Selasa, 24 November 2015

PENGARUH TERAPI OKSIGEN HIPERBARIK TERHADAP KADAR GULA DARAH PASIEN DIABETES MELLITUS DI INSTALASI KESEHATAN PENYELAMAN DAN HIPERBARIK KANTOR KESEHATAN PELABUHAN KELAS II MATARAM

PENGARUH TERAPI OKSIGEN HIPERBARIK TERHADAP KADAR GULA DARAH PASIEN DIABETES MELLITUS DI INSTALASI KESEHATAN PENYELAMAN DAN HIPERBARIK KANTOR KESEHATAN PELABUHAN KELAS II MATARAM oleh : Siti Zaetun, Lalu Bambang Kerti, Lalu Srigede Jurusan Analis Kesehatan Poltekkes Kemenkes Mataram Abstract: Background: Diabetes Mellitus (DM) has become a serious threat to society. In theory hyperbaric oxygen at 2.4 ATA pressure may increase tissue sensitivity to insulin and cause hypoglycemia in patients with diabetes mellitus where hyperbaric oxygen therapy at 2.4 ATA caused a decrease in blood sugar levels. Objective: To identify the effect of hyperbaric oxygen therapy on blood sugar levels of patients with Diabetes Mellitus (DM) in Diving and Hyperbaric Medical Installing Port Health Office Class II Mataram. Methods: This study is a cross-sectional design with pre-experimental one group pretest and post-test design in which each experimental unit was treated as well as the control group (reflective control) with the goal of all diabetic patients undergoing hyperbaric oxygen therapy who meet the criteria in the span of time between the months of June to August 2013 Results: Paired Sample Test Results of the analysis of the data showed the blood sugar levels of patients before and after undergoing hyperbaric oxygen therapy has a significant difference because the probability value is 0.001 <0.05 Conclusions: Based on the results of statistical tests concluded that no effect of hyperbaric oxygen therapy on blood sugar levels of patients with Diabetes Mellitus (DM) in Diving and Hyperbaric Medical Installing Port Health Office Class II Mataram. Keywords: Hyperbaric Oxygen Therapy, Blood Sugar, Diabetes Mellitus PENDAHULUAN Diabetes Mellitus (DM) adalah penyakit metabolik yang kebanyakan herediter, dengan tanda – tanda hiperglikemia dan glukosuria, disertai dengan atau tidak adanya gejala klinik akut ataupun kronik, sebagai akibat dari kurangnya insulin efektif di dalam tubuh, gangguan primer terletak pada metabolisme karbohidrat yang biasanya disertai juga gangguan metabolisme lemak dan protein. Berbagai macam pengobatan akan dilakukan untuk mencapai derajat kesehatan yang setinggitingginya. Ilmu pengetahuan dan teknologi pun semakin maju untuk menunjang kebutuhan manusia akan kesehatan. Salah satu teknologi terkini yaitu terapi oksigen hiperbarik yang menggunakan oksigen 100% dalam ruangan bertekanan tinggi yang ampuh untuk berbagai penyakit. Terapi oksigen hiperbarik adalah terapi dimana penderita harus berada dalam suatu ruangan bertekanan tinggi dan bernafas dengan oksigen murni (100%) pada tekanan udara lebih besar daripada udara atmosfir normal yaitu sebesar 1 ATA (Atmosfir Absolut) sama dengan 760 mmHg. Pemberian terapi oksigen tekanan tinggi dilaksanakan di dalam chamber atau Ruang Udara Bertekanan Tinggi (RUBT). Semula terapi ini dikhususkan untuk penyelam yang mengalami kelainan atau penyakit akibat penyelaman, kemudian dikembangkan untuk terapi penyakit klinis serta dapat meningkatkan kebugaran. Berbagai manfaat di bidang kesehatan bisa didapatkan dengan terapi oksigen hiperbarik ini. Dua efek penting yang mendasar pada terapi oksigen hiperbarik adalah efek mekanik yaitu meningkatnya tekanan lingkungan atau ambient yang memberikan manfaat penurunan volume gelembung gas atau udara seperti pada penderita dekompresi akibat kecelakaan kerja penyelaman dan gas emboli yang terjadi pada beberapa tindakan medis rumah sakit. Efek peningkatan tekanan parsial oksigen dalam darah dan jaringan yang memberikan manfaat terapeutik bakteriostatik pada infeksi kuman anaerob, detoksifikasi pada keracunan karbon monoksida, sianida dan hidrogensulfida, reoksigenisasi pada kasus iskemia akut dan kronis, nekrosis radiasi, luka bakar, kecantikan, serta gas ganggren. Secara teori terapi oksigen hiperbarik pada tekanan 2,4 ATA dapat meningkatkan sensitifitas jaringan terhadap insulin dan menimbulkan hipoglikemik pada penderita DM dimana terapi HBO pada 2,4 ATA menimbulkan penurunan kadar gula darah [6]. Teori lain juga menyebutkan terapi oksigen hiperbarik juga dapat meningkatkan 14 Media Bina Ilmiah ISSN No. 1978-3787 _____________________________________________ Volume 9, No. 2, April 2015 http://www.lpsdimataram.com jumlah oksigen bentuk larut secara sedemikian rupa sehingga akan lebih mudah dikonsumsi oleh jaringan lewat difusi langsung. Berdasarkan uraian di atas peneliti tertarik untuk melakukan penelitian mengenai pengaruh pemberian terapi oksigen hiperbarik terhadap kadar gula darah pasien Diabetes Mellitus (DM). Penelitian ini bertujuan melihat pengaruh terapi oksigen hiperbarik terhadap kadar gula darah pasien Diabetes Mellitus dengan cara mengukur kadar gula darah pasien Diabetes Mellitus sebelum dan sesudah pemberian terapi oksigen hiperbarik. METODE DAN BAHAN Penelitian ini dilaksanakan di Instalasi Kesehatan Penyelaman dan Hiperbarik Kantor Kesehatan Pelabuhan Kelas II Mataram pada bulan Juli – Agustus 2013. Penelitian ini adalah penelitian yang bersifat cross sectional dengan desain pre experimental one group pretest and post test design dimana tiap unit percobaan diperlakukan sekaligus sebagai kelompok kontrol (Reflective control). O1 P O2 Keterangan : O1 : Pengukuran gula darah pertama sebelum menjalani terapi P : Perlakuan pada sampel berupa pemberian terapi oksigen hiperbarik O2 : Pengukuran gula darah ke dua setelah pasien menjalani terapi oksigen hiperbarik Populasi dalam penelitian ini adalah Seluruh pasien DM yang menjalani terapi oksigen hiperbarik selama bulan Juli s/d Agustus 2013. Sampel dalam penelitian ini adalah keseluruhan dari total populasi yaitu jumlah pasien Diabetes Mellitus yang menjalani terapi oksigen hiperbarik selama bulan Juli s/d Agustus 2013. Besar sampel dalam penelitian ini yaitu berdasarkan data terakhir pada bulan Juni 2013 adalah sebanyak 6 orang. Kriteria sampel terdiri dari Kriteria Inklusi meliputi: Pasien yang mengidap penyakit Diabetes Mellitus, Berumur diatas 30 tahun, Pasien tidak sedang hamil, Bersedia untuk menjadi responden. Kriteria Eklusi : Pasien berumur di bawah 30 tahun, Bukan penderita Diabetes Mellitus, Pasien dalam keadaan hamil, Tidak bersedia untuk menjadi responden. Variabel Penelitian meliputi: Variabel Independent : Terapi Oksigen Hiperbarik dan Variabel Dependent : Kadar gula darah pasien Diabetes Mellitus (DM) a. Definisi Operasional 1. Terapi oksigen hiperbarik : Keadaan pasien yang ditempatkan dalam suatu tabung bertekanan 2,4 ATA dan menghirup oksigen murni selama 1,5 jam; Alat ukur : Gauge pressure; Skala Data: Nominal 2. Kadar gula darah: Kadar gula darah sewaktu dari penderita Diabetes mellitus yang di ukur sebelum dan sesudah melakukan terapi oksigen hiperbarik; Alat Ukur: Accuchek; Skala Data: Rasio. 3. Diabetes Mellitus (DM): keadaan dimana seseorang memiliki kadar gula darah sewaktu diatas 200 mg/dl kemudian mendatangi Kantor Kesehatan Pelabuhan Kelas II Mataram untuk melakukan terapi oksigen hiperbarik.; Alat Ukur: Accuchek; Skala Data: Nominal b. Alur kerja a. Cara Pengumpulan Data Kadar gula darah pada pasien Diabetes Mellitus sebelum dan sesudah menjalani terapi oksigen hiperbarik diukur dengan menggunakan alat pembaca gula accuchek test stick. Persiapan pasien dilakukan dengan prosedur sebagai berikut : - Pasien diberikan waktu istirahat sejenak - Diukur tekanan darah pasien oleh perawat jaga - Diperiksa keadaan/kesehatan umum pasien oleh dokter jaga - Pasien diperkenalkan dengan tabel klinis Kinwall yang memuat besar tekanan dan waktu terapi yang akan dijalani oleh pasien Persiapan pasien Pemeriksaan kadar gula darah sebelum terapi Terapi hiperbarik Pengambilan darah kapiler Persiapan Alat dan Bahan Pengambilan darah kapiler Pengumpulan data Pengolahan dan analisis data Kesimpulan Pemeriksaan kadar gula darah setelah terapi ISSN No. 1978-3787 Media Bina Ilmiah 15 _____________________________________ http://www.lpsdimataram.com Volume 9, No. 2, April 2015 Gambar 1. Tabel Klinis Kinwall - Pasien diajari tehnik valsava yang berguna mengatasi rasa sakit pada liang telinga pasien saat menjalani terapi Pengukuran kadar gula darah sebelum menjalani terapi oksigen hiperbarik, pengukuran ini melalui darah kapiler di ujung jari manis dengan menggunakan alat pembaca gula darah portable accuchek test stick dengan langkah sebagai berikut : - Ditempatkan alat ukur pada daerah yang datar - Dimasukkan kode alat pada slot kode yang terletak disamping alat - Dimasukkan stik pemeriksaan pada slot yang terletak dibagian tengah alat - Ditunggu beberapa saat sampai layar berkedip menampakkan kode stik yang kita gunakan dan meminta tetesan sampel - Diteteskan darah yang berasal dari jari manis pasien di area kuning pada stik - Ditunggu beberapa detik sampai alat menampilkan kadar gula darah dari pasien - Dicatat hasil pengukuran - Alat dimatikan dengan cara mencabut stik yang telah kita gunakan tadi. Gambar 2. Accuchek Terapi Oksigen Hiperbarik, setelah pasien merasa benar-benar siap selanjutnya pasien menjalani terapi oksigen hiperbarik dengan menggunakan tabel klinis Kinwall dengan tekanan 2,4 ATA atau setara dengan tekanan pada kedalaman 14 meter di bawah permukaan air laut selama 3 X 30 menit dengan prosedur : - Pasien dimasukkan kedalam ruang chamber dengan bantuan perawat - Pintu ruangan chamber ditutup rapat - Diberikan tekanan menggunakan udara tekan sedikit demi sedikit sambil memperhatikan keadaan umum pasien melalui celah kaca pada alat atau dengan berkomunikasi melalui radio sampai tekanan mencapai 2,4 ATA pada skala manometer tekanan yang terletak di bagian tengah alat - Pasien diminta untuk mulai memasang masker dan menghirup oksigen murni selama 30 menit pertama dengan nafas yang teratur - Pasien diminta untuk istirahat selama 5 menit dengan melepas masker oksigen yang dipakai dan bernafas secara teratur - Pasien diminta untuk memasang masker dan mulai menghirup oksigen murni untuk 30 menit ke 2 dan bernafas secara teratur - Pasien diminta untuk istirahat ke 2 selama 5 menit dengan melepas masker oksigen yang dipakai - Pasien diminta untuk memasang masker dan mulai menghirup oksigen murni untuk 30 menit ke 3 dan bernafas secara teratur - Pasien diminta untuk melepas masker oksigen yang dipakai untuk selanjutnya secara perlahan-perlahan petugas mengurangi tekanan yang ada di dalam alat sampai pintu chamber terbuka dengan sendirinya yang menandakan proses terapi telah selesai Gambar 3.3 Chamber hyperbaric Pengukuran kadar gula darah setelah menjalani terapi oksigen hiperbarik, pengukuran ini melalui darah kapiler di ujung jari manis dengan menggunakan alat pembaca gula darah portable accuchek test stick dengan langkah sebagai berikut : - Ditempatkan alat ukur pada daerah yang datar - Dimasukkan kode alat pada slot kode