tidak stabil juga dapat memicu tekanan darah tinggi.

7. Rokok
Faktor ini bisa Anda kendalikan. Merokok juga dapat meningkatkan tekanan darah menjadi tinggi. Kebiasan merokok dapat meningkatkan risiko diabetes, serangan jantung dan stroke. Karena itu, kebiasaan merokok yang terus dilanjutkan ketika memiliki tekanan darah tinggi, merupakan kombinasi yang sangat berbahaya yang akan memicu penyakit-penyakit yang berkaitan dengan jantung dan darah.

8. Kafein
Faktor ini bisa Anda kendalikan. Kafein yang terdapat pada kopi, teh maupun minuman cola bisa menyebabkan peningkatan tekanan darah.

9. Alkohol
Faktor ini bisa Anda kendalikan. Konsumsi alkohol secara berlebihan juga menyebabkan tekanan darah tinggi. Alkohol HARAM !!

10. Kurang Olahraga
Faktor ini bisa Anda kendalikan. Kurang olahraga dan bergerak bisa menyebabkan tekanan darah dalam tubuh meningkat. Olahraga teratur mampu menurunkan tekanan darah tinggi Anda namun jangan melakukan olahraga yang berat jika Anda menderita tekanan darah tinggi.

Untuk mencegah darah tinggi bagi Anda yang masih memiliki tekanan darah normal ataupun mengatasi darah tinggi bagi Anda yang sudah memiliki tekanan darah tinggi, maka saran praktis berikut ini dapat Anda lakukan:
1. Kurangi konsumsi garam dalam makanan Anda. Jika Anda sudah menderita tekanan darah tinggi sebaiknya Anda menghindari makanan yang mengandung garam.

2. Konsumsi makanan yang mengandung kalium, magnesium dan kalsium. Kalium, magnesium dan kalsium mampu mengurangi tekanan darah tinggi.

3. Kurangi minum minuman atau makanan beralkohol. Jika Anda menderita tekanan darah tinggi, sebaiknya hindari konsumsi alkohol secara berlebihan. Untuk pria yang menderita hipertensi, jumlah alkohol yang diijinkan maksimal 30 ml alkohol per hari sedangkan wanita 15 ml per hari. (Lebih baik tidak usah minum, HARAM !!)

4. Olahraga secara teratur bisa menurunkan tekanan darah tinggi. Jika Anda menderita tekanan darah tinggi, pilihlah olahraga yang ringan seperti berjalan kaki, bersepeda, lari santai, dan berenang. Lakukan selama 30 hingga 45 menit sehari sebanyak 3 kali seminggu.

5. Makan sayur dan buah yang berserat tinggi seperti sayuran hijau, pisang, tomat, wortel, melon, dan jeruk.

6. Jalankan terapi anti stres agar mengurangi stres dan Anda mampu mengendalikan emosi Anda.

7. Berhenti merokok juga berperan besar untuk mengurangi tekanan darah tinggi atau hipertensi.

8. Kendalikan kadar kolesterol Anda.

9. Kendalikan diabetes Anda.

Darah Tinggi dapat Dikendalikan
Tekanan darah tinggi atau hipertensi bukan suatu penyakit yang tidak dapat dihilangkan. Anda bisa mengendalikannya dan mencegah darah tinggi.

http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/174-mengatasi-tekanan-darah-tinggi-atau-hipertensi.html

Mengatasi Kanker Payudara

2010-03-28T06:07:00.000+07:00

Kanker payudara adalah pertumbuhan sel yang abnormal pada jaringan payudara seseorang. Bila sudah sampai stadium lanjut, pengangkatan payudara kadang-kadang dilakukan untuk keselamatan pasien. Hal ini tentu menjadi sesuatu yang menakutkan bagi seorang wanita.

Hampir semua jenis kanker memiliki penyebab spesifik. Misalnya sebagian besar kasus kanker kulit disebabkan oleh sinar ultraviolet matahari. Sedangkan kanker paru-paru disebabkan karena rokok. Namun tidak ada penyebab tunggal yang pasti untuk kanker payudara.

Beberapa faktor bisa menjadi penyebab kanker payudara. Misalnya faktor genetika, lingkungan, dan hormon kemungkinan turut berperan dalam kanker payudara. Wanita yang rentan terhadap faktor-faktor tadi bisa jadi memiliki risiko yang lebih tinggi.

Faktor Risiko Kanker Payudara
Tidak ada yang tahu pasti apa penyebab kanker payudara. Berdasarkan hasil statistik, kebanyakan penderita kanker payudara adalah wanita dengan usia diatas 50 tahun. Ini berarti semakin tua seseorang, maka peluang terkena penyakit ini semakin besar. Faktor lain yang mempengaruhi adalah riwayat keluarga. Bila ada keluarga yang menderita penyakit ini seperti ibu atau saudara kandung maka peluangnya akan semakin besar. Kanker payudara juga bisa disebabkan karena sebelumnya menderita kanker di organ tubuh lainnya sehingga menyebar ke bagian payudara. Atau bila sebelumnya ada riwayat menderita kanker pada organ tubuh lainnya.

Hal lain yang dapat memicu kanker adalah gaya hidup. Sering mengkonsumsi makanan yang mengandung bahan kimia atau bersifat karsinogen, alkohol, atau merokok.

Mencegah Kanker Payudara
Salah satu pencegahan kanker payudara adalah pola makan yang sehat. Diperkirakan satu dari tiga kasus kanker payudara karena faktor pola makan. Pola makan yang baik yang akan membantu mempertahankan sistem kekebalan tubuh Anda dan ini merupakan pencegahan penyakit yang paling ampuh. Meskipun belum diketahui adanya makanan yang dapat menyembuhkan kanker, memakan makanan tertentu dan mengurangi makanan tertentu lainnya dapat menjadi tindakan pencegahan.

Makanan yang kaya serat, dapat membantu menurunkan kadar prolaktin dan estrogen, kemungkinan dengan mengikatkan diri pada hormon-hormon ini lalu membuangnya ke luar tubuh. Ini dapat menekan fase lanjut dari karsinogenesis (pembentukan kanker). Selain itu, mengurangi makanan berlemak jenuh dapat menurunkan risiko. Kacang kedelai dan produk kedelai tanpa difermentasi dapat menghambat pertumbuhan tumor.

Sayur-sayuran yang kaya vitamin A, seperti wortel, labu siam, ubi jalar, dan sayur-sayuran berdaun hijau tua seperti bayam, kangkung dan sawi hijau, mungkin dapat membantu. Vitamin A mencegah pembentukan mutasi penyebab kanker. Sedangkan buah-buahan dan sayuran yang kaya akan vitamin C menurunkan risiko kanker payudara.

Deteksi Dini Kanker Payudara
Timbulnya benjolan pada daerah payudara dapat merupakan indikasi kemungkinan adanya jenis kanker payudara. Tetapi belum tentu semua benjolan berarti kanker karena harus diperiksa lebih lanjut untuk kepastiannya di rumah sakit atau dokter.

Indikasi lain dari penyakit ini adalah benjolan pada bagian ketiak, rasa nyeri pada payudara, perubahan warna atau tekstur pada payudara, puting tertarik ke dalam, areola (daerah di sekitar putting susu yang berwarna coklat), atau pada puting susu. Pada beberapa kasus, kanker payudara dideteksi dari keluarnya cairan dari puting susu yang berwarna kekuningan, kehijauan atau bernanah.

Kunci untuk bertahan hidup adalah mendeteksi kanker payudara sedini mungkin, sebelum ia memiliki kesempatan untuk menyebar. Salah satu penyebab kematian yang tinggi akibat penyakit ini disebabkan karena kurangnya kesadaran untuk mendeteksi gejala-gejala yang ada. Umumnya setelah sampai pada keluhan-keluhan yang berat, penderita baru berkonsultasi ke dokter yang sering kali berarti kanker sudah dalam stadium lanjut. Sehingga apabila penyakit ini sudah sampai stadium lanjut, maka akan sulit untuk disembuhkan.

Periksa Payudara Sendiri
Agar masyarakat, khususnya wanita dapat melakukan pemeriksaan pada payudara secara teratur, maka dibuat gerakan yang dinamakan Sadari atau Sarari yang merupakan singkatan dari "Periksa Payudara Sendiri". Dianjurkan agar pemeriksaan dilakukan 1 bulan sekali setelah menstruasi kira-kira 4-7 hari setelah menstruasi.

Pada pemeriksaan ini, hal yang dilakukan adalah:
1. Berdiri di depan cermin dengan posisi bahu lurus dan kedua tangan di pinggang. Perhatikan apakah ada perubaan fisik payudara Anda, misalnya perubahan bentuk, ukuran atau warna payudara.

2. Angkat kedua tangan ke atas dan perhatikan kembali apakah ada perubahan fisik payudara yang tampak.

3. Tekan puting susu dan lihat apakah ada cairan yang keluar dari puting susu.

4. Berbaring dan raba payudara bagian kanan dengan tangan kiri dan sebagainya. Buat pola memutar dan rasakan apakah pada payudara terdapat benjolan dan lainnya.

5. Saat duduk atau berdiri coba pijat payudara untuk menemukan apakah ada benjolan yang mencurigakan. Raba daerah ketiak sampai perut untuk memeriksanya.

Gerakan Sadari dapat dilakukan oleh pasangan hidup kepada istrinya. Atau para suami dapat mengingatkan istrinya agar melakukan pemeriksaan Sadari secara teratur. Peranan keluarga tentu dapat memudahkan terdeteksinya penyakit ini.

Jika Anda Terkena Kanker Payudara
Saat seseorang dinyatakan menderita kanker payudara, kebanyakan penderita akan langsung terpukul secara emosi. Mereka merasa mendapat vonis mati, walaupun sebenarnya bisa saja penderita disembuhkan terlebih lagi bila masih dalam stadium dini. Pada tahap lanjut, dampak emosi dan psikologis dapat menyebabkan seorang penderita kanker mengalami depresi. Hal ini dapat memperburuk keadaannya. Untuk itu, perlu adanya dukungan dari pihak keluarga atau teman.

Penderita kanker payudara sebaiknya memberitahu keluarga atau teman mereka karena penderita membutuhkan dukungan dari orang-orang terdekat akibat dampak emosi yang dialaminya. Adalah hal yang wajar apabila penderita tidak mau memberitahu keluarga atau temannya tentang penyakit mereka. Alasannya karena mereka tidak mau merepotkan atau membuat orang yang mendengarnya menjadi sedih atau khawatir. Tetapi, bayangkanlah keadaan sebaliknya, bila Anda yang tidak diberitahu oleh keluarga atau teman dekat Anda bahwa ternyata dia menderita kanker, tentu Anda akan semakin sedih karena Anda tidak tahu dan mungkin tidak memberikan bantuan yang dibutuhkan.

Teman hidup adalah seseorang yang paling dekat dan bisa Anda ajak bicara untuk menemukan pengobatan terbaik dan dampak yang mungkin harus dialami. Penderita kanker payudara mungkin merasa minder dengan keadaannya sehingga mempengaruhi saat melakukan hubungan suami istri. Sebaiknya, hal ini juga dibicarakan dengan suami Anda agar dapat dimengerti dan dapat memberi bantuan dengan memberikan pelukan atau ungkapan sayang lainnya.

Anak-anak yang masih kecil mungkin tidak mengerti apa yang sedang terjadi. Tetapi, bila anak Anda sudah dapat diajak bicara, Anda dapat menceritakan dengan bahasa yang sederhana apa yang dimaksud dengan kanker payudara dan efek yang mungkin akan terjadi pada fisik Anda seperti kebotakan akibat kemoterapi atau perubahan pada payudara. Hal ini penting agar anak-anak yang masih lugu tidak mendapatkan informasi yang salah dari orang yang tidak bertanggung jawab yang dapat membuat mereka mennjadi takut atau benci kepada Anda atau merasa bahwa apa yang Anda alami akibat kesalahan mereka.

Tidak semua teman atau keluarga yang tidak terlalu dekat perlu diberitahu apabila Anda merasa tidak nyaman untuk menyampaikannya. Anda juga tidak perlu menanggapi seluruh komentar yang diberikan oleh teman, keluarga atau orang lain yang mengetahui penyakit Anda. Selalu ada komentar yang positif dan negatif. Jadi, hal itu tidak perlu dipikirkan secara berlebihan yang dapat merusak ketahanan tubuh Anda.

Untuk menambah semangat, Anda dapat bergabung dengan kelompok sesama penderita kanker payudara. Di Indonesia, Yayasan Kanker Indonesia dapat mengakomodasi kebutuhan ini. Dalam kelompok ini, mereka dapat memberi semangat dan keyakinan agar Anda dapat sembuh. Cerita-cerita dari penderita lain mungkin dapat membuat Anda merasakan keadaan Anda masih lebih baik. Atau cerita dari penderita lain yang gigih untuk melawan penyakitnya dan dapat memperoleh kesembuhan dapat membantu Anda memperoleh kekuatan untuk tidak menyerah pada keadaan.

Jadi, tetaplah bersemangat untuk melawan penyakit Anda. Bila ada anggota keluarga atau teman Anda yang menderita tumor atau kanker payudara, Anda dapat memberikan dukungan yang diperlukan karena mengetahui penderitaan yang mereka alami. Dukungan tersebut dapat membantu kesembuhan mereka.

http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/260-mengatasi-kanker-payudara.html

Kanker Serviks Pembunuh Banyak Wanita

2010-03-28T06:03:00.000+07:00

Di Indonesia, setiap 1 jam seorang meninggal karena kanker serviks

Kanker serviks atau kanker leher rahim (sering juga disebut kanker mulut rahim) merupakan salah satu penyakit kanker yang paling banyak terjadi bagi kaum wanita. Setiap satu jam, satu wanita meninggal di Indonesia karena kanker serviks atau kanker leher rahim ini. Fakta menunjukkan bahwa jutaan wanita di dunia terinfeksi HPV, yang dianggap penyakit lewat hubungan seks yang paling umum di dunia.

Menurut Organisasi Kesehatan Dunia (WHO), infeksi ini merupakan faktor risiko utama kanker leher rahim. Setiap tahun, ratusan ribu kasus HPV terdiagnosis di dunia dan ribuan wanita meninggal karena kanker serviks, yang disebabkan oleh infeksi itu. Mengingat fakta yang mengerikan ini, maka berbagai tindakan pencegahan dan pengobatan telah dibuat untuk mengatasi kanker serviks atau kanker leher rahim.

Kanker serviks atau kanker leher rahim terjadi di bagian organ reproduksi seorang wanita. Leher rahim adalah bagian yang sempit di sebelah bawah antara vagina dan rahim seorang wanita. Di bagian inilah tempat terjadi dan tumbuhnya kanker serviks. Apa penyebab kanker serviks atau kanker leher rahim? Bagaimana cara pencegahannya? Serta bagaimana cara mengatasinya jika sudah terinfeksi HPV?

HPV
Kanker serviks disebabkan infeksi virus HPV (human papillomavirus) atau virus papiloma manusia. HPV menimbulkan kutil pada pria maupun wanita, termasuk kutil pada kelamin, yang disebut kondiloma akuminatum. Hanya beberapa saja dari ratusan varian HPV yang dapat menyebabkan kanker. Kanker serviks atau kanker leher rahim bisa terjadi jika terjadi infeksi yang tidak sembuh-sembuh untuk waktu lama. Sebaliknya, kebanyakan infeksi HPV akan hilang sendiri, teratasi oleh sistem kekebalan tubuh.

Penyebab dan Gejala Kanker Serviks
Kanker serviks menyerang daerah leher rahim atau serviks yang disebabkan infeksi virus HPV (human papillomavirus) yang tidak sembuh dalam waktu lama. Jika kekebalan tubuh berkurang, maka infeksi HPV akan mengganas dan bisa menyebabkan terjadinya kanker serviks. Gejalanya tidak terlalu kelihatan pada stadium dini, itulah sebabnya kanker serviks yang dimulai dari infeksi HPV dianggap sebagai "The Silent Killer".

Beberapa gejala bisa diamati meski tidak selalu menjadi petunjuk infeksi HPV. Keputihan atau mengeluarkan sedikit darah setelah melakukan hubungan intim adalah sedikit tanda gejala dari kanker ini. Selain itu, adanya cairan kekuningan yang berbau di area genital juga bisa menjadi petunjuk infeksi HPV. Virus ini dapat menular dari seorang penderita kepada orang lain dan menginfeksi orang tersebut. Penularannya dapat melalui kontak langsung dan karena hubungan seks.

Ketika terdapat virus ini pada tangan seseorang, lalu menyentuh daerah genital, virus ini akan berpindah dan dapat menginfeksi daerah serviks atau leher rahim Anda. Cara penularan lain adalah di closet pada WC umum yang sudah terkontaminasi virus ini. Seorang penderita kanker ini mungkin menggunakan closet, virus HPV yang terdapat pada penderita berpindah ke closet. Bila Anda menggunakannya tanpa membersihkannya, bisa saja virus kemudian berpindah ke daerah genital Anda.

Buruknya gaya hidup seseorang dapat menjadi penunjang meningkatnya jumlah penderita kanker ini. Kebiasaan merokok, kurang mengkonsumsi vitamin C, vitamin E dan asam folat dapat menjadi penyebabnya. Jika mengkonsumsi makanan bergizi akan membuat daya tahan tubuh meningkat dan dapat mengusir virus HPV.

Risiko menderita kanker serviks adalah wanita yang aktif berhubungan seks sejak usia sangat dini, yang sering berganti pasangan seks, atau yang berhubungan seks dengan pria yang suka berganti pasangan. Faktor penyebab lainnya adalah menggunakan pil KB dalam jangka waktu lama atau berasal dari keluarga yang memiliki riwayat penyakit kanker.

Sering kali, pria yang tidak menunjukkan gejala terinfeksi HPV itulah yang menularkannya kepada pasangannya. Seorang pria yang melakukan hubungan seks dengan seorang wanita yang menderita kanker serviks, akan menjadi media pembawa virus ini. Selanjutnya, saat pria ini melakukan hubungan seks dengan istrinya, virus tadi dapat berpindah kepada istrinya dan menginfeksinya.

Deteksi Kanker Serviks
Bagaimana cara mendeteksi bahwa seorang wanita terinfeksi HPV yang menyebabkan kanker serviks? Gejala seseorang terinfeksi HPV memang tidak terlihat dan tidak mudah diamati. Cara paling mudah untuk mengetahuinya dengan melakukan pemeriksaan sitologis leher rahim. Pemeriksaan ini saat ini populer dengan nama Pap smear atau Papanicolaou smear yang diambil dari nama dokter Yunani yang menemukan metode ini yaitu George N. Papanicolaou. Namun, ada juga berbagai metode lainnya untuk deteksi dini terhadap infeksi HPV dan kanker serviks seperti berikut:
1. IVA
IVA yaitu singkatan dari Inspeksi Visual dengan Asam asetat. Metode pemeriksaan dengan mengoles serviks atau leher rahim dengan asam asetat. Kemudian diamati apakah ada kelainan seperti area berwarna putih. Jika tidak ada perubahan warna, maka dapat dianggap tidak ada infeksi pada serviks. Anda dapat melakukan di Puskesmas dengan harga relatif murah. Ini dapat dilakukan hanya untuk deteksi dini. Jika terlihat tanda yang mencurigakan, maka metode deteksi lainnya yang lebih lanjut harus dilakukan.

2. Pap smear
Metode tes Pap smear yang umum yaitu dokter menggunakan pengerik atau sikat untuk mengambil sedikit sampel sel-sel serviks atau leher rahim. Kemudian sel-sel tersebut akan dianalisa di laboratorium. Tes itu dapat menyingkapkan apakah ada infeksi, radang, atau sel-sel abnormal. Menurut laporan sedunia, dengan secara teratur melakukan tes Pap smear telah mengurangi jumlah kematian akibat kanker serviks.

3. Thin prep
Metode Thin prep lebih akurat dibanding Pap smear. Jika Pap smear hanya mengambil sebagian dari sel-sel di serviks atau leher rahim, maka Thin prep akan memeriksa seluruh bagian serviks atau leher rahim. Tentu hasilnya akan jauh lebih akurat dan tepat.

4. Kolposkopi
Jika semua hasil tes pada metode sebelumnya menunjukkan adanya infeksi atau kejanggalan, prosedur kolposkopi akan dilakukan dengan menggunakan alat yang dilengkapi lensa pembesar untuk mengamati bagian yang terinfeksi. Tujuannya untuk menentukan apakah ada lesi atau jaringan yang tidak normal pada serviks atau leher rahim. Jika ada yang tidak normal, biopsi — pengambilan sejumlah kecil jaringan dari tubuh — dilakukan dan pengobatan untuk kanker serviks segera dimulai.

Mengobati Kanker Serviks
Jika terinfeksi HPV, jangan cemas, karena saat ini tersedia berbagai cara pengobatan yang dapat mengendalikan infeksi HPV. Beberapa pengobatan bertujuan mematikan sel-sel yang mengandung virus HPV. Cara lainnya adalah dengan menyingkirkan bagian yang rusak atau terinfeksi dengan pembedahan listrik, pembedahan laser, atau cryosurgery (membuang jaringan abnormal dengan pembekuan).

Jika kanker serviks sudah sampai ke stadium lanjut, maka akan dilakukan terapi kemoterapi. Pada beberapa kasus yang parah mungkin juga dilakukan histerektomi yaitu operasi pengangkatan rahim atau kandungan secara total. Tujuannya untuk membuang sel-sel kanker serviks yang sudah berkembang pada tubuh.

Namun, mencegah lebih baik daripada mengobati. Karena itu, bagaimana cara mencegah terinfeksi HPV dan kanker serviks? Berikut ini beberapa cara yang dapat Anda lakukan untuk mencegah kanker serviks.

Mencegah Kanker Serviks
Meski kanker serviks menakutkan, namun kita semua bisa mencegahnya. Anda dapat melakukan banyak tindakan pencegahan sebelum terinfeksi HPV dan akhirnya menderita kanker serviks. Beberapa cara praktis yang dapat Anda lakukan dalam kehidupan sehari-hari antara lain:
1. Miliki pola makan sehat, yang kaya dengan sayuran, buah dan sereal untuk merangsang sistem kekebalan tubuh. Misalnya mengkonsumsi berbagai karotena, vitamin A, C, dan E, dan asam folat dapat mengurangi risiko terkena kanker leher rahim.

2. Hindari merokok. Banyak bukti menunjukkan penggunaan tembakau dapat meningkatkan risiko terkena kanker serviks.

3. Hindari seks sebelum menikah atau di usia sangat muda atau belasan tahun.

4. Hindari berhubungan seks selama masa haid terbukti efektif untuk mencegah dan menghambat terbentuknya dan berkembangnya kanker serviks.

5. Hindari berhubungan seks dengan banyak partner. ( Jangan mendekati zina !!!)

6. Secara rutin menjalani tes Pap smear secara teratur. Saat ini tes Pap smear bahkan sudah bisa dilakukan di tingkat Puskesmas dengan harga terjangkau.

7. Alternatif tes Pap smear yaitu tes IVA dengan biaya yang lebih murah dari Pap smear. Tujuannya untuk deteksi dini terhadap infeksi HPV.

8. Pemberian vaksin atau vaksinasi HPV untuk mencegah terinfeksi HPV.

9. Melakukan pembersihan organ intim atau dikenal dengan istilah vagina toilet. Ini dapat dilakukan sendiri atau dapat juga dengan bantuan dokter ahli. Tujuannya untuk membersihkan organ intim wanita dari kotoran dan penyakit.

Hidup Sehat Tanpa Kanker Serviks
Kanker serviks bisa dicegah dan bisa diobati. Deteksi sejak dini dan rutin melakukan Pap smear akan memperkecil risiko terkena kanker serviks. Ubah gaya hidup Anda dan juga pola makan Anda agar terhindar dari penyakit yang membunuh banyak wanita di dunia ini. Dengan demikian, maka kesehatan serviks atau leher rahim lebih terjamin. Dengan penanganan yang tepat, kanker serviks bukanlah sesuatu yang menakutkan.

http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/237-kanker-serviks-leher-rahim-pembunuh-wanita.html

Mengatasi Sakit Jantung dan Serangan Jantung

2010-03-26T07:06:00.000+07:00

Setiap tahun, jutaan orang di seluas dunia mengalami serangan jantung. Tidak semua serangan jantung mengakibatkan kematian. Namun, umumnya setiap pasien yang pernah mengalami serangan jantung menderita beberapa dampak lanjutannya. Sedangkan sisanya tidak tertolong lagi.

Jantung
Jantung adalah sebuah otot yang memompa darah ke seluruh tubuh. Dalam suatu serangan jantung (myocardial infarction), bagian dari otot jantung mati sewaktu tidak mendapatkan darah. Untuk tetap sehat, jantung membutuhkan oksigen dan zat-zat gizi lain yang dibawa oleh darah. Ini didapatkan melalui arteria (pembuluh darah) koroner, yang membungkus bagian luar jantung.

Penyakit Jantung
Penyakit-penyakit dapat mempengaruhi bagian mana pun dari jantung. Tetapi, penyakit yang paling umum adalah penyakit kronis pada arteria koroner yang disebut aterosklerosis. Karena itu, sakit jantung yang umum dikenal dan paling banyak diderita adalah penyakit jantung koroner atau penyakit arteria koroner. Penyakit ini paling sering menyebabkan serangan jantung pada seseorang yang bisa menyebabkan kematian. Penyebabnya adalah penyempitan pada pembuluh darah koroner, dimana pembuluh ini berfungsi untuk menyediakan darah ke otot jantung. Penyempitan disebabkan oleh tumpukan kolesterol atau protein lain yang berasal dari makanan yang masuk dalam tubuh. Penumpukan ini juga menyebabkan pembuluh darah koroner menjadi kaku. Kekakuan ini disebut sebagai aterosklerosis.

Aterosklerosis terjadi jika terjadi penumpukan plak atau timbunan lemak pada dinding-dinding arteri. Selang beberapa waktu, plak dapat menumpuk, mengeras dan mempersempit arteri, dan menghambat aliran darah ke jantung. Penyakit arteria koroner atau coronary artery disease (CAD) inilah yang pada dasarnya menuntun kepada sebagian besar serangan jantung.

Penyumbatan dalam satu arteri koroner atau lebih dapat menimbulkan serangan jantung secara tiba-tiba. Penyebabnya karena jantung meminta oksigen melebihi yang tersedia sehingga memicu serangan jantung. Mengapa? Apabila otot jantung tidak menerima oksigen untuk waktu yang cukup lama, jaringan di sekitarnya dapat rusak. Tidak seperti jaringan yang lain, otot jantung tidak mengalami regenerasi. Semakin lama serangannya, semakin banyak kerusakan pada jantung dan semakin besar kemungkinan meninggal.

Bahkan dalam arteri yang tidak terlalu sempit karena timbungan plak dan lemak, timbunan plak dapat pecah dan membentuk kerak darah atau trombus. Selain itu, arteri yang berpenyakit juga cenderung mengalami kontraksi otot secara mendadak. Sehingga, sekeping kerak darah dapat terbentuk di tempat kontraksi, melepaskan zat kimia yang kemudian mengakibatkan dinding arteri menyempit, memicu sebuah serangan jantung.

Jika sistem kerja dari jantung rusak, irama normal jantung dapat menjadi kacau dan jantung mulai bergetar dengan tidak menentu atau mengalami fibrilasi. Irama tidak normal ini disebut sebagai aritmia yaitu penyimpangan dari irama jantung normal. Hal ini akan menyebabkan jantung kehilangan kesanggupannya untuk memompa darah dengan efektif ke otak. Dalam waktu sepuluh menit, otak mati dan si pasien pun tidak tertolong lagi.

Selain penyakit jantung koroner yang disebabkan karena penumpukan lemak di dinding arteri, ada juga penyakit jantung lainnya yang disebabkan kelainan semenjak lahir. Misalnya jantung yang tidak sempurna, kelainan katup jantung, melemahnya otot jantung. Penyebab lain adalah bakteri yang menyebabkan infeksi pada jantung.