yang terletak disamping alat 16 Media Bina Ilmiah ISSN No. 1978-3787 _____________________________________________ Volume 9, No. 2, April 2015 http://www.lpsdimataram.com - Dimasukkan stik pemeriksaan pada slot yang terletak dibagian tengah alat - Ditunggu beberapa saat sampai layar berkedip menampakkan kode stik yang kita gunakan dan meminta tetesan sampel - Diteteskan darah yang berasal dari jari manis pasien di area kuning pada stik - Ditunggu beberapa detik sampai alat menampilkan kadar gula darah dari pasien - Dicatat hasil pengukuran - Alat dimatikan dengan cara mencabut stik yang telah kita gunakan. d. Analisis Data Data dari hasil pemeriksaan kadar gula darah pasien Diabetes Mellitus sebelum dan sesudah menjalani terapi oksigen hiperbarik dianalisis statistik menggunakan uji T-berpasangan (Paired T test) dengan tingkat kepercayaan 95% (p α 0,05). HASIL PENELITIAN a. Hasil Pengukuran kadar gula darah pasien sebelum dan setelah menjalani proses terapi oksigen hiperbarik. Tabel 1 Hasil Pengukuran kadar gula darah pasien sebelum dan sesudah menjalani proses terapi oksigen hiperbarik No Kadar Gula darah pasien Sebelum Menjalani proses terapi (gr/dl) Setelah Menjalani proses terapi (gr/dl) 1 367 203 2 354 259 3 424 206 4 412 316 5 390 206 6 392 290 7 265 241 8 354 234 Total 2958 1955 Rerata 369,75 244,38 Dari data tabel diatas menunjukkan bahwa rerata kadar gula darah pasien sebelum menjalani proses terapi oksigen hiperbarik adalah 369,75 gr/dl dan rerata kadar gula darah pasien setelah menjalani proses terapi oksigen hiperbarik adalah 244,38 gr/dl b. Hasil Uji Statistik Data hasil pemeriksaan perbedaan kadar gula darah pasien sebelum dan setelah menjalani proses terapi oksigen hiperbarik dilakukan analisis data menggunakan uji statistik pada tingkat kepercayaan 95% diperoleh hasil analisis sebagai berikut : c. Hasil Uji Shapiro Wilk Hasil uji Shapiro Wilk menunjukkan data kadar gula darah pasien sebelum menjalani proses terapi oksigen hiperbarik dengan nilai probabilitasnya adalah 0,177 > 0.15 yang menunjukkan bahwa data tersebut berdistribusi normal. Data kadar kadar gula darah pasien setelah menjalani proses terapi oksigen hiperbarik dengan nilai probabilitasnya adalah 0.271 > 0.15 yang menunjukkan bahwa data tersebut berdistribusi normal. d. Hasil uji Paired sample Test Hasil analisis Paired Sample Test menunjukkan data kadar kadar gula darah pasien sebelum dan setelah menjalani proses terapi oksigen hiperbarik memiliki perbedaan yang bermakna karena nilai probabilitasnya adalah 0.001 < 0.05, dengan demikian Ha yang menyatakan ada pengaruh pemberian terapi oksigen hiperbarik terhadap kadar gula darah pasien Diabetes Mellitus (DM) di Instalasi Kesehatan Penyelaman dan Hiperbarik Kantor Kesehatan Pelabuhan Kelas II Mataram diterima, yang artinya pemberian terapi oksigen hiperbarik efektif terhadap penurunan kadar gula darah pasien Diabetes Mellitus (DM) di Instalasi Kesehatan Penyelaman dan Hiperbarik Kantor Kesehatan Pelabuhan Kelas II Mataram. PEMBAHASAN Penelitian ini merupakan penelitian Cross sectional dengan desain pre experimental one group pretest and post test design dimana tiap unit percobaan diperlakukan sekaligus sebagai kelompok kontrol. Hasil penelitian menunjukkan rerata kadar gula darah pasien Diabetes Mellitus (DM) sebelum menjalani proses terapi oksigen hiperbarik adalah 369,75 mg/dl sedangkan rerata kadar gula darah pasien Diabetes Mellitus (DM) setelah menjalani proses terapi oksigen hiperbarik adalah 244,38 mg/dl. Hasil penelitian ini diperiksa metode stik dengan alat accuchek test strip dan dianalisis dengan uji statistik menunjukkan adanya perbedaan yang bermakna. Hal ini menunjukkan bahwa pemberian terapi oksigen hiperbarik mampu menurunkan kadar gula darah pasien Diabetes Mellitus (DM) sebesar 21,55%. Hiperbarik oksigen (HBO) adalah suatu cara terapi dimana penderita harus berada dalam suatu ruangan bertekanan, dan bernafas dengan oksigen 100 % pada suasana tekanan ruangan yang lebih ISSN No. 1978-3787 Media Bina Ilmiah 17 _____________________________________ http://www.lpsdimataram.com Volume 9, No. 2, April 2015 besar dari 1 ATA (Atmosfer absolute). Dasar dari terapi hiperbarik sedikit banyak mengandung prinsip fisika. Teori Toricelli yang mendasari terapi digunakan untuk menentukan tekanan udara 1 atm adalah 760 mmHg. Dalam tekanan udara tersebut komposisi unsur-unsur udara yang terkandung di dalamnya mengandung Nitrogen (N2) 79 % dan Oksigen (O2) 21%. Dalam pernafasan kita pun demikian. Pada terapi hiperbarik oksigen ruangan yang disediakan mengandung Oksigen (O2) 100%. Sedangkan prinsip yang dianut secara fisiologis adalah bahwa tidak adanya O2 pada tingkat seluler akan menyebabkan gangguan kehidupan pada semua organisme. Oksigen yang berada di sekeliling tubuh manusia masuk ke dalam tubuh melalui cara pertukaran gas. Diabetes Mellitus merupakan penyakit metabolik kronis yang paling banyak diderita dan menjadi “The Giant Killer” karena menimbulkan komplikasi pada berbagai organ tubuh seperti mata, saraf, ginjal, jantung dan pembuluh darah. Penyakit ini ditandai dengan kadar gula yang tinggi di dalam darah, diikuti oleh perubahan metabolik lemak dan protein. Hal tersebut berhubungan dengan gangguan sekresi insulin maupun kerja insulin. Didapatkan juga kelainan aktivitas sel-sel darah yang menghambat aliran darah dan berakibat kerusakan bahkan kematian jaringan tubuh. Diabetes yang ditandai dengan peningkatan kadar gula darah merupakan penyebab kematian nomor 6 di Indonesia dengan proporsi kematian 5,8 persen setelah stroke, tuberkulosis, hipertensi, cedera, dan perinatal. Jumlah diabetes di Indonesia 8,4 juta penderita dan diperkirakan terus meningkat sampai 21,3 juta orang di tahun 2030. Gangguan kesehatan ini timbul karena tubuh kekurangan insulin atau reseptor insulin tubuh tidak berfungsi baik. Insulin adalah hormon yang diproduksi sel beta di pankreas yang mengatur metabolisme glukosa menjadi energi serta mengubah kelebihan glukosa menjadi glikogen yang disimpan pada hati dan otot. Dalam jangka panjang, kadar glukosa darah yang tinggi akan menaikkan kadar kolesterol dan trigliserida darah. Selanjutnya akan terjadi aterosklerosis (penyempitan pembuluh darah) yang membuat aliran darah tidak lancar sehingga tubuh kekurangan oksigen. Menurut Mayor Laut (K) Titut Harnanik, dokter dan Kepala Sub departemen Faal Penyelaman TNI AL Armada Timur, terapi hiperbarik oksigen (HBO) pada Penderita diabetes, terutama tipe II (gangguan pada reseptor insulin) mampu mempercepat kesembuhan dan mengurangi dosis obat yang diminum penderita diabetes. Dari hasil penelitiannya pada tahun 2008 pada 13 orang pasien diabetes diterapi memakai oksigen 100 persen dan tekanan 2,4 atmosfir (setara kedalaman 14 meter di bawah permukaan laut) selama lima hari berturut-turut, diberi perlakuan ini selama 2 jam, terjadi penurunan gula darah secara signifikan. Jika biasanya tak pernah kurang dari 200 miligram per desiliter (mg/dl), kadar gula darah mereka bisa sampai 60 mg/dl. Pada pasien diabetes tipe I yang mengalami kerusakan pada fungsi pankreas sehingga tak bisa menghasilkan insulin, setelah menjalani terapi oksigen hiperbarik beberapa waktu, pasien yang harus disuntik insulin itu bisa lepas dari ketergantungan pada insulin dari luar, namun pasien wajib diterapi 3-5 kali per bulan seumur hidup guna menjamin pasokan oksigen ke pankreas. Menurut Suyanto Sidik, dokter spesialis penyakit dalam dari RS TNI AL dr Mintohardjo, terapi oksigen hiperbarik bersifat memperbaiki jumlah oksigen di dalam tubuh. Diabetes membuat kondisi pembuluh darah penderitanya buruk sehingga aliran darah tak lancar. Contohnya, ada pasien diabetes dengan luka terbuka yang tak sembuh atau tak kunjung kering. Hal itu terjadi karena pembuluh darah tak mendapat pasokan oksigen sehingga tak berfungsi normal dalam memperbaiki kerusakan sel. Sedangkan menurut dr. Susan Manungkalit, yang juga dokter di Pusat Hiperbarik RS TNI AL dr Mintohardjo Jakarta mengatakan, HBO mampu meningkatkan kandungan oksigen pada plasma darah. Pada kondisi oksigen normal di udara bebas (20 persen) dengan tekanan normal (1 atmosfir), jumlah oksigen pada hemoglobin 20,1 persen dan plasma darah 0,32 persen. Jika diberi oksigen 100 persen dan tekanan normal 1 atmosfir, oksigen hemoglobin tetap 20,1 persen dan oksigen plasma darah jadi 2,14 persen. Ketika tekanan oksigen 100 persen dinaikkan jadi 3 atmosfir, jumlah oksigen dalam plasma darah jadi tiga kali lipat (6,42 persen). Meningkatnya tekanan dan volume oksigen menimbulkan oksigenasi pada jaringan yang mengalami kekurangan pasokan oksigen (hipoksia). Dampak lain, terjadinya pembaruan pembuluh darah, mendorong perkembangbiakan sel, dan meningkatkan ”kemampuan tempur” sel darah putih (leukosit). Pengobatan Diabetes mellitus (DM) adalah pengobatan seumur hidup yang bertujuan untuk meningkatkan kualitas hidup penderita, agar tetap produktif dan tidak menjadi beban masyarakat. Terapi ini dapat memberikan manfaat antara lain: 1. Meningkatkan sekresi insulin dan menurunkan sekresi hormon kontra insulin. 2. Meningkatkan metabolisme aerob sehingga menurunkan kadar gula darah. 18 Media Bina Ilmiah ISSN No. 1978-3787 _____________________________________________ Volume 9, No. 2, April 2015 http://www.lpsdimataram.com 3. Menurunkan kadar HbAlc, hal ini menunjukkan perbaikan pengolahan gula darah penderita Diabetes mellitus (DM) untuk jangka panjang. 4. Memperlancar aliran darah terutama didaerah mikrosirkulasi sehingga mencegah komplikasi pada organ tubuh vital. 5. Meningkatkan kebugaran penderita Diabetes mellitus. Terlepas dari semua hal diatas penelitian ini masih memiliki kelemahan terutama pada tidak adanya kelompok kontrol pada sampel yang dipakai dan tidak adanya kontrol terhadap obatobatan yang dikonsumsi oleh pasien sebelum menjalani sesi terapi oksigen hiperbarik. Seberapa besar pengaruh pasca sesi terapi oksigen hiperbarik juga perlu menjadi perhatian lebih lanjut, sehingga tidak terkesan efek terapi oksigen hiperbarik ini hanya terasa pada saat menjalani sesi terapi saja. PENUTUP a. Simpulan Pemberian terapi oksigen hiperbarik selama satu seri/ 5 hari berturut- turut efektif terhadap penurunan kadar gula darah pada pasien Diabetes mellitus (DM) dengan nilai p (0.000 < 0.05 ). b. Saran Perlu penjelasan yang lebih mendetail mengenai tehnik valsava/ ekwalisasi pada saat penyesuaian tekanan didalam tubuh dengan keadaan didalam lingkungan pesawat chamber sehingga pasien dapat lebih tenang pada saat menjalani proses terapi. DAFTAR RUJUKAN Tjokroprawiro. Buku Ajar Ilmu Penyakit Dalam. Surabaya. Airlangga University Press. 2007 Rijadi. Penuntun Praktikum Kimia Klinik II, Analis Kesehatan Bandung, 2009. Lakesla. Ilmu Kesehatan Bawah Air dan Hiperbarik. Surabaya. Lembaga Kesehatan Angkatan Laut. 2009. Pennefather. Hyperbaric equipment ; Diving and sub quatic medicine. London. Oxford university press 2002. Neubauer. Hyperbaric oxygen therapy. New York. Avery Publishing Group Inc. 1998.

Selasa, 17 November 2015

Obati Diabetes dengan "Selam"

Obati Diabetes dengan "Selam" Selasa, 6 September 2011 | 09:34 WIB KOMPAS.COM Ichwan Susanto Tekanan udara tinggi membuat oksigen lebih leluasa memasuki jaringan tubuh. Oksigen, zat yang dibutuhkan tubuh untuk metabolisme, digunakan untuk perbaikan sel yang rusak. Prinsip tersebut digunakan pada terapi hiperbarik oksigen untuk menyembuhkan berbagai macam penyakit. Salah satu penyakit yang diupayakan sembuh dengan terapi hiperbarik adalah diabetes melitus (penyakit kencing manis). diabetes yang ditandai dengan peningkatan kadar gula darah merupakan penyebab kematian nomor 6 di Indonesia dengan proporsi kematian 5,8 persen setelah stroke, tuberkulosis, hipertensi, cedera, dan perinatal (Kementerian Kesehatan 2007). Jumlah diabetes di Indonesia 8,4 juta penderita dan diperkirakan terus meningkat sampai 21,3 juta orang di tahun 2030. Gangguan kesehatan ini timbul karena tubuh kekurangan insulin atau reseptor insulin tubuh tidak berfungsi baik. Insulin adalah hormon yang diproduksi sel beta di pankreas yang mengatur metabolisme glukosa menjadi energi serta mengubah kelebihan glukosa menjadi glikogen yang disimpan pada hati dan otot. Dalam jangka panjang, kadar glukosa darah yang tinggi akan menaikkan kadar Kolesterol dan trigliserida darah. Selanjutnya akan terjadi aterosklerosis (penyempitan pembuluh darah) yang membuat aliran darah tidak lancar sehingga tubuh kekurangan oksigen. Penderita diabetes, terutama tipe II (gangguan pada reseptor insulin), telah banyak tertolong oleh terapi ini. Mayor Laut (K) Titut Harnanik, dokter dan Kepala Subdepartemen Faal Penyelaman TNI AL Armada Timur, mengatakan, terapi hiperbarik oksigen (HBO) mampu mempercepat kesembuhan dan mengurangi dosis obat yang diminum penderita diabetes. Tahun 2008, Titut melakukan penelitian atas biaya Kementerian Kesehatan. Sebanyak 13 pasien diabetes diterapi memakai oksigen 100 persen dan tekanan 2,4 atmosfir (setara kedalaman 14 meter di bawah permukaan laut). Selama lima hari berturut-turut, para penderita diabetes tanpa luka terbuka diberi perlakuan ini selama 2 jam. ”Selama menjalani terapi HBO, pasien tetap mengonsumsi obat. Setelah menjalani HBO, terjadi penurunan gula darah secara signifikan. Jika biasanya tak pernah kurang dari 200 miligram per desiliter (mg/dl), kadar gula darah mereka bisa sampai 60 mg/dl. Maka dosis obat harus diturunkan,” kata Titut. Di luar penelitian itu, Titut punya pasien diabetes tipe I (mengalami kerusakan pada fungsi pankreas sehingga tak bisa menghasilkan insulin). Setelah menjalani HBO beberapa waktu, pasien yang harus disuntik insulin itu bisa lepas dari ketergantungan pada insulin dari luar. ”HBO mengembalikan fungsi pankreas sebab sifat antioksidan pada oksigen,” ujarnya. Namun, pasien wajib diterapi HBO 3-5 kali per bulan, seumur hidup. Hal ini guna menjamin pasokan oksigen ke pankreas. Menurut Suyanto Sidik, dokter spesialis penyakit dalam dari RS TNI AL dr Mintohardjo, HBO bersifat memperbaiki jumlah oksigen di dalam tubuh. diabetes, tutur Suyanto, membuat kondisi pembuluh darah penderitanya buruk sehingga aliran darah tak lancar. Contohnya, ada pasien diabetes dengan luka terbuka yang tak sembuh atau tak kunjung kering. Hal itu terjadi karena pembuluh darah tak mendapat pasokan oksigen sehingga tak berfungsi normal dalam memperbaiki kerusakan sel. Oksigen sebagai obat Terapi HBO modern diperkenalkan peneliti Belanda, Ite Boerema, dalam artikel penelitian Life without blood tahun 1956. Dalam hal ini, molekul oksigen diberi tekanan tinggi sehingga mampu masuk ke pembuluh darah yang tersumbat atau peredaran darahnya terganggu. Oksigen lalu memicu metabolisme jaringan tubuh dan memperbaiki sel yang rusak. ”HBO merupakan pengobatan, seperti halnya dengan obat. Bedanya, ini memasukkan oksigen ke tubuh,” kata Suyanto. Di RS Mintohardjo, ruang hiperbarik (ruang dengan udara bertekanan tinggi) berdaya tampung 12 orang, termasuk seorang perawat. Dalam ruangan mirip kapsul kapal selam itu, pasien diberi oksigen lewat selang di hidung, kemudian tekanan udara diatur oleh operator di luar kapsul. Dokter di Pusat Hiperbarik RS TNI AL dr Mintohardjo Jakarta, Susan Manungkalit, mengatakan, HBO mampu meningkatkan kandungan oksigen pada plasma darah. Pada kondisi oksigen normal di udara bebas (20 persen) dengan tekanan normal (1 atmosfir), jumlah oksigen pada hemoglobin 20,1 persen dan plasma darah 0,32 persen. Jika diberi oksigen 100 persen dan tekanan normal 1 atmosfir, oksigen hemoglobin tetap 20,1 persen dan oksigen plasma darah jadi 2,14 persen. Ketika tekanan oksigen 100 persen dinaikkan jadi 3 atmosfir, jumlah oksigen dalam plasma darah jadi tiga kali lipat (6,42 persen). ”Jumlah oksigen sangat cukup untuk bertahan hidup meski tanpa kehadiran hemoglobin darah,” tulis peneliti Catherine A Heyneman, dalam jurnal Critical Care Nurse (2002), yang juga melakukan penelitian hiperbarik oksigen. Meningkatnya tekanan dan volume oksigen menimbulkan oksigenasi pada jaringan yang mengalami kekurangan pasokan oksigen (hipoksia). Dampak lain, terjadinya pembaruan pembuluh darah, mendorong perkembangbiakan sel, dan meningkatkan ”kemampuan tempur” sel darah putih (leukosit). Susan merekomendasikan agar pasien sebelum menjalani terapi hiperbarik oksigen harus menjalani scan kepala untuk mendeteksi kemungkinan ada kelainan pada tengkorak. Jika ada kelainan, bisa membahayakan pasien, misalnya bisa terjadi stroke. Syarat lain menjalani terapi HBO mirip dengan persyaratan umum menyelam, yaitu tidak boleh ada sinusitis (radang di hidung), dan tekanan darah normal. Karena itu, terapi ini juga disebut selam kering.