Gejala Sakit Jantung
Gejala-gejala yang dirasakan jika mengalami penyakit jantung koroner antara lain rasa sakit atau nyeri di dada di mana kebanyakan orang menyangka itu hanya sebagai gangguan pencernaan. Lalu gejala lain yaitu merasa tertekan di tengah dada selama 30 detik sampai 5 menit. Hal lainnya adalah keringat dingin, berdebar-debar, pusing, dan merasa mau pingsan. Gejala ini tidak selalu dirasakan penderitanya. Tanda peringatan lain adalah napas tersengal-sengal pada saat berolahraga.

Selama beberapa bulan sebelum serangan jantung biasanya penderita penyakit jantung sering merasa sangat lelah. Jangan menganggap gejala ini disebabkan oleh kurang tidur dan stres akibat pekerjaan.

Rasa nyeri atau rasa ditekan di dada, yang disebut angina, memberikan peringatan kepada setengah dari mereka yang menderita serangan jantung. Beberapa orang mengalami napas tersengal-sengal atau kelelahan dan perasaan lunglai sebagai gejalanya, mengindikasikan bahwa jantung tidak mendapatkan cukup oksigen karena penyumbatan koroner.

Biasanya beberapa hari menjelang mengalami serangan jantung hebat, seseorang akan mengalami kontraksi otot secara tiba-tiba di dada yang merupakan serangan kecil atau serangan jantung ringan. Serangan jantung ringan umum terjadi sebelum serangan besar beberapa hari kemudian.

Tips Mencegah Penyakit Jantung
Agar terhindar dari penyakit jantung koroner, Anda dapat melakukan hal-hal berikut:

Pola makan sehat
Hindari makanan yang banyak mengandung lemak atau yang mengandung kolesterol tinggi. Seafood memiliki kandungan kolesterol tinggi yang dapat membahayakan jantung. Kurangi menyantap makanan yang digoreng yang banyak mengandung lemak, sebaliknya makanan dapat diolah dengan cara direbus, dikukus atau dipanggang.

Sebisa mungkin, produk makanan yang kita makan rendah lemak atau tanpa lemak. Pilih susu, keju, mentega atau makanan lain yang rendah lemak. Menggoreng dengan menggunakan minyak zaitun memiliki kandungan lemak yang sedikit sehingga bisa menjadi pilihan bila harus mengolah makanan dengan cara digoreng.

Selain menghindari makanan berlemak, hindari juga makanan dengan kandungan gula tinggi seperti soft drink. Jangan pula tertalu banyak mengkonsumsi karbohirat, karena dalam tubuh, karbohidrat akan dipecah menjadi lemak. Sebaliknya, konsumsi oat atau gandum yang dapat membantu menjaga jantung tetap sehat.

Jaga pola makan tidak berlebihan agar terhindar dari kegemukan, karena seseorang yang memiliki lingkar pinggang lebih dari 80 cm, berisiko lebih besar terkena penyakit ini.

Berhenti merokok
Mengisap rokok sangat tidak baik untuk kesehatan jantung, maka segera hentikan kebiasaan ini agar jantung tetap sehat.

Hindari Stres
Stres memang sangat sulit dihindari jika hidup di kota besar seperti Jakarta yang dikenal karena kemacetan dan kesibukannya. Saat seseorang mengalami stres, tubuhnya akan mengeluarkan hormon cortisol yang menyebabkan pembuluh darah menjadi kaku. Hormon norepinephrine akan diproduksi tubuh saat menderita stres, yang akan mengakibatkan naiknya tekanan darah. Maka, sangat baik bila Anda menghindari stres baik di kantor atau di rumah.

Hipertensi
Problem hipertensi atau tekanan darah tinggi juga bisa menyebabkan penyakit jantung. Hipertensi dapat melukai dinding arteri dan memungkinkan kolesterol LDL memasuki saluran arteri dan meningkatkan penimbunan plak.

Obesitas
Kelebihan berat atau obesitas meningkatkan tekanan darah tinggi dan ketidaknormalan lemak. Menghindari atau mengobati obesitas atau kegemukan adalah cara utama untuk menghindari diabetes. Diabetes mempercepat penyakit jantung koroner dan meningkatkan risiko serangan jantung.

Olahraga secara teratur
Anda dapat melakukan kegiatan olahraga seperti berjalan kaki, jalan cepat, atau jogging. Kegiatan olahraga yang bukan bersifat kompetisi dan tidak terlalu berlebihan dapat menguatkan kerja jantung dan melancarkan peredaran darah ke seluruh tubuh.

Konsumsi antioksidan
Polusi udara, asap kendaraan bermotor atau asap rokok menciptakan timbulnya radikal bebas dalam tubuh. Radikal bebas dapat menyebabkan bisul atau endapan pada pembuluh darah yang dapat menyebabkan penyumbatan. Untuk mengeluarkan kandungan radikal bebas dalam tubuh, perlu adanya antioksidan yang akan menangkap dan membuangnya. Antioksidan dapat diperoleh dari berbagai macam buah-buahan dan sayuran.

Keturunan
Seorang yang orang tua atau saudara kandungnya pernah mengalami serangan jantung sebelum usia 60 memiliki risiko lebih besar menderita penyakit ini. Karena itu, jika Anda memiliki kerabat yang pernah mengalami serangan jantung, sebaiknya Anda lebih berhati-hati dalam menjaga agar pola makan dan gaya hidup Anda dapat menunjang jantung sehat.

Mengatasi Penyakit Jantung
Jika Anda merasakan gejala awal penyakit jantung ataupun pernah mengalami serangan jantung ringan, jangan abaikan itu. Anda sangat membutuhkan penanganan dini oleh personel medis yang terlatih. Ini dapat menyelamatkan jantung dari kerusakan yang lebih parah dan bahkan dapat menghindari akibat yang lebih fatal seperti kematian.

Namun jika gejala serangan jantung mulai terjadi, sangat penting untuk segera mencari bantuan medis. Risiko kematian terbesar dari serangan jantung adalah dalam kurun waktu satu jam setelah terjadi serangan jantung. Perawatan yang cepat dan tepat dari tim medis dapat menyelamatkan otot jantung dari kerusakan yang tidak dapat diperbaiki. Semakin banyak otot jantung yang terselamatkan, semakin efektif jantung akan kembali memompa setelah serangan. Jangan menunda-nunda untuk mendapatkan bantuan medis karena merasa takut dianggap mengada-ada.

Bila telah terjadi penyumbatan, tindakan medis yang umumnya diambil adalah dengan pemasangan kateterisasi dan cincin yang menjaga agar pembuluh darah koroner tidak tersumbat. Tetapi, ada kemungkinan terjadi penyumbatan pada pembuluh lainnya.

Sayangi Jantung Anda
Melihat berharganya organ jantung ini untuk kelangsungan hidup, maka segeralah perbaiki gaya hidup Anda agar tetap sehat. Mulailah menikmati makanan yang sehat, bergizi dan rendah kolesterol. Hindari merokok dan stres. Serta berolahragalah secara teratur. Mulailah dengan gaya hidup yang sehat sejak hari ini untuk menyayangi jantung Anda.

http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/189-mengatasi-penyakit-jantung-dan-serangan-jantung.html

Tips Mengendalikan Kolesterol

2010-03-26T04:11:00.000+07:00

Dalam tubuh terdapat lemak terdiri dari kolesterol jahat yang biasa disebut LDL (Low Density Lipoprotein) dimana lemak ini dapat menempel pada pembuluh darah. Sedangkan kolesterol baik yang dikenal dengan HDL (High Density Lipoprotein) merupakan lemak yang dapat melarutkan kandungan LDL dalam tubuh. Kolesterol normal dalam tubuh adalah 160-200 mg, maka penumpukan kandungan LDL harus dicegah agar tetap dalam keadaan normal. Berikut beberapa tips agar Anda dapat mengontrol kolesterol dalam darah.

Tips Mengendalikan Kolesterol

Berikut ini beberapa tips yang bisa Anda lakukan untuk mengendalikan kolesterol Anda:

Diet
Konsumsi makanan yang rendah lemak dan kolesterol. Misalnya dengan mengkonsumsi susu tanpa lemak dan mengurangi konsumsi daging. Pilihlah makanan dengan kandungan lemak tak jenuh daripada kandungan lemak jenuh. Minyak yang digunakan untuk menggoreng secara berulang-ulang dapat meningkatkan kadar kolesterol, maka ada baiknya Anda mengurangi konsumsi makanan yang digoreng.
Konsumsi makanan berserat
Lebih banyak mengkonsumsi makanan berserat seperti gandum, kacang-kacangan, sayur-sayuran dan buah-buahan. Jenis makanan ini dapat menyerap kolesterol yang ada dalam darah dan mengeluarkannya dari tubuh.
Konsumsi antioksidan
Antioksidan banyak terdapat dalam buah-buahan seperti jeruk, strawbery, pepaya, wortel, atau labu. Mengkonsumsi bawang putih secara teratur juga dapat menurunkan kadar kolesterol.

Hindari alkohol dan merokok
Dengan merokok atau mengkonsumsi alkohol, kolesterol akan mudah menumpuk dalam aliran darah.

Olahraga
Berolahraga secara teratur sesuai dengan umur dan kemampuan. Jaga agar berat tubuh Anda tetap ideal.

Makanan sehat, hati-hati, berbahaya atau pantang?

Seperti disebutkan diatas, makanan merupakan hal penting yang dapat menyebabkan kolesterol. Tabel berikut dapat Anda jadikan acuan makanan apa saja yang sebaiknya Anda makan atau dapat dikurangi konsumsinya.

Tabel Jumlah Kolestrol pada Makanan
Jenis makanan yang aman dikonsumsi karena kadar kolestrol yang rendah
Putih telur ayam:0
Teripang:0
Susu sapi non fat:0
Daging ayam / daging bebek pilihan tanpa kulit:50
Ikan air tawar
Daging sapi tanpa lemak
Daging kambing tanpa lemak
Ikan ekor kuning

Jenis makanan yang boleh dikonsumsi sekali-kali
Daging asap (ham / smoke beef)
Iga sapi
Daging sapi
Burung dara
Ikan bawal

Jenis makanan yang perlu diperhatikan untuk dikonsumsi karena kadar kolestrol yang cukup tinggi
Daging sapi berlemak
Gajih sapi
Gajih kambing
Keju
Sosis daging:150
Kepiting
Udang
Kerang
Siput
Belut

Jenis makanan yang berbahaya untuk dikonsumsi karena kandungan kolestrol yang tinggi.
Santan
Susu sapi:250
Susu sapi cream:280
Coklat
Margarin / Mentega
Jeroan sapi
Kerang putih / tiram
Jeroan kambing

Jenis makanan yang pantang untuk dikonsumsi karena kandungan kolestrol yang sangat tinggi.
Cumi-cumi:1170
Kuning telur ayam:2000
Otak sapi:2300
Telur burung puyuh:3640

Catatan: Untuk kategori berbahaya dan pantang sebaiknya tidak dikonsumsi oleh penderita masalah hipertensi atau problem jantung, karena dapat menyebabkan serangan jantung, stroke dan bahkan kematian.

URL: http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/83-tips-mengontrol-kolestrol.html

Mengenal Asam Urat

2010-03-26T03:25:00.001+07:00

Yang dimaksud dengan asam urat adalah sisa metabolisme zat purin yang berasal dari makanan yang kita konsumsi. Ini juga merupakan hasil samping dari pemecahan sel dalam darah.

Purin sendiri adalah zat yang terdapat dalam setiap bahan makanan yang berasal dari tubuh makhluk hidup. Dengan kata lain, dalam tubuh makhluk hidup terdapat zat purin ini, lalu karena kita memakan makhluk hidup tersebut, maka zat purin tersebut berpindah ke dalam tubuh kita. Berbagai sayuran dan buah-buahan juga terdapat purin. Purin juga dihasilkan dari hasil perusakan sel-sel tubuh yang terjadi secara normal atau karena penyakit tertentu.

Normalnya, asam urat ini akan dikeluarkan dalam tubuh melalui feses (kotoran) dan urin, tetapi karena ginjal tidak mampu mengeluarkan asam urat yang ada menyebabkan kadarnya meningkat dalam tubuh. Hal lain yang dapat meningkatkan kadar asam urat adalah kita terlalu banyak mengkonsumsi bahan makanan yang mengandung banyak purin. Asam urat yang berlebih selanjutnya akan terkumpul pada persendian sehingga menyebabkan rasa nyeri atau bengkak.

Penderita asam urat setelah menjalani pengobatan yang tepat dapat diobati sehingga kadar asam urat dalam tubuhnya kembali normal. Tapi karena dalam tubuhnya ada potensi penumpukan asam urat, maka disarankan agar mengontrol makanan yang dikonsumsi sehingga dapat menghindari makanan yang banyak mengandung purin.

Kesimpulan singkat tentang asam urat

Gejala Asam Urat
Kesemutan dan linu
Nyeri terutama malam hari atau pagi hari saat bangun tidur
Sendi yang terkena asam urat terlihat bengkak, kemerahan, panas dan nyeri luar biasa pada malam dan pagi.

Solusi Mengatasi Asam Urat
Melakukan pengobatan hingga kadar asam urat kembali normal. Kadar normalnya adalah 2.4 hingga 6 untuk wanita dan 3.0 hingga 7 untuk pria.
Kontrol makanan yang dikonsumsi.
Banyak minum air putih. Dengan banyak minum air putih, kita dapat membantu membuang purin yang ada dalam tubuh.

Makanan yang Dihindari (mengandung banyak purin)
Lauk pauk seperti jeroan, hati, ginjal, limpa, babat, usus, paru dan otak.
Makanan laut seperti udang, kerang, cumi, kepiting.
Makanan kaleng seperi kornet dan sarden.
Daging, telur, kaldu atau kuah daging yang kental.
Kacang-kacangan seperti kacang kedelai (termasuk hasil olahannya seperti tempe, tauco, oncom, susu kedelai), kacang tanah, kacang hijau, tauge, melinjo, emping.
Sayuran seperti daun bayam, kangkung, daun singkong, asparagus, kembang kol, buncis.
Buah-buahan seperti durian, alpukat, nanas, air kelapa.

Minuman dan makanan yang mengandung alkohol seperti bir, wiski, anggur, tape, tuak.

http://kumpulan.info/sehat/artikel-kesehatan/48-artikel-kesehatan/64-asam-urat.html

Pericarditis, Constrictive-Effusive

2010-02-22T11:50:00.001+07:00

Introduction
Background

Effusive-constrictive pericarditis is a clinical syndrome characterized by concurrent pericardial effusion and pericardial constriction where constrictive hemodynamics are persistent after the pericardial effusion is removed. The mechanism of effusive-constrictive pericarditis is thought to be visceral pericardial constriction. Pericardial effusions vary in size and age and may be transudative, exudative, sanguineous, or chylous. An effusion persisting for months to years may evolve into effusive-constrictive pericarditis.1,2,3,4,5,6,7,8,9,10

The pericardium consists of two layers, a parietal layer and visceral layer. The visceral pericardium is composed of 1 or 2 cell layers of mesothelial cells and adheres closely with the epicardium. The parietal pericardium is separated from the visceral pericardium by a small amount of fluid that serves as a lubricant. Any supraphysiological accumulation of this fluid is identified as a pericardial effusion.1,2,11,12,13 In general, a pericardial effusion should be evaluated to determine its etiology and hemodynamic significance.

Patients with effusive-constrictive pericarditis may present with symptoms caused from a limitation of intercardiac end-diastolic volume. These findings are secondary to not only the pericardial effusion but also pericardial constriction. Symptoms, as well as history and physical findings, vary and a moderate-to-large pericardial effusion may occur.

Jugular venous and arterial pressures may be within the reference range, with or without signs of cardiac tamponade. This syndrome can evolve as part of a clinical continuum initiated by pericarditis or a pericardial effusion; thus, its etiologies mirror those of pericarditis, pericardial tamponade, and chronic constrictive pericarditis (see Pericarditis, Constrictive). The hemodynamic definition of this syndrome is the continued elevation of right atrial, end-diastolic right ventricular and left ventricular diastolic pressures after the removal of pericardial fluid returns the pericardial pressure to zero (or near zero).1,3,14

Recognition of effusive-constrictive pericarditis is clinically important because treatment with pericardiocentesis or a pericardial window may be inadequate as it would not address the visceral pericardium. Rather, a visceral pericardiectomy may be indicated for optimal therapy since it is the visceral pericardium that is constricting.

Importantly, not all cases of effusive-constrictive pericarditis progress to chronic constrictive pericarditis. In some clinical situations, relief from the effusion is obtained by means of pericardiocentesis or a pericardial window, and medical treatment is used to manage the underlying condition. The constriction may be transitory and surgical pericardiectomy may be avoided. These situations usually occur in the first months of a chronic effusion and close monitoring is required.

The effusive-constrictive variant of pericarditis was first described in the 1960s. Hancock popularized this definition of a constrictive physiology with a coexisting pericardial effusion.3 In 2004, Sagrista-Sauldea et al reported 15 subjects from Barcelona, Spain who were identified as having effusive-constrictive pericarditis.14 These individuals were among 190 consecutive subjects with clinical tamponade who underwent pericardiocentesis and concurrent catheterization. The etiologies of the effusive-constrictive pericarditis were infectious causes, irradiation, cardiac surgery, and idiopathic. Consistent with Hancock's data, Sagrista-Sauldea reported that most cases were due to idiopathic factors.
Pathophysiology

Constrictive pericarditis and cardiac tamponade both restrict filling of the cardiac chambers, thereby increasing both systemic and pulmonary filling pressures. In tamponade, single forward flow occurs during systole (prominent x descent in atrial pressure tracings), whereas in constriction, a biphasic pressure tracing is greater during diastole (prominent y descent). Patients with effusive-constrictive pericarditis may have tamponadelike pressure tracings, which change to constrictivelike tracings after pericardiocentesis. This is because the visceral pericardium, not the parietal, is constrictive. In rare cases, a loculated effusion may lead to constriction with regional tamponade of 1 or more cardiac chambers. Almost any form of chronic pericardial effusion has the potential to organize into an effusive-constrictive state even though the absolute number of cases is relatively low.4

Effusive-constrictive pericarditis may be part of a clinical continuum. Stages of infective pericarditis have been observed that range from acute pericarditis and tamponade with effusion to constrictive pericarditis without effusion. Effusive-constrictive pericarditis is likely a middle phase in this evolution. Therefore, suspicion for this entity should be high in cases of indolent, subacute pericarditis, as well in cases of chronic pericardial effusion.
Frequency
United States

Effusive-constrictive pericarditis is a rare disorder. As a complication of pericarditis, pericardial effusion, pericardial tamponade, or chronic constrictive pericarditis, the incidence of effusive-constrictive pericarditis is proportional to the incidence of each of these entities. Cases in the United States are more often secondary to irradiation, cardiac surgery, uremia, or malignancy, or are idiopathic (see Differentials).6
International

Effusive-constrictive pericarditis is a rare disorder. As a complication of pericarditis, pericardial effusion, pericardial tamponade, or chronic constrictive pericarditis, the incidence of effusive-constrictive is proportional to the incidence of each of these entities. Cases in the developing countries are more often secondary to infectious causes (eg, tuberculosis) than other causes (see Differentials).15 In a prospective study of 1184 patients with pericarditis, Sagrista-Sauldea et al reported that 6.9% of 218 patients with tamponade had confirmed effusive-constrictive pericarditis.14
Mortality/Morbidity

* The mortality of effusive-constrictive disease is directly related to its etiology. For example, patients with metastatic carcinoma in the pericardial space usually have a prognosis much poorer than that of patients with postviral or idiopathic pericardial effusion with constriction.
* Constrictive physiology increases the risk of morbidity, but no definitive statistics are available.
* Noncardiac metastatic effusions are often end-stage, with reported mortality rates of 47% and 80% at 3 and 6 months, respectively.

Race

No reported racial predilection exists.
Sex

No reported sex predilection exists.
Age

Since the incidences of many of the diseases that can cause effusive-constrictive pericarditis occur more frequently in older age groups, an age association exists. However, this disease can affect people of any age.
Clinical
History

* Symptoms of effusive-constrictive pericarditis can be hard to interpret but may include atypical or typical chest pain, chest heaviness, or pressure.
* Other symptoms include dyspnea on exertion, fatigability, or peripheral edema.
* Many patients are asymptomatic until the advanced stages of disease. In more severe cases, impaired mental status may be evident as a result of decreased cardiac output.
* Specific etiologies of effusive-constrictive pericarditis may have characteristic antecedent histories that may suggest pericardial disease (eg, tuberculosis, renal failure, malignancy, radiation therapy, cardiovascular surgery).2

Physical

* Physical findings may be a continuum, including findings common with cardiac tamponade (see Cardiac Tamponade).16
* Findings may include hypotension, jugular venous distension, and diminished heart sounds (classic Beck triad).
* Other common findings may include pulsus paradoxus (paradoxical pulse), jugular venous pulse with a prominent x descent and absent y descent, tachycardia, tachypnea, hepatomegaly, ascites, peripheral edema, pleural effusion (in the absence of left-sided congestive signs), renal dysfunction, liver dysfunction and/or auscultation of a pericardial friction rub.
* The classic description of percussible cardiac dullness at the apex may be unreliable.
* Careful attention to all physical findings is required to find clues as to the underlying etiology of the pericardial disease.

Causes

Because effusive-constrictive pericarditis is rare, the differential diagnosis is guided by few published series and case reports (see Pericarditis, Constrictive). Effusive-constrictive pericarditis likely occurs at any point along a clinical continuum, from the occurrence of an effusion to the development of chronic pericardial constriction.

* Leading causes
o Idiopathic factors
o Irradiation
o Cardiac surgery
o Neoplasm - Most commonly lung, breast, or hematologic
o Infectious disease - Particularly in immunocompromised states (most commonly tuberculosis and fungal, although streptococcus species have been reported)17,18
o Myocardial infiltration
o Connective tissue disease
o Uremia
* The etiology can often be suspected from the clinical setting in which the effusion occurs.
* The differential diagnosis of effusive-constrictive pericarditis requires a consideration of all the causes for pericardial effusions and pericardial tamponade and then a determination if the particular patient has constrictive physiology.

http://emedicine.medscape.com/article/157216-overview

Pericarditis, Constrictive

2010-02-22T11:48:00.000+07:00

Introduction
Background

The thousand mysteries around us would not trouble but interest us, if only we had cheerful, healthy hearts.

–Nietzche

If we all had healthy hearts, the mysteries of the heart would not trouble us; however, constrictive pericarditis certainly has been a mystery and remains a diagnostic challenge to this day.

The history of constrictive pericarditis is replete with some of the most famous names in medicine. Richard Lower described a patient with dyspnea and an intermittent pulse in 1669. Lancisi first reported on the constrictive syndrome in 1828. Corrigan described the pericardial knock in 1842. Kussmaul described his sign and the associated paradoxical pulse in 1873.1,2,3

Constrictive pericarditis has symptoms that overlap a variety of diseases as diverse as myocardial infarction, aortic dissection, pneumonia, influenza, and connective tissue disorders. This overlap can confuse the most skilled diagnostician. An increased suspicion for constriction helps move it to the top of the broad differential diagnosis and provides for a correct diagnosis and timely therapy.

Constrictive pericarditis occurs when a thickened fibrotic pericardium, of whatever cause, impedes normal diastolic filling. This usually involves the parietal pericardium, although it can involve the visceral pericardium (see Pericarditis, Constrictive-Effusive). Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which may, in turn, evoke a pericardial effusion. This often leads to pericardial organization, chronic fibrotic scarring, calcification, and restricted cardiac filling.4

The classic diagnostic conundrum of constrictive pericarditis is the difficulty in distinguishing it from restrictive cardiomyopathy (see Cardiomyopathy, Restrictive) and other syndromes associated with elevated right-sided pressures that all share similar symptoms, physical findings, and hemodynamics. Although obtaining a careful history and performing a physical examination remain the cornerstones of evaluation, technologic advances have facilitated diagnosis, particularly with the appropriate use of Doppler echocardiography, high-resolution computed tomography (CT), magnetic resonance imaging (MRI), and invasive hemodynamic measurement.
Pathophysiology

The normal pericardium is composed of 2 layers: the tough fibrous parietal pericardium and the smooth visceral pericardium. Usually, approximately 50 mL of fluid (plasma ultrafiltrate) is present in the intrapericardial space to minimize friction during cardiac motion.5

Acute and subacute forms of pericarditis (which may or may not be symptomatic) may deposit fibrin, which may, in turn, evoke a pericardial effusion. This often leads to pericardial organization, chronic fibrotic scarring, and calcification, most often involving the parietal pericardium (see Pericarditis, Constrictive-Effusive).6

This thickened fibrotic pericardium, regardless of cause, impedes normal late diastolic filling, distinguishing constrictive from restrictive pericarditis. Since the myocardium is unaffected, early ventricular filling during the first third of diastole is unimpeded, but afterwards, the stiff pericardium affects flow and hemodynamics. In other words, the ventricular pressure decreases rapidly early (producing a steep y descent on right atrial pressure waveform tracings) and then increases abruptly to a level that is sustained until systole ("dip-and-plateau waveform" or "square root sign" seen on right or left ventricular pressure waveform tracings).7

The clinical symptoms and classic hemodynamic findings can be explained by early rapid diastolic filling and elevation and equalization of the diastolic pressures in all of the cardiac chambers restricting late diastolic filling, leading to venous engorgement and decreased cardiac output, all secondary to a confining pericardium.

Frequency
United States

Similar to many diseases that in the past were predominantly infectious in origin, the clinical spectrum of constrictive pericarditis has changed in recent years. Approximately 9% of patients with acute pericarditis for any reason go on to develop constrictive physiology.8 T he true frequency is therefore dependent on the incidence of the specific causes of pericarditis, but since acute pericarditis is only clinically diagnosed in 1 in 1,000 hospital admissions, the frequency of a diagnosis of constrictive pericarditis is less than 1 in 10,000 hospital admissions.

International

In the developing world, infectious etiologies remain more prominent (tuberculosis has the highest total incidence).
Mortality/Morbidity

* Scant data exist because the disease is rare.
* The underlying disease usually determines the prognosis. Poorer prognoses are associated with malignancy and New York Heart Association (NYHA) class III or IV heart failure symptoms.
* Long-term survival after pericardiectomy depends on the underlying cause. Of common causes, idiopathic constrictive pericarditis has the best prognosis (88% survival at 7 years), followed by constriction due to cardiac surgery (66% at 7 years). The worst postpericardiectomy prognosis occurs in postradiation constrictive pericarditis (27% survival at 7 years). This likely represents confounding comorbidities. Predictors of poor outcomes in patients who undergo pericardiectomy including history of prior radiation, worsening renal function, pulmonary hypertension, systolic heart failure, hyponatremia, and advanced age.9

Race

* No race predilection exists for this disorder.

Sex

* Most likely a male predominance exists, with a male-to-female ratio of 3:1 in some studies.

Age

* Cases have been reported in persons aged 8-70 years. Predilection is likely reflective of the underlying disease.
* Historical studies suggest a median age of 45 years, while more recent studies suggest a median age of 61 years. This likely reflects a demographic change that is likely to continue.

Clinical
History

* Constrictive pericarditis presents with a myriad of symptoms, making a diagnosis based solely on clinical history virtually impossible. Additionally, these symptoms may develop slowly over a number of years such that patients may not be aware of all of their symptoms until questioned.
* Dyspnea tends to be the most common presenting symptom and occurs in virtually all patients. Fatigue and orthopnea are common.
* Lower-extremity edema and abdominal swelling and discomfort are other common symptoms. Nausea, vomiting, and right upper quadrant pain, if present, are thought to be due to hepatic congestion, bowel congestion, or both.
* The initial history may be more compatible with liver disease (cryptogenic cirrhosis) than with pericardial constriction because of the predominance of findings related to the venous system.
* Chest pain, presumably due to active inflammation, may be present, although this is observed in a minority of patients.