Selasa, 10 November 2015

DIABETUS MELITUS DAN HIPERBARIK OKSIGEN TERAPI

Vemale.com - Oleh Risma M. Tambunan Lewat penelitian, terapi ini dinyatakan mampu menyembuhkan diabetes mellitus. Diabetes Mellitus (DM) atau kencing manis atau gula darah, merupakan penyakit kronis, sistemis dan degeneratif. Kronis: mampu berkembang dan dapat berimplikasi. Sistemis: memiliki luas penyebaran/ menyerang hampir seluruh organ tubuh manusia. Degeneratif: para ahli menyimpulkan DM ada hubungannya dengan faktor keturunan. Seseorang yang kedua orangtuanya menderita DM hampir dipastikan akan menderita penyakit ini. Hasil riset kesehatan dasar (Riskesdas) Depkes RI tahun 2007, DM merupakan penyebab kematian nomor enam di Indonesia dengan proporsi kematian 5,8 persen setelah stroke, tuberkulosis, hipertensi, cedera, dan perinatal. Jumlah diabetes mellitus di Indonesia 5,4 juta penderita, dan diperkirakan terus meningkat sampai 21,3 juta di tahun 2030. Dikatakan sebagai lifelong disease atau penyakit seumur hidup karena DM memang tidak dapat disembuhkan. Namun, gejala dan komplikasi yang ditimbulkannya dapat diminimalkan jika penderita rajin dan disiplin mengatur pola diet, olahraga, dan rutin memeriksakan kadar gula darah, serta disiplin makan obat sesuai anjuran dokter. Menurut dr. Suyanto Sidik, SpPD, KGEH, spesialis penyakit dalam di Rumah Sakit Premier Bintaro, DM ditandai dengan tingginya kadar gula darah sebab tidak dapat digunakan oleh tubuh. Pada orang normal, karbohidrat yang dimakan akan diubah menjadi glukosa di dalam saluran pencernaan. Glukosa di bawa oleh darah ke seluruh tubuh dan masuk ke sel untuk dimanfaatkan antara lain sebagai energi. Masuknya glukosa ke dalam sel dibantu oleh insulin, sejenis hormon yang diproduksi oleh kelenjar pankreas. Pada penderita DM, gula susah masuk ke dalam sel karena sedikitnya hormon insulin yang diproduksi, atau karena sel tidak dapat memberikan respon yang baik terhadap insulin meski jumlah insulinnya cukup. Akibatnya, gula menumpuk di dalam darah, tidak dapat dimanfaatkan oleh tubuh, dan akhirnya dibuang melalui air seni. Gangguan metabolisme karbohidrat ini menyebabkan tubuh kekurangan energi. Terapi Awet Muda Pengobatan yang umumnya dijalani pasien diabetes mellitus adalah terapi insulin yang berkesinambungan, konsumsi obat. Penderita juga wajib melakukan berolahraga dan mengontrol pola serta menu makanan. Kini, terapi hiperbarik oksigen (HBO) direkomendasikan oleh penderita DM. Terapi hiperbarik oksigen berfungsi untuk meningkatkan konsentrasi oksigen pada seluruh jaringan tubuh, dan merangsang pertumbuhan pembuluh darah baru untuk meningkatkan aliran darah/ pada sirkulasi yang berkurang. Karena fungsinya, terapi ini juga dapat dilakukan pada penyakit kronis lainnya, seperti stroke, pembuluh darah perifer, cerebral palsy, trauma otak, slerosis multiple, dan penyembuhan luka bakar. Makin meluas pula pemakaiannya sebagai terapi kebugaran tubuh dan terapi awet muda. “HBO bersifat memperbaiki jumlah oksigen di dalam tubuh. Diabetes akan membuat kondisi pembuluh darah penderitanya buruk sehingga aliran darah tak lancar. Contohnya, ada pasien diabetes dengan luka terbuka yang tak sembuh atau tak kunjung kering. Hal itu terjadi karena pembuluh darah tak mendapat pasokan oksigen sehingga tak berfungsi normal dalam memperbaiki kerusakan sel,” ujar dokter Suyanto. Salah satu rumah sakit yang mempunyai fasilitas terapi HBO adalah RS TNI AL Mintohardjo, Jakarta. Menurut salah satu penderita diabetes yang sedang menjalani terapi HBO di sana, ruangan mirip kapsul selam dengan udara bertekanan tinggi itu berdaya tampung 12 orang termasuk seorang perawat. Pasien diberi oksigen lewat selang hidung, lalu tekanan udara diatur oleh operator di luar kapsul. “Saya hanya wajib meneruskan terapi saja. Tidak perlu suntik insulin lagi,” aku si pasien, tanpa mau merinci lamanya masa terapi yang sudah dijalani, dan besarnya biaya yang dikeluarkan. Dosis Obat Berkurang Tahun 2008, atas biaya dari Depkes RI, beberapa peneliti melakukan terapi HBO terhadap 13 pasien DM Tipe 2 tanpa luka terbuka. Para pasien diterapi menggunakan oksigen 100 persen dalam tekanan 2,4 atmosfir (setara kedalaman 14 meter di bawah permukaan laut), selama lima hari berturut-turut dengan waktu dua jam. Selama terapi, pasien tetap mengonsumsi obat. Usai menjalani terapi HBO, terjadi penurunan gula darah. Jika biasanya tidak pernah kurang dari 200 miligram per desiliter (mg/dl), saat itu bisa turun hingga mencapai 60 mg/dl, dan dosis obat pun dikurangi. Penelitian menghasilkan klaim bahwa terapi hiperbarik oksigen mampu mempercepat kesembuhan dan mengurangi dosis obat yang diminum penderita DM Tipe 2. Penelitian berikutnya dilakukan pada pasien DM Tipe 1. Hasilnya, pasien bisa lepas dari ketergantungan pada insulin dari luar setelah beberapa kali menjalani terapi HBO. Dikatakan, HBO mengembalikan fungsi pankreas sebab sifat antioksidan pada oksigen. Pasien itu hanya wajib melakukan terapi HBO sebanyak 3-5 kali per bulan, untuk menjamin pasokan oksigen ke pankreas. Dokter Suyanto menyebutkan, “Sebelum terapi, pasien harus menjalani scan kepala untuk mendeteksi kemungkinan adanya kelainan pada tengkorak. Jika ada, bisa membahayakan, misalnya bisa terjadi stroke.” Syarat lainnya sama seperti persyaratan umum menyelam, yaitu tidak boleh ada sinusitis (radang di bagian hidung), dan tekanan darah normal. Karena itu, terapi ini juga disebut selam kering. Source: Good Housekeeping, edisi November 2011, halaman 34-www.goodhousekeeping.co.id (vem/tik)

Selasa, 03 November 2015

Cerebral Palsy- New Study demonstrates effectiveness of hyperbaric oxygen therapy in treating neurological and motor dysfunction

Cerebral Palsy- New Study demonstrates effectiveness of hyperbaric oxygen therapy in treating neurological and motor dysfunction By TomFox | Posted May 1, 2014 | Montreal Quebec Montreal Quebec, April 22, 2014 – A new study published in the current issue of the Undersea and Hyperbaric Medicine Journal demonstrates the beneficial effect of hyperbaric oxygen therapy in addressing motor and neurological dysfunction due to cerebral palsy (CP). CP is a non progressive condition that can be attributed to a neurological injury just prior to or at the time of birth. Affecting more than 2000 children in Quebec, this study confirms the positive results of two previous studies conducted by physicians from Quebec’s Sainte Justine’s hospital. The concept of using Hyperbaric oxygen to treat brain injury in children with cerebral palsy is not new. For over 25 years, numerous clinical trials have reported significant improvement in study groups worthy of additional study. What makes the current study’s finding’s impressive is the rigorous , methodical, multifaceted comparison of the study design. Standard Intensive Rehabilitation given children with cerebral palsy was compared to groups where hyperbaric oxygen therapy of differing doses HBOT). Dr. Pierre Marois, a physiatrist from Sainte Justine Hospital in Montreal collaborated on this new study. The clinical trials conducted in India examined 150 children from which 20 received standard intensive rehabilitative therapy only. The remaining 130 children were divided into three different groups distinquished by different doses of hyperbaric oxygen. His work as a principle investigator in studies since 1998 has helped to document the significant beneficial effects of hyperbaric oxygen in children with Cerebral Palsy. This study found that the children treated in hyperbarics improved three times more than those that received standard intensive rehabilitative therapy. “Some have been able to walk for the first time, others have spoken the first words of their lives following hyperbaric treatments, says Dr Marois. The current study followed the children for eight months after the completion of treatment and found the improvements “seemed to be permanent “ These results which appear in the Undersea and Hyperbaric Medicine Journal concur with those recently obtained in studies of adults in Israel with residual effects of strokes and traumatic brain injury. “Some patients have begun to use arms or legs that were paralyzed. In viewing images of the brains of these patients, we have seen that areas that previously were completely inactive worked again after hyperbaric treatment , "said Dr. Marois . With this new study, it becomes clear that this treatment can significantly improve the quality of life of patients , insists Dr. Marois . Hopefully, as evidence continues to accumulate RAMQ will agree to pay for these treatments for children. Point of Contact: Thomas M. Fox MAS, MS, CHT 514-453-7978

Selasa, 27 Oktober 2015

Hyperbaric Oxygen Therapy for Diabetic Foot Wounds

Hyperbaric Oxygen Therapy for Diabetic Foot Wounds Has hope hurdled hype? Benjamin A. Lipsky, MD, FACP, FIDSA, FRCP1 and Anthony R. Berendt, BM, BCH, FRCP2 + Author Affiliations 1University of Washington, VA Puget Sound, Seattle, Washington; 2Bone Infection Unit, Nuffield Orthopaedic Centre NHS Trust, Oxford, U.K. Corresponding author: Benjamin A. Lipsky, dblipsky@hotmail.com. “One must always hope when one is desperate, and doubt when one hopes.” Gustave Flaubert. Hyperbaric oxygen therapy (HBOT) has been promoted as an effective treatment for diabetic foot wounds, and the first controlled trial for this indication was reported (in Diabetes Care) over 20 years ago (1). Advocates have suggested that the experimentally demonstrated effects of HBOT on improving wound tissue hypoxia, enhancing perfusion, reducing edema, downregulating inflammatory cytokines, promoting fibroblast proliferation, collagen production, and angiogenesis make it a useful adjunct in clinical practice for “problem wounds,” such as diabetic foot ulcers (2,3). HBOT is also touted for eradicating difficult to treat soft tissue and bone infections by mechanisms that include killing microorganisms, improving leukocyte and macrophage function, and enhancing the effect of antimicrobials (4). If realized clinically, these beneficial effects, although requiring expensive technology, might powerfully reduce the risk of lower-extremity amputation in diabetic patients with foot wounds. Thus, rigorously assessing the clinical effectiveness of HBOT in diabetic foot ulceration is an important enterprise. But, because both patients and clinicians are strongly motivated to avoid the devastating outcome of amputation, there is a high potential for bias in poorly designed trials. Proof of benefit requires properly conducted clinical trials that minimize the possibility that preexisting prejudices will influence the allocation of patients, diligence of foot care, or other key management decisions. Most of the published reports on the effect of HBOT for treating diabetic foot wounds have been case series or nonrandomized trials with major methodological limitations. Although these are a poor source of evidence, the consistency of positive results is noteworthy. More recently, several randomized controlled trials have been conducted. A Cochrane database systematic review published in 2004 concluded, based on results from four such trials, that “HBOT significantly reduced the risk of major amputation and may improve the chance of healing at 1 year” but, “… the small number of studies … modest numbers of patients, methodological and reporting inadequacies … demand a cautious interpretation” (5). A more recent systematic review and meta-analysis that included 10 studies (6 of which were not randomized, controlled trials) concluded that HBOT reduces the risk of amputation (odds ratio 0.24, seven studies) and increases the likelihood of wound healing (odds ratio 10.0, six studies) (6). But there are concerns. HBOT is available in only a minority of communities, is very expensive (a full course of treatment in the U.S. typically costs $50,000 [Medicare] to $200,000 [private pay]), and is time-consuming (an average of 60 total hours in the chamber). Limited economic analyses using the flawed primary clinical data have suggested, however, that HBOT is potentially cost-effective (7,8) or even cost-saving (9). The more skeptical view is best summarized in a counterpoint commentary (10) on hyperbaric oxygen treatment for diabetic foot wounds published 4 years ago that concluded “[it] is time that the advocates of this therapy organized large, randomized, placebo-controlled trials to provide definitive answers to the questions: which, if any, patients would benefit from HBOT for a diabetic foot wound, and how great is any measurable benefit?” Have there been investigations designed to answer these questions published since that challenge, and, specifically, has the study from Lund, Sweden, by Löndahl et al. (11) in this issue of Diabetes Care provided the proof that HBOT naysayers are seeking? One new study that addressed this issue by Duzgun et al. (12) was published in 2008. This randomized trial compared the effects of HBOT with standard wound care alone on 100 patients with a diabetic foot ulcer that had not responded to a month of appropriate treatment. They found that HBOT was associated with statistically significantly higher rates of wound healing (66% vs. 0%), lower rates of operative interventions (debridement, amputation, or skin flap or graft; 16% vs. 100%), and fewer lower extremity amputations (8% vs. 82%). This study, in common with most others previously published, had several important limitations, including a lack of investigator or patient blinding, minimal descriptions of the types of wounds enrolled, and disparities in treatment allocation that were presumed to be by chance. Nevertheless, it provided useful data and increased by two-thirds the number of patients on which the previously cited Cochrane systematic review of HBOT for diabetic wounds reported. The study by Löndahl et al. (11) builds on work their team began in the early 1990s, when they demonstrated in a randomized controlled study of 16 nondiabetic patients with a nonischemic chronic leg ulcer, that HBOT significantly reduced the size of the wounds during a 6-week observation period (13). This study, unlike all previous ones except that by Abidia et al. (9), was double-blinded; all enrolled patients were treated in a multiplace hyperbaric chamber, but the masks for half the subjects delivered air while those for the other half delivered 100% oxygen. This method, although technically complex, allowed for a placebo-controlled and blinded evaluation of HBOT, thus eliminating many of the potential confounders that plagued other trials. Fortunately, the investigators kept this design for the current trial in patients with diabetic foot ulcers. In this study, the authors enrolled 94 diabetic patients with a foot ulcer (Wagner grades 2–4) that had been present for at least 3 months and who did not need or could not have reconstructive vascular surgery. They excluded only those patients for whom HBOT was contraindicated or who had a substance abuse problem and stratified enrolled patients by their arterial toe blood pressure. Hyperbaric sessions were given for 8 to10 weeks (aiming for 40 sessions), in conjunction with appropriate foot care provided by a multidisciplinary diabetic foot clinic. The primary end point was ulcer healing, properly defined as complete epithelial regeneration, and patients were followed for a year. Patients randomized to the two treatment groups were similar at baseline; of note is that over half had previously had vascular surgery to the affected lower limb. It was disappointing that only 56% of eligible patients were enrolled, and only 57% of those enrolled completed the 40 treatments (although most had at least 35). The results of the Löndahl study clearly support the benefit of HBOT. Complete ulcer healing at the 1-year follow-up was noted in significantly more HBOT-treated than hyperbaric air- treated patients (52% vs. 29% [P = 0.03] in the intention-to-treat analysis, and 61% vs. 27% [P = 0.009] in the per-protocol analysis). The number needed to treat to avert nonhealing was only 4.2 (3.1 in the per-protocol analysis). Among their secondary outcomes, the rates during the study period of major amputation (∼4%) and death (∼7%) were relatively low (for these elderly diabetic patients with a high prevalence of comorbidities) and were similar for the two groups. Although patients with infected wounds (presumably including osteomyelitis) could be enrolled, and ∼70% of the patients were receiving oral antibiotic therapy at the time of enrollment, the authors, unfortunately, did not comment on the rates or speed of resolution of infection in the two groups. The rate of adverse reactions to hyperbaric therapy in this study was notable; one patient died (in the HBOT group, possibly related to treatment), 5% had significant barotrauma, and 6% had symptomatic hypoglycemia (one of whom was hospitalized), a known potential risk of HBOT. The authors of this study are certainly to be commended on the strong study design they used—it was fully blinded and placebo-controlled, with concealed allocation that was maintained until the end of a 1-year follow-up period, the exclusion criteria were limited, and patients were stratified by arterial vascular status. The number of patients enrolled was larger than any but the methodologically inferior study by Duzgun et al. (12). There were, however, some important limitations. Only 55% of potentially eligible patients were available for analysis at the 1-year follow-up. The Wagner system used to grade wound severity, while also used in previous HBOT studies and by Medicare to determine eligibility for treatment, has largely been superseded by other systems that provide more information (14,15). We are given no information regarding how many patients in each group had osteomyelitis, a clinically important variable that was neither a reason for exclusion nor used for stratification of enrolled patients. The enrolled patients were relatively unique in some ways: the mean age was a decade older than in most studies of patients with diabetic foot ulcers, all had ulcers that had failed prolonged attempts at treatment, and most had previously had vascular surgery on the affected leg. The description of the severity of infection in the two groups, or how HBOT affected the resolution of infection, was inadequate. There were too few amputations to judge the effect of HBOT on this crucial end point. No data supporting the statement that arterial toe blood pressure did not predict outcomes were provided, and transcutaneous oxymetry would have been a better means of determining adequacy of wound perfusion and oxygenation than toe pressures (16). Finally, the authors made no attempt to address the cost-effectiveness of this expensive technology. What are we to conclude about the place of HBOT in treating patients with diabetic foot wounds? It seems clear that in a center of excellence of both HBOT and diabetic foot care, like the one in Lund, HBOT can help heal refractory wounds. It is unnecessary for the great majority of patients, however, who will respond to appropriate wound care (cleansing, debridement, off-loading, antimicrobials, as needed). But, for chronic diabetic foot wounds that are not responding to months of appropriate therapy, the present study, together with most of those previously published, suggests that HBOT improves long-term healing. Although HBOT is approved in the U.S. for treatment of chronic osteomyelitis, there is little published support for this treatment for treating infectious complications in the diabetic foot. The potential benefit of HBOT comes at a high financial cost; it would be reasonable for payers to ask if treating four patients to deliver one additional healed ulcer at 1 year is cost-effective. Further randomized controlled trials would, of course, be welcomed. In light of the expense of conducting properly designed clinical trials, alternative methods of assessment, such as theoretical modeling, may be helpful (17). The study by Löndahl et al., standing on the shoulders of previous trials, has placed HBOT on firmer ground. While this article may not be the one to untie the purse strings of health care payment agencies, it does provide cause for hope and serves to prove that large, properly designed trials are both possible and necessary. Key issues that we must yet address to better understand the place of HBOT in treating diabetic foot wounds include developing robust criteria to determine which patients are likely to benefit, determining at what point in their treatment HBOT should be considered (or abandoned), and deciding which treatment protocols are most appropriate (18). This landmark study at last demonstrates not only that answering these questions is possible using standards of evidence appropriate for the 21st century, but that seeking the answers to these questions is no longer of interest only to the hyperbaric industry. The answers are important for, and eagerly awaited by, all “stakeholders” in the diabetic foot world. Next Section Acknowledgments No potential conflicts of interest relevant to this article were reported. © 2010 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. Previous Section References ↵ Baroni G, Porro T, Faglia E, Pizzi G, Mastropasqua A, Oriani G, Pedesini G, Favales F : Hyperbaric oxygen in diabetic gangrene treatment. Diabetes Care 1987; 10: 81– 86 Abstract/FREE Full Text ↵ Gill AL, Bell CN : Hyperbaric oxygen: its uses, mechanisms of action and outcomes. QJM 2004; 97: 385– 395 FREE Full Text ↵ Barnes RC : Point: hyperbaric oxygen is beneficial for diabetic foot wounds. Clin Infect Dis 2006; 43: 188– 192 FREE Full Text ↵ Cimşit M, Uzun G, Yildiz S : Hyperbaric oxygen therapy as an anti-infective agent. Expert Rev Anti Infect Ther 2009; 7: 1015– 1026 CrossRefMedlineGoogle Scholar ↵ Kranke P, Bennett M, Roeckl-Wiedmann I, Debus S : Hyperbaric oxygen therapy for chronic wounds. Cochrane Database Syst Rev 2004; 1: CD004123 Google Scholar ↵ Goldman RJ : Hyperbaric oxygen therapy for wound healing and limb salvage: a systematic review. PM R 2009; 1: 471– 489 CrossRefMedlineGoogle Scholar ↵ Chow I, Lemos EV, Einarson TR : Management and prevention of diabetic foot ulcers and infections: a health economic review. Pharmacoeconomics 2008; 26: 1019– 1035 CrossRefMedlineGoogle Scholar ↵ Chuck AW, Hailey D, Jacobs P, Perry DC : Cost-effectiveness and budget impact of adjunctive hyperbaric oxygen therapy for diabetic foot ulcers. Int J Technol Assess Health Care 2008; 24: 178– 183 MedlineGoogle Scholar ↵ Abidia A, Laden G, Kuhan G, Johnson BF, Wilkinson AR, Renwick PM, Masson EA, McCollum PT : The role of hyperbaric oxygen therapy in ischaemic diabetic lower extremity ulcers: a double-blind randomised-controlled trial. Eur J Vasc Endovasc Surg 2003; 25: 513– 518 CrossRefMedlineGoogle Scholar ↵ Berendt AR : Counterpoint: hyperbaric oxygen for diabetic foot wounds is not effective. Clin Infect Dis 2006; 43: 193– 198 Abstract/FREE Full Text ↵ Löndahl M, Katzman P, Nilsson A, Hammarlund C : Hyperbaric oxygen therapy facilitates healing of chronic foot ulcers in patients with diabetes. Diabetes Care 2010; 33: 998– 1003 Abstract/FREE Full Text ↵ Duzgun AP, Satir HZ, Ozozan O, Saylam B, Kulah B, Coskun F : Effect of hyperbaric oxygen therapy on healing of diabetic foot ulcers. J Foot Ankle Surg 2008; 47: 515– 519 CrossRefMedlineGoogle Scholar ↵ Hammarlund C, Sundberg T : Hyperbaric oxygen reduced size of chronic leg ulcers: a randomized double-blind study. Plast Reconstr Surg 1994; 93: 829– 833 CrossRefMedlineGoogle Scholar ↵ Gul A, Basit A, Ali SM, Ahmadani MY, Miyan Z : Role of wound classification in predicting the outcome of diabetic foot ulcer. J Pak Med Assoc 2006; 56: 444– 447 MedlineGoogle Scholar ↵ Parisi MC, Zantut-Wittmann DE, Pavin EJ, Machado H, Nery M, Jeffcoate WJ : Comparison of three systems of classification in predicting the outcome of diabetic foot ulcers in a Brazilian population. Eur J Endocrinol 2008; 159: 417– 422 Abstract/FREE Full Text ↵ Niinikoski J : Hyperbaric oxygen therapy of diabetic foot ulcers, transcutaneous oxymetry in clinical decision making. Wound Repair Regen 2003; 11: 458– 461 CrossRefMedlineGoogle Scholar ↵ Flegg JA, McElwain DL, Byrne HM, Turner IW : A three species model to simulate application of hyperbaric oxygen therapy to chronic wounds. PLoS Comput Biol 2009; 5: e1000451 CrossRefMedlineGoogle Scholar ↵ Wang C, Schwaitzberg S, Berliner E, Zarin DA, Lau J : Hyperbaric oxygen for treating wounds: a systematic review of the literature. Arch Surg 2003; 138: 272– 279 CrossRefMedlineGoogle Scholar

Selasa, 20 Oktober 2015

Study the effect of hyperbaric oxygen therapy in Egyptian autistic children: A clinical trial

Study the effect of hyperbaric oxygen therapy in Egyptian autistic children: A clinical trial Farida El-baza, , , Reham M. Elhossinya, , , Yasser Abdel Azeemb, , Marianne Girgisa Show more doi:10.1016/j.ejmhg.2014.01.004 Get rights and content Open Access funded by Ain Shams University Under a Creative Commons license Abstract Background Numerous studies of autistic individuals have revealed evidence of cerebral hypoperfusion, neuroinflammation, gastrointestinal inflammation, immune dysregulation, oxidative stress, relative mitochondrial dysfunction, and neurotransmitter abnormalities. Many of these findings have been correlated with core autistic symptoms. For example, cerebral hypoperfusion in autistic children has been correlated with repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication. Specifically, hyperbaric oxygen therapy (HBOT) has been used and can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues. The aim of this work was to study the effect of hyperbaric oxygen therapy in autistic Egyptian children. Patients and methods This prospective clinical trial study was conducted on 20 children diagnosed as autism based on DSM-IV-TR criteria (diagnostic and statistical manual of mental disorders, 4th edition criteria, text revised). All patients received at least 20 sessions of hyperbaric oxygen therapy. Sessions were done at pressure 1.5 ATA (atmosphere absolute) with 100% oxygen concentration each lasting for 1–1.5 h either in multiplace chamber or monoplace chamber. MRI Perfusion of the brain was done before and after at least 20 HBOT sessions only for 6 cases. Results There was a statistically significant increase in the ratio of regional cerebral blood flow (RCBF) to white matter after HBOT in different brain regions when compared to their levels before HBOT. Conclusion HBOT is a treatment that has recently become quite popular in the autism spectrum disorder (ASD) community. Its benefits cross a wide range of autistic traits as: improved language, increased awareness, behavior and socialization by affecting the pathophysiological findings in autism. Keywords Autism; Hyperbaric oxygen therapy; Oxidative stress; Behavior