Physical

* General findings
o In the early stages, physical findings may be subtle, requiring close examination to avoid missing the diagnosis.
o In more advanced stages, the patient may appear ill, with marked muscle wasting, cachexia, or jaundice.
o Constriction should be considered in the presence of otherwise unexplained jugular venous distention, pleural effusion, hepatomegaly, or ascites.
* Cardiovascular findings
o Elevated jugular venous pressures are an almost universal finding.
o Avoid examining the patient only in the supine position because venous pressures may be above the angle of the jaw and inadvertently mistaken for normal.
o Sinus tachycardia is common while the blood pressure is normal or low, depending on the stage of the disease process.
o The apical impulse is often impalpable, and the patient may have distant or muffled heart sounds.
o A pericardial knock, which corresponds with the sudden cessation of ventricular filling early in diastole, occurs in approximately half the cases and may be mistaken for an S3 gallop. However, a knock is of higher frequency than an S3 and occurs slightly earlier in diastole.
o A cardiac murmur is typically not present unless concomitant valvular heart disease or a fibrous band that constricts the right ventricular outflow tract is present.
o Pulsus paradoxicum (paradoxus) is a variable finding and, if present, rarely exceeds 10 mm Hg unless a concomitant pericardial effusion with an abnormally elevated pressure exists.
o The Kussmaul sign (ie, elevation of systemic venous pressures with inspiration) is a common nonspecific finding, but this sign is also observed in patients with right ventricular failure, restrictive cardiomyopathy, right ventricular infarction, and tricuspid stenosis, although, importantly, not in patients with cardiac tamponade.
* Gastrointestinal, pulmonary, and other organ system findings
o Hepatomegaly with prominent hepatic pulsations can be detected in as many as 70% of patients.
o Other signs that result from chronic hepatic congestion include ascites, spider angiomata, and palmar erythema, which can contribute to the common but erroneous diagnosis of primary liver disease.
o Peripheral edema is a common finding, although it may be less prominent in younger patients with competent venous valves.

Causes

The varied etiologies of constrictive pericarditis parallel those of acute pericarditis (see Pericarditis, Acute), which is a common precipitant. All forms of pericarditis may eventually lead to pericardial constriction. Generally, these can be broken down by frequency into common, less common, and rare forms. The top 3 causes of constrictive pericarditis are idiopathic (presumably viral), postcardiothoracic surgery, and irradiation therapy, which, according to a recent study, are responsible for 46%, 37%, and 9%, respectively, of cases of constrictive pericarditis (in patients who underwent surgical therapy).9

* The following are common etiologies:
o Idiopathic: In many cases, particularly in developed countries, no antecedent diagnosis can be found. These cases are termed idiopathic. Reports by many authors indicate that a high percentage of idiopathic cases of constrictive pericarditis may be related to previously recognized or unrecognized viral pericarditis. Of the viruses, coxsackievirus A and B, other echoviruses, and adenoviruses are most commonly implicated.8
o Infectious (bacterial): Tuberculosis is the leading cause of constrictive pericarditis in developing nations but represents only a minority of causes in the United States and other developed countries. Bacterial infections that lead to purulent pericarditis are also declining in frequency. In the past, purulent pericarditis associated with pneumococcal pneumonia was the most common presentation of a bacterial source. However, the widespread use of antibiotics has drastically changed the frequency and spectrum of purulent pericarditis such that the most common presentation now occurs following cardiac surgery. An increasing number of gram-positive organisms, including multiple resistant strains of staphylococci, may be isolated. Group A and B streptococci and gram-negative rods (eg, Pseudomonas species, Escherichia coli, and Klebsiella species) have also been documented.
o Infectious (viral [see also Idiopathic]): Coxsackievirus, hepatitis, adenovirus, and echovirus.
o Radiation-induced: The long-term effects of thoracic and mediastinal radiation therapy (eg, used in the treatment of hematological, breast, and other malignancies) are being increasingly realized. The common features of radiation-induced cardiac complications stem from microcirculation injury with endothelial damage, capillary rupture, and platelet adhesion. This sets up an inflammatory response, which may either resolve or organize to form adhesions between the visceral pericardium and the parietal pericardium, which leads to constriction. Generally, radiation-induced constrictive pericarditis presents 5-10 years after radiation therapy and is more likely to present with an associated pericardial effusion. In a study by Bertog in 2004, the median time between radiation and pericardiectomy was 11 years, with a broad range of 2-30 years, which is consistent with other previous studies.9
o Postsurgical: Any operative or invasive (catheterization) procedure in which the pericardium is opened, manipulated, or damaged may invoke an inflammatory response, leading to constrictive pericarditis. The most common example is constrictive pericarditis in the setting of previous coronary artery bypass grafting.
* The following are less common etiologies:
o Infectious (fungal): Fungal infections are an uncommon source of constrictive pericarditis in patients who are immunocompetent. Nocardia species can be causative organisms, especially in endemic areas such as the Ohio Valley. Aspergillus, Candida, and Coccidioides species are important pathogens in patients infected with HIV and in other immunocompromised hosts.
o Neoplasms: Malignant involvement may also manifest as pericardial effusion (with or without tamponade) or as an encased heart with thickening of both visceral and parietal layers, resulting in constrictive physiology. Although many types of neoplasms have been reported, breast and lung carcinomas and lymphomas are the most common metastatic malignancies associated with constrictive pericarditis. Other malignancies that involve the pericardium with relative frequency include melanoma and mesothelioma.
o Uremia: Constrictive pericarditis may develop in association with long-term hemodialysis.
o Connective tissue disorders: Autoimmune disorders that involve the pericardium are not unusual, typically manifesting as a small pericardial effusion or as an episode of acute pericarditis. Chronic pericardial involvement is less common but can occur in patients with rheumatoid arthritis, usually associated with the presence of subcutaneous nodules. Systemic lupus erythematosus and scleroderma also may lead to constrictive pericarditis, and, in the latter, this carries a poor prognosis.
o Drug-induced: Procainamide and hydralazine have been reported to cause constrictive pericarditis through a drug-induced lupuslike syndrome. Methysergide therapy also has been implicated as a cause of constrictive pericarditis.
o Trauma: Although uncommon, both blunt and penetrating trauma to the chest wall have been reported to cause constrictive pericarditis, presumably through an inflammatory mechanism.
o Myocardial infarction: Postmyocardial infarction constrictive pericarditis has been reported. The patient typically has a history of Dressler syndrome or hemopericardium after thrombolytic therapy.
* The following are rare etiologies:
o Toxic or metabolic: Uremia with chronic hemodialysis can lead to constrictive pericarditis and is usually associated with a pericardial effusion.
o Intrapericardial instrumentation: Constrictive pericarditis after implantation of an epicardial pacemaker or automated implantable cardiac defibrillator is a rare but reported phenomenon.
o Hereditary: Mulibrey nanism is an autosomal recessive disorder characterized by multiple abnormalities, including dwarfism, constrictive pericarditis, abnormal fundi, and fibrous dysplasia of the long bones.
o Chemical trauma: Constrictive pericarditis following sclerotherapy for esophageal varices is rare.
o Chylopericardium: This is a rare cause of constrictive pericarditis.

http://emedicine.medscape.com/article/157096-overview

Aortitis

2010-02-22T11:47:00.000+07:00

Introduction
Background

Aortitis is literally inflammation of the aorta, and it is representative of a cluster of large-vessel diseases that have various or unknown etiologies. While inflammation can occur in response to any injury, including trauma, the most common known causes are infections or connective tissue disorders. Infections can trigger a noninfectious vasculitis by generating immune complexes or by cross-reactivity. The etiology is important because immunosuppressive therapy, the main treatment for vasculitis, could aggravate an active infectious process.

Inflammation of the aorta can cause aortic dilation, resulting in aortic insufficiency. Also, it can cause fibrous thickening and ostial stenosis of major branches, resulting in reduced or absent pulses, low blood pressure in the arms, possibly with central hypertension due to renal artery stenosis. Depending on what other vessels are involved, ocular disturbances, neurological deficits, claudication, and other manifestations of vascular impairment may accompany this disorder.

Agents known to infect the aorta include Neisseria (eg, gonorrhea), tuberculosis, Rickettsia (eg, Rocky Mountain spotted fever) species, spirochetes (eg, syphilis), fungi (eg, aspergillosis, mucormycosis), and viruses (eg, herpes, varicella-zoster, hepatitis B, hepatitis C).

Immune disorders affecting the aorta include Takayasu arteritis, giant cell arteritis, polyarteritis nodosa, Behcet disease, Cogan syndrome, sarcoidosis, spondyloarthropathy, serum sickness, cryoglobulinemia, systemic lupus erythematosus (SLE), rheumatoid arthritis, Henoch-Schönlein purpura, and postinfectious or drug-induced immune complex disease.

Also, anti-neutrophil cytoplasmic autoantibody (ANCA) can affect the large vessels, as in Wegener granulomatosis, polyangiitis, and Churg-Strauss syndrome. Other antibodies such as anti-glomerular basement membrane (ie, Goodpasture syndrome) and anti-endothelial (ie, Kawasaki disease) also can be culprits. Transplant rejection, inflammatory bowel diseases, and paraneoplastic vasculitis also may afflict the large vessels.

The cause or causes of giant cell or temporal arteritis, Takayasu arteritis, and polyarteritis nodosa are unknown.
Pathophysiology

The disease has 3 phases. Phase I is the prepulseless inflammatory period characterized by nonspecific systemic symptoms including low-grade fever, fatigue, arthralgia, and weight loss. Phase II involves vascular inflammation associated with pain (eg, carotidynia) and tenderness over the arteries. Phase III is the fibrosis stage, with predominant ischemic symptoms and signs secondary to dilation, narrowing, or occlusion of the proximal or distal branches of the aorta. Bruits frequently are heard, especially over carotid arteries and the abdominal aorta. The extremities become cool, and pain develops with use (ie, arm or leg claudication). Even in phase III, a significant number of patients seem to have insidious vascular inflammation, which has been demonstrated in surgical specimens and postmortem series.

In advanced cases, occlusion of the vessels to the extremities may result in ischemic ulcerations or gangrene, and with the involvement of cerebral arteries, strokes can occur. Because of the chronic nature of the disease, however, collateral circulation usually develops in the areas involved by vasculitis.

Pathologic changes involved in Takayasu arteritis are the same as for giant cell arteritis. Involved vessel walls develop irregular thickening and intimal wrinkling. Early in the disease, mononuclear infiltration with perivascular cuffing is seen. That extends to the media, followed by granulomatous changes and patches of necrosis and scarring (fibrosis) of all layers, especially the intima. Late stages have lymphocytic infiltration.

The distinction between Takayasu and giant cell arteritis is primarily the clinical pattern of vessels involved. Giant cell arteritis commonly involves the temporal artery, whereas Takayasu arteritis primarily involves the aorta, its main branches, and, in 50% of cases, the pulmonary artery. The initial vascular lesions frequently occur in or at the origin of the left subclavian artery, which can cause weakened radial pulse and easy fatigability in the left arm. As the disease progresses, the left common carotid, vertebral, brachiocephalic, right-middle or proximal subclavian, right carotid, and vertebral arteries, as well as the aorta, also are affected, as well as retinal vessels.

When the abdominal aorta and its branches, eg, the renal arteries, are involved, central hypertension may develop. Accurate blood pressure measurement may be difficult because of arterial lesions affecting supply to the extremities.

Varying degrees of narrowing and occlusion or dilation of involved portions of the arteries result in a wide variety of symptoms.
Frequency
United States

In the United States and Europe, incidence is 1-3 new cases per year per million population. In a cohort of 1204 surgical aortic specimens described by Rojo-Leyva et al1 , 168 (14%) had inflammation and 52 (4.3%) were classified as having idiopathic aortitis. Among 383 individuals with thoracic aortic aneurysms, 12% had idiopathic aortitis.
International

Vasculitis has a worldwide distribution, with the greatest prevalence among Asians. An extensive epidemiological study conducted in Japan in 1984 identified 20 cases per million population. In 1990, Takayasu arteritis was added to the list of intractable diseases maintained by the Japanese Ministry of Health and Welfare; by the year 2000, 5000 patients were registered (the reported prevalence increased 2.5-fold).
Mortality/Morbidity

The 2 major predictors of poor outcome are complications (eg, Takayasu retinopathy, hypertension, aortic regurgitation, aneurysm) and progressive course.

* Patients with no complications or with mild to moderately severe complications have a 10-year survival rate of 100% and a 15-year survival rate of 93-96%. With notable complications or progression, the 10-year survival rate is 80-90% and the 15-year survival rate is 66-68 %.
* The occurrence of both a major complication and progressive course predicts the worst outcome (43% survival rate at 15 y).

Sex

Vasculitis is most common among women of reproductive age (female cases outnumber male at a ratio of 9:1).
Age

Aortitis is most commonly discovered at age 10-40 years.
Clinical
History

In 1905, at the 12th Annual Meeting of the Japanese Ophthalmology Society, Mikito Takayasu, an ophthalmologist, described a 21-year-old Japanese woman with a peculiar retinal arteriovenous anastomosis. At the same meeting, Onishi described a patient with similar funduscopic findings and absence of radial pulses. Giovan B. Morgagni, an Italian pathologist, reported the first case with signs and symptoms consistent with Takayasu arteritis. In 1948, Shimizu and Sano described a condition characterized by absent pulses, peripapillary arteriovenous anastomosis of the retina, and accelerated carotid sinus reflex, which they called pulseless disease. The name "Takayasu's disease" was applied by Caccamis in 1954, and that eponym held.

* Vanoli et al2 reported a study of 104 Italian patients (91 female, 13 male) with Takayasu arteritis. Median delay in diagnosis was 15.5 months. The main clinical features and laboratory findings were arterial bruit (90%), decreased or absent pulse (85%), blood pressure deference over 10 mm Hg (70%), claudication of extremities (45%), hypertension (40%), asthenia (50%), fever (30%), arthralgia/arthritis (25%), weight loss over 5 kg (20%), headache (20%), erythrocyte sedimentation rate greater than 30 mm/hr (85%), anemia (60%), and leukocytosis (20%). Vascular involvement based on full aortography revealed involvement of the left subclavian (65%), right subclavian (52%), left carotid (44%), abdominal aorta (39%), and right carotid (36%).
* Many patients have ischemia of the upper extremities that may manifest as arm claudication or numbness at the time of disease recognition. Claudication of the lower limbs is less common as a presenting symptom.
* Hall et al3 reported arthralgias or myalgias in about one half of patients at the early stage of disease. Symmetric inflammatory polyarthritides resembling rheumatoid arthritis were observed in 5 of 32 patients. Articular symptoms were either transient or continual for several months or longer. Myalgia sometimes dominates the clinical presentation and may mislead clinicians.
* Neurologic symptoms are generally caused by decreased cerebral blood flow in the carotid and vertebral arteries. Neurologic manifestations include vertigo, syncope, orthostasis, headaches, convulsions, transient ischemic attacks, stroke, and dementia. Seizures are often attributed to hypertensive encephalopathy. Because of central retinal hypoperfusion, visual impairment is most often bilateral and 48% of patients with vertebral artery involvement and 40% with common carotid artery involvement have visual aberrations.
* In a minority of cases (8-18% of pooled series), skin lesions resembling erythema nodosum or pyoderma gangrenosum were found over the legs. Upon biopsy, the lesions frequently showed vasculitis of the small vessels. Erythema nodosum is the predominant dermatologic finding in the United States and Europe, whereas pyoderma gangrenosum is found more frequently in Japan. Raynaud phenomenon has also been reported in 8-14% of patients.
* Angina pectoris occurs as a result of coronary artery ostial narrowing from aortitis or coronary arteritis and can lead to myocardial infarction, heart failure, or sudden death. Congestive heart failure may be caused by valvular disease. Aortic regurgitation that results from dilation of the aortic root is common.
* In cases of documented pulmonary artery involvement, fewer than 25% of patients had related clinical manifestations and only 20% had pulmonary hypertension. Pulmonary symptoms include cough, dyspnea, and hemoptysis.
* Abdominal pain, diarrhea, and gastrointestinal hemorrhage may result from mesenteric artery ischemia, but this is rare.
* Specific arteries that are inflamed may be tender to the touch (eg, carotid, temporal).

Physical

Patients frequently appear chronically ill. Mild to moderate fever may be present. Heart rate and rhythm are unaffected. Reduced blood pressure in one or both arms is common. Laterality of blood pressure (ie, a difference between left and right arms greater than 10 mm Hg) suggests vascular obstruction, and the difference may be greater than 30 mm Hg. Maneuvers can distinguish this pressure drop and/or pulse weakness from scalenus anticus syndrome, in which arm elevation and turning of the head are influential.

* Arterial pulse intensity in any of the limbs may be diminished, often asymmetrically. Bruits may be audible over the carotid arteries, abdominal aorta, and sometimes the subclavian and brachial arteries. In a North American study by Kerr et al, bruit was the most common clinical finding (80%), and the most common site was in the carotid vessels (70%). A diastolic decrescendo murmur may signal aortic valve insufficiency. The cardiac apex may be displaced laterally. Rales, edema, liver congestion, elevated venous pressure, and hepatojugular reflux, if present, signify the complication of heart failure.
* Hypertension develops in 33-76% of patients, most frequently resulting from narrowing of the renal artery, but narrowing and decreased elasticity of the aorta and branches also can be exacerbating factors. As narrowing or occlusion may lower the pressure in the arms, all limbs must be checked, and measuring central pressure by catheterization may be required to identify hypertension.
* Synovitis mimicking rheumatoid arthritis may be noticeable over larger joints, such as the knees or wrists, early in the course of disease.

Causes

The pathogenesis of Takayasu arteritis has not been elucidated completely. Genetic influences and immunological mechanisms have received the most attention. The associations of Takayasu arteritis with other autoimmune diseases, such as connective tissue diseases and ulcerative colitis, provide clinical support for the importance of autoimmunity in the pathogenesis.

* High titers of anti-endothelial antibodies were detected in patients clinically diagnosed as having Takayasu arteritis.
o In a study of 19 patients by Eichorn et al4 , anti-endothelial antibodies were found in 18, and the titers were approximately 20 times higher than normal. Chauhan et al5 showed that the antibodies are directed against 60-65 kd antigens and may induce expression of endothelial adhesion molecules, cytokine production, and apoptosis.
o The only patient who did not have a positive titer for the antibody had inactive disease. However, whether this antibody is pathogenic or merely an epiphenomenon secondary to the vascular injury remains unclear.
o The presence of elevated anti-cardiolipin antibody titer also has been reported.
* Cell-mediated immunological mechanisms are thought to be of primary importance.
o Histopathologic examination has shown heavily infiltrating cells in all layers of the aorta, including alpha-beta T cells, gamma-delta T cells, and natural killer (NK) cells.
o In comparison to the cells found in a patient with an atherosclerotic aortic aneurysm, the proportion of gamma-delta T cells (ie, cytotoxic cells) was exceedingly high.
o Enhanced expression of human leukocyte antigen (HLA) molecules and restricted usage of alpha-beta T-cell receptor genes and gamma-delta T-cell receptor genes in the infiltrating cells suggest the existence of a targeted specific antigen. Gamma-delta T cells can recognize the major histocompatability complex (MHC) class I (MIC) chain-related molecules MICA and MICB, whose expression is known to be increased by stress. The MICA gene was found to be located near the HLA-B gene. MICA-1.2 is strongly associated with Takayasu arteritis, even in the absence of HLA-B52, which is highly prevalent in Japanese patients. Expression of heat shock protein-65, a stress-induced protein, also is increased in the tissue. These findings suggest that unknown stress, such as infection, may trigger the autoimmune process involved in patients with Takayasu arteritis.

http://emedicine.medscape.com/article/150755-overview

Aortic Dissection

2010-02-22T11:45:00.000+07:00

Introduction

Aortic dissection is defined as separation of the layers within the aortic wall. Tears in the intimal layer result in the propagation of dissection (proximally or distally) secondary to blood entering the intima-media space.

This disease was first described long ago (>200 y), but new challenges have arisen since the advent of advanced diagnostic and therapeutic modalities. The clinical manifestations are diverse, making the diagnosis difficult and requiring a high clinical index of suspicion.1,2,3

Aortic dissection can be diagnosed premortem or postmortem because many patients die before presentation to the emergency department (ED) or before diagnosis is made in the ED.

Aortic dissection is more common in males than in females, with a male-to-female ratio of 2:1. The condition commonly occurs in persons in the sixth and seventh decades of life.3 Patients with Marfan syndrome present earlier, usually in the third and fourth decades of life.

Aortic dissection. CT scan showing a flap (right ...
Aortic dissection. CT scan showing a flap (right side of image).

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Aortic dissection. CT scan showing a flap (right ...

Aortic dissection. CT scan showing a flap (right side of image).

Aortic dissection. CT scan showing a flap (center...
Aortic dissection. CT scan showing a flap (center of image).

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Aortic dissection. CT scan showing a flap (center...

Aortic dissection. CT scan showing a flap (center of image).

Aortic dissection. CT scan showing a flap (center...
Aortic dissection. CT scan showing a flap (center of image).

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Aortic dissection. CT scan showing a flap (center...

Aortic dissection. CT scan showing a flap (center of image).

For more examples of aortic dissection visible on CT scans, see the Multimedia section.

History of the Procedure

Morgagni first described aortic dissection more than 200 years ago. The condition was associated with a high mortality rate before the introduction of the cardiopulmonary bypass in the 1950s, which led to aortic arch repair and construction.

Recent advancements in the field of stent placements and percutaneous aortic fenestrations have further reduced mortality rates. However, despite recent advancements, the mortality rate associated with aortic dissection remains high.1,3
Problem

An aortic dissection is a split or partition in the media of the aorta; this split is frequently horizontal or diagonal. An intimal tear connects the media with the aortic lumen, and an exit tear creates a true lumen and a false lumen. The true lumen is lined by intima, and the false lumen is within the media.

Aortic dissection. True lumen and false lumen sep...
Aortic dissection. True lumen and false lumen separated by an intimal flap.

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Aortic dissection. True lumen and false lumen sep...

Aortic dissection. True lumen and false lumen separated by an intimal flap.

Typically, flow in the false lumen is slower than in the true lumen, and the false lumen often becomes aneurysmal when subjected to systemic pressure. The dissection usually stops at an aortic branch vessel or at the level of an atherosclerotic plaque.

An acute aortic dissection (<2 wk) is associated with high morbidity and mortality rates (highest mortality in the first 7 d) compared with chronic aortic dissection (>2 wk), which has a better prognosis.
Frequency

In the United States, aortic dissection is an uncommon disease. The true prevalence of aortic dissection is difficult to estimate, and most estimates are based on autopsy studies. Evidence of aortic dissection is found in 1-3% of all autopsies (1 in 350 cadavers). The incidence of aortic dissection is estimated to be 5-30 cases per 1 million people per year. Aortic dissection occurs once per 10,000 patients admitted to the hospital; approximately 2,000 new cases are reported each year in the United States.4
Etiology

* Arterial hypertension:3 Of patients with aortic dissection, 70% have elevated blood pressure.
* Aortic dilatation and wall thinning: Aortic aneurysm is defined as a pathologic dilatation of a segment of a blood vessel. A true aneurysm involves all 3 layers of the aortic wall.
* Iatrogenic: Aortic dissection can be caused by cardiac surgery, including aortic and mitral valve replacements, coronary artery bypass graft surgery, or percutaneous catheter placement (eg, cardiac catheterization, percutaneous transluminal coronary angioplasty). Aortic dissection occurs when the layers are split in the process of cannulation or aortotomy.
* Aortic atherosclerosis: Factors include cystic medial necrosis and aortic medial disease.
* Congenital aortic valve anomalies: These may include unicommissural or bicuspid aortic valves or aortic coarctation.
* Marfan syndrome
* Advanced age
* Pregnancy
* Ehlers-Danlos syndrome
* Syphilitic aortitis
* Deceleration injury possibly with related chest trauma
* Aortic arch hypoplasia
* Cocaine use

Pathophysiology

The aortic wall is continuous and is exposed to high pulsatile pressure and shear stress (the steep slope of the pressure curve, ie, the water hammer effect), making the aorta particularly prone to injury and disease from mechanical trauma. The aorta is more prone to rupture than any other vessel, especially with the development of aneurysmal dilatation, because its wall tension, as governed by the Laplace law (proportional to the product of pressure and radius), is intrinsically high.

An intimal tear connects the media with the aortic lumen, and an exit tear creates a true lumen and a false lumen. The true lumen is lined by intima, and the false lumen is lined by media. The true lumen is frequently smaller than the false lumen, but not invariably. The false lumen is indeed within the media, but suggesting that it is "lined" with it is misleading; if the aortic dissection becomes chronic, the lining becomes a serosal pseudointima. Typically, flow in the false lumen is slower than flow in the true lumen, and the false lumen often becomes aneurysmal when subjected to systemic pressure.

Aortic dissection. True lumen versus false lumen ...
Aortic dissection. True lumen versus false lumen in an intimal flap.

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Aortic dissection. True lumen versus false lumen ...

Aortic dissection. True lumen versus false lumen in an intimal flap.

The dissection usually stops at an aortic branch vessel or at the level of an atherosclerotic plaque. Most classic aortic dissections begin at 1 of 3 distinct anatomic locations, including (1) the aortic arch, (2) approximately 2.2 cm above the aortic root, or (3) distal to the left subclavian artery.

Ascending aortic involvement may result in death from wall rupture, hemopericardium and tamponade, occlusion of the coronary ostia with myocardial infarction, or severe aortic insufficiency. The nervi vascularis (ie, bundles of nerve fibers found in the aortic adventitia) are involved in the production of pain.

DeBakey and coworkers classify aortic dissection into 3 types, as follows:

* Type I: The intimal tear occurs in the ascending aorta, but the descending aorta is also involved.
* Type II: Only the ascending aorta is involved.
* Type III: Only the descending aorta is involved.
o Type IIIA involves the descending aorta that originates distal to the left subclavian artery and extends as far as the diaphragm.
o Type IIIB involves the descending aorta below the diaphragm.

The Stanford classification has 2 types, as follows:

* Type A: The ascending aorta is involved (DeBakey types I and II).
* Type B: The descending aorta is involved (DeBakey type III).

This system also helps delineate treatment. Type A dissections usually require surgery, whereas type B dissections are managed medically under most conditions.5

Image A represents a Stanford A or a DeBakey type...
Image A represents a Stanford A or a DeBakey type 1 dissection. Image B represents a Stanford A or DeBakey type II dissection. Image C represents a Stanford type B or a DeBakey type III dissection. Image D is classified in a manner similar to A but contains an additional entry tear in the descending thoracic aorta. Note that a primary arch dissection does not fit neatly into either classification.

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Image A represents a Stanford A or a DeBakey type...

Image A represents a Stanford A or a DeBakey type 1 dissection. Image B represents a Stanford A or DeBakey type II dissection. Image C represents a Stanford type B or a DeBakey type III dissection. Image D is classified in a manner similar to A but contains an additional entry tear in the descending thoracic aorta. Note that a primary arch dissection does not fit neatly into either classification.

Presentation

Patients with acute aortic dissection present with the sudden onset of severe and tearing chest pain, although this description is not universal. Some patients present with only mild pain, often mistaken for a symptom of musculoskeletal conditions located in the thorax, groin, or back. Some patients present with no pain.6

Consider thoracic aortic dissection in the differential diagnosis of all patients presenting with chest pain. The pain is usually localized to the front or back of the chest, often the interscapular region, and typically migrates with propagation of the dissection.

The pain of aortic dissection is typically distinguished from the pain of acute myocardial infarction by its abrupt onset, although the presentations of the two conditions overlap to some degree and are easily confused. Aortic dissection can be presumed in patients with symptoms and signs suggestive of myocardial infarction but without classic ECG findings.

Presenting signs and symptoms in acute thoracic aortic dissection include the following:

Anterior chest pain is a manifestation of ascending aortic dissection. Neck or jaw pain is a manifestation of aortic arch dissection. Interscapular tearing or ripping pain is a manifestation of descending aortic dissection.

Neurologic deficits are a presenting sign in up to 20% of cases. Syncope is part of the early course of aortic dissection in approximately 5% of patients and may be the result of increased vagal tone, hypovolemia, or dysrhythmia.6 Cerebrovascular accident (CVA) symptoms include hemianesthesia and hemiparesis or hemiplegia.6 Altered mental status is also reported. Other causes of syncope or altered mental status include (1) CVA from compromised blood flow to the brain or spinal cord or (2) ischemia from interruption of blood flow to the spinal arteries.

Patients with peripheral nerve ischemia can present with numbness and tingling in the extremities, limb paresthesias, pain, or weakness.

Horner syndrome is caused by interruption in the cervical sympathetic ganglia and manifests as ptosis, miosis, and anhidrosis.

Hoarseness from recurrent laryngeal nerve compression has also been described.

Cardiovascular manifestations involve symptoms and signs suggestive of congestive heart failure6 secondary to acute severe aortic regurgitation or dyspnea, orthopnea, bibasilar crackles, or elevated jugular venous pressure. Signs of aortic regurgitation include bounding pulses, wide pulse pressure, and diastolic murmurs. Hypertension may result from a catecholamine surge or underlying essential hypertension.7,6 Hypotension is an ominous finding and may be the result of excessive vagal tone, cardiac tamponade, or hypovolemia from rupture of the dissection.

Other cardiovascular manifestations include findings suggestive of cardiac tamponade (eg, muffled heart sounds, hypotension, pulsus paradoxus, jugular venous distension); these may be present and must be recognized quickly. Superior vena cava syndrome can result from compression of the superior vena cava from a large, distorted aorta. Wide pulse pressure and pulse deficit or asymmetry of peripheral pulses is reported. Patients with right coronary artery ostial dissection may present with acute myocardial infarction, commonly inferior myocardial infarction. Pericardial friction rub may occur secondary to pericarditis.

Respiratory symptoms can include dyspnea and hemoptysis if dissection ruptures into the pleura or if tracheal or bronchial obstruction has occurred. Physical findings of a hemothorax may be found if the dissection ruptures into the pleura.

GI symptoms include dysphagia, flank pain, and/or abdominal pain. Dysphagia may occur from compression of the esophagus. Flank pain may be present if the renal artery is involved. Abdominal pain may be present if the dissection involves the abdominal aorta.

Other nonspecific clinical presentations include fever or anxiety and premonitions of death.8
Indications

Emergent surgical correction is the preferred treatment for the following classifications of aortic dissection:

* Stanford type A (DeBakey type I and II) ascending aortic dissection
* Complicated Stanford type B (DeBakey type III) aortic dissections with clinical or radiological evidence of the following conditions:
o Propagation (increasing aortic diameter)
o Increasing size of hematoma
o Compromise of major branches of the aorta
o Impending rupture
o Persistent pain despite adequate pain management
o Bleeding into the pleural cavity
o Development of saccular aneurysm

Relevant Anatomy

From outside to inside, the aorta is composed of the intima, media, and adventitia. The intima, the innermost layer, is thin, delicate, lined by endothelium, and easily traumatized.

The media is responsible for imparting strength to the aorta and is composed of laminated but intertwining sheets of elastic tissue. The arrangement of these sheets in a spiral provides the aorta with its maximum allowable tensile strength. The aortic media contains very little smooth muscle and collagen between the elastic layers and thus has increased distensibility, elasticity, and tensile strength. This contrasts with peripheral arteries, which, in comparison, have more smooth muscle and collagen between the elastic layers.

The outermost layer of the aorta is adventitia. This largely consists of collagen. The vasa vasorum, which supplies blood to the outer half of the aortic wall, lies within the adventitia. The aorta does not have a serosal layer.

The aorta plays an integral role in the forward circulation of the blood in diastole. During left ventricular contraction, the aorta is distended by blood flowing from the left ventricle, and kinetic energy from the ventricle is transformed into potential energy stored in the aortic wall. During recoil of the aortic wall, this potential energy is converted to kinetic energy, propelling aortic lumen blood into the periphery.

The volume of blood ejected into the aorta, the compliance of the aorta, and resistance to blood flow are responsible for the systolic pressures within the aorta. Resistance is mainly due to the tone of the peripheral vessels, although the inertia exerted by the column of blood during ventricular systole also plays a small part.

The aorta has thoracic and abdominal regions. The thoracic aorta is divided into the ascending, arch, and descending segments; the abdominal aorta is divided into suprarenal and infrarenal segments.

The ascending aorta is the anterior tubular portion of the thoracic aorta from the aortic root proximally to the innominate artery distally. The ascending aorta is 5 cm long and is made up of the aortic root and an upper tubular segment. The aortic root consists of the aortic valve, sinuses of Valsalva, and left and right coronary arteries. The aortic root extends from the aortic valve to the sinotubular junction. The aortic root supports the base of the aortic leaflets and allows the 3 sinuses of Valsalva to bulge outward, facilitating the full excursion of the leaflets in systole. The left and right coronary arteries arise from these sinuses.

The upper tubular segment of the ascending aorta starts at the sinotubular junction and ends at the beginning of the aortic arch. The ascending aorta lies slightly to the right of the midline, with its proximal portion in the pericardial cavity. Structures around the aorta include the pulmonary artery anteriorly; the left atrium, right pulmonary artery, and right mainstem bronchus posteriorly; and the right atrium and superior vena cava to the right.

The arch of the aorta curves upward between the ascending and descending aorta. The brachiocephalic arteries originate from the aortic arch. Arteries that arise from the aortic arch carry blood to the brain via the left common carotid, innominate, and left subclavian arteries. Initially, the aortic arch lies slightly left and in front of the trachea and ends posteriorly to the left of the trachea and esophagus. Inferior to the arch is the pulmonary artery bifurcation, the right pulmonary artery, and the left lung. The recurrent laryngeal nerve passes beneath the distal arch, and the phrenic and vagus nerves lie to the left. The junction between the aortic arch and the descending aorta is called the aortic isthmus. The isthmus is a common site for coarctations and trauma.

The descending aorta extends from distal to the left subclavian artery to the 12th intercostal space. Initially, the descending aorta lies in the posterior mediastinum to the left of the course of the vertebral column. It passes in front of the vertebral column in its descent and ends behind the esophagus before passing through the diaphragm at the level of the 12th thoracic vertebra. The abdominal aorta extends from the descending aorta at the level of the 12th thoracic vertebra to the level of bifurcation at the fourth lumbar vertebra. The splanchnic arteries branch from the abdominal aorta. The thoracoabdominal aorta is the combination of the descending thoracic and abdominal aorta.

With increasing age, the elasticity and distensibility of the aorta decline, thus inducing the increase in pulse pressure observed in elderly individuals. The progression of this process is exacerbated in patients with hypertension, coronary artery disease, or hypercholesterolemia. The loss of physiologic distensibility is observed anatomically by fragmentation of elastin and the resultant increase in collagen. This results in an increased collagen-to-elastin ratio. This, along with impairment in flow in the vasa vasorum, may be responsible for the age-related changes. These factors cumulatively lead to increased left ventricular systolic pressure and wall tension with associated increases in end-diastolic pressure and volume.
Contraindications

Cautions and relative contraindications to surgery include the following:

* Cerebrovascular accident
* Severe left ventricular dysfunction
* Coagulopathy
* Pregnancy
* Postmyocardial infarction ( <6 mo)
* Significant arrhythmias
* Advanced age
* Severe valvular disease

http://emedicine.medscape.com/article/425118-overview

Loeffler Endocarditis

2010-02-22T11:43:00.000+07:00

Introduction
Background

Loeffler endocarditis and endomyocardial fibrosis are restrictive cardiomyopathies, defined as diseases of the heart muscle that result in impaired ventricular filling with normal or decreased diastolic volume of either or both ventricles. Systolic function and wall thickness may remain normal, especially early in the disease, as reported by Richardson and associates.1 Both conditions are associated with eosinophilia.

The associations among eosinophilia, active carditis, and multiorgan involvement were first described by Loeffler in 1936.2 Pathologic specimens in Loeffler endocarditis show eosinophilic myocarditis, a tendency toward endomyocardial fibrosis and clinical manifestations of thromboembolism, and acute heart failure.

Eosinophilic states that may occur in association with Loeffler endocarditis include hypereosinophilic syndrome, eosinophilic leukemia, carcinoma, lymphoma, drug reactions or parasites, as reported in multiple case series.

Although eosinophilic endocardial disease has been well described, myocardial and vascular damage due to eosinophilic infiltration and degranulation is rarely diagnosed during life, as reported by Oakley et al and others.3 Herzog et al and Tonnesen et al have proposed that the reason for this situation may be the rapidly fatal evolution of most cases of eosinophilic arteritis and myocarditis.4,5 These conditions are usually diagnosed based on postmortem examination and nonspecificity of clinical manifestations, as reported by Kim et al, Isaka et al, and Seshadri et al.6,7,8

Pathophysiologically, the fibrotic stage of Loeffler endocarditis is very similar to the disease entity described as endomyocardial fibrosis, which is indolent in comparison to Loeffler endocarditis. The tropical form of endomyocardial fibrosis is associated with eosinophilia, a common finding in Loeffler endocarditis.
Pathophysiology

Endomyocardial damage in Loeffler endocarditis is well known and described in a study by Solley and associates.9 Myocardial involvement is less well known and has been considered a manifestation of an acute necrotic stage of eosinophilic endomyocardial disease, as reported by Olsen and colleagues.10 More recently, cases of isolated eosinophilic myocarditis have been reported without signs of endomyocardial involvement, with or without vasculitis.

Additionally, idiopathic eosinophilic endomyocarditis, in the absence of peripheral eosinophilia, has been reported by Priglinger et al.11

Morphologic abnormalities of eosinophils have been noted in patients with Loeffler endocarditis, suggesting that these eosinophils were mature or stimulated. The intracytoplasmic granular content of activated eosinophils is thought to be responsible for the toxic damage to the heart, as reported by Tai and associates.12 Spry et al reported eosinophilic degranulation of basic proteins causing myocardial damage in tissue cultures in vitro.13 Gliech et al reported a dose-dependent cytotoxic effect of the eosinophilic granular proteins, inhibiting multiple enzyme systems.14

The cationic eosinophilic proteins bind to the anionic endothelial protein, thrombomodulin. This complex impairs anticoagulant activities, leading to enhanced endocardial thrombus formation, as reported by Slungaard and colleagues.15

Toxins released by the eosinophils include eosinophil-derived neurotoxin, cationic protein, major basic protein, reactive oxygen species, and arachidonic acid derivatives. As described by Cunningham et al, these toxins may cause endothelial and myocyte damage, resulting in thrombosis, fibrosis, and infarction.16

The intensity and timing of the active carditis is related closely to the severity of the circulating eosinophilia. Some have suggested that, particularly in the tropics, patients who present with later fibrotic stages of endomyocardial disease may have had either transient earlier bouts of moderate eosinophilia with spontaneous resolution, or only moderate levels of eosinophilia leading to a low-grade endomyocarditis with gradual progressive fibrosis, as reported by Olsen et al.10

Molecular pathophysiology

Cools et al reported a landmark finding by treating patients with hypereosinophilic syndrome (HES) with imatinib, a tyrosine kinase inhibitor.17

* The gene defect is localized to an interstitial chromosomal deletion on chromosome band 4q12, resulting in fusion of the Fip1-like1 (FIP1L1) gene to the platelet-derived growth factor gene alpha (PDGFRA). The protein product of this gene is a tyrosine kinase enzyme that transforms the hematopoietic stem cells. This FIP1L1-PDGFRA fusion gene defect was identified in 9 of 16 patients treated with imatinib.
* This study also highlights the importance of reclassifying HES as a myeloproliferative disorder of a possible single clone based on genotyping, as the FIP1L1-PDGFRA gene rearrangement is a clonal abnormality.
* Treatment with imatinib caused rapid regression of eosinophilic proliferation and endomyocardiopathy in subsequent cases reported by Vandenberghe et al and Rotoli et al.18,19

The following list summarizes the initial clinical presentations of eosinophilic endomyocardial disease in relation to the predominant pathologic stage of the disease as reported by Alderman et al in the Textbook of Cardiovascular Medicine.20 Death is usually related to multiorgan dysfunction in the presence of congestive heart failure. (See Medscape's Heart Failure Resource Center.)

The initial clinical presentation and stages of eosinophilic endomyocardial disease are as follows:20

* Necrotic stage (early stage)
o Hypereosinophilia with systemic illness (20-30%)
+ Fever
+ Sweating
+ Chest pain (as described by Bestetti et al21 )
+ Lymphadenopathy
+ Splenomegaly
o Acute carditis (20-50%)
+ Anorexia
+ Weight loss
+ Cough
+ Pulmonary infiltrates
+ Skin and retinal lesion
+ Atrioventricular valve (AV) valve regurgitation
+ Biventricular failure
* Thrombotic stage
o Thrombotic emboli (10-20%)
+ Cerebral, splenic, renal, and coronary infarction
+ Splinter hemorrhages
* Fibrotic stage (late stage)
o Restrictive myopathy (10%)
+ AV valvular regurgitation
+ Right and left heart failure

The image shows dense fibrosis of ventricle in a postmortem dissected heart.

Myocardial as well as valvular involvement with L...
Myocardial as well as valvular involvement with Loffler endocarditis. This image shows dense fibrosis of ventricle in a postmortem dissected heart.

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Myocardial as well as valvular involvement with L...

Myocardial as well as valvular involvement with Loffler endocarditis. This image shows dense fibrosis of ventricle in a postmortem dissected heart.

Frequency
United States

The condition is rare and is seen mostly in immigrants from Africa, Asia, and South America.
International

Loeffler endocarditis is primarily confined to the rain forest (tropical and temperate) belts of Africa, Asia, and South America.
Mortality/Morbidity

The literature reports a 35-50% 2-year mortality rate in patients with advanced myocardial fibrosis. Substantially better survival rates may be seen in less symptomatic patients who have milder forms of the disease. As noted, this rate may reflect underdiagnosis of clinically inapparent disease, as for other types of cardiomyopathy.
Race

The condition has a predilection for African and African American populations, notably the Rwanda tribe in Uganda, and for people of low socioeconomic status. Whether this is due to genetic factors or the epidemiology of underlying environmental factors is not known.
Sex

Loeffler endocarditis has a predilection for males. However, endomyocardial fibrosis, which has similar clinical manifestations, is found equally frequently in both sexes.
Age

The reported age range is 4-70 years. Loeffler endocarditis particularly affects young males, as does its close counterpart, endomyocardial fibrosis, which is more common in children and young adults.
Clinical
History

Patients with Loeffler endocarditis may present with weight loss, fever, cough, rash, and symptoms related to congestive heart failure. Initial cardiac involvement has been reported in about 20-50% of cases; however, cardiac involvement rarely presents with chest pain, as reported by Bestetti et al.21
Physical

Signs of biventricular failure (eg, pedal edema, elevated jugulovenous pressure, pulmonary edema, third heart sound [S3] gallop) are commonly seen once congestive heart failure develops.

* Cardiomegaly may be present without overt signs of congestive heart failure.
* Murmur of mitral regurgitation may be present, as reported by multiple authors, including Weller et al.22
* Systemic embolism is frequent and may lead to neurologic and renal dysfunction.
* The Kussmaul sign may be present.
* S 3 gallop may be present, but rarely fourth heart sound (S4).
* Restrictive cardiomyopathy, such as Loeffler endocarditis, is sometimes difficult to differentiate from constrictive pericarditis. Physical signs in constrictive pericarditis that may help differentiate the 2 conditions include a nonpalpable apex (usually), presence of pericardial knock, and usually absent regurgitation murmurs.
* Published case reports highlight presentations with unusual ECG changes mimicking posterior myocardial infarction as described by Maruyoshi et al23 , acute myocardial infarction as described by Mor et al24 , and aortic valve regurgitation secondary to valve fibrosis and fibrotic vegetations on the aortic valve as described by Gudmundsson et al

http://emedicine.medscape.com/article/155340-overview

Sudden Cardiac Death

2010-02-22T11:32:00.000+07:00

Introduction
Background

Sudden cardiac death (SCD) is an unexpected death due to cardiac causes occurring in a short time period (generally within 1 h of symptom onset) in a person with known or unknown cardiac disease. Most cases of SCD are related to cardiac arrhythmias. Approximately half of all cardiac deaths can be classified as SCDs. SCD represents the first expression of cardiac disease in many individuals presenting with out-of-hospital cardiac arrest. This article explores the epidemiology, pathophysiology, diagnostic approach, and treatment of patients who experience SCD.

Pathophysiology

The most common electrophysiologic mechanisms leading to SCD are tachyarrhythmias such as ventricular fibrillation (VF) or ventricular tachycardia (VT). Interruption of tachyarrhythmias, using either an automatic external defibrillator (AED) or an implantable cardioverter defibrillator (ICD), has been shown to be an effective treatment for VF and VT.1 The implantable defibrillator has become the central therapeutic factor in the prevention and treatment of sudden cardiac death. Patients with tachyarrhythmias, especially VT, carry the best overall prognosis among patients with sudden cardiac arrest (SCA).

There are multiple factors at the organ (eg imbalance of autonomic tone), tissue (eg reentry, wave break, and action potential duration alternans), cellular (eg triggered activity, and automaticity) and subcellular (abnormal activation or deactivation of ion channels) level involved in generation of VT or VF in different conditions. An anatomical or a functional block in the course of impulse propagation may create a circuit with the wave front circling around it and resulting in VT. Other mechanisms such as wave break and collisions are involved in generating VF from VT. While at the tissue level the above-mentioned reentry and wave break mechanisms are the most important known mechanisms of VT and VF, at the cellular level increased excitation or decreased repolarization reserve of cardiomyocytes may result in ectopic activity (eg automaticity, triggered activity), contributing to VT and VF initiation.

At the subcellular level, altered intracellular Ca2+ currents, altered intracellular K+ currents (especially in ischemia), or mutations resulting in dysfunction of a sodium channel (Na+ channelopathy) can increase the likelihood of VT and VF.

Approximately 20-30% of patients with documented sudden death events have bradyarrhythmia or asystole at the time of initial contact. Oftentimes, it is difficult to determine with certainty the initiating event in a patient presenting with a bradyarrhythmia because asystole and pulseless electrical activity (PEA) may result from a sustained VT. Less commonly, an initial bradyarrhythmia producing myocardial ischemia may then provoke VT or VF.

Most cases of SCD occur in patients with structural abnormalities of the heart. Myocardial infarction (MI) and post-MI remodeling of the heart is the most common structural abnormality in patients with SCD. In patients who survive a myocardial infarction, the presence of premature ventricular contractions (PVCs), particularly complex forms such as multiform PVCs, short coupling intervals (R-on-T phenomenon), or VT (salvos of 3 or more ectopic beats), reflect an increased risk of sudden death. However suppression of the PVCs with antiarrhythmic drugs increases mortality, owing to the proarrhythmic risk of currently available medications.

Hypertrophic cardiomyopathy and dilated cardiomyopathy are associated with an increased risk of SCD. Various valvular diseases such as aortic stenosis are associated with increased risk of SCD. Acute illnesses, such as myocarditis, may provide both an initial and sustained risk of SCD due to inflammation and fibrosis of the myocardium.

Less commonly, SCD happens in patients who may not have apparent structural heart disease. These conditions are usually inherited arrhythmia syndromes.

Even though many patients have anatomic and functional cardiac substrates that predispose them to develop ventricular arrhythmias, only a small percentage develop SCD. Identifying the patients at risk for SCD remains a challenge. The strongest known predictor of SCD is significant left ventricular dysfunction of any cause. The interplay between the regional ischemia, LV dysfunction, and transient inciting events (eg, worsened ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic disturbances) has been proposed as being the precipitator of sudden death (see Media file 1).

Interplay of various risk factors that can lead t...
Interplay of various risk factors that can lead to sudden cardiac death.

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Interplay of various risk factors that can lead t...

Interplay of various risk factors that can lead to sudden cardiac death.

Frequency
United States

SCD accounts for approximately 325,000 deaths per year in the United States; more deaths are attributable to SCD than to lung cancer, breast cancer, or AIDS. This represents an incidence of 0.1-0.2% per year in the adult population. SCD is often the first expression of CAD and is responsible for approximately 50% of deaths from CAD.

In several population-based studies, the incidence of out-of-hospital cardiac arrest has been noted as declining in the past 2 decades, but the proportion of sudden CAD deaths in the United States has not changed. A high incidence of SCD occurs among certain subgroups of high-risk patients (congestive heart failure with ejection fraction <30%, convalescent phase after myocardial infarction, patients who survived cardiac arrest). However, these populations are much smaller than patients with minimal or even inapparent coronary artery disease. Consequently, in the overall population, most SCD occurs in lower risk patients. The time dependence of risk for SCD has been noted in several studies, with an increased number of events in the first 6-24 months after surviving a major cardiovascular event.
International

The frequency of SCD in Western industrialized nations is similar to that in the United States. The incidence of SCD in other countries varies as a reflection of the prevalence of coronary artery disease or other high-frequency cardiomyopathies in those populations. The trend toward increasing SCD events in developing nations of the world is thought to reflect a change in dietary and lifestyle habits in these nations. It has been estimated that SCD claims more than 7,000,000 lives per year worldwide.2

Mortality/Morbidity

Of more than 300,000 deaths attributed to SCD in the United States each year, a large portion (as many as 40%) are unwitnessed. For most people who experience SCD, their survival depends on the presence of individuals who are competent in performing basic life support, the rapid arrival of personnel and apparatus for defibrillation and advanced life support, and transfer to a hospital. Even under ideal circumstances, only an estimated 20% of patients who have out-of-hospital cardiac arrest survive to hospital discharge. In a study of out-of-hospital cardiac arrest survival in New York City, only 1.4% of patients survived to hospital discharge. Other studies in suburban and rural areas have indicated higher rates of survival (as high as 35%). Placement of automatic external defibrillators throughout communities and training people to use them has the potential to markedly improve outcomes from SCD.

* Upon emergency department (ED) presentation, the most important determinants of survival include (1) an unsupported systolic blood pressure (SBP) greater than 90 mm Hg, (2) a time from loss of consciousness to return of spontaneous circulation (ROSC) of less than 25 minutes, and (3) some degree of neurological responsiveness.
* A major adverse outcome from a SCD event is anoxic encephalopathy, which occurs in 30-80% of cases.

Race

Most studies demonstrate inconclusive data with regard to racial differences as they relate to the incidence of sudden death. Some studies suggest that a greater proportion of coronary deaths were "sudden" in blacks compared to whites. In a report by Gillum et al on SCD from 1980-1985, the percentage of coronary artery disease deaths occurring out of the hospital and in EDs was found to be higher in blacks than in whites (see Media file 2).3

Cardiac death, sudden. Plots of mortality rates (...
Cardiac death, sudden. Plots of mortality rates (deaths per 1000 persons) for ischemic heart disease occurring out of the hospital or in the emergency department (top) and occurring in the hospital (bottom) by age, sex, and race in 40 states during 1985.

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Cardiac death, sudden. Plots of mortality rates (...

Cardiac death, sudden. Plots of mortality rates (deaths per 1000 persons) for ischemic heart disease occurring out of the hospital or in the emergency department (top) and occurring in the hospital (bottom) by age, sex, and race in 40 states during 1985.

Sex

Men have a higher incidence of SCD than women, with a ratio of 3:1. This ratio generally reflects the higher incidence of obstructive coronary artery disease in men. Recent evidence suggests that a major sex difference may exist in the mechanism of myocardial infarction. Basic and observational data point to the fact that men tend to have coronary plaque rupture, while women tend to have plaque erosion. Whether this biologic difference accounts for the male predominance of SCD is unclear.
Age

The incidence of SCD parallels the incidence of coronary artery disease, with the peak of SCD occurring in people aged 45-75 years. The incidence of SCD increases with age in men, women, whites, and nonwhites as the prevalence of coronary artery disease increases with age. However, the proportion of deaths that are sudden from coronary artery disease decreases with age. In the Framingham study, the proportion of coronary artery disease deaths that were sudden was 62% in men aged 45-54 years, but this percentage fell to 58% in men aged 55-64 years and to 42% in men aged 65-74 years.4 According to Kuller et al, 31% of deaths are sudden in people aged 20-29 years.5

Clinical
History

Obtaining a thorough history from the patient, family members, or other witnesses is necessary to obtain insight into the events surrounding the sudden death. Patients at risk for SCD may have prodromes of chest pain, fatigue, palpitations, and other nonspecific complaints. History and associated symptoms, to some degree depend on the underlying etiology of SCD. For example, SCD in an elderly patient with significant coronary artery disease may be associated with preceding chest pain due to a myocardial infarction, while SCD in a young patient may be associated with history of prior syncopal episodes and/or a family history of syncope and SCD and due to inherited arrhythmia syndromes. As many as 45% of persons who have SCD were seen by a physician within 4 weeks before death, although as many as 75% of these complaints were not related to the cardiovascular system. A prior history of LV impairment (ejection fraction <30-35%) is the most potent common risk factor for sudden death.

Risk factors that relate to coronary artery disease and subsequent myocardial infarction and ischemic cardiomyopathy also are important and include a family history of premature coronary artery disease, smoking, dyslipidemia, hypertension, diabetes, obesity, and a sedentary lifestyle. Specific considerations include the following:

* Coronary artery disease
o Previous cardiac arrest
o Syncope
o Prior myocardial infarction, especially within 6 months
o Ejection fraction less than 30-35%
o History of frequent ventricular ectopy (more than 10 PVCs per h or nonsustained VT)
* Dilated cardiomyopathy
o Previous cardiac arrest
o Syncope
o Ejection fraction less than 30-35%
o Use of inotropic medications
* Hypertrophic cardiomyopathy
o Previous cardiac arrest
o Syncope
o Family history of SCD
o Symptoms of heart failure
o Drop in SBP or ventricular ectopy upon stress testing
o Palpitations
o Most are asymptomatic
* Valvular disease
o Valve replacement within 6 months
o Syncope
o History of frequent ventricular ectopy
o Symptoms associated with severe uncorrected aortic stenosis or mitral stenosis
* Long QT syndrome
o Family history of long QT and SCD
o Medications that prolong the QT interval
o Bilateral deafness
* Wolff-Parkinson-White (WPW) syndrome (with atrial fibrillation or atrial flutter with extremely rapid ventricular rates): With extremely rapid conduction over an accessory pathway, degeneration to VF can occur.
* Brugada syndrome, arrhythmogenic right ventricular (RV) cardiomyopathy/dysplasia, and others

Physical

The physical examination may reveal evidence of underlying myocardial disease or may be entirely normal, depending on the underlying cause. Initial evaluation studies show that patients who survive to ED presentation can be stratified by a cardiac arrest score, which has excellent diagnostic value. The cardiac arrest score, developed by Thompson and McCullough, can be used for patients with witnessed out-of-hospital cardiac arrest and is defined by the following criteria6,7 :

* Clinical characteristic points
o ED SBP greater than 90 mm Hg = 1 point
o ED SBP less than 90 mm Hg = 0 points
o Time to ROSC less than 25 minutes = 1 point
o Time to ROSC more than 25 minutes = 0 points
o Neurologically responsive = 1 point
o Comatose = 0 point
o Maximum score = 3 points
* Patients with a score of 3 points can be expected to have an 89% chance of neurologic recovery and an 82% chance of survival to discharge (see Media file 3).

Cardiac death, sudden. Figure a shows neurologic ...
Cardiac death, sudden. Figure a shows neurologic outcome stratified by initial cardiac arrest score. Neurologic recovery is defined as discharged home and able to care for self. Figure b shows overall survival stratified by initial cardiac arrest score.

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Cardiac death, sudden. Figure a shows neurologic ...

Cardiac death, sudden. Figure a shows neurologic outcome stratified by initial cardiac arrest score. Neurologic recovery is defined as discharged home and able to care for self. Figure b shows overall survival stratified by initial cardiac arrest score.
* McCullough indicates that even in the setting of ST elevation and early invasive management with primary angioplasty and intraaortic balloon pump insertion, patients with low cardiac scores are unlikely to survive.8
* Severe anoxic encephalopathy in patients with scores of 0, 1, or 2 mitigates conservative management with empiric supportive and medical therapy. Given the very poor actuarial survival rates for these patients, invasive management with catheterization and electrophysiology studies (EPS) is rarely justified.