Selasa, 13 Oktober 2015

Oxygen Chamber Therapy May Ease Fibromyalgia, Study Suggests By Maureen Salamon

Oxygen Chamber Therapy May Ease Fibromyalgia, Study Suggests By Maureen Salamon HealthDay Reporter WEDNESDAY, June 24, 2015 (HealthDay News) -- The majority of women with fibromyalgia who underwent hyperbaric oxygen therapy -- best known for treating "the bends" in scuba divers -- experienced relief from pain and other symptoms, a small study found. Brain scans of the patients showed that two months of hyperbaric oxygen therapy may have also repaired abnormal brain activity in pain-related areas of the brain, the researchers said. "Seventy percent of the patients could not be categorized as suffering from fibromyalgia at the end of the treatment," said study author Dr. Shai Efrati, director of the Sagol Center for Hyperbaric Medicine and Research in Tel Aviv, Israel. "The good correspondence between the physiological improvements and the changes in brain functionality ... make the results particularly convincing," Efrati added. The research is published in the June issue of the journal PLOS ONE. Fibromyalgia is a pain syndrome that affects nine times more women than men. Symptoms include chronic widespread pain, intense pain in response to pressure on certain body parts, fatigue and poor sleep, according to the American College of Rheumatology (ACR). The condition is poorly understood because no single cause has been traced. Physical or emotional factors may trigger symptoms, the ACR says. Fibromyalgia is typically treated with a combination of therapies, including drugs, lifestyle changes and cognitive behavioral therapy. The new study included 48 women who had been diagnosed with fibromyalgia at least two years earlier. Half underwent 40 hyperbaric oxygen therapy treatments over two months. The treatments were given five times a week. They lasted 90 minutes each session. During the treatment, patients breathed 100 percent oxygen pressurized to twice the normal air pressure. The therapy is thought to increase oxygen flow to body tissues, improving healing. Administered in cylindrical chambers, the therapy has been approved by the U.S. Food and Drug Administration to treat 14 conditions, including decompression sickness among scuba divers, diabetic wounds, radiation injury from cancer treatments, serious infections, severe burns, and carbon monoxide poisoning. Fibromyalgia is not one of the currently FDA-approved conditions for hyperbaric oxygen therapy, which continues to be tested for this and other "off-label" conditions. After a two-month delay, the other 24 women in the study were then exposed to the same hyperbaric oxygen therapy treatment as the first group, after which they experienced similar symptom relief and brain scan changes, Efrati said. Patients were able to significantly reduce or even eliminate their use of pain medications, he said. One U.S. expert not involved with the study said the new finding has potential. "I think this could give patients another option to help manage their pain from fibromyalgia," said Dr. Michelle Dang, a pain management specialist and anesthesiologist at Houston Methodist Hospital. "It's a debilitating pain where there aren't a whole lot of treatment options available," she said, "and these patients will experience pain for pretty much the whole day." But health insurance or Medicare are unlikely to cover the cost of hyperbaric oxygen therapy for fibromyalgia at this point, since it's not one of the FDA-approved uses. According to the Duke Center for Hyperbaric Medicine and Environmental Physiology in North Carolina, the total cost of the 30 to 60 treatments required for most conditions can approximate that of a major surgical procedure -- tens of thousands of dollars. Dang said some of her fibromyalgia patients who use a continuous positive airway pressure (CPAP) machine to treat their coexisting sleep apnea also experience an improvement in their fibromyalgia symptoms. This improvement may be due to the increased oxygen flow to their brain and other tissues, she said. "Fibromyalgia isn't a well-understood disorder and there are a lot of different components to it," Dang said. "This [oxygen chamber therapy] may be one good option for these patients." More information The U.S. National Library of Medicine offers more information on hyperbaric oxygen therapy. SOURCES: Shai Efrati, M.D., director, research and development unit, and director, Sagol Center for Hyperbaric Medicine and Research, Assaf-Harofeh Medical Center, Tel Aviv, Israel; Michelle Dang, M.D., anesthesiologist and pain management specialist, Houston Methodist Hospital, Houston, Texas; June 2015, PLOS ONE Last Updated: Jun 24, 2015 Copyright © 2015 HealthDay. All rights reserved.

Selasa, 06 Oktober 2015

New Study Reaffirms: Hyperbaric Oxygen Therapy Should Be Standard Treatment for Veterans 41

New Study Reaffirms: Hyperbaric Oxygen Therapy Should Be Standard Treatment for Veterans 41 BY ANH-USA ON DECEMBER 6, 2011 TELL THE TRUTH, YES TO HYPERBARIC OXYGEN THERAPY - ESPECIALLY FOR BRAIN DAMAGED SOLDIERS HBOTSo why does the government keep blocking its use? Research from health pioneer (and former ANH-USA board member) Dr. Paul G. Harch published in the Journal of Neurotrauma indicates that hyperbaric oxygen therapy, or HBOT, is able to dramatically help veterans with post-concussion syndrome (a form of traumatic brain injury) and post-traumatic stress disorder (PTSD). Dr. Harch is an associate clinical professor of medicine at Louisiana State University in New Orleans. Since January 2007, ANH-USA has been bringing attention to a project to have veterans treated with HBOT. In HBOT, the patient is put in a hyperbaric oxygen chamber, which saturates the tissues with twelve times more oxygen than can be absorbed by breathing. This greatly enhances the body’s own healing process. Under normal circumstances, oxygen is transported throughout the body only by red blood cells. With HBOT, oxygen is dissolved into all of the body’s fluids, the plasma, the central nervous system fluids, the lymph, and the bone, and can be carried to areas where circulation is diminished or blocked. In this way, extra oxygen can reach all of the damaged tissues and the body can support its own healing process. The increased oxygen greatly enhances the ability of white blood cells to kill bacteria, reduces swelling, and allows new blood vessels to grow more rapidly into the affected areas. It is a simple, non-invasive, and painless treatment. According to Dr. Harch’s new study, even three years after the vets sustained brain injury, one month of HBOT was able to induce improvements in brain blood flow, cognition, symptoms, and quality of life, while the veterans experienced fewer suicidal thoughts. Specifically, improvements were seen in 92% of vets experiencing short-term memory problems, 87% of those complaining of headaches, 93% of those with cognitive deficits, 75% with sleep disruption, and 93% with depression. There were also improvements in irritability, mood swings, impulsivity, balance, motor function, IQ, and blood flow in the brain, as well as the reduction in PTSD symptoms and suicidal thoughts. And there was a reduction in—or complete elimination of—psychoactive and narcotic prescription medication usage in 64% of those previously prescribed the medication. One major problem is that the HBOT treatment is currently “off-label.” In other words, it is an FDA-approved treatment for some conditions—but not for traumatic brain injury (TBI) or PTSD. Because of this, the Department of Defense does not allow HBOT to be prescribed for its veterans—they say they don’t prescribe off-label medications and treatments for these diagnoses, and claim that they can only use HBOT after it has been approved by the FDA for this use. This is a completely false and misleading statement! The Department of Defense often uses off-label antipsychotic drugs for treatment of TBI and PTSD. This should not surprise us. The FDA receives a large proportion of its budget from pharmaceutical manufacturers. And the government turns to drugs, often very inappropriate and damaging drugs, to treat damaged veterans without even considering alternatives. Nearly 280,000 individuals received antipsychotic medication in 2007. Yet over 60% of them had no record of a diagnosis for which these drugs are approved. Antipsychotic drugs were prescribed off-label for PTSD (42% of the patients), minor depression (40%), major depression (23%), and anxiety disorder (20%)—with about 20% having more than one condition. About 20% of veterans diagnosed with PTSD—or nearly 87,000 patients—are prescribed an antipsychotic each year even though it is an off-label use. TBI and PTSD severely and disproportionally affect military who have served in Iraq and Afghanistan—approximately 546,000 have TBI, post-concussion syndrome (PCS), and PTSD, and yet their treatment options are limited. HBOT is an effective and economical treatment for PCS and PTSD, without the very dangerous and negative side effects of antipsychotic medication. The off-label use of HBOT is a huge freedom of choice issue in medicine. But even more important, if we really want to support our troops rather than just pay lip service, don’t we need to give them the safest, most economical, and most effective treatment for their traumatic brain injuries and PTSD?

Selasa, 29 September 2015

Hyperbaric Oxygen Therapy for Post-Concussion Syndrome: Contradictory Conclusions from a Study Mischaracterized as Sham-Controlled