Causes

Ischemic heart disease

* Cardiac arrest due to ventricular arrhythmias may be due to post-MI remodeling of the heart with scar formation and interstitial fibrosis (intramyocardial collagen deposition) or to acute MI/ischemia. A chronic infarct scar can serve as the focus for reentrant ventricular tachyarrhythmias. This can occur shortly after the infarct or years later. Interestingly, post-MI remodeling and ischemic cardiomyopathy may be associated with increased interstitial fibrosis even in noninfarcted areas of the heart.9 Interstitial fibrosis can provide anatomical block similar to a scar. Fibroblasts and myocytes shown to be coupled through gap junctions and fibroblasts can reduce repolarization reserve of myocytes. In addition to post-MI remodeling, many other structural heart diseases associated with SCD (eg, dilated cardiomyopathy, hypertrophic cardiomyopathy, and aortic stenosis) are also associated with increased myocardial fibrosis.10,11,12
* Many studies support the relationship of symptomatic and asymptomatic ischemia as a factor for risk of SCD. Patients resuscitated from out-of-hospital cardiac arrest represent a group of patients with increased recurrence of cardiac arrest and have been shown to express an increased incidence of silent ST-segment depression. Experiments inducing myocardial ischemia in animal models have a strong relationship with the development of VF. However, in patients with prior myocardial infarction and scarring, ventricular arrhythmias, especially VT, do not require an acute ischemic trigger.
* In postmortem studies of people who have died from SCD, extensive atherosclerosis is a common pathologic finding. In survivors of cardiac arrest, coronary heart disease with vessels showing greater than 75% stenosis is observed in 40-86% of patients, depending on the age and sex of the population studied. Autopsy studies show similar results; in one study of 169 hearts, approximately 61% of patients died of SCD, and more than 75% stenosis in 3 or 4 vessels and similar severe lesions were present in at least 2 vessels in another 15% of cases. No single coronary artery lesion is associated with an increased risk for SCD. Despite these findings, only approximately 20% of SCD-related autopsies have shown evidence of a recent MI. A greater proportion of autopsies (40-70%) show evidence of a healed MI. Many of these hearts also reveal evidence of plaque fissuring, hemorrhage, and thrombosis.
* The Cardiac Surgery Study (CASS) showed that improving or restoring blood flow to an ischemic myocardium decreased the risk of SCD, especially in patients with 3-vessel disease and heart failure, when compared with medical treatment over a 5-year period.
* The efficacy of beta-blocking agents, such as propranolol, in decreasing sudden death mortality, especially when administered to patients who had MI with VF, VT, and high-frequency PVCs, may be due in part to the ability of beta-blockers to decrease ischemia, but they are also effective in patients with nonischemic cardiomyopathy for reduction of SCD. Beta-blockers also increase the VF threshold in ischemic animals and decrease the rate of ventricular ectopy in patients who had MI.
* Reperfusion of ischemic myocardium with thrombolysis or direct percutaneous coronary intervention can induce transient electrical instability by several different mechanisms.
* Coronary artery spasm is a condition that exposes the myocardium to both ischemia and reperfusion insults. It is occasionally associated with VT, VF, and SCD. Since some of the episodes of coronary vasospasm may be silent, this disease should be considered in a patient with unexplained SCA.13 The exact mechanism of ventricular arrhythmia in coronary vasospasm is not known, but factors associated with both ischemia and reperfusion may contribute in induction of arrhythmia.
* Nonatherosclerotic coronary artery abnormalities, including congenital lesions, coronary artery embolism, coronary arteritis, and mechanical abnormalities of the coronary artery, have been associated with an increased incidence of sudden death.

Nonischemic cardiomyopathies

Patients with nonischemic cardiomyopathies represent the second largest group of patients who experience SCD in the United States. Nonischemic myopathies, for the purpose of this article, can be divided into the categories dilated and hypertrophic.

* Dilated cardiomyopathy
o Dilated cardiomyopathy can result from prior ischemia and myocardial infarction or from nonischemic causes. Nonischemic dilated cardiomyopathy (DCM) is becoming increasingly more common, with an incidence of approximately 7.5 cases per 100,000 persons each year. Of cases of SCD, 10% are estimated to be attributable to DCM. The prognosis is very poor for these patients, with a 1-year mortality rate of 10-50%, depending on the New York Heart Association functional class; approximately 30-50% of these deaths are SCD.
o The causes of DCM are uncertain; viral, autoimmune, genetic, and environmental (alcohol) origins are implicated. The predominant mechanism of death appears to be ventricular tachyarrhythmia, although bradyarrhythmia and electromechanical dissociation also have been observed, especially in patients with advanced LV dysfunction. Extensive fibrosis of the subendocardium, leading to dilated ventricles and subsequent generation of reentrant tachyarrhythmias, is a proposed factor in mechanism of sudden death. Multiple factors have been shown to contribute to increased risk for SCD in this population. The most important hemodynamic predictor is an increase in end-diastolic pressure and subsequent wall tension. Other important factors are increased sympathetic tone, neurohumoral activation, and electrolyte abnormalities.
o Many drugs used in the treatment of heart failure, such as antiarrhythmics, inotropic agents, and diuretics, have direct or indirect (eg, through electrolyte abnormalities) proarrhythmic properties, which may provoke arrhythmias in some cases. Potassium-sparing diuretics may be helpful in decreasing SCD.
o Nonsustained ventricular tachycardia (NSVT) is common in patients with dilated cardiomyopathy and approximately 80% of persons with DCM have abnormalities on Holter monitoring. Although NSVT may be a marker, it has not been shown to be a reliable predictor of SCD in these patients. Recent studies have shown possibility of increased mortality following suppression of NSVT by antiarrhythmic medications due to proarrhythmic properties of these medications and involvement of several other factors in generation of VT and VF. Given the possibility of sustained VT being the underlying cause, a history of syncope should be aggressively pursued. Unexplained syncope, especially in patients with class 3 or 4 heart failure, has been shown to be a predictor of SCD in most patients with cardiomyopathy
* Hypertrophic cardiomyopathy
o Hypertrophic cardiomyopathy (HCM) is an autosomal-dominant, incompletely penetrant genetic disorder resulting from a mutation in one of the many (>45) genes encoding proteins of the cardiac muscle sarcomere. Among the genetic abnormalities described, mutations in the genes coding for the beta-myosin heavy chains, and cardiac troponin T make up most cases. Other mutations may include alpha-myosin heavy chain MYH6), cardiac troponin C (TNNC1), alpha-tropomyosin (TPM1), myosin binding protein-C (MYBPC3), cardiac troponin (TNNI3), essential and regulatory light-chain genes (MYL 3 and MYL 2, respectively), cardiac alpha-actin gene (ACTC), and titin (TTN). The incidence of SCD in this population is 2-4% per year in adults and 4-6% per year in children and adolescents. HCM is the most common cause of SCD in people younger than 30 years.
o The vast majority of young people who die of HCM are previously asymptomatic. The patients may experience SCD while at rest or with mild exertional activity; however, in a significant portion of these patients, the SCD event occurs after vigorous exertion. HCM is the single greatest cause of SCD in young athletes and, hence, is the major entity for which to screen during the physical examination of an athlete.
o The mechanism of SCD in HCM is not entirely understood. Initially, it was thought to be due to obstruction of the outflow tract because of catecholamine stimulation. However, later studies suggested that individuals with nonobstructive HCM are at high risk for SCD as well, primarily related to VT or VF. The mechanism of arrhythmia in this setting is not clear, and hypertrophy may be a part of cardiac remodeling in these patients that provides the substrate for lethal arrhythmia.
o Rapid or polymorphic symptomatic NSVT may have better predictive value compared with asymptomatic and monomorphic NSVT. Other clinical markers that may have predictive value for SCD in patients with HCM are young age at onset, thickness of the septum, and family history of SCD.
* Arrhythmogenic right ventricular cardiomyopathy
o Arrhythmogenic RV cardiomyopathy is characterized by replacement of the RV wall with fibrofatty tissue. Involvement of the interventricular septum and left ventricle is associated with poorer outcomes.
o About 30-50% of cases occur as a phenotypically apparent familial disorder. Several genetic defects, including mutations in the desmoplakin domain locus on chromosome 6 and the ryanodine receptor locus on chromosome 1 (although this has been debated), have been correlated with SCD. Again, interstitial fibrosis plays an important role in ventricular arrhythmia in this condition. Autosomal dominant inheritance is common, but autosomal recessive transmission has been reported for select mutations. The autosomal recessive form, Naxos disease (named after the Greek Island), has been reported in a geographically isolated area mainly in Mediterranean countries and is usually associated with wooly hair and palmoplantar keratoderma or similar skin disorder. This disorder is associated with mutation in the gene for plakoglobin, a protein involved in cellular adhesion, found on chromosome 17p.
o Arrhythmogenic RV dysplasia affects men more often than women. The annual incidence rate of SCD in this population is approximately 2%. Patients may present with signs and symptoms of RV hypertrophy and dilation, often with sustained monomorphic or polymorphic VT of a left bundle-branch block morphology with an axis usually between negative 90-100°
o Atrial arrhythmias may be present in as many as 25% of patients. Syncope and sudden death often are associated with exercise. In many patients, sudden death is the first manifestation of the disease. Clinicians should be alerted to the epsilon wave finding on ECG studies (see Media file 4). The epsilon wave can be present in as many as 23% of patients after the first VT event. The percentage of patients with the epsilon wave finding on ECG increases to 27% and 34% at 5 and 10 years, respectively, after the first VT event.

Cardiac death, sudden. Epsilon wave in a patient ...
Cardiac death, sudden. Epsilon wave in a patient with arrhythmogenic right ventricular dysplasia.

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Cardiac death, sudden. Epsilon wave in a patient ...

Cardiac death, sudden. Epsilon wave in a patient with arrhythmogenic right ventricular dysplasia.
o Uhl anomaly is a condition in which the RV wall is extremely thin secondary to apposition of endocardial and epicardial layers.

Valvular disease

* Prior to the advent of surgical therapy for valvular heart disease, SCD was fairly common in patients with progressive aortic stenosis.
o Most aortic stenosis deaths were sudden. In a study by Chizner et al of 42 patients who had isolated aortic stenosis and did not undergo valve replacement, as many as 56% of deaths were sudden at 5 years of follow-up. Of these 42 patients, 32 were symptomatic and 10 were asymptomatic.14
o The mechanism of sudden death is unclear, and both malignant ventricular arrhythmia and bradyarrhythmia have been documented.
o The incidence of SCD has decreased significantly with advent of aortic valve replacement. However, it still accounts for the second most common cause of death postoperatively in this population and especially in those with prosthetic and heterograft aortic valve replacement. The incidence of SCD after aortic valve surgery is highest in the first 3 weeks after the procedure and then plateaus at 6 months of follow-up.

Other valvular lesions

The risk of SCD is much lower in other valvular diseases compared with aortic stenosis.

* Aortic insufficiency usually presents with signs of heart failure and progressive LV dilatation. As part of this process, reentrant or automatic ventricular foci may develop and ultimately lead to a symptomatic ventricular arrhythmia. After valve replacement, LV wall tension can be expected to reduce and the risk of arrhythmia can be expected to decrease.
* Mitral stenosis is becoming increasingly uncommon in the United States because of widespread use of antibiotics in primary streptococcal infections. SCD due to mitral stenosis is very rare.
* The incidence of SCD is low in patients with mitral valve prolapse (MVP). MVP has a 5-7% incidence in the general population. In clinically significant MVP, the risk of SCD seems to rise along with total mortality. Kligfield et al estimated that the incidence of sudden death varies with the presence of symptoms and the severity of mitral regurgitation. Ventricular tachyarrhythmias are the most frequent arrhythmia in patients with SCD. Risk factors for SCD to consider in these patients include a family history of SCD, echocardiographic evidence of a redundant mitral valve, repolarization abnormalities, and lengthening of the corrected QT interval (>420 ms in women and >450 ms in men).

Congenital heart disease

In the pediatric and adolescent age groups, SCD occurs with an incidence of 1.3-8.5 cases per 100,000 patients annually, accounting for approximately 5% of all deaths in this group. The causes of SCD are much more diverse in children than adults. In reviewing 13 studies involving 61 children and adolescents with SCD, Driscoll found 50% of cases were due to HCM; 25% were due to anomalous origin of the left coronary artery; and the remaining patients had aortic stenosis, cystic medial necrosis, and sinus node artery obstruction. The following is a classification of SCD in the pediatric population.

* In patients with known, previously recognized (including repaired) congenital heart disease, abnormalities associated with SCD include the following:
o Tetralogy of Fallot
o Transposition of the great arteries
o Fontan operation
o Aortic stenosis
o Marfan syndrome
o Mitral valve prolapse
o Hypoplastic left heart syndrome
o Eisenmenger syndrome
o Congenital heart block
o Ebstein anomaly
* In patients with known, previously recognized (including repaired) heart disease, acquired causes of SCD include the following:
o Kawasaki syndrome
o DCM or myocarditis
* In patients with previously unrecognized heart disease who have structural heart disease, causes of SCD include the following:
o HCM
o Congenital coronary artery abnormalities
o Arrhythmogenic RV cardiomyopathy
* In patients with previously unrecognized heart disease who do not have structural heart disease, causes of SCD include the following:
o Long QT syndrome
o WPW syndrome
o Primary ventricular tachycardia and ventricular fibrillation
o Primary pulmonary hypertension
o Commotio cordis - Traumatic blow to the chest wall (eg, from a hockey puck or baseball) causing VT/VF and SCD in the absence of significant identifiable trauma
* The predominant mechanism is ventricular arrhythmias. In tetralogy of Fallot after postoperative correction of the anomaly, as many as 10% of these patients have VT and the incidence of sudden death is 2-3%. In the Fontan procedure, ie, to correct a physiologic single ventricle, even atrial arrhythmias can cause severe hemodynamic compromise and arrhythmic death. Patients who develop secondary pulmonary hypertension (Eisenmenger syndrome), despite attempted correction of the anatomic defects, have a very poor prognosis. The terminal event may be bradycardia or VT progressing to VF.

Primary electrophysiologic abnormalities

This generally represents a group of abnormalities in which patients have no apparent structural heart disease but have a primary electrophysiologic abnormality that predisposes them to VT or VF. Some imaging techniques have detected abnormal sympathetic neural function in these patients. An ECG study can provide clues to the diagnosis; consider a familial component to these conditions. Normal early repolarization may be associated with increased SCD, though this often represents a benign finding.15

* Long QT syndrome
o Idiopathic long QT syndrome, in which patients have a prolonged QT with a propensity to develop malignant ventricular arrhythmias, is a rare familial disorder.
o Two inheritance patterns of congenital long QT syndrome have been described. The Jervell-Lange-Nielsen syndrome, associated with congenital deafness, has an autosomal-recessive pattern of inheritance. The Romano-Ward syndrome is not associated with deafness and has an autosomal dominant pattern of inheritance with variable penetration. This syndrome accounts for 90% of long QT syndrome cases. More than 200 mutations in the 10 or more genes related to long QT syndrome have been found. Among the most common are mutations of SCN5A on chromosome 3, the HERG gene on chromosome 7, and the KVLTQT1 gene on chromosome 11.
o Alteration in the function of a myocellular channel protein that regulates the potassium flux during electrical repolarization is thought to be causative, though in some subsets of long QT syndrome, such as those with mutations in SCN5A (long QT3), Na channels are primarily impaired. A relationship with sympathetic nervous system imbalance also appears to exist. The prolongation that occurs makes these patients susceptible to develop a specific form of VT called torsade de pointes.
o The clinical course of patients with long QT syndrome is quite variable, with some patients remaining asymptomatic while others develop torsade de pointes with syncope and sudden death. Symptoms and SCD are more common among homozygous individuals (those with two copies of the mutant allele), compared with heterozygous individuals (who have a single mutant allele). The risk of SCD is impacted by environmental factors such as hypokalemia, medications and the presence of sinus pauses. SCD in these patients also has been associated with emotional extremes, auditory auras or stimulation, and vigorous physical activity. Symptoms usually begin in childhood or adolescence.
o The probability that a specific patient has congenital long QT syndrome is divided to low, intermediate, and high probability based on the following criteria: (1) ECG criteria including long QT, torsade de pointes, notched T wave, T wave alternans, bradycardia for age; (2) clinical criteria including syncope with or without stress, deafness; and (3) family history of long QT syndrome or SCD.
o When measuring QTc, selecting rhythm strips that have minimal variability of RR intervals and a stable heart rate is important.
o Treatment for long QT syndrome includes beta-blockers and often pacemaker or ICD implantation. Beta-blockers decrease the overall mortality in patients with long QT syndrome. However, they do not eliminate the risk of syncope, cardiac arrest, and SCD completely. They are not effective in patients with mutation in Na channel genes (long QT3). Torsade de pointes in patients with long QT syndrome is associated with bradycardia and pauses. Therefore, a pacemaker can prevent torsade de pointes in these patients by preventing bradycardia. ICD therapy may be indicated in patients with recurrent symptoms despite treatment with beta-blockers.
* Acquired long QT syndrome
o A number of antiarrhythmics (especially class Ia and class III) and other medications, electrolyte abnormalities, cerebrovascular diseases, and altered nutritional states are known to cause QT prolongation and put patients at risk for torsade de pointes. This usually occurs when QT prolongation is associated with a slow heart rate and hypokalemia.
o The QT interval is prolonged in as many as 32% of patients with intracranial hemorrhage (especially in subarachnoid hemorrhages). Lesions in the hypothalamus are thought to lead to this phenomenon.
o Reports of sudden death due to ventricular arrhythmia in patients with hypocalcemia, hypothyroidism, nutritional deficiencies associated with modified starvation diets, and in patients who are obese and on severe weight-loss programs have been reported.
o Class Ia antiarrhythmic drugs that cause acquired long QT syndrome include quinidine, disopyramide, and procainamide. Class III antiarrhythmic drugs that cause acquired long QT syndrome include sotalol, N -acetyl procainamide, bretylium, amiodarone, and ibutilide.
o Other drugs that cause acquired long QT syndrome include bepridil, probucol, tricyclic and tetracyclic antidepressants, phenothiazines, Haldol, antihistamines (eg, terfenadine, astemizole), antibiotics (eg, erythromycin, sulfamethoxazole/trimethoprim), chemotherapeutics (eg, pentamidine, anthracycline), serotonin antagonists (eg, ketanserin, zimeldine), and organophosphorus insecticides.
o Electrolyte abnormalities that cause acquired long QT syndrome include hypokalemia, hypomagnesemia, and hypocalcemia.
o Altered nutritional states and cerebrovascular disease that cause acquired long QT syndrome include intracranial and subarachnoid hemorrhages, stroke, and intracranial trauma.
o Hypothyroidism and altered autonomic status (eg, diabetic neuropathy) can cause acquired long QT syndrome.
o Hypothermia can cause acquired QT prolongation. The ECG will typically also demonstrate an Osborn wave, a distinct bulging of the J point at the beginning of the ST segment. This ECG finding resolves upon warming.
* Short QT syndrome
o The short QT syndrome is a newly recognized syndrome, first time described in 2000, which can lead to lethal arrhythmias and SCD. Three mutations in potassium channels have been described that lead to gain of function in potassium channels and shortening of action potential and decreased QT interval.
o To diagnose short QT syndrome, the QTc should be less than 330 msec and tall and peaked T waves should be present. Clinical manifestations are variable from no symptoms, to palpitations due to atrial fibrillation, syncope due to VT, and SCD. VF is easily inducible at electrophysiology study in these patients, and SCD can happen at any age.
o Although antiarrhythmic medications, such as sotalol, ibutilide, and procainamide, have been proposed as a therapy (to prolong the QT), data to support this approach are insufficient at present. ICD placement may be considered to prevent VT and SCD, although T-wave oversensing, resulting in inappropriate ICD discharges, has been problematic.
* Wolff-Parkinson-White syndrome
o WPW syndrome is a recognized but rare cause of sudden death. The existence of an atrioventricular accessory pathway in this syndrome results in ventricular preexcitation, which appears with short PR interval, wide QRS complex, and delta wave on ECG. The refractory period in the anterograde direction of accessory pathway determines the ventricular rate in the setting of atrial fibrillation and WPW. Most patients with WPW syndrome and SCD develop atrial fibrillation with a rapid ventricular response over the accessory pathway, which induces VF (see Media file 5). In a study by Klein et al of 31 patients with VF and WPW syndrome, a history of atrial fibrillation or reciprocating tachycardia was an important predisposing factor. The presence of multiple accessory pathways, posteroseptal accessory pathways, and a preexcited R-R interval of less than 220 ms during atrial fibrillation are associated with higher risk for SCD.

Cardiac death, sudden. Ventricular fibrillation a...
Cardiac death, sudden. Ventricular fibrillation appeared during rapid atrial fibrillation in a patient with Wolff-Parkinson-White syndrome.

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Cardiac death, sudden. Ventricular fibrillation a...

Cardiac death, sudden. Ventricular fibrillation appeared during rapid atrial fibrillation in a patient with Wolff-Parkinson-White syndrome.
o Symptomatic patients should be treated by antiarrhythmic medications (eg, procainamide), catheter ablation of the accessory pathway, or electrical cardioversion depending on the severity and frequency of symptoms. Asymptomatic patients may be observed without treatment.
o Medications such as digoxin, adenosine, and verapamil that block the AV node are contraindicated in patients with WPW and atrial fibrillation because they may accelerate conduction through the accessory pathway, potentially causing VF and SCD.
* Brugada syndrome
o In 1992, Brugada and Brugada described a syndrome of a specific ECG pattern of right bundle-branch block and ST-segment elevation in leads V1 through V3 without any structural abnormality of the heart, that was associated with sudden death.
o In 25-30% of these patients, a mutation in SCN5A on chromosome 3 is detected. This mutation results in a sodium channelopathy. The most common clinical presentation is syncope, and this mutation is most common in young males and in Asians. It is associated with VT, VF, and SCD.
o Three ECG types of Brugada pattern are described. Only type 1,- which consists of a coving ST elevation in V1 to V3 with downsloping ST segment and inverted T waves, pseudo RBBB pattern with no reciprocal ST changes and normal QTc, is specific enough to be diagnostic for Brugada syndrome when it is associated with symptoms. The other two ECG patterns of Brugada are not diagnostic, but they merit further evaluation.
o The Brugada ECG pattern can be dynamic and not found on an index ECG. When clinical suspicion is high, a challenge test with procainamide or some other Na channel blocker may be diagnostic by reproducing the type 1 ECG pattern.
* Although antiarrhythmic medications, catheter ablation and pacemaker therapies all have potential, in young and symptomatic patients, an ICD should be implanted to prevent VF and SCD. ICD therapy is the only proven treatment to date. Whether ICD placement is indicated in older or asymptomatic patients is controversial at present.
o Catecholaminergic polymorphic ventricular tachycardia
+ Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a syndrome that presents with polymorphic VT, syncope, or SCD, and in about half of these patients, a mutation in one of two different genes have been detected.
+ The polymorphic VT is characteristically induced by emotional or physical stress (eg, exercise stress test). The medical therapy of choice is administration of beta-blockers, and ICD may be indicated. New data may support the use of flecainide in the treatment of this disease.16
* Primary ventricular fibrillation occurs in a structurally normal heart due to idiopathic etiology.
o An estimated 3-9% of cases of VT and VF occur in the absence of myocardial ischemia. As many as 1% of patients with out-of-hospital cardiac arrest have idiopathic VF with no structural heart disease. As many as 15% of patients younger than 40 years who experience VF have no underlying structural heart disease. Viskin and Behassan noted that of 54 patients with idiopathic VF, 11 patients had histologic abnormalities on endomyocardial biopsy.
o SCD is often the first presentation of VF in patients at risk but who have had no preceding symptoms. In those patients who survive, VF may recur in as many as one third of patients.
o The options for medical therapy include beta-blockers and class 1A antiarrhythmic drugs, but limited data are available regarding their efficacy. The mainstay of treatment is preventing VF by ICD placement. Mapping and radiofrequency ablation of the triggering foci is an option for those patients who experience frequent episodes of VF following ICD placement.
* Right ventricular outflow tract ventricular tachycardia
o Right ventricular outflow tract (RVOT) tachycardia is the most common form of idiopathic VT, comprising 70-80% of all idiopathic VTs. RVOT tachycardia is a very rare cause of SCD. It also has been referred to as exercise-induced VT, adenosine-sensitive VT, and repetitive monomorphic VT.
o RVOT tachycardia occurs in patients without structural heart disease and arises from the RV outflow region. Current data suggest that triggered activity is the underlying mechanism of RVOT tachycardia. RVOT tachycardia is believed to be receptor-mediated because exogenous and endogenous adenosine can terminate this process. Maneuvers that increase endogenous acetylcholine also have been demonstrated to antagonize this process.
o Symptoms typical of RVOT tachycardia include palpitations and presyncope or syncope, often occurring during or after exercise or emotional stress. VT also can occur at rest. The ECG during VT displays a left bundle-branch block/inferior axis morphology.
o Treatment is based on frequency and severity of symptoms. The first line of therapy is a beta-blocker or calcium channel blocker. Patients with symptoms not relieved by medical therapy are best treated with radiofrequency catheter ablation. Successful ablation is reported in 83-100% of cases.

Other causes of sudden death

Two major causes of sudden cardiopulmonary death deserve mention.

* Pulmonary embolism is a frequent cause of sudden death in people at risk. Risk factors include previous personal or family history of deep venous thromboembolism, malignancy, hypercoagulable states, and recent mechanical trauma such as hip or knee surgery.
* Aortic dissection or aneurysmal rupture is the other major cause of out-of-hospital nonarrhythmic cardiovascular death. Predisposing factors for aortic dissection include genetic deficiencies of collagen such as Marfan syndrome, Ehlers-Danlos syndrome, and aortic cystic medial necrosis.

http://emedicine.medscape.com/article/151907-overview

Brugada Syndrome

2010-02-22T11:30:00.000+07:00

Introduction
Background

Brugada syndrome is a disorder characterized by sudden death associated with one of several ECG patterns characterized by incomplete right bundle branch block and ST elevations in the anterior precordial leads. (See Media file 2.) In the initial description of Brugada syndrome, the heart was reported to be structurally normal, but this has been challenged.1 Moreover, subtle structural abnormalities in the right ventricular outflow tract can also be observed. The typical patient with Brugada syndrome is young, male, and otherwise healthy, with normal general medical and cardiovascular physical examinations.

Patients with Brugada syndrome are prone to develop ventricular tachyarrhythmias that may lead to syncope, cardiac arrest, or sudden cardiac death.2,3,4 Infrahisian conduction delay and atrial fibrillation may also be manifestations of the syndrome.5,6 Brugada syndrome is genetically determined and has an autosomal dominant pattern of transmission in about 50% of familial cases. About 5% of survivors of cardiac arrest have no clinically identified cardiac abnormality; about half of these cases are thought to be due to Brugada syndrome.7
Pathophysiology

Brugada syndrome is an example of a channelopathy; a disease caused by an alteration in the transmembrane ion currents that together constitute the cardiac action potential. Specifically, in 10-30% of cases, mutations in the SCN5A gene, which encodes the cardiac voltage-gated sodium channel Nav 1.5, have been found. These loss-of-function mutations reduce the sodium current (INa) available during the phases 0 (upstroke) and 1 (early repolarization) of the cardiac action potential. This decrease in INa is thought to affect the right ventricular endocardium differently from the epicardium, thus underlying both the Brugada ECG pattern and the clinical manifestations of the Brugada syndrome.

The mechanisms underlying the ECG alterations and arrhythmogenesis in Brugada syndrome are disputed.8 The repolarization-defect theory is based on the fact that right ventricular epicardial cells display a more prominent notch in the action potential than endocardial cells. This is thought to be due to an increased contribution of the transient outward current (Ito) to the action potential waveform in that tissue. A decrease in INa accentuates this difference, causing a voltage gradient during repolarization and the characteristic ST elevations on ECG. When the usual relative durations of repolarization are not altered, the T wave remains upright, causing a saddleback ECG pattern (Type 2 or 3). When the alteration in repolarization is sufficient enough to cause a reversal of the normal gradient of repolarization, the T wave inverts, and the coved (Type 1) ECG pattern is seen.

In a similar way, a heterogeneous alteration in cardiac repolarization may predispose to the development of reentrant arrhythmias, termed phase 2 reentry, that can clinically cause ventricular tachycardia and ventricular fibrillation.9

Human evidence for a repolarization gradient in patients with Brugada syndrome using simultaneous endocardial and epicardial unipolar recordings was recently published.10

On the other hand, the depolarization/conduction disorder hypothesis proposes that the typical ECG signs can be explained by slow conduction and activation delays in the right ventricle (in particular in the right ventricular outflow tract).8
Frequency
United States

Because of its recent identification, the incidence of Brugada syndrome is not well established. In a large university hospital on the west coast of the US, the incidence of a Brugada ECG pattern among unselected, mainly Caucasian and Hispanic adults, was 2 of 1348 patients (0.14%), both of which were type 2 EKGs.11 The prevalence in other ethnic populations may be higher.
International

In Asia (eg, the Philippines, Thailand, Japan), Brugada syndrome seems to be the most common cause of natural death in men younger than 50 years. It is known as Lai Tai (Thailand), Bangungut (Philippines), and Pokkuri (Japan). In Northeast Thailand, the mortality rate from Lai Tai is approximately 30 per 100,000 population per year.12
Mortality/Morbidity

Brugada syndrome is a leading cause of death, aside from accidents, in men under 40. The true incidence is not known due to reporting biases.An estimated 4% of all sudden deaths and at least 20% of sudden death in patients with structurally normal hearts are due to the sydrome. Those with the syndrome have a mean age of sudden death of 41±15 years.13

The major manifestation of Brugada syndrome is polymorphic ventricular tachycardia that can degenerate into ventricular fibrillation and cause sudden cardiac death. Patients in whom sudden death has been aborted may have neurologic sequela of prolonged ischemia. Patients in whom an automatic internal defibrillator is implanted are subject to the risks of that procedure, and may receive shocks from the device that can cause physical pain and psychological trauma.

Race

Brugada syndrome is most common in people from Asia. The reason for this observation is not yet fully understood but may be due to an Asian-specific sequence in the promoter region of SCN5A.14
Sex

Brugada syndrome is 8-10 times more prevalent in men than in women, although the probability of having a mutated gene does not differ by sex. The penetrance of the mutation therefore appears to be much higher in men than in women.
Age

Brugada syndrome most commonly affects otherwise healthy men aged 30-50 years, but affected patients aged 0-84 years have been reported. The mean age of patients who die suddenly is 41 years.9
Clinical
History

Syncope and cardiac arrest are the most common clinical manifestations leading to the diagnosis of Brugada syndrome. Nightmares or thrashing at night may occur. However, sometimes no symptoms have been recognized and the diagnosis of Brugada syndrome is based on a routine ECG showing ST-segment elevation in leads V1 through V3. A family history of sudden cardiac death is common, though not required, as the syndrome can occur sporadically.

The context of the cardiac event is important. In many cases, cardiac arrest occurs during sleep or rest. Cases occurring during physical activity are rare. In addition, fever is often reported to trigger or exacerbate the clinical manifestations of Brugada syndrome.
Physical

The physical examination is usually normal in patients with the Brugada syndrome. Nevertheless, physical examination is required to rule out other possible cardiac causes (eg, heart murmurs from hypertrophic cardiomyopathy or from a valvular or septal defect) that may be associated with syncope or cardiac arrest in an otherwise healthy patient.
Causes

The prototypical case of Brugada syndrome has been associated with alterations in the SCN5A gene, of which well more than 100 mutations have been found. Mutations in other genes have been proposed to cause a variant of Brugada syndrome, including the genes coding for alpha1- and beta2b-subunits of the L-type calcium channel (CACNA1C and CACNB2), which are thought to cause a syndrome of precordial ST elevation, sudden death, and short QT.15 Cases in which a mutation in the SCN5A gene cannot be demonstrated may be due to mutations of these genes, other genes that have not yet been identified, or in regions of the coding sequence or promoter region of SCN5A that are not routinely sequenced in lab tests. More recently, mutations in the genes GPD1-L16 and SCN1B17 have been identified in a few familial cases.

Many clinical situations may unmask or exacerbate the ECG pattern of Brugada syndrome. Examples are hyperkalemia, hypokalemia, hypercalcemia, alcohol or cocaine intoxication, a febrile state, and the use of sodium-channel blockers, vagotonic agents, alpha-adrenergic agonists, beta-adrenergic blockers, heterocyclic antidepressants, and a combination of glucose and insulin.9

http://emedicine.medscape.com/article/163751-overview

Polycystic Kidney Disease

2010-02-13T08:41:00.000+07:00

Introduction
Background
Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common inherited disorders in humans. It is the most frequent genetic cause of renal failure in adults, accounting for 6-8% of patients on dialysis in the United States.
ADPKD is a multisystemic and progressive disorder characterized by the formation and enlargement of renal cysts in the kidney (as seen in the image below) and other organs (eg, liver, pancreas, spleen). Clinical features usually begin in the third to fourth decade of life, but cysts may be detectable in childhood and in utero.
Pathophysiology
The main feature of ADPKD is bilateral progressive cystic dilation of the renal tubules, which may lead to end-stage renal disease (ESRD). Hepatic cysts, cerebral aneurysms, and cardiac valvular abnormalities also may occur.
Although ADPKD is a systemic disease, it shows a focal expression because less than 1% of nephrons become cystic. In ADPKD, each epithelial cell within a renal tubule harbors a germ-line mutation, yet only a tiny fraction of the tubules develop renal cysts. It is currently held that the cells are protected by the allele inherited from the parent without ADPKD. When this allele is inactivated by a somatic event (mutation or otherwise) within a solitary renal tubule cell, the cell divides repeatedly until a cyst develops, with an aberrant growth program causing endless expansion. The severity of ADPKD is thought to be a direct consequence of the number of times and the frequency with which this cystogenic process occurs within the kidneys over the life of the patient.
The hyperplastic cells cause an out-pocketing of the tubule wall, with the formation of a saccular cyst that fills with fluid derived from glomerular filtrate that enters from the afferent tubule segment. Progressive expansion eventually causes most of the emerging cysts to separate from the parent tubule, leaving an isolated sac that fills with fluid by transepithelial secretion. This isolated cyst expands relentlessly as a result of continued proliferation of the mural epithelium together with the transepithelial secretion of sodium chloride and water into the lumen.
The expanding fluid-filled tumor masses elicit secondary and tertiary changes within the renal interstitium evinced by thickening and lamination of the tubule basement membranes, infiltration of macrophages, and neovascularization. Fibrosis within the interstitium begins early in the course of the disease. Cellular proliferation and fluid secretion may be accelerated by cAMP and growth factors, such as epidermal growth factor (EGF). In summary, cysts function as autonomous structures and are responsible for progressive kidney enlargement in ADPKD.
Approximately 85-90% of patients with ADPKD have an abnormality on the short arm of chromosome 16 (ie, ADPKD type 1 [ADPKD1]). A second defect, termed ADPKD type 2 (ADPKD2), is responsible for 5-15% of ADPKD cases and is found on the long arm of chromosome 4. A third genotype may exist, but no genomic locus is assigned.
PKD1 and PKD2 are expressed in most organs and tissues of the human body. The proteins that are encoded by PKD1 and PKD2, polycystin 1 and polycystin 2, seem to function together to regulate the morphologic configuration of epithelial cells. The polycystins are expressed in development as early as the blastocyst stage and are expressed in a broad array of terminally differentiated tissues. The functions of the polycystins have been scrutinized to the greatest extent in epithelial tissues of the kidneys and liver and in vascular smooth muscle.
Frequency
International
ADPKD is responsible for 6-10% of ESRD cases in North America and Europe. Approximately 1 per 800-1000 people carries the mutation for this condition. Approximately 85-90% of patients with ADPKD have ADPKD1; most of the remaining patients have ADPKD2.
Mortality/Morbidity
The major cause of morbidity is progressive renal dysfunction, resulting in grossly enlarged kidneys and kidney failure. In general, half of patients with ADPKD undergo renal replacement therapy by age 60 years. Cardiovascular pathology and infections account for approximately 90% of deaths of those patients treated by hemodialysis or peritoneal dialysis and after renal transplantation.
Another cause of mortality is subarachnoidal hemorrhage from intracranial aneurysms (ICAs). This complication is rare and severe.
In a retrospective, observational study of 88 patients with ADPKD who died sometime between 1981 and 1999, Rahman et al determined that almost half of the patients died of cardiovascular problems.1 More specifically, the investigators found, using data from the Sheffield Kidney Institute, in the United Kingdom, and clinical notes, that the causes of death included the following:
Cardiovascular problems - 46.6% of patients
Infection - 15.9% of patients, with 42% of these deaths resulting from septicemia
Central nervous system disorders - 11.36% of patients, with 60% of these deaths caused by cerebrovascular events
Uremia - 2.2% of patients
Other, miscellaneous causes - 11.36%
The median age of the nonsurviving patients was 60.5 years.
Sex : ADPKD is slightly more severe in males than in females, but it is not statistically significant.
Age
Symptoms generally increase with age. Children very rarely present with renal failure from ADPKD.
The mean age of onset of ESRD in patients with ADPKD1 is 53 years; in patients with ADPKD2, it is 74 years.
Clinical
History
Renal manifestations
A decrease in urine-concentrating ability is an early manifestation of the disease.
Microalbuminuria occurs in 35% of patients with ADPKD. However, nephrotic-range proteinuria is uncommon.
Patients may develop renal failure, usually in the fourth to sixth decade of life. The development of renal insufficiency is highly variable in ADPKD. Renal failure has been reported in children, and, conversely, individuals with the condition may live a normal life expectancy without knowing that they have the disease. An early study estimated that approximately 70% of patients with ADPKD would develop renal insufficiency if they survived to age 65 years. There is an inverse association between the size of polycystic kidneys and the level of glomerular filtration.
Hypertension2,3
Hypertension is one of the most common early manifestations of ADPKD. Even when renal function is normal, hypertension has been found in 50-75% of patients. In fact, the clinical course of hypertension in ADPKD is very unlike that of hypertension in chronic glomerulonephritis or tubulointerstitial nephropathies. In ADPKD, the hypertension is usually more severe early in the course of the disease and becomes less problematic with the progression of the renal insufficiency. Studies of the renin-angiotensin-aldosterone system have not convincingly demonstrated that they play an important role in its pathogenesis. A rise in diastolic blood pressure is the rule in ADPKD.
Doulton and colleagues have demonstrated that activation of the classic circulating renin-angiotensin system (RAS) is no greater in patients with hypertensive ADPKD than in individuals with essential hypertension.4 In spite of this evidence, angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers are still the most indicated drugs to treat hypertension in patients with ADPKD.
Pain
Pain, located in the abdomen, the flank, or the back, is the most common initial complaint, and it is almost universally present in patients with ADPKD. The pain can be caused by enlargement of one or more cysts, bleeding, either confined inside the cyst or leading to gross hematuria with passage of clots, or a perinephric hematoma; urinary tract infection (eg, acute pyelonephritis, infected cysts, perinephric abscess); nephrolithiasis and renal colic; and, rarely, a coincidental hypernephroma.
In addition, patients with ADPKD may have abdominal pain related to definitively or presumably associated conditions. Dull aching and an uncomfortable sensation of heaviness may result from a large polycystic liver. Although rare, hepatic cysts may become infected, especially after renal transplantation. Abdominal pain can also result from diverticulitis, which has been reported to occur with increased frequency in patients with ADPKD maintained on dialysis.
Patients with ADPKD may be at a higher risk of developing thoracic aortic aneurysms. Abdominal aortic aneurysms are not increased among these patients.
These patients may also develop pain for reasons completely unrelated to their underlying disease; thus, abdominal pain in patients with ADPKD may be a diagnostic challenge.
Hematuria
Hematuria frequently is the presenting manifestation and usually is self-limited (lasting less than or equal to 1 wk).
Polycystic kidneys are unusually susceptible to traumatic injury, with hemorrhage occurring in approximately 60% of individuals. Mild trauma can lead to intrarenal hemorrhage or bleeding into the retroperitoneal space accompanied by intense pain that often requires narcotics for relief. The cysts are associated with excessive angiogenesis evinced by fragile vessels stretched across their distended walls. When traumatized, these vessels may leak blood into the cyst, causing it to expand rapidly, resulting in excruciating pain. If bleeding continues, then the cyst may rupture into the collecting system, causing gross hematuria. Alternatively, it may rupture into the subcapsular compartment and eventually dissect through the renal capsule to fill the retroperitoneal space.
Stroke - A family history of stroke (or cerebrovascular accident), the presence of symptoms that may be related to an aneurysm, or a job or hobby in which a loss of consciousness may be lethal indicates the need for aneurysm screening with magnetic resonance angiography.
Physical
Palpable, bilateral flank masses occur in patients with advanced ADPKD.
Nodular hepatomegaly occurs in those with severe polycystic liver disease.
Symptoms related to renal failure (eg, pallor, uremic fetor, dry skin, edema) are rare upon presentation.
Causes
ADPKD is a hereditary disorder. The pattern of inheritance is autosomal dominant. Because the disorder occurs equally in both sexes, each offspring has a 50% chance of inheriting the affected chromosome and, hence, the disease.
ADPKD is a genetically heterogeneous condition that involves at least 2 genes.
PKD1 is located on 16p13.3 and accounts for most ADPKD cases.
PKD2 is located on 4q21-q22 and accounts for 15% of ADPKD cases.
PKD1 codes for a 4304–amino acid protein (polycystin 1) with as yet undefined function but interacts with polycystin 2 and is involved in cell cycle regulation and intracellular calcium transport. Polycystin 1 localizes in the primary cilia of renal epithelial cells, which function as mechanosensors and chemosensors.
PKD2 codes for a 968–amino acid protein (polycystin 2) that is structurally similar to polycystin 1 and colocalizes to the primary cilia of renal epithelial cells. It is a member of the family of voltage-activated calcium channels.
Polycystin 1 and polycystin 2 are highly conserved ubiquitous transmembrane proteins that, in the kidney, are located in the epithelial cells of the renal tubules, in particular in the primary cilia at the luminal side of the tubules, as well as in other areas of the renal cell epithelium.
Polycystin 1 is a large protein with a long extracellular N-terminal region, 11 transmembrane domains, and a short intracellular C-terminal tail. Polycystin 2 is structurally related to the transient receptor potential (TRP) channel family, and it is known to function as a nonselective cation channel permeable to Ca2+.
Polycystin 1 and polycystin 2 form heteromeric complexes and colocalize in the primary cilium of renal epithelial cells. The primary cilium is a long, nonmotile tubular structure located in the apical surface of the epithelial cells in the renal tubules. Its function was unknown for a long time. However, studies now indicate that the primary cilium may be a mechanoreceptor that senses changes in apical fluid flow and that transduces them into an intracellular Ca2+ signaling response.
This model involves the participation of polycystin 1 as a mechanical sensor of ciliary bending induced by luminal fluid flow. Bending of the cilium would cause a conformational change in polycystin 1 that would, in turn, activate the polycystin 2-associated Ca2+ channel, increasing the intracellular Ca2+ concentration and triggering intracellular signaling pathways leading to normal kidney development.
A good genotype-phenotype correlation has not been well established for ADPKD1 and ADPKD2.
ADPKD1 is more severe than ADPKD2. The mean age of ESRD for patients with ADPKD1 is 53 years. The mean age of ESRD for patients with ADPKD2 is 74 years.
Differential Diagnoses Cystic Diseases of the Kidney, von Hippel-Lindau Disease
Other Problems to Be Considered
Acquired renal cystic disease, Autosomal recessive polycystic kidney disease, Medullary cystic disease, Orofaciodigital type II syndrome, Renal dysplasia, Simple renal cysts, Tuberous sclerosis
Workup
Laboratory Studies
Genetic testing is available by means of DNA linkage analysis and has an accuracy rate of greater than 95% for ADPKD1 and ADPKD2.
To perform this analysis, obtain blood from at least 2 affected individuals (if they are parent and child, 1 more affected family member is needed) and 2 unaffected individuals from one family.
The major indication for genetic screening is in young adults with negative ultrasonographic findings who are being considered as potential kidney donors.
Mutation screening is commercially available (Athena Diagnostics, Inc, Worchester, Mass).
Other studies to perform include a serum chemistry profile, including calcium and phosphorus; a complete blood cell count; urinalysis; urine culture; uric acid determination; and intact parathyroid hormone value.
An increased hematocrit may result from increased erythropoietin secretion from cysts.
Imaging Studies
Ultrasonography5
This is the most widely used imaging technique to help diagnose ADPKD, and it can detect cysts from 1-1.5 cm.
This study avoids the use of radiation or contrast material, is widely available, and is inexpensive.
Ultrasonographic imaging is likely to remain a widely applied modality for diagnosing ADPKD.
Sensitivity for ADPKD1 is 99% for at-risk patients older than 20 years, but ultrasonography often yields false-negative results in younger patients.
Sensitivity for ADPKD2 is lower and is still not well defined.
Ultrasonography is also useful for exploring abdominal extrarenal features of ADPKD (eg, liver cysts, pancreatic cysts).
The presence of hepatic or pancreatic cysts supports the diagnosis of ADPKD.
Ultrasonographic diagnostic criteria for ADPKD1 were established by Ravine et al in 1994 and are as follows:6
At least 2 cysts in 1 kidney or 1 cyst in each kidney in an at-risk patient younger than 30 years
At least 2 cysts in each kidney in an at-risk patient aged 30-59 years
At least 4 cysts in each kidney for an at-risk patient aged 60 years or older
Computed tomography (CT) scan
This study is more sensitive than ultrasonography and can detect cysts as small as 0.5 cm.
It involves radiation and is more expensive; therefore, it is not used routinely for diagnosis or for follow-up studies of ADPKD.
This study may be useful in doubtful cases in children or in complicated cases (eg, kidney stone, suspected tumor).
Magnetic resonance imaging (MRI)
This study is also more sensitive than either ultrasonography or CT scanning. It may be more helpful in distinguishing renal cell carcinoma from simple cysts.
MRI is the best imaging tool to monitor kidney size after treatment to assess progress. However, it is not routinely used because it is expensive and tedious. It should not be used unless the patient is in a protocol or similar situation.
MRI is the criterion standard to help determine renal volume for clinical trials when testing drugs for ADPKD.
Intravenous urography
This was once used widely to diagnose ADPKD.
It involves contrast and only helps in the diagnosis of advanced-stage ADPKD because of the distortion of calyces.
It is no longer indicated to establish a diagnosis of the disease.
Magnetic resonance angiography
This is the preferred imaging technique for diagnosing ICAs.
This study is recommended when a member of the family is diagnosed with an ICA, if the patient refers to symptoms related to an ICA, when the patient has a high-risk job, or when the patient has had a previous ICA.
Procedures
Barium enema - To help diagnose colonic diverticula
Doppler studies and 2-dimensional echocardiography - To exclude mitral prolapse, which is often associated with ADPKD
Staging
Staging of renal failure is as follows:
Stage 1 - GFR >90 mL/min
Stage 2 - GFR 60-90 mL/min
Stage 3 - GFR 30-60 mL/min
Stage 4 - GFR 15-30 mL/min
Stage 5 - GFR <15 mL/min
Treatment
Medical Care
Ensure that a patient with ADPKD who is nonhypertensive and has normal renal function undergoes blood testing and ultrasonographic scanning once a year.
Schedule more frequent follow-up studies for patients with high blood pressure. Hypertension is common, occurring in as many as 50-70% of patients before the onset of renal failure.
Patients with renal failure require more frequent monitoring, based on the severity of their condition.
Medical therapy is necessary to accomplish the following:
Control blood pressure. In patients with renal disease, the goal is a blood pressure of less than 130/88 mm Hg. If more than 1 g/d of urinary protein is present, the target blood pressure is less than 125/75 mm Hg. Achieving good blood pressure control helps slow the progression of renal disease.
The best drugs for this condition are ACE inhibitors (ie, captopril, enalapril, lisinopril) or angiotensin II receptor antagonist blockers (ie, telmisartan, losartan, irbesartan, candesartan). Calcium channel blockers are not recommended.
Control abnormalities related to renal failure (ie, hyperkalemia, hyperphosphatemia, hypocalcemia, hyperparathyroidism, acidosis).
Treat urinary tract infections, which occur in 30-50% of patients and most frequently in women. Gram-negative bacteria are the most common pathogens.
Reduce abdominal pain produced by enlarged kidneys.
Avoid nonsteroidal anti-inflammatory drugs (NSAIDs).
With heart murmurs, institute routine American Heart Association antibiotic prophylaxis.
Treatment involves surgical cyst decompression, which is effective for pain relief in 60-80% of patients. See Surgical Care.
Distinguishing between infections of the bladder, renal parenchyma, and cysts is important because the treatment for each condition is different. Treating infected cysts requires antibiotics that penetrate into the cyst. Useful agents are ciprofloxacin, trimethoprim-sulfamethoxazole, clindamycin, and chloramphenicol.
Patients with ADPKD and ESRD may undergo hemodialysis, peritoneal dialysis, or renal transplantation.
Surgical Care
Infected renal or hepatic cysts
If infected cysts do not respond to conventional antibiotic therapy, surgical drainage may be necessary.
This procedure is usually performed with ultrasonographically guided puncture.
Large cysts causing abdominal pain
Cysts may become large enough to cause abdominal discomfort or pain. Typically, acute pain is from cyst hemorrhage or an obstruction by a clot, stone, or infection.7
When one or more cysts can be identified as causing the pain, the symptoms can often be abated by open- or fiber optic–guided surgery to excise the outer walls and to drain them.
In approximately one half of patients, however, candidate cysts cannot be identified as directly causing the pain. In these cases, indiscriminate excision of dozens of cyst walls that abut the capsule have produced complete symptomatic relief for months or years. Volumetric reduction of these kidneys usually exceeds 50% but still leaves kidneys larger than normal size. Not every cyst can be removed, and, with time, the residual cysts enlarge and symptoms may reappear.
Approximately one quarter of patients with the most severe pain do not gain relief from surgery or pharmacologic therapy with narcotics. These individuals usually have inaccessible cysts in the medullary portions of the kidneys. Nephrectomy is used as a last resort to control the pain in these patients.
Massive polycystic liver diseases (See the image below.)
When the liver becomes so large that it prevents the patient from obtaining normal nutrition or causes severe abdominal discomfort, a surgical procedure is necessary.
Surgical intervention may range from unroofing several cysts to a partial hepatectomy.
Partial hepatectomy is difficult because of the characteristics of the polycystic liver. Only expert surgeons should proceed with this surgical procedure.
When the polycystic liver causes portal hypertension or is very large with nonresectable areas, liver transplantation may be necessary.
Special attention should be paid when bilateral nephrectomy has to be carried out in patients with severe liver involvement. Several cases of refractory ascites after bilateral nephrectomy have been reported in these patients.
Consultations
Nephrologist upon evidence of renal insufficiency, hypertension, microalbuminuria, or concentrating defect
Invasive radiologist for cyst sclerosis or drainage
General surgeon for nephrectomy, cyst decompression, unroofing, or surgical hepatic procedures
Neurosurgeon for ICAs
Cardiologist for valvular abnormalities
Diet = Although a low-salt diet is recommended when hypertension or renal failure is present, no other special diet reportedly is of benefit.
Activity
Patients should avoid contact sports in which direct trauma to the back or abdomen is likely. This is especially important with larger, palpable kidneys in order to minimize the risk of rupture.
Medication
No specific medication is available for ADPKD; however, clinical trials with vasopressin 2 receptor antagonists (Tolvaptan), somatostatin, and rapamycin are ongoing. The drugs of choice for hypertension are ACE inhibitors and angiotensin II receptor antagonist blockers. Do not treat abdominal pain with NSAIDs because of its potential nephrotoxic effect.
Cyst infections require gyrase inhibitors (eg, ciprofloxacin, chloramphenicol, clindamycin). Trimethoprim-sulfamethoxazole is also an effective antibiotic for reaching the inner cavity of the cyst. Renal failure requires drugs to maintain electrolyte levels (eg, calcium carbonate, calcium acetate, sevelamer, lanthanum carbonate, calcitriol [possibly], diuretics, blood pressure medications). Approximately 62% of patients with renal insufficiency require at least 2 antihypertensive agents for optimal blood pressure control.
ACE inhibitors
These peptides suppress the renin-angiotensin-aldosterone system.
Enalapril (Vasotec)
Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.
Dosing
Adult
2.5-5 mg/d PO, increase prn
Dosing range: 10-40 mg/d PO in 1-2 divided doses
Alternatively: 1.25 mg/dose IV over 5 min q6h
Pediatric
Not established
Interactions
NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics
Contraindications
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Renal impairment, valvular stenosis, or severe congestive heart failure

Lisinopril (Prinivil, Zestril)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Dosing
Adult
10 mg/d PO; increase 5-10 mg/d at 1- to 2-wk intervals; not to exceed 40 mg
Pediatric
Not established
Interactions
NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Renal impairment, valvular stenosis, or severe congestive heart failure

Captopril (Capoten)
Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.
Dosing
Adult
12.5-25 mg PO bid/tid; may increase by 12.5-25 mg/dose at 1- to 2-wk intervals; not to exceed 50 mg tid
Pediatric
6.25-12.5 mg/dose PO q12-24h; not to exceed 6 mg/kg/d
Interactions
NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics
Contraindications
Documented hypersensitivity; renal impairment
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Renal impairment, valvular stenosis, or severe congestive heart failure
Electrolyte supplements
Administer to maintain electrolyte levels in renal failure.

Calcium carbonate (Oystercal)
Reduces phosphorus load.
Dosing
Adult
1-2 g divided PO bid/qid
Pediatric
45-65 mg/kg/d PO divided qid

Interactions
May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels
Contraindications
Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; patients with digitalis toxicity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Digitalized patients and respiratory failure or acidosis
Antibiotics
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Ciprofloxacin (Cipro)
Inhibits bacterial DNA synthesis and, consequently, growth. Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms, but no activity against anaerobes. Levofloxacin (Levaquin) overcomes many of these limitations. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared
Dosing
Adult
250-500 mg PO bid for 7-14 d
Pediatric
<18 years: Not recommended
>18 years: Administer as in adults
Interactions
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Levofloxacin (Levaquin)
Inhibits growth of susceptible organisms by inhibiting DNA gyrase and promoting breakage of DNA strands.
Dosing
Adult
750 mg PO q24h for 7-14 d
Pediatric
Not established
Interactions
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS, Cotrim C)
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
Dosing
Adult
20 mg TMP/kg/d IV divided qid
Pediatric
Administer as in adults
Interactions
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration with diuretics increases incidence of thrombocytopenic purpura in elderly people; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Contraindications
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly people, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation
Clindamycin (Cleocin)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Dosing
Adult
150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d
600-1200 mg/d IV/IM divided q6-8h depending on degree of infection
Pediatric
8-20 mg/kg/d PO as hydrochloride and 8-25 mg/kg/d as palmitate divided tid/qid
20-40 mg/kg/d IV/IM divided tid/qid
Interactions
Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption
Contraindications
Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis
Precautions
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis

Chloramphenicol (Chloromycetin)
Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.
Dosing
Adult
50-100 mg/kg/d PO/IV divided q6h for 10 d; not to exceed 4 g/d
Pediatric
50-75 mg/kg/d PO/IV divided q6h
Interactions
With concurrent administration with barbiturates, serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity (chloramphenicol levels may increase or decrease)
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately q2d while on therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)
Phosphate binders
Administer to maintain phosphate levels in renal failure.