Journal of Neurotrauma J Neurotrauma. 2013 Dec 1; 30(23): 1995–1999. doi: 10.1089/neu.2012.2799 PMCID: PMC3837504 Hyperbaric Oxygen Therapy for Post-Concussion Syndrome: Contradictory Conclusions from a Study Mischaracterized as Sham-Controlled Paul G. Harchcorresponding author Author information ► Copyright and License information ► This article has been cited by other articles in PMC. Dear Editor, The recent study by Wolf and associates1 has affirmed the effectiveness of hyperbaric (oxygen) therapy in the treatment of patients with mild traumatic brain injury (mTBI)/post-concussion syndrome (PCS) and post-traumatic stress disorder (PTSD). This affirmation emerges from analysis of the study data, rather than from the study's stated conclusions. Mischaracterized as a sham-controlled (placebo implied) design, the study errs in concluding that “HBO2 at 2.4 ATA pressure had no effect on post-concussive symptoms after mild TBI.” A reconsideration of the science of hyperbaric therapy reveals that the study by Wolf and colleagues1 is neither a sham nor placebo-controlled study. Rather, it is a Phase II study of two composite doses of hyperbaric therapy that demonstrated significant improvements in PCS and PTSD symptoms at the 2.4 atmospheres absolute (ATA) pure oxygen dose as well as the low-pressure 1.3 ATA air/oxygen dose. Hyperbaric (oxygen) therapy (HBOT) is a combination product of increased pressure and increased pressure of oxygen above ambient atmospheric pressure, according to scientific principles and current Food and Drug Administration understanding. Although traditionally misdefined as a treatment for diseases based on the increased oxygen component alone (>1.4 ATA oxygen),2 it is a treatment with hyperbaric pressure and hyperoxia for disease processes2,3 whose primary targets are oxygen and pressure sensitive genes.4–6 Evidence for this dual component nature of hyperbaric therapy is found in the 351-year history of hyperbaric air therapy7 and the recent 60-year history of animal, human tissue, and human experiments that have documented biological effects of pressure, especially in the micropressure range8,9 of the Wolf and coworkers1 “sham” control group and the control groups of the Department of Defense (DoD) HBOT TBI studies.10 Examples of this literature are listed in Tables 1 and ​and22.11–28 Pressures from 1.21–1.26 ATA delivered to human29–31 and 1.0015–1.015 ATA to animal endothelial cells,32 and 1.10 and 1.20 ATA to human platelets33,34 for 15 min or longer have caused the elaboration or suppression of vasoactive substances,29–31 and the elaboration of growth factors,32 inflammatory mediators,33 oxidation products,34 and cell proliferation.32 This literature and biological effects from a 1-min exposure to 1.09 ATA or 3 min at 1.04 ATA17 inform the symptomatic improvements noted in the Wolf and associates1 “sham” group, as do benefits of hyperbaric air on spinal function and PTSD in spinal cord injured veterans during a SCUBA diving training course.28 Table 1. Table 1. In vitro and In vivo Studies on Hyperbaric (Pressure and Oxygen) Effects Table 2. Table 2. Continuation of Table 1 In vitro and in Vivo Studies on Hyperbaric (Pressure and Oxygen) Effects To meet the definition of a true sham,35 any controlled experiment to test HBOT must omit in its control groups the active ingredients of increased pressure and hyperoxia. The Wolf and colleagues1 “sham” control group does neither; rather, it includes both. The “sham” control group is exposed to 1.3/1.2 ATA of air, which is a 20–30% increase in pressure and 28–43% increase in plasma oxygen36 over sea level plasma oxygen and a slightly greater increase over San Antonio (hyperbaric treatment site) atmospheric pressure.37 Because pressure and hyperoxia are non-inert—i.e., are biologically active—the Wolf and coworkers1 “sham” control group cannot test for placebo effects; placebo/placebo response is defined as “The effect that an inactive or inert substance has on a clinical condition.”38 Wolf and associates1 allude to possible bioactivity of the control group, but the lack of discussion indicates a lack of appreciation that the presence of hyperoxia and pressure negate Wolf and colleagues1 characterization as a “sham” control group. Restating the design of the Wolf and coworkers1 study, it is a Phase II comparative dosing study of two composite doses of hyperbaric therapy (four actual doses), compressed air (low dose increased pressure and increased oxygen), and compressed oxygen (high dose pressure and high dose oxygen). Both doses were efficacious in the treatment of mTBI PCS and PTSD. The PTSD data demonstrated 18% and 22% reductions in the PCL-M (interpolated from the Figure 1 graph in Wolf and colleagues1) in the HBOT and “sham” groups, respectively, after 30 2 h treatments. These reductions compared favorably with five other therapies/six studies for PTSD39–44 that used the PCL-M (6–45% reductions). The PCS ImPACT data were similarly significantly improved in both groups, but it is the disparity in component and pattern change on the ImPACT results for the two groups that underscore the dual dose design of the study and efficacy of these two doses: 10 IMPACT scores significantly improved in the low dose group compared with 2 in the high dose group. For all 22 items of the ImPACT, 20 improved, 1 was unchanged, and 1 was worse in the low dose group, while 11 improved, 3 were unchanged, and 8 were worse in the high dose group (Table 1 in Wolf and associates1). The pattern of composite ImPACT scores over the course of the study is also different for the two groups (Figure 2 in Wolf and coworkers1). Subjects in the low dose group experienced initial deterioration then steady improvement until the end of the study while the high dose group showed improvement then a steady reversal of benefit to near baseline, followed by rebound improvement 6 weeks post-treatment. This sinusoidal trajectory in the high dose group suggests a differential dosing effect and possibly an overdose response with partial recovery after removal of the high dose, and is consistent with the worsening of eight scores in this group. It is also consistent with a phenomenon previously described and documented in multiple cases of HBOT treatment of chronic cerebral disorders.45 Since the initial submission of this Letter to the Editor, Wolf and colleagues1 have now confirmed this overdosing effect on PCS symptoms in the 2.4 ATA group in a subset analysis presented on June 14, 2013.46 This demonstration of low dose effectiveness and progressive high dose overdosing is also evident in other animal and clinical studies.25,47,48 Wolf and associates1 list multiple possibilities for the improvements in PCS and PTSD, including “placebo, Hawthorne effect, the natural resolution of symptoms over time,…exposure to sham-control partial pressures of oxygen and nitrogen,…and change in living environment…and daily routine.” While 30 chamber experiences and change in living environment and daily routine are theoretical placebo contributions, the myriad standard clinical pressure/hyperoxia2 and micropressure-induced biological effects demonstrated in both animal and human studies8,9 and Tables 1 and ​and22 suggest that placebo is not the majority effect. At the same time, placebo effects were also present in all six of the aforementioned PTSD/PCL-M studies. Hawthorne effect is also theoretically possible, but the foundation/proofing of the Hawthorne effect has been undermined by re-evaluation of the initial data set.49 Symptoms in veterans with TBI and PTSD, in fact, do not resolve over time, as acknowledged by Wolf and coworkers1 in their conclusion “improved more than would be expected greater than 6 months after mTBI,” and reports on persistent care and even worsening of condition over time in the Veterans Affairs system.50,51 All of the explanations by Wolf and colleagues,1 however, do not explain the disparity in component and pattern change in the ImPACT data and transient overdose effect in the high dose oxygen group. If placebo, Hawthorne effect, and other non-biological etiologies are causally entertained, why wouldn't the component and pattern changes be identical in the two groups? The last choice, effects of increased partial pressures of oxygen and nitrogen, seems most plausible as the dominant etiology for the statistically significant improvements in both groups, but it is not necessarily nitrogen pressure, but pressure, per se, that is involved. Wolf and associates1 state, however, “…it seems very unlikely such a minimal dose of oxygen and nitrogen could influence brain function favorably.” The preceding argument and studies in Table 1 and ​and22 suggest the opposite. In conclusion, the study by Wolf and colleagues1 is a non-sham/non-placebo/non-controlled Phase II two composite dose study of hyperbaric therapy (hyperbaric air and hyperbaric oxygen) in U.S. veterans with PCS from mTBI with or without PTSD. The study demonstrated significant net improvements in PCS and PTSD symptoms with both doses of hyperbaric therapy, improvements that are similar in magnitude to other therapies for PTSD and greater than would be expected for PTSD and PCS over time without treatment based on the natural history of the diseases and published persistence rates in veterans.50,51 Their results are thus comparatively effective to other existing therapies for PTSD and possibly PCS of mTBI. If further evidence for the efficacy of hyperbaric therapy in mTBI PCS and PTSD is deemed necessary, as alternatives to the “pivotal” trial,10 and in light of nearly $1 billion dollars of research and development money already spent by the Department of Defense (DoD) on research seeking effective treatments for TBI and PTSD, this author would suggest two options: (1) Abandoning the pursuit of a “sham” hyperbaric control group and prioritizing the data from the wait-list group in the DoD HOPP study10 (Wolf and coworkers1 mention a wait-list group in their recommendations for future studies). This option is based on the physical impossibility of controlling for a chamber experience because of the inability to control for pressure (no method to duplicate middle ear pressure changes without placement of pressure equalization tubes and no commercially available mechanisms to duplicate adiabatic heating and cooling on compression and decompression). Continued attempts at a “sham” pressure control group will only further confuse the scientific and lay community; and (2) an economical Civilian/DoD/Veterans Affairs (VA) off-label networked hyperbaric treatment program using a Medicare-like Coverage with Evidence Development52 pathway. The safety of HBOT 1.5 and even higher doses is not in issue; hyperbaric oxygen therapy in mTBI PCS/PTSD has satisfied one of the cardinal rules of medicine, “First, Do No Harm.” The Coverage with Evidence pathway would allow the DoD and VA to immediately begin treating active military and veteran casualties with hyperbaric therapy in both military and civilian clinics/hospitals such that this health and quality of life improving therapy can be delivered without further delay to the hundreds of thousands of injured PCS/PTSD casualties and veterans now in need. Go to: Author Disclosure Statement Dr. Harch owns a small consulting company, Harch Hyperbarics, Inc., and is president of a non-profit corporation, The International Hyperbaric Medical Foundation (IHMF). He derives no income, salary, or benefits from the IHMF. Go to: References 1. Wolf G. Cifu D. Baugh L. Carne W. Profenna L. The effect of hyperbaric oxygen on symptoms after mild traumatic brain injury. J. Neurotrauma. 2012;29:2606–2612. [PubMed] 2. Gesell L.B. The Hyperbaric Oxygen Therapy Committee Committee Report. Hyperbaric Oxygen Therapy Indications. 12th. Undersea and Hyperbaric Medical Society; Durham, NC: 2009. pp. 4–5. 3. Harch P.G. Neubauer R.A. Hyperbaric oxygen therapy in global cerebral ischemia/anoxia and coma. In: Jain K.K., editor. Textbook of Hyperbaric Medicine. 3rd. Chapter 18. Hogrefe and Huber Publishers; Seattle: 1999. pp. 319–345. revised. 4. Godman C.A. Chheda K.P. Hightower L.E. Perdrizet G. Shin D.G. Giardina C. Hyperbaric oxygen induces a cytoprotective and angiogenic response in human microvascular endothelial cells. Cell Stress Chaperones. 2010;15:431–442. [PMC free article] [PubMed] 5. Chen Y. Nadi N.S. Chavko M. Auker C.R. McCarron R.M. Microarray analysis of gene expression in rat cortical neurons exposed to hyperbaric air and oxygen. Neurochem. Res. 2009;34:1047–1056. [PubMed] 6. Kendall A.C. Whatmore J.L. Harries L.W. Winyard P.G. Eggleton P. Smerdon G.R. Different oxygen treatment pressures alter inflammatory gene expression in human endothelial cells. Undersea Hyper. Med. 2013;40:115–123. [PubMed] 7. Jain K.K. The history of hyperbaric medicine. In: Jain K.K., editor. Textbook of Hyperbaric Medicine. 4th. Hogrefe and Huber Publishers; Cambridge, MA: 2004. pp. 3–8. revised and expanded edition. 8. Dean J.B. Mulkey D.K. Garcia A.J., III Putnam R.W. Henderson R.A., III Neuronal sensitivity to hyperoxia, hypercapnia, and inert gases at hyperbaric pressures. J. Appl. Physiol. 2003;95:883–909. [PubMed] 9. Macdonald A.G. Fraser P.J. The transduction of very small hydrostatic pressures. Comp. Biochem. Physiol. A. Mol. Integr. Physiol. 1999;122:13–36. [PubMed] 10. Weaver L.K. Cifu D. Hart B. Wolf G. Miller S. Hyperbaric oxygen for post-concussion syndrome: design of Department of Defense clinical trials. Undersea Hyperb. Med. 2012;39:807–814. [PubMed] 11. Trimble V.H. The Uncertain Miracle: Hyperbaric Oxygenation. Doubleday & Company, Inc.; Garden City, NY: 1974. 12. Dowell R.T. McManus R.E., III Pressure-induced cardiac enlargement in neonatal and adult rats. Left ventricular functional characteristics and evidence of cardiac muscle cell proliferation in the neonate. Circ. Res. 1978;42:303–310. [PubMed] 13. Hishikawa K. Nakaki T. Marumo T. Hayashi M. Suzuki H. Kato R. Saruta T. Pressure promotes DNA synthesis in rat cultured vascular smooth muscle cells. J. Clin. Invest. 1994;93:1975–1980. [PMC free article] [PubMed] 14. Mattana J. Singhal P.C. Applied pressure modulates mesangial cell proliferation and matrix synthesis. Am. J. Hypertens. 1995;8:1112–1120. [PubMed] 15. Teiger E. Than V.D. Richard L. Wisnewsky C. Tea B.S. Gaboury L. Tremblay J. Schwartz K. Hamet P. Apoptosis in pressure overload-induced heart hypertrophy in the rat. J. Clin. Invest. 1996;97:2891–2897. [PMC free article] [PubMed] 16. Kramer M.R. Springer C. Berkman N. Glazer M. Bublil M. Bar-Yishay E. Godfrey S. Rehabilitation of hypoxemic patients with COPD at low altitude at the Dead Sea, the lowest place on earth. Chest. 1998;113:571–575. [PubMed] 17. Kawata Y. Mizukami Y. Fujii Z. Sakumura T. Yoshida K. Matsuzaki M. Applied pressure enhances cell proliferation through mitogen-activated protein kinase activation in mesangial cells. J. Biol. Chem. 1998;273:16905–16912. [PubMed] 18. Agar A. Yip S.S. Hill M.A. Coroneo M.T. Pressure related apoptosis in neuronal cell lines. J. Neurosci. Res. 2000;60:495–503. [PubMed] 19. Dean J.B. Mulkey D.K. Continuous intracellular recording from mammalian neurons exposed to hyperbaric helium, oxygen, or air. J. Appl. Physiol. 2000;89:807–822. [PubMed] 20. Heal R.D. Rogers A.T. Lunt G.G. Pointer S.A. Parsons A.T. Development of a neuronal pressure sensor. Biosens. Bioelectron. 2001;16:905–909. [PubMed] 21. Collet J.P. Vanasse M. Marois P. Amar M. Goldberg J. Lambert J. Lassonde M. Hardy P. Fortin J. Tremblay S.D. Montgomery D. Lacroix J. Robinson A. Majnemer A. HBO-CP Research Group. Hyperbaric oxygen for children with cerebral palsy: a randomized multicentre trial. Lancet. 2001;357:582–586. [PubMed] 22. Yu H.A.I. Tian R.L. Pan X.W. Luan Z. Song L.W. Effects of hyperbaric oxygen on brain bFGF and bFGF mRNA expression of neonatal rats after hypoxia-ischemia injury. In: Joiner J.T., editor. The Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child; Flagstaff: Best Publishing Co; 2002. pp. 57–66. 23. Heuser G. Heuser S.A. Rodelander D. Aguilera O. Uszler M. Treatment of neurologically impaired adults and children with “mild” hyperbaric oxygen (1.3ATA and 24% oxygen). In: Joiner J.T., editor. The Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child; Flagstaff: Best Publishing Co; 2002. pp. 109–116. 24. Kazantseva N.V. Mechanisms of curative effect of minimized hyperbaric treatment in cerebral ischemia. In: Joiner J.T., editor. The Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child; Flagstaff: Best Publishing Co; 2002. pp. 199–212. 25. Rusyniak D.E. Kirk M.A. May J.D. Kao L.W. Brizendine E.J. Welch J.L. Cordell W.H. Alonso R.J. Hyperbaric oxygen therapy in acute ischemic stroke: results of the Hyperbaric Oxygen in Acute Ischemic Stroke Trial Pilot Study. Stroke. 2003;34:571–574. [PubMed] 26. Stanley A.C. Lounsbury K.M. Corrow K. Callas P.W. Zhar R. Howe A.K. Ricci M.A. Pressure elevation slows the fibroblast response to wound healing. J. Vasc. Surg. 2005;42:546–551. [PubMed] 27. Rossignol D.A. Rossignol L.W. Smith S. Schneider C. Logerquist S. Usman A. Neubrander J. Madren E.M. Hintz G. Grushkin B. Mumper E.A. Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial. BMC Pediatr. 2009;13:9–21. [PMC free article] [PubMed] 28. Kaplin A. Becker D. Scuba diving improves function of body, mind in vets with spinal cord injury. http://www.newswise.com/articles/view/580607. [Sep 21;2013 ]. http://www.newswise.com/articles/view/580607 29. Tokunaga O. Watanabe T. Properties of endothelial cells and smooth muscle cell cultured in ambient pressure. In Vitro Cell Dev. Biol. 1987;23:528–534. [PubMed] 30. Tokunaga O. Fan J.L. Watanabe T. Atherosclerosis and endothelium. Part II. Properties of aortic endothelial and smooth muscle cells cultured at venous ambient pressures. Acta Pathol Jpn. 1989;39:356–362. [PubMed] 31. Hishikawa K. Nakaki T. Suzuki H. Saruta T. Kato R. New method of investigating functional roles of pressure sensitive mechanoreceptor in human endothelial cells. J. Cardiovasc. Pharmacol. 1992;20(Suppl. 12):S66–S67. [PubMed] 32. Acevedo A.D. Bowser S.S. Gerritsen M.E. Bizios R. Morphological and proliferative responses of endothelial cells to hydrostatic pressure: role of fibroblast growth factor. J. Cell Physiol. 1993;157:603–614. [PubMed] 33. Torsellini A. Belvicci A. Citti S. Cozzolino F. Guidi G. Lombardi V. Vercilli D. Veloci M. Effects of pressure excursions on human platelets. In vitro studies on beta-thromboglobulin (β-TG) and platelet factor 4 (PF4) release and on platelet sensitivity to ADP-aggregation. Haematologica. 1982;67:860–866. [PubMed] 34. Torsellini A. Donc L. Palinski W. Guidi G. Lombardi V. Pressure-induced metabolic activation of platelets demonstrated in vitro by determination of malondialdehyde formation. Thromb. Haemostas. 1984;52:4–6. [PubMed] 35. Sham. http://www.merriam-webster.com/medical/sham. [Sep 13;2013 ]. http://www.merriam-webster.com/medical/sham 36. Alveolar gas equation. http://en.wikipedia.org/wiki/Alveolar_gas_equation. [Sep 13;2013 ]. http://en.wikipedia.org/wiki/Alveolar_gas_equation 37. San Antonio. http://en.wikipedia.org/wiki/San_Antonio#Geography. [Sep 21;2013 ]. http://en.wikipedia.org/wiki/San_Antonio#Geography 38. Placebo effect. http://medical-dictionary.thefreedictionary.com/placebo+effect. [Sep 21;2013 ]. http://medical-dictionary.thefreedictionary.com/placebo+effect 39. Alvarez J. Mclean C. Harris A.H. Rosen C. Ruzek J.I. Kimerling R. The comparative effectiveness of cognitive processing therapy for male veterans treated in a VHA posttraumatic stress disorder residential rehabilitation program. J. Consult. Clin. Psychol. 2011;79:590–599. [PubMed] 40. Chard K.M. Schumm J.A. McIlvain S.M. Bailey G.W. Parkinson R.B. Exploring the efficacy of a residential treatment program incorporating cognitive processing therapy-cognitive for veterans with PTSD and traumatic brain injury. J. Trauma. Stress. 2011;24:347–351. [PubMed] 41. Macdonald A. Monson C.M. Doron-Lamarca S. Resick P.A. Palfai T.P. Identifying patterns of symptom change during a randomized controlled trial of cognitive processing therapy for military-related posttraumatic stress disorder. J. Trauma. Stress. 2011;24:268–276. [PubMed] 42. Rizzo A. Parsons T.D. Lange B. Kenny P. Buckwalter J.G. Rothbaum B. Difede J. Frazier J. Newman B. Williams J. Reger G. Virtual reality goes to war: a brief review of the future of military behavioral healthcare. J. Clin. Psychol. Med. Settings. 2011;18:176–187. [PubMed] 43. Rosenthal J.A. Grosswald S. Ross R. Rosenthal N. Effects of transcend-dental meditation in veterans of Operation Enduring Freedom and Operation Iraqi Freedom with posttraumatic stress disorder: a pilot study. Mil. Med. 2011;176:626–630. [PubMed] 44. Wolf G.K. Stron T.Q. Kehle S.M. Eftekhari A. A preliminary examination of prolonged exposure therapy with Iraq and Afghanistan veterans with a diagnosis of posttraumatic stress disorder and mild to moderate traumatic brain injury. J. Head Trauma Rehabil. 2012;27:26–32. [PubMed] 45. Harch P.G. The dosage of hyperbaric oxygen in chronic brain injury. In: Joiner J.T., editor. The Proceedings of the 2nd International Symposium on Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child; Flagstaff: Best Publishing Co.; 2002. pp. 31–56. 46. Scorza K.A. McCarthy W. Miller R.S. Carne W. Wolf G. Hyperbaric oxygen effects on PTSD and mTBI symptoms: a subset analysis. Presented at the Undersea and Hyperbaric Medical Society Annual Meeting; Orlando, FL. 2013. 47. Gordillo G.M. Roy S. Khanna S. Schlanger R. Khandelwal S. Phillips G. Sen C.K. Topical oxygen therapy induces vascular endothelial growth factor expression and improves closure of clinically presented chronic wounds. Clin. Exp. Pharmacol. Physiol. 2008;35:957–964. [PMC free article] [PubMed] 48. Patel V. Chivukula I.V. Roy S. Khanna S. He G. Ojha N. Mehrotra A. Dias L.M. Hunt T.K. Sen C.K. Oxygen: from the benefits of inducing VEGF expression to managing the risk of hyperbaric stress. Antioxid. Redox Signal. 2005;7:1377–1387. [PubMed] 49. Questioning the Hawthorne effect. Light work. Being watched may not affect behaviour, after all. http://www.economist.com/node/13788427?story_id=13788427. [Sep 21;2013 ]. http://www.economist.com/node/13788427?story_id=13788427 50. For combat vets, brain injury symptoms can last years. http://health.usnews.com/health-news/news/articles/2012/06/20/for-combat-vets-brain-injury-symptoms-can-last-years. [Sep 21;2013 ]. http://health.usnews.com/health-news/news/articles/2012/06/20/for-combat-vets-brain-injury-symptoms-can-last-years 51. The Veterans Health Administration's treatment of PTSD and traumatic brain injury among recent combat veterans. http://www.cbo.gov/sites/default/files/cbofiles/attachments/02-09-PTSD.pdf. [Sep 21;2013 ]. http://www.cbo.gov/sites/default/files/cbofiles/attachments/02-09-PTSD.pdf 52. Tunis S.R. Pearson S.D. Coverage options for promising technologies: Medicare's ‘coverage with evidence development.’ Health Aff. (Millwood) 2006;25:1218–1230. [PubMed] Articles from Journal of Neurotrauma are provided here courtesy of Mary Ann Liebert, Inc.