Lanthanum carbonate (Fosrenol)
Noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with ESRD. Directly binds dietary phosphorus in upper GI tract, thereby inhibiting phosphorus absorption.
Dosing
Adult
Initial: 250-500 mg PO tid pc (chewable tabs); adjust dose q2-3wk to target serum phosphorus level
Maintenance: 500-1000 mg PO tid pc
Pediatric
Not established
Interactions
Drugs known to interact with antacids (eg, alendronate, amprenavir, ciprofloxacin, itraconazole, tetracycline, thyroid hormones) should not be administered within 2 h
Contraindications
Documented hypersensitivity; bowel obstruction; hypophosphatemia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Deposited into developing bone, including growth plate (long-term effects unknown); common adverse effects typically diminish over time but include headache, abdominal pain, nausea, diarrhea, constipation, and vomiting; in clinical trials, dialysis graft occlusion occurred more frequently than with placebo; caution with GI motility diseases (eg, Crohn disease, ulcerative colitis) or recent GI surgery

Sevelamer hydrochloride (Renagel)
Polymeric phosphate binder for oral administration. Does not contain aluminum and, thus, aluminum intoxication is not a concern.
Dosing
Adult
2-4 cap PO pc; adjust based on serum phosphorus concentrations to lower serum phosphorus to <6 mg/dL
Pediatric
Not established
Interactions
May reduce absorption of drugs co-administered with sevelamer
Contraindications
Documented hypersensitivity; bowel obstruction; hypophosphatemia
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with dysphagia, severe GI motility disorders, or swallowing disorders; can cause hypophosphatemia in patients with low or normal serum phosphate levels; when changes in absorption of oral medications may have clinical consequences (eg, antiseizure or antiarrhythmic drugs), medications should be taken 1 h before or 3 h after a dose of sevelamer
Angiotensin II receptor antagonists
These agents interfere with the binding of formed angiotensin II to its endogenous receptor.
Valsartan (Diovan)
Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACE inhibitors.
Dosing
Adult
80 mg/d PO; may increase to 160 mg/d if needed
Pediatric
<6 years: Not established
>6 years: 1.3 mg/kg PO qd initially, not to exceed 40 mg/d; may adjust dose according to blood pressure response up to 2.7 mg/kg/d (not to exceed 160 mg/d)

Interactions
May increase digoxin, lithium, and allopurinol levels; probenecid may increase valsartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of valsartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics
Contraindications
Documented hypersensitivity; severe hepatic insufficiency; biliary cirrhosis or obstruction; primary hyperaldosteronism; bilateral renal artery stenosis
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Pregnancy category D in second and third trimesters; caution in hyperkalemia, suspected bilateral renal artery stenosis, or suspected solitary kidney with unilateral renal artery stenosis

Losartan (Cozaar)
Angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.
Dosing
Adult
25-100 mg PO qd or divided bid
Pediatric
<6 years: Not established
6-16 years: 0.7 mg/kg PO qd; not to exceed 50 mg/d if <50 kg or 100 mg/d if >50 kg
CrCl <30 mL/min: Not established
Interactions
May increase digoxin, lithium, and allopurinol levels; probenecid may increase losartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of losartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Pregnancy category D in second and third trimesters; caution in patients with unilateral or bilateral renal artery stenosis
Candesartan (Atacand)
Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.
Angiotensin II receptor antagonist blockers reduce blood pressure and proteinuria, protecting renal function and delaying onset of ESRD.
Dosing
Adult
8-16 mg/d PO initially; not to exceed 32 mg/d
Pediatric
Not established
Interactions
May increase digoxin, lithium, and allopurinol levels; probenecid may increase candesartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of candesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Pregnancy category D in second and third trimesters; caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium

Olmesartan (Benicar)
Blocks vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to AT-1 receptor in vascular smooth muscle. Action is independent of pathways for angiotensin II synthesis.
Dosing
Adult
20 mg PO qd initially; may increase to 40 mg/d after 2 wk if further BP reduction required; lower dose in volume- or salt-depleted patients
Pediatric
Not established
Follow-up
Further Inpatient Care
Admit patients with cyst infections.
Admit patients for surgical procedures.
Further Outpatient Care
Carefully monitor blood pressure and renal function.
Perform an ultrasonogram of the kidneys every 1-2 years.
Inpatient & Outpatient Medications
Institute antihypertensive therapy with ACE inhibitors or angiotensin II receptor antagonist blockers. In patients with advanced renal disease, ACE inhibitors and/or angiotensin II receptor antagonist blockers can exacerbate renal failure or increase serum potassium; therefore, regularly monitor use with serum chemistry values.
If renal failure is present, drugs directed towards normalization of electrolyte levels are necessary.
Avoid NSAIDs because they can worsen renal function and potentiate hyperkalemia.
Hematuria is frequent among patients with ADPKD, usually resulting from cyst rupture or stone passage. Instruct the patient to drink large amounts of water, to rest, and to take a pain killer if necessary. Hospitalization is necessary if the patient is still bleeding after several days or if the amount of blood is substantial.
Transfer
Surgical interventions
Invasive procedures
Complications
ESRD - This is the most frequent complication of ADPKD; 50% of patients require renal replacement therapy by age 60 years.
Hypertension
The cause of an early rise in blood pressure remains controversial.
The rise in blood pressure is likely secondary to renal damage by cysts. A direct relationship exists between the volume of the kidneys and the severity of the hypertension.
The prevalence of hypertension increases with age, with a rate of approximately 85% when patients enter ESRD.
Extrarenal cysts
The presence of extrarenal cysts in the liver, pancreas, and spleen is a well-known feature of polycystic liver disease, which is a frequent condition in persons with ADPKD.
Polycystic liver disease belongs to a family of liver diseases characterized by an overgrowth of biliary epithelium and supportive connective tissue. It is characterized by multiple cysts that may be microscopic or can occupy most of the abdominal cavity. Liver size may range from normal to enlarged.
Women are more likely to have more and larger hepatic cysts than men; this correlates with estrogen exposure and increases with gravidity in women. Liver size in massive polycystic liver disease tends to stabilize after menopause.
Hepatic cysts occur in almost 50% of affected patients, are more common in women, and are exceptional in children with ADPKD.
The frequency of liver cysts increases with age; cysts occur in approximately 20% of patients during the third decade of life and in 75% during the seventh decade of life.
The presence of liver cysts does not involve hepatic failure.
Pain and infection are the only symptoms that occur from the presence of hepatic cysts, and most frequently, cysts are asymptomatic.
Massive polycystic liver disease may manifest predominantly in women, and portal hypertension (ie, ascites, esophageal varices) may occur in these patients.
The enlarged liver may cause malnutrition. These patients may need a partial resection of the liver or hepatic transplantation.
Bilateral nephrectomy in patients with massively enlarged livers may cause portal hypertension and severe ascites.
Pancreatic cysts occur at a rate of 9% in patients older than 20 years.
Cerebral aneurysms
Cerebral aneurysms are among the most serious complications of ADPKD; they occur in 4-10% of patients with ADPKD. (In the aforementioned study by Rahman et al, the mortality rate from cerebrovascular events was approximately 7%;1 see Morbidity/Mortality.)
Rupture usually occurs in patients younger than 50 years who have uncontrolled hypertension; however, a stroke from hypertension and intracerebral hemorrhage is more common.
There is no relationship between the risk of rupture and the severity of renal disease.
Colonic diverticula - Patients with ADPKD develop colonic diverticula, probably from altered connective tissue, at an estimated rate of 80%. However, this rate has not been demonstrated to be higher than the rate among other patients on dialysis.
Mitral valve prolapse - Patients with ADPKD occasionally develop mitral valve prolapse at a rate that is probably no higher than that of the normal population.
Nephrolithiasis - This occurs in 20-30% of patients with ADPKD. Consider this condition in patients with acute pain and hematuria. Unlike the most common form of kidney stones, calcium oxalate, uric acid stones form in as many as 50% of patients with ADPKD. Establishing a diagnosis by ultrasonogram is often difficult; therefore, an intravenous pyelogram or a CT scan is preferred because of the presence of large cysts.
Metabolic abnormalities (eg, decreased urinary citrate) - These contribute to uric acid stone formation.
Prognosis
Half of all patients with ADPKD require renal replacement therapy by age 60 years. Risk factors for progression include PKD1 genotype, large kidneys, several episodes of gross hematuria, severe and frequent kidney infections, hypertension, multiple pregnancies, black racial background, and male sex. The presence of more than one risk factor increases the risk of progression to ESRD.
The 2 forms of ADPKD are ADPKD1 and ADPKD2. Although they share similar clinical features, renal prognosis is strikingly different. Studies confirm that ADPKD2 is a milder disease, based on the age of onset of ESRD. The median age of renal survival for those with ADPKD2 is 68 years, which is significantly older than for those with ADPKD1 where the median age of renal survival is 53 years. Although ADPKD2 is milder than ADPKD1, it has an overall impact on survival and shortens life expectancy.
Patient Education
Ensure that patients are aware that this disease is hereditary and that their children have a 50% chance of acquiring the disease. Although several treatments are being tested, this disease currently has no cure. Only interventions that slow the progression of renal disease (eg, adequate blood pressure control) are of benefit. Hopefully, effective specific therapy will be available in a few years.
Prenatal diagnosis is available through DNA linkage studies if enough family members cooperate or through a mutation search. Suggest that family members who are not screened for ADPKD have annual blood pressure checks and urine screenings for hematuria.
For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education articles Blood in the Urine, Chronic Kidney Disease, and Kidney Transplant.
Miscellaneous
Medicolegal Pitfalls
Failure to inform patients that the disease is hereditary
Failure to inform patients that they may eventually develop ESRD
Performing genetic testing without informed consent

http://emedicine.medscape.com/article/244907-overview

Happy Birthday - Selamat Ulang Tahun 1102

2010-02-11T07:21:00.001+07:00

Vitamin A Deficiency

2010-01-21T07:48:00.000+07:00

Introduction
Background

The word vitamin was originally derived from Funk's term "vital amine." In 1912, he was referring to Christian Eijkman's discovery of an amine extracted from rice polishings that could prevent beriberi. Funk's recognition of the antiberiberi factor as vital for life was indeed accurate. Researchers have since found that vitamins are essential organic compounds that the human body cannot synthesize. Vitamins A, D, K, and E are classified as fat-soluble vitamins, whereas others are classified as water-soluble vitamins.1,2

Vitamin A was the first fat-soluble vitamin to be discovered. Early observations by ancient Egyptians recognized that night blindness could be treated with consumption of liver. Two independent research teams, Osborne and Mendel at Yale University and McCollum and Davis at the University of Wisconsin, simultaneously discovered vitamin A in 1913. Vitamin A is made up of a family of compounds called the retinoids. The retinoid designation resulted from finding that vitamin A had the biologic activity of retinol, which was originally isolated from the retina.

There are essentially 3 forms of vitamin A: retinols, beta carotenes, and carotenoids. Retinol, also known as preformed vitamin A, is the most active form and is mostly found in animal sources of food. Beta carotene, also known as provitamin A, is the plant source of retinol from which mammals make two-thirds of their vitamin A. Carotenoids, the largest group of the 3, contain multiple conjugated double bonds and exist in a free alcohol or in a fatty acyl-ester form.

In the human body, retinol is the predominant form, and 11-cis -retinol is the active form. Retinol-binding protein (RBP) binds vitamin A and regulates its absorption and metabolism. Vitamin A is essential for vision (especially dark adaptation), immune response, bone growth, reproduction, the maintenance of the surface linings of the eyes, epithelial cell growth and repair, and the epithelial integrity of the respiratory, urinary, and intestinal tracts. Vitamin A is also important for embryonic development and the regulation of adult genes. It functions as an activator of gene expression by retinoid alpha-receptor transcription factor and ligand-dependent transcription factor.

Deficiency of vitamin A is found among malnourished, elderly, and chronically sick populations in the United States, but it is more prevalent in developing countries. Abnormal visual adaptation to darkness, dry skin, dry hair, broken fingernails, and decreased resistance to infections are among the first signs of vitamin A deficiency (VAD).3
Pathophysiology

Once ingested, provitamins A are released from proteins in the stomach. These retinyl esters are then hydrolyzed to retinol in the small intestine, because retinol is more efficiently absorbed. Carotenoids are cleaved in the intestinal mucosa into molecules of retinaldehyde, which is subsequently reduced to retinol and then esterified to retinyl esters. The retinyl esters of retinoid and carotenoid origin are transported via micelles in the lymphatic drainage of the intestine to the blood and then to the liver as components of chylomicrons. In the body, 50-80% of vitamin A is stored in the liver, where it is bound to the cellular RBP. The remaining vitamin A is deposited into adipose tissue, the lungs, and the kidneys as retinyl esters, most commonly as retinyl palmitate.

Vitamin A can be mobilized from the liver to peripheral tissue by a process of deesterification of the retinyl esters. In blood, vitamin A is bound to RBP, which transports it as a complex with transthyretin. The hepatic synthesis of RBP is dependent on the presence of zinc and amino acids to maintain its narrow serum range of 40-50 mcg/dL. Through a receptor-mediated process, the retinol is taken up by the peripheral tissues from the RBP-transthyretin complex.

VAD may be secondary to decreased ingestion, defective absorption and altered metabolism, or increased requirements. An adult liver can store up to a year's reserve of vitamin A, whereas a child's liver may have enough stores to last only several weeks. Serum retinol concentration reflects an individual's vitamin A status. Because serum retinol is homeostatically controlled, its levels do not drop until the body's stores are significantly limited. The serum concentration of retinol is affected by several factors, including RBP synthesis in the liver, infection, nutritional status, and the existing level of other nutrients, such as zinc and iron.4

In zinc deficiency, impaired synthesis of proteins occurs with rapid turnover (eg, RBP). In turn, this impairment affects retinol transport by RBP from the liver to the circulation and to other tissues. The mechanism by which iron affects vitamin A metabolism has not been identified, but randomized, double-blind studies have shown that vitamin A supplementation alone is not sufficient to improve VAD in the presence of coexisting iron deficiency.

The bioavailability of the carotenoids varies; this availability depends on absorption and on their yield of retinol. Only 40-60% of ingested beta carotene from plant sources is absorbed by the human body, whereas 80-90% of retinyl esters from animal proteins are absorbed. Carotenoid absorption is affected by dietary factors, including zinc deficiency, abetalipoproteinemia, and protein deficiency.

Because vitamin A is a fat-soluble vitamin, any GI diseases affecting the absorption of fats also affect vitamin A absorption. Patients with cystic fibrosis, sprue, pancreatic insufficiency, inflammatory bowel disorder (IBD), or cholestasis, as well as persons who have undergone small-bowel bypass surgery, are at increased risk for VAD. These patients should be advised to consume vitamin A.

One factor affecting the metabolism of vitamin A is alcoholism. Alcohol dehydrogenase catalyzes the conversion of retinol to retinaldehyde, which is then oxidized to retinoic acid. The affinity of alcohol dehydrogenase to ethanol impedes the conversion of retinol to retinoic acid.

Increased requirements of vitamin A most commonly occur among sick children. The American Academy of Pediatrics has recommended vitamin A supplementation for infants aged 6-24 months who are hospitalized with measles and for all hospitalized children older than 6 months. In the 1960s, the World Health Organization (WHO) undertook the first global survey of VAD with associated xerophthalmia and complicated measles.5 In 1973, an international vitamin A board was set up to alleviate global malnutrition.

The WHO and the United Nations International Children's Emergency Fund (UNICEF) have issued joint statements recommending that vitamin A be administered to all children, especially those younger than 2 years, who are diagnosed with measles. Coexistent VAD in young children increases the risk of death. The Cochrane Database Systemic Review concluded that daily treatment with 200,000 IU of vitamin A for at least 2 days reduces mortality rates.6,7

Pregnant women do not require increased vitamin A supplementation. In fact, the Teratology Society advocates that women be informed of the possible risk of cranial neural crest defects and other malformations resulting from excessive use of vitamin A shortly before or during pregnancy.8 The recommended daily allowance (RDA) of 800 mcg for all adult females is also appropriate for pregnant women, because their stores of vitamin A meet the fetal accretion rate. The requirements for lactating women have been debated, but the current RDA is 1300 mcg in the first 6 months and 1200 mcg in the second 6 months.

The RDAs of vitamin A for various age groups are as follows:

* Infants aged 1 year or younger - 375 mcg
* Children aged 1-3 years - 400 mcg
* Children aged 4-6 years - 500 mcg
* Children aged 7-10 years - 700 mcg
* All males older than 10 years - 1000 mcg
* All females older than 10 years - 800 mcg

Frequency
United States

Statistics from the US Centers for Disease Control and Prevention, based on a 1988-1991 survey, showed that age-specific intakes of carotenes were higher among males than females during that period and were higher among adults than children.9 Significant differences in intake existed among different ethnic groups.
International

Clinical and subclinical VAD are problems in at least 75 countries.10 In 1994, the WHO classified countries as having clinical or subclinical, severe, moderate, or mild VAD. Clinical VAD (in which children demonstrate ophthalmic signs and symptoms, including blindness) occurs mainly in countries in Southeast Asia and sub-Saharan Africa.5 Severe VAD is also found in persons in refugee settlements and in displaced populations.
Mortality/Morbidity

* United States - VAD is uncommon in the general population, but subgroups of patients suffering from fat malabsorption, cholestasis, or IBD or who have undergone small-bowel bypass may have subclinical deficiency with dark-adaptation abnormalities in the range of 60%. Vegans, persons with alcoholism, toddlers and preschool children living below the poverty line, and recent immigrants or refugees from developing countries all have increased risk of VAD secondary to decreased ingestion.
* Developing countries - An estimated 250 million children are at risk for vitamin deficiency syndromes. The most widely affected group includes up to 10 million malnourished children, who develop xerophthalmia and have an increased risk of complications and death from measles. Each year, 250,000-500,000 children become blind because of VAD. Improving the vitamin A status of children with deficiencies (aged 6-59 mo) can reduce measles and diarrhea mortality rates by 50% and 33%, respectively, and can decrease risk rates from all causes of mortality by 23%.

Clinical
History

Subclinical forms of VAD may not cause any symptoms, but the risk of developing respiratory and diarrheal infections is increased, the growth rate is decreased, and bone development is slowed. Patients may have a recent history of increased infections, infertility secondary to impaired spermatogenesis, or recent spontaneous abortion secondary to impaired embryonic development. The patient may also report increased fatigue, as a manifestation of VAD anemia.
Physical

Signs and symptoms of vitamin A deficiency include the following:

* Bitot spots - Areas of abnormal squamous cell proliferation and keratinization of the conjunctiva can be seen in young children with VAD.
* Blindness due to retinal injury - Vitamin A has a major role in phototransduction. The cone cells are responsible for the absorption of light and for color vision in bright light. The rod cells detect motion and are responsible for night vision. In the rod cells of the retina, all-trans-retinol is converted into 11-cis -retinol, which then combines with a membrane-bound protein called opsin to yield rhodopsin.11 A similar type of reaction occurs in the cone cells of the retina to produce iodopsin. The visual pigments absorb light at different wavelengths, according to the type of cone cell they occupy. VAD leads to a lack of visual pigments; this reduces the absorption of various wavelengths of light, resulting in blindness.
* Poor adaptation to darkness (nyctalopia)
* Dry skin
* Dry hair
* Pruritus
* Broken fingernails
* Keratomalacia
* Xerophthalmia
* Corneal perforation
* Follicular hyperkeratosis (phrynoderma) secondary to blockage of hair follicles with plugs of keratin.
* Other signs of VAD include excessive deposition of periosteal bone secondary to reduced osteoclastic activity, anemia, keratinization of mucous membranes, and impairment of the humoral and cell-mediated immune system.

Causes

The risk of VAD is increased in patients suffering from fat malabsorption, cystic fibrosis, sprue, pancreatic insufficiency, IBD, or cholestasis, as well as in persons who have undergone small-bowel bypass surgery. The risk is also increased in vegans, refugees, recent immigrants, persons with alcoholism, and toddlers and preschool children living below the poverty line. These patients should be advised to consume vitamin A.

http://emedicine.medscape.com/article/126004-overview

Head Trauma

2010-01-21T07:47:00.000+07:00

Introduction

Traumatic brain injury (TBI) continues to be an enormous public health problem, even with modern medicine in the 21st century. Most patients with TBI (75-80%) have mild head injuries; the remaining injuries are divided equally between moderate and severe categories.

The cost to society of TBI is staggering, from both an economic and an emotional standpoint. Almost 100% of persons with severe head injury and as many as two thirds of those with moderate head injury will be permanently disabled in some fashion and will not return to their premorbid level of function. In the United States, the direct cost of care for patients with TBI, excluding inpatient care, is estimated at more than $25 billion annually. The impact is even greater when one considers that most severe head injuries occur in adolescents and young adults.

For excellent patient education resources, visit eMedicine's Back, Ribs, Neck, and Head Center, Back, Neck, and Head Injury Center, and Eye and Vision Center. Also, see eMedicine's patient education articles Concussion, Bicycle and Motorcycle Helmets, and Black Eye.
Frequency

The annual incidence of TBI in the United States has been estimated to be 180-220 cases per 100,000 population. In the United States, with a population of almost 300 million, approximately 600,000 new TBIs occur per year. As many as 10% of these injuries are fatal, resulting in almost 550,000 persons hospitalized annually in the United States with head injuries.
Etiology

While various mechanisms may cause TBI, the most common causes include motor vehicle accidents (eg, collisions between vehicles, pedestrians struck by motor vehicles, bicycle accidents), falls, assaults, sports-related injuries, and penetrating trauma.

Motor vehicle accidents account for almost half of the TBIs in the United States, and in suburban/rural settings, they account for most TBIs. In cities with populations greater than 100,000, assaults, falls, and penetrating trauma are more common etiologies of head injury.

The male-to-female ratio for TBI is nearly 2:1, and TBI is much more common in persons younger than 35 years.

Motorcycle-related head injury

Motorcycle-related head injuries deserve special mention. Motorcycle rights organizations dedicated to promoting safety and to preserving individual freedom suggest that safety should be a choice rather than a requirement; safety is a good choice, but individual motorcyclists should have the right to make a bad choice that ends in disaster if they so choose. A hallmark of the antihelmet movement is the argument that motorcyclists who do not wear helmets can perceive (ie, see and hear) their environment more effectively and, thus, can avoid impending accidents by anticipating them earlier. This argument is fallacious.

Most accidents involving adult, otherwise responsible, motorcyclists are caused by moving objects hitting motorcyclists or by motorcyclists hitting a stationary object after being forced into an unusual position in an attempt to avoid something in their path. A full-face helmet restricts a relatively small portion of inconsequential downward and lateral peripheral vision. Similarly, it is highly improbable that a motorcyclist will hear an impending accident. A marginal increase in the ability to hear road noise and to see downward and laterally is not an improvement in the ability to avoid most accidents.

The medical literature regarding motorcyclists’ head injury is clear. Head trauma is a devastating injury for motorcyclists and their families, and rehabilitation for survivors is prolonged and expensive. Injury expenses for motorcyclists who do not wear helmets far exceed that of motorcyclists who wear helmets. More importantly, the burden of caring for a motorcyclist with a head injury is frequently borne by the taxpayers, regardless of the insurance status of the injured motorcyclist.
Pathophysiology

Appropriate management of TBI requires an understanding of the pathophysiology of head injury. In addition to the obvious functional differences, the brain has several features that distinguish it from other organ systems. The most important of these differences is that the brain is contained within the skull, a rigid and inelastic container. Because the brain is housed within this inelastic container, only small increases in volume within the intracranial compartment can be tolerated before pressure within the compartment rises dramatically. This concept is defined by the Monro-Kellie doctrine, which states that the total intracranial volume is fixed because of the inelastic nature of the skull. The intracranial volume (V i/c) is equal to the sum of its components, as follows:

V i/c = V (brain) + V (cerebrospinal fluid) + V (blood)

In the typical adult, the intracranial volume is approximately 1500 mL, of which the brain accounts for 85-90%, intravascular cerebral blood volume accounts for 10%, and cerebrospinal fluid (CSF) accounts for the remainder (<3%). When a significant head injury occurs, cerebral edema often develops, which increases the relative volume of the brain. Because the intracranial volume is fixed, the pressure within this compartment rises unless some compensatory action occurs, such as a decrease in the volume of one of the other intracranial components. This is intimately related to the concept of intracranial compliance, which is defined as the change in pressure due to changes in volume.

Compliance = Change in volume / change in pressure

Compliance is based on the pressure volume index (PVI) within the intracranial compartment. The PVI describes the change in intracranial pressure (ICP) that occurs when a small amount of fluid is added to or withdrawn from the intracranial compartment. Simply stated, the brain has very limited compliance and cannot tolerate significant increases in volume that can result from diffuse cerebral edema or from significant mass lesions, such as a hematoma. The rationale for each treatment of head injury is based on the concept of the Monro-Kellie doctrine and how a particular intervention affects the intracranial compliance. When the volume of any of the components of the total intracranial volume is decreased, the ICP may be decreased.

A second crucial concept in TBI pathophysiology is the concept of cerebral perfusion pressure (CPP). CPP is defined as the difference between the mean arterial pressure (MAP) and the ICP.

CPP = MAP - ICP

In practical terms, CPP is the net pressure of blood delivery to the brain. In the noninjured brain in individuals without long-standing hypertension, cerebral blood flow (CBF) is constant in the range of MAPs of 50-150 mm Hg. This is due to autoregulation by the arterioles, which will constrict or dilate within a specific range of blood pressure to maintain a constant amount of blood flow to the brain.

When the MAP is less than 50 mm Hg or greater than 150 mm Hg, the arterioles are unable to autoregulate and blood flow becomes entirely dependent on the blood pressure, a situation defined as pressure-passive flow. The CBF is no longer constant but is dependent on and proportional to the CPP. Thus, when the MAP falls below 50 mm Hg, the brain is at risk of ischemia due to insufficient blood flow, while a MAP greater than 160 mm Hg causes excess CBF that may result in increased ICP. While autoregulation works well in the noninjured brain, it is impaired in the injured brain. As a result, pressure-passive flow occurs within and around injured areas and, perhaps, globally in the injured brain.

TBI may be divided into 2 categories, primary brain injury and secondary brain injury. Primary brain injury is defined as the initial injury to the brain as a direct result of the trauma. This is the initial structural injury caused by the impact on the brain, and, like other forms of neural injury, patients recover poorly. Secondary brain injury is defined as any subsequent injury to the brain after the initial insult. Secondary brain injury can result from systemic hypotension, hypoxia, elevated ICP, or as the biochemical result of a series of physiologic changes initiated by the original trauma. The treatment of head injury is directed at either preventing or minimizing secondary brain injury.

Elevated ICP may result from the initial brain trauma or from secondary injury to the brain. In adults, normal ICP is considered 0-15 mm Hg. In young children, the upper limit of normal ICP is lower, and this limit may be considered 10 mm Hg. Elevations in ICP are deleterious because they can result in decreased CPP and decreased CBF, which, if severe enough, may result in cerebral ischemia. Severe elevations of ICP are dangerous because, in addition to creating a significant risk for ischemia, uncontrolled ICP may cause herniation. Herniation involves the movement of the brain across fixed dural structures, resulting in irreversible and often fatal cerebral injury.

Maloney-Wilensky et al found that in patients with TBI, brain hypoxia as measured by brain tissue oxygen levels is associated with worse outcome.1 Their review showed that, in 150 patients with severe TBI, those with brain tissue oxygen levels below 10 mm Hg had worse outcomes (odds ratio [OR], 4.0) and higher mortality (OR, 4.6). However, use of direct brain tissue oxygen probes proved to be safe, with only 2 adverse events in 292 patients.1 The researchers suggest that treatment to increase brain tissue oxygen levels deserves investigation as a possible means of improving outcome in severe TBI.
Presentation

TBI may be divided into 2 broad categories, closed head injury and penetrating head injury. This is not purely a mechanistic division because some aspects of the treatment of these 2 types of TBIs differ. The clinical presentation of the patient with TBI varies significantly, from an ambulatory patient complaining of a sports-related head injury to the moribund patient arriving via helicopter following a high-speed motor vehicle accident.

The Glasgow Coma Scale (GCS) developed by Jennett and Teasdale is used to describe the general level of consciousness of patients with TBI and to define broad categories of head injury.2 The GCS is divided into 3 categories, eye opening (E), motor response (M), and verbal response (V). The score is determined by the sum of the score in each of the 3 categories, with a maximum score of 15 and a minimum score of 3, as follows:

GCS score = E + M + V

Glasgow Coma Scale

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Table
Eye Opening
Score 1 Year or Older 0-1 Year
4 Spontaneously Spontaneously
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best Motor Response
Score 1 Year or Older 0-1 Year
6 Obeys command

5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
Best Verbal Response
Score >5 Years 2-5 Years 0-2 Years
5 Oriented and converses Appropriate words Cries appropriately
4 Disoriented and converses Inappropriate words Cries
3 Inappropriate words; cries Screams Inappropriate crying/screaming
2 Incomprehensible sounds Grunts Grunts
1 No response No response No response
Eye Opening
Score 1 Year or Older 0-1 Year
4 Spontaneously Spontaneously
3 To verbal command To shout
2 To pain To pain
1 No response No response
Best Motor Response
Score 1 Year or Older 0-1 Year
6 Obeys command

5 Localizes pain Localizes pain
4 Flexion withdrawal Flexion withdrawal
3 Flexion abnormal (decorticate) Flexion abnormal (decorticate)
2 Extension (decerebrate) Extension (decerebrate)
1 No response No response
Best Verbal Response
Score >5 Years 2-5 Years 0-2 Years
5 Oriented and converses Appropriate words Cries appropriately
4 Disoriented and converses Inappropriate words Cries
3 Inappropriate words; cries Screams Inappropriate crying/screaming
2 Incomprehensible sounds Grunts Grunts
1 No response No response No response

Patients who are intubated are unable to speak, and their verbal score cannot be assessed. They are evaluated only with eye opening and motor scores, and the suffix T is added to their score to indicate intubation. In intubated patients, the maximal GCS score is 10T and the minimum score is 2T. The GCS is often used to help define the severity of TBI. Mild head injuries are generally defined as those associated with a GCS score of 13-15, and moderate head injuries are those associated with a GCS score of 9-12. A GCS score of 8 or less defines a severe head injury. These definitions are not rigid and should be considered as a general guide to the level of injury.
Indications

Traumatic injury and brain failure

As a type of organ system failure, brain failure invariably affects consciousness. Consciousness is structurally produced in the cerebral hemispheres, including the pons and the medulla. These structures are all interconnected by the reticular formation, which begins in the medulla and extends to the midbrain, where it forms the reticular activating system. This pathway modulates the perception of events and controls integrated responses.

Clinical evaluation of consciousness states is heavily dependent on the findings from the physical examination. When the physical examination yields visual and palpable clues to the integrity of consciousness, impairment thereof may be classified into one of the following categories:

* Cloudy consciousness: This state is defined as a mild deficit in the speed of information processing by the brain. This results from macrotearing and histological-level disruption of cell-to-cell connectivity occurring throughout the brain disrupting physical connectivity between brain regions, exacerbated by vascular compromise of a mechanical and/or biochemical nature causing islands of nonfunctional or impaired tissue in the brain parenchyma. Cloudy consciousness may be noted after mild-to-moderate head trauma and may persist for several months. Memory of recent events is often diminished, but long-term memory typically remains intact.
* Lethargy: This state is defined as a decrease in alertness, resulting in impaired ability to perform tasks that are normally accomplished without effort. Patients rouse briefly in response to stimuli and then settle back into inactivity when left alone. They retain awareness of their immediate environment.
* Obtundation: This state is defined as a decrease in awareness and alertness, in which patients rouse briefly in response to stimuli and follow simple commands but are unaware of their immediate surroundings. When stimulation ceases, they settle back into inactivity.
* Stupor: In this state, patients cannot communicate clearly but can be aroused by continued painful stimulation. Arousal may be manifested only as withdrawal from painful stimuli. As soon as stimuli are removed, the patient settles back into inactivity.
* Coma: In this state, patients do not respond to even the most vigorous stimuli.
* Brain death: This state is equivalent to functional decapitation and is characterized by irreversible cessation of whole-brain function and hemisphere and brainstem function.

The efficacy of the physical examination in the evaluation of consciousness diminishes when visual clues disappear (eg, during heavy sedation, therapeutic musculoskeletal paralysis). In such situations, monitoring of cerebral function by compressed spectral array is helpful in assessing the effect of therapy on neuronal function.
Processed electroencephalogram (compressed spectral array) in consciousness assessment

The processed electroencephalogram (EEG) does not require as many head electrodes to generate a satisfactory signal that can be used for clinical data in the intensive care unit (ICU). Brain wave monitoring by portable, noninvasive computer processed monitors allow quick recognition of some brain functions under titrated suspended animation in real time. These parameters are not effectively evaluated by raw signal EEG monitors, but some progress has been made using computerized processed signal EEGs. Advantages of the processed EEG during neuromuscular blockade are that data are more easily interpreted by clinicians not specifically trained in electroencephalography.

The continuum from wakefulness to sleep involves a progressive decrease in the alpha band followed by increased activity in the beta, theta, and delta bands. The alpha rhythm contains waves of 8-12 Hz and is very responsive to volitional mental activity, increasing with excitement and decreasing with tranquility. These rhythms occur mainly in the posterior head and are the predominant brain activity in the normal brain.

A technique has been developed to simplify pattern recognition and interpretation of the brain electrical activity using the key word SAFE:

* S - SYMMETRY - Compare the pattern of asymmetrical patterns. Can indicate diminished perfusion to one hemisphere, cerebral embolism, or thrombosis.
* A - AMPLITUDE - Compare the altitude of the vectors. Asymmetric hemispherical amplitude suggests agitation under paralysis. Low amplitude suggests sedation and quiescence.
* F - FREQUENCY - Compare the distribution of vectors throughout all frequency bands. Absent or attenuated activity in the “conscious” side suggests sedation or anesthesia.
* E - EDGE - Observe the activity edge. Significant dips in one hemisphere compared to the other suggest focal brain ischemia.

Agitation is represented by linear activity depicting intensity of brain activity and position of this activity within the brain topography. Sedation can be effectively titrated until this activity is reduced to normalcy using continuous infusion of sedative agents, while ensuring patient comfort under paralysis as the search for underlying pathology follows. Different classifications and combinations of sedatives, analgesics, or antipsychotics can be tried until the combination that brings about the most appropriately calm cerebral function tracing is discovered. Attention can then be turned to protecting other organs from damage.
Relevant Anatomy

Several aspects of neuroanatomy and neurophysiology require review in a discussion of TBI. Although a comprehensive review of neuroanatomy is beyond the scope of this discussion, a few key concepts are reviewed.

The brain essentially floats within the CSF; as a result, the brain can undergo significant translation and deformation when the head is subjected to significant forces. In a deceleration injury, in which the head impacts a stationary object, such as the windshield of a car, the skull stops moving almost instantly. However, the brain continues to move within the skull toward the direction of the impact for a very brief period after the head has stopped moving. This results in significant forces acting on the brain as it undergoes both translation and deformation.

In an acceleration injury, as in a direct blow to the head, the force applied to the skull causes the skull to move away from the applied force. The brain does not move with the skull, and the skull impacts the brain, causing translation and deformation of the brain. The forces that result from either deceleration or acceleration of the brain can cause injury by direct mechanical effects on the various cellular components of the brain or by shear-type forces on axons. In addition to the translational forces, the brain can experience significant rotational forces, which can also lead to shear injuries.

The intracranial compartment is divided into 3 compartments by 2 major dural structures, the falx cerebri and the tentorium cerebelli. The tentorium cerebelli divides the posterior fossa or infratentorial compartment (the cerebellum and the brainstem) from the supratentorial compartment (cerebral hemispheres). The falx cerebri divides the supratentorial compartment into 2 halves and separates the left and right hemispheres of the brain. Both the falx and the tentorium have central openings and prominent edges at the borders of each of these openings. When a significant increase in ICP occurs, caused by either a large mass lesion or significant cerebral edema, the brain can slide through these openings within the falx or the tentorium, a phenomenon known as herniation. As the brain slides over the free dural edges of the tentorium or the falx, it is frequently injured by the dural edge.

Several types of herniation exist, as follows: (1) transtentorial herniation, (2) subfalcine herniation, (3) central herniation, (4) upward herniation, and (5) tonsillar herniation.

Transtentorial herniation occurs when the medial aspect of the temporal lobe (uncus) migrates across the free edge of the tentorium. This causes pressure on the third cranial nerve, interrupting parasympathetic input to the eye and resulting in a dilated pupil. This unilateral dilated pupil is the classic sign of transtentorial herniation and usually (80%) occurs ipsilateral to the side of the transtentorial herniation. In addition to pressure on the third cranial nerve, transtentorial herniation compresses the brainstem.

Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx. This may compromise the blood flow through the anterior cerebral artery complexes, which are located on the medial side of each frontal lobe. Subfalcine herniation does not cause the same brainstem effects as those caused by transtentorial herniation.

Central herniation occurs when a diffuse increase in ICP occurs and each of the cerebral hemispheres is displaced through the tentorium, resulting in significant pressure on the upper brainstem.

Upward, or cerebellar, herniation occurs when either a large mass or an increased pressure in the posterior fossa is present and the cerebellum is displaced in an upward direction through the tentorial opening. This also causes significant upper brainstem compression.

Tonsillar herniation occurs when increased pressure develops in the posterior fossa. In this form of herniation, the cerebellar tonsils are displaced in a downward direction through the foramen magnum, causing compression on the lower brainstem and upper cervical spinal cord as they pass through the foramen magnum.

Another aspect of the intracranial anatomy that has a significant role in TBI is the irregular surface of the skull underlying the frontal and temporal lobes. These surfaces contain numerous ridges that can cause injury to the inferior aspect of the frontal lobes and the temporal lobes as the brain glides over these irregular ridges following impact. Typically, these ridges cause cerebral contusions. The roof of the orbit has many ridges, and, as a result, the inferior frontal lobe is one of the most common sites of traumatic cerebral contusions.

http://emedicine.medscape.com/article/433855-overview

Burns, Thermal

2010-01-21T07:45:00.000+07:00

Introduction
Background

Burn injuries account for an estimated 700,000 annual ED visits per year. Of these, 45,000 require hospitalization. Approximately half of these patients are hospitalized at one of the 125 specialized burn treatment centers in the United States.

Most burns are not life threatening, but each burn causes a significant amount of pain for the patient and often some degree of psychological trauma. At temperatures greater than 120 º F, a child's skin is burned severely enough to require surgery in 3 seconds. Rapid evaluation by the emergency physician (EP) is essential to address pain management, provide initial wound care, evaluate appropriate disposition, mitigate the psychological impact of the burn, and identify intentional burns. Follow-up for even superficial thickness burns is imperative, particularly when involving the hands, feet, face, genital area, or other particularly sensitive areas.

To effectively evaluate, treat, and prevent potential future burns, understanding the different methods of categorizing burns is helpful. The general categories include life-threatening versus non–life-threatening, accidental versus intentional, recreational versus occupational, and domestic (home or residence) versus industrial.

Identifying the type of burn is essential because interventions must be appropriately tailored to the underlying cause. Type of burns include thermal burns, chemical burns, and radiation burns. Thermal burns can be further classified according to skin depth and percentage of total body area burned. Additional descriptions for thermal burns include contact, flame, heat, and scalding. Accurate documentation of the burn location (such as ophthalmic, hand, face, inhalation, soles, or perineum) and measurement of involved surface area are essential for follow-up and specialist referral/consultation.
Pathophysiology

The skin is the largest organ of the body. Although not very active metabolically, the skin serves multiple functions essential to the survival of the organism, which may be compromised by the presence of a burn, including the following:

* Thermal regulation and prevention of fluid loss by evaporation
* Hermetic barrier against infection
* Sensory receptors that provide information about environment

The skin is divided into 3 layers, as follows:

* Epidermis: This is the outermost layer of skin composed of cornified epithelial cells. Outer surface cells die and are sloughed off as newer cells divide at the stratum germinativum.
* Dermis: This is the middle layer of skin composed of primarily connective tissue. It contains capillaries that nourish the skin, nerve endings, and hair follicles.
* Hypodermis: This is a layer of adipose and connective tissue between the skin and underlying tissues.

The most common type of burns are thermal burns. Soft tissue is burned when it is exposed to temperatures above 115ºF (46°C). The extent of damage depends on surface temperature and contact duration. A thermal burn causes coagulation of soft tissue. As the marginally perfused areas become reperfused, it is thought that there is a release of vasoactive substances causing formation of reactive oxygen species, which leads to increases in capillary permeability. This causes fluid loss as well as increasing plasma viscosity with resultant microthrombi formation.1

This third spacing of fluid "seals" at 18-24 hours, which is why the guidelines for fluid resuscitation are based on a 24-hour time scale. After the initial 24 hours, the fluid requirements abruptly drop as the capillary permeability returns to normal. Underresuscitation in this initial 24-hour time period leads to significant morbidity from hypovolemia and shock.

Burns may cause a hypermetabolic state manifested by fever, increased metabolic rate, increased minute ventilation, increased cardiac output, decreased afterload, increased gluconeogenesis resistant to glucose infusion, and increased skeletal and visceral muscle catabolism. Patients need support in this state, which continues until wound closure is complete.1 To a large degree, how the individual responds to the increased energy demands determine recovery.
Frequency
United States

Nearly one million Americans seek ED treatment of burns each year. According to data provided by the American Burn Association, the incidence of burn injuries in the United States has declined from 2 million annual injuries estimated from 1957-1961.

According to 2007 data from the US Fire Administration, in 2006, 3,245 Americans lost their lives, and another 16,400 were injured as the result of fire. Notably, although the number of fires and deaths due to fires has decreased from 1997 to 2006, the direct dollar loss in millions has significantly increased from $8,525 to $11,307. Not included in these data are the deaths or the monetary value attributed to fires caused by the terrorist attacks of September 11, 2001. In 2002-2004, the United States had one of the highest fire death rates reported in the industrialized world at 12.4 deaths per million population, a slight decrease from 12.9 deaths per million population last reported in 2003.2 Most of these fatalities (79.5%) occurred in the home.

Slightly different findings were released by the World Fire Statistics in 2007.3 They reported that the fire-related death rate in the United States was 1.39 deaths per 100,000 (18.6 per million) in the years 2002-2004. For comparison, fire-related death rates per 100,000 were higher in Finland and Hungary at 2.08 and 2.10, respectively.

States with the highest death rates in 2004 were the District of Columbia (36.1 per million), Mississippi (32.1 per million), and Alabama (25.6 per million). The states with the lowest rates were Colorado (4.3 per million), Vermont (3.2 per million), and Wyoming (2 per million).2 Interestingly, in 2006, fire killed more Americans than all natural disasters combined.2

From 1990-2006, an estimated 2,054,563 patients aged 20 years or younger were treated in US EDs for burn-related injuries, with an average of 120,856 cases per year.4
International

The incidence of burn injuries varies from country to country, typically peaking during the country's holiday period.

In 2007, the World Fire Statistics Centre released fire-related death data by country (from lowest to highest number of deaths per 100,000 person) from 2002-2004.3 The countries with the lowest incidences include Singapore (0.08) and Switzerland (0.51). Those with the highest include Finland (2.08) and Hungary (2.10).3

In the United Kingdom, more than 47 fire-related injuries occur every day.

In Greece, the estimated annual incidence of childhood firework injuries treated in EDs is 7 injuries per 100,000 children per year. Seventy percent of injuries occur in children aged 10-14 years. Boys sustain self-inflicted accidental injuries; girls are typically injured as bystanders. A sharp peak of firework injuries occurs in the spring when the Greek Orthodox Easter is celebrated.5

Interesting data from Northern Ireland allows a comparison of burn incidence before and after the enactment of firework legislation. In the prelegislation series, the mean number of patients admitted annually was 0.38 per 100,000, whereas in the postlegislation series, the mean was 0.43 per 100,000. The authors concluded that legislation did not significantly affect the incidence of burns. Also in Northern Ireland, blast injuries to the hand account for more than 50% of injuries in this series.6
Mortality/Morbidity

Although fire-related deaths still rank fifth in the leading causes of unintentional injury-related deaths,7 the number of deaths from fires and burns has declined since the 1960s. Improvements in burn care (ie, quality burn centers, recognition, and effective management of burn shock) have reduced the number of deaths in the early postburn period. Improved wound management and antibiotics have decreased deaths from burn wound infection as well. The legislature has passed acts aimed at the prevention of injury due to fires. In 1971, the Flammable Fabrics Act was passed in an attempt to regulate the sale of flammable children’s clothing, especially that of sleepwear in infants, as it was noted to be a major cause of morbidity and mortality. Over time, this decreased the number of fire-related deaths and injuries in children.8

However, the greatest factors in the reduction of burn-related deaths is the use of smoke detectors and regulations on hot water heater temperature. In the United States, most people killed in house fires die from smoke inhalation rather than from burns (see Smoke Inhalation and Toxicity, Carbon Monoxide).

Race

Native American and black children are more than 2 times and 3 times as likely to die in a fire than white children, respectively.7 Black children and adolescents had the highest rates of burn and fire-related deaths. This is attributed to the decreased likelihood of minorities to engage in safe practices (fireplace guards, smoke alarm use, and adjusting water heater temperature).7
Age

Minor burns are more common in younger adults, often as a result of cooking or occupational exposures. Teenaged males are at increased risk of injury from fireworks; scald injuries are more common in young children. Most scald injuries in young children result from improper setting of domestic hot water heaters and spillage of cooking pots or beverages. Both types of injuries are easily prevented.

Most children aged 4 years and younger who are hospitalized for burn-related injuries suffer from scald burns (65%) or contact burns (20%). Most scald burns to children, especially small children aged 6 months to 2 years, are caused by hot foods or liquids spilled in the kitchen or other areas where food is prepared and served.

Water heater temperature must be set lower than 120°F. Within 3 seconds, a child's skin can be burned severely enough to require surgery when they are scalded with water temperature greater than 120°F.

The EP must consider intentional injury when burn patterns, such as absence of splash marks, stocking glove distribution, sharply defined wound margins, soles, palms, and pinpoint "cigarette ash" burns, are identified. Children aged 4 years and younger and children with disabilities are at the greatest risk of burn-related death and injury, especially scald and contact burns.

The leading cause of residential fire-related death and injury among children aged 9 years and younger is due to carelessness. Fires kill more than 600 children aged 14 years and younger each year and injure approximately 47,000 other children. Approximately 88,000 children aged 14 years and younger were treated at hospital EDs for burn-related injuries; 62,500 were thermal burns and 25,500 were scald burns. The most common causes of product-related thermal burn injuries among children aged 14 years and younger are hair curlers, curling irons, room heaters, ovens and ranges, irons, gasoline, and fireworks.

Elderly persons are also at increased risk not only for having a burn-related injury but for having increased morbidity due to their thinner skin and decreased healing abilities.
Clinical
History

The EP must consider the type of burn (thermal, chemical, radiation) and the location during early burn management. Once it has been determined that the burn is a thermal burn, the EP can add to the description: contact (with source name), scald (with fluid or gas type), heat, and flame. Systemic injury, duration, intentional versus accidental, and location of the burn must all be considered during the critical early burn period.

Other important points to determine include the patient's tetanus immunization status as well as the components of the history including past medical history, medications, and allergies.

Ascertain the history early because often the paramedics may be the only source of information about the event.

History should also include the following:

* Medical personnel must consider abuse as a cause of burns in all children. As many as 10% of abuse cases involve burns (see Pediatrics, Child Abuse).
* Components of the history that should raise suspicion of abuse include the
o Multiple/conflicting stories of how injury was sustained
o Injury attributed to a sibling
o Injury claimed to be unwitnessed
o Injury incompatible with developmental level of the child
o Presence of adult male who is not child's father (such as mother's boyfriend) living in household
* Characteristics of the burn that should raise suspicion of abuse include the following:
o Pattern burns that suggest contact with an object
o Cigarette burns
o Stocking, glove, or circumferential burns
o Burns to genitalia or perineum
* All health care personnel are obligated to contact appropriate law enforcement and protective services if they suspect the burn was intentional.
* Medical personnel must be aware that burns resulting from abuse or neglect may also be seen in the geriatric population.

Physical

* Burn depth is described as superficial, partial thickness, or full thickness (corresponding to first, second, or third degree). (See Causes for more information.)
* Superficial (first-degree) burns involve only the epidermis.
o Tissue blanches with pressure.
o Tissue is erythematous.
o Tissue damage is minimal.
o Edema may be present; generally blisters do not form.
o Sunburn is a classic example of this type of burn (see Sunburn for more details and management).
o These wounds are red, dry, painful, and generally heal in 3-6 days without scarring.9
* Partial-thickness burns (second-degree) are often further delineated into superficial and deep types.;
o Epidermis and portions of the dermis are involved.
o Blisters usually form either very quickly or within 24 hours.
o Superficial and deep partial-thickness can be difficult to differentiate at the bedside. The difference lies in the depth of penetrance into the dermis with the transition occurring at about half of dermal depth. Superficial partial-thickness burns usually blanch and do not result in scarring. Deep partial-thickness burns often do not blanch and do scar. The deeper the injury, the longer the healing time, which may vary from 7-21 days in the more superficial dermis burns to greater than 21 days in the deep dermis burns.
o Adnexal structures (eg, sweat glands, hair follicles) are often involved, but enough of these structures are preserved for function, and the epithelium lining them can proliferate and allow for regrowth of skin.
o If deep second-degree burns are not cared for properly, edema, which accompanies the injury, and decreased blood flow in the tissue can result in conversion to full-thickness burn.
o These wounds are red, wet, and painful (with decreasing pain, color, and moisture with increasing depth into the dermis).9
* Full-thickness (third-degree) burns extend completely through the skin to subcutaneous tissue. They may involve underlying structures including tendon, nerves, muscle, or bone (sometimes previously referred to as fourth-degree burn). Full-thickness and partial thickness burns are shown in the image below.
*

Partial- and full-thickness burns from a structur...
Partial- and full-thickness burns from a structure fire. Note facial involvement.

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Partial- and full-thickness burns from a structur...

Partial- and full-thickness burns from a structure fire. Note facial involvement.

o These burns are characterized by charring of skin or a translucent white color, with coagulated vessels visible below.
o The area is insensate, but the patient complains of pain, which is usually a result of surrounding second-degree burn.
o As all of the skin tissue and structures are destroyed, healing is very slow. Full-thickness burns are often associated with extensive scarring because epithelial cells from the skin appendages are not present to repopulate the area.
o These wounds vary from waxy white, to charred and black often with a leathery texture, they are dry and usually painless to touch. These wounds generally do not heal on their own.9
* Burn extent
o The more body surface area (BSA) involved in a burn, the greater the morbidity and mortality rates and the difficulty in management. Emergency medical services (EMS) personnel tend to overestimate the extent of the burn, whereas ED personnel tend to underestimate it.
o An individual's palmar surface classically represents 1% of the BSA, but, in actuality, it represents about 0.4%, whereas the entire hand represents about 0.8%.10,11 A simple method to estimate burn extent is to use the patient's palmar surface including fingers to measure the burned area. Burn extent is calculated only on individuals with partial-thickness or full-thickness burn.
o Another quick method is to use the Rule of Nines to estimate the extent of burn injury (as is shown in the image below).
o

Rule of nines for calculating burn area.
Rule of nines for calculating burn area.

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Rule of nines for calculating burn area.

Rule of nines for calculating burn area.
o The head represents a greater portion of body mass in children than it does in adults. Lund and Browder first described a method for compensating for the differences, and the Lund and Browder Chart is used to calculate BSA in children (as is shown in the image below).
o

Lund and Browder chart illustrating the method fo...
Lund and Browder chart illustrating the method for calculating the percentage of body surface area affected by burns in children.

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Lund and Browder chart illustrating the method fo...

Lund and Browder chart illustrating the method for calculating the percentage of body surface area affected by burns in children.
o If the chart is unavailable, estimate BSA by the Rule of Nines and adjust for age as follows:
+ In children younger than 1 year, the head and neck are 18% of BSA and each leg is 15% of BSA. The torso and arms represent the same percentages as in adults (10% and 16%, respectively).
+ For each year older than 1 year, add 0.5% to each leg and decrease percentage for the head by 1% until adult values are reached.
* On the basis of burn extent and depth, EPs can determine the severity of burn injury and whether the patient requires transfer to a burn center. The American Burn Association has developed criteria for burn center admission, as follows:
o Full-thickness (third-degree) burns over 5% BSA
o Partial-thickness (second-degree) burns over 10% BSA
o Any full-thickness or partial-thickness burn involving critical areas (eg, face, hands, feet, genitals, perineum, skin over any major joint), as these have significant risk for functional and cosmetic problems
o Circumferential burns of the thorax or extremities
o Significant chemical injury, electrical burns, lightning injury, coexisting major trauma, or presence of significant preexisting medical conditions
o Presence of inhalation injury
o Greater than 15% BSA in adults
o Greater than 10% BSA in children
o Hand and foot burns can lead to significant morbidity if not properly treated; therefore, most are treated with aggressive therapy. However, with careful follow-up, the patient may be monitored on an outpatient basis.

Causes

* Flame burns
o Contact with open flame causes direct injury to tissue.
o Flame may ignite clothing. Although natural fibers tend to burn, synthetic fibers may melt or ignite, adding a contact burn component to the injury.
o If the burn occurs in an enclosed area, the patient is also at risk for CO poisoning and cyanide poisoning as well as inhalational injury from the smoke and heat.
* Contact burns
o Contact burns result from direct contact with a hot object.
o Burn injury is confined to the point of contact.
o Examples are burns from cigarettes and tools (eg, soldering irons, cooking appliances, curling irons).
* Scalds
o Scalds result from contact with hot liquids (as is shown in the image below).
o

Child with burns from a scald. Hot soup was spill...
Child with burns from a scald. Hot soup was spilled when the child grabbed the handle of a pot. Note the full-thickness burn to left upper part of the chest. Edema of the lips and blisters on the face and nose indicate second-degree burns of the face.

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Child with burns from a scald. Hot soup was spill...

Child with burns from a scald. Hot soup was spilled when the child grabbed the handle of a pot. Note the full-thickness burn to left upper part of the chest. Edema of the lips and blisters on the face and nose indicate second-degree burns of the face.
o The more viscous the liquid and the longer the contact with the skin, the greater the damage.
o Accidental scalds often show a pattern of splashing, with burns separated by patches of uninjured skin.
o In contrast, intentional scalds often involve the entire extremity, appearing in a circumferential pattern with a line that marks the liquid surface.
* Steam burns
o Steam burns most often occur in industrial accidents or result from automobile radiator accidents.
o These burns produce extensive injury from the high heat-carrying capacity of steam and the dispersion of pressurized steam and liquid.
o Steam inhalation can actually cause thermal injury to the distal airways of the lung.
* Gas burns
o Inhalation of hot gas normally does not injure distal airways, as the heat-exchange capacity of the upper airway is excellent.
o In this situation, the upper airway is at risk for thermal injury and subsequent occlusion due to edema.
o Distal airway injury is more likely to be due to the direct effects of the products of combustion on the mucosa and alveoli.
* Electrical burns, including lightning12
o Electrical burns produce heat injury by passing through tissue.
o Most problems from these burns present in patients exposed to more than 1000V.
o Children can have significant injury after exposure to 200-1000V.
o Ignition of clothing may produce some flame burn, but most of the injury is deep in the skin (see Electrical Injuries).
o Cardiac injury is prominent, and patients must be monitored for 4-72 hours depending on the strength of the voltage and the age of the patient.
o The EP must consider visceral injuries, long bone and spine fractures, myoglobinuria, and compartment syndromes.
* Flash burns
o Flash burns are a subset of flame burns and are a result of rapid ignition of a flammable gas or liquid.
o The body parts involved are those exposed to the agent when it ignites.
o Areas covered by clothing are usually spared.
o The face may be involved, but if this type of injury takes place outside, then the risk for inhalation injury is low. A careful examination of the airway is indicated.
o A classic example of this type of injury occurs when a person pours gasoline on a trash or leaf fire to increase the flame and is burned by the subsequent fireball.
* Tar burns (see Emergency Department Care)
* Chemical burns12
o Alkaline substances and acid substances can burn the skin and can be associated with systemic toxicity.
o Alkaline burns produce liquefactive necrosis and are considered higher risk burns due to their likelihood to penetrate deeper.
o Acid burns are the result of coagulation necrosis, limiting the depth and penetration of the burn.
o The upper GI tract and oropharynx may also be at risk if the chemicals were ingested; therefore, the EP should be aware that the airway may occlude due to edema.
o Circumoral burns may be present if the agent was ingested.

http://emedicine.medscape.com/article/769193-overview