Selasa, 22 September 2015

A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury.

J Neurosurg. 2010 May;112(5):1080-94. doi: 10.3171/2009.7.JNS09363. A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury. Rockswold SB1, Rockswold GL, Zaun DA, Zhang X, Cerra CE, Bergman TA, Liu J. Author information Abstract OBJECT: Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain under normobaric as well as hyperbaric conditions. In this study the authors directly compare hyperbaric oxygen (HBO2) and normobaric hyperoxia (NBH) treatment effects. METHODS: Sixty-nine patients who had sustained severe TBIs (mean Glasgow Coma Scale Score 5.8) were prospectively randomized to 1 of 3 groups within 24 hours of injury: 1) HBO2, 60 minutes of HBO(2) at 1.5 ATA; 2) NBH, 3 hours of 100% fraction of inspired oxygen at 1 ATA; and 3) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue PO(2), microdialysis, and intracranial pressure were continuously monitored. Cerebral blood flow (CBF), arteriovenous differences in oxygen, cerebral metabolic rate of oxygen (CMRO2), CSF lactate and F2-isoprostane concentrations, and bronchial alveolar lavage (BAL) fluid interleukin (IL)-8 and IL-6 assays were obtained pretreatment and 1 and 6 hours posttreatment. Mixed-effects linear modeling was used to statistically test differences among the treatment arms as well as changes from pretreatment to posttreatment. RESULTS: In comparison with values in the control group, the brain tissue PO2 levels were significantly increased during treatment in both the HBO2 (mean +/- SEM, 223 +/- 29 mm Hg) and NBH (86 +/- 12 mm Hg) groups (p < 0.0001) and following HBO2 until the next treatment session (p = 0.003). Hyperbaric O2 significantly increased CBF and CMRO2 for 6 hours (p < or = 0.01). Cerebrospinal fluid lactate concentrations decreased posttreatment in both the HBO2 and NBH groups (p < 0.05). The dialysate lactate levels in patients who had received HBO2 decreased for 5 hours posttreatment (p = 0.017). Microdialysis lactate/pyruvate (L/P) ratios were significantly decreased posttreatment in both HBO2 and NBH groups (p < 0.05). Cerebral blood flow, CMRO2, microdialysate lactate, and the L/P ratio had significantly greater improvement when a brain tissue PO2 > or = 200 mm Hg was achieved during treatment (p < 0.01). Intracranial pressure was significantly lower after HBO2 until the next treatment session (p < 0.001) in comparison with levels in the control group. The treatment effect persisted over all 3 days. No increase was seen in the CSF F2-isoprostane levels, microdialysate glycerol, and BAL inflammatory markers, which were used to monitor potential O2 toxicity. CONCLUSIONS: Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 > or = 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were prese

Selasa, 15 September 2015

Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial

Hyperbaric treatment for children with autism: a multicenter, randomized, double-blind, controlled trial Daniel A RossignolEmail author, Lanier W Rossignol, Scott Smith, Cindy Schneider, Sally Logerquist, Anju Usman, Jim Neubrander, Eric M Madren, Gregg Hintz, Barry Grushkin and Elizabeth A Mumper BMC Pediatrics20099:21 DOI: 10.1186/1471-2431-9-21© Rossignol et al. 2009 Received: 20 January 2009Accepted: 13 March 2009Published: 13 March 2009 Abstract Background Several uncontrolled studies of hyperbaric treatment in children with autism have reported clinical improvements; however, this treatment has not been evaluated to date with a controlled study. We performed a multicenter, randomized, double-blind, controlled trial to assess the efficacy of hyperbaric treatment in children with autism. Methods 62 children with autism recruited from 6 centers, ages 2–7 years (mean 4.92 ± 1.21), were randomly assigned to 40 hourly treatments of either hyperbaric treatment at 1.3 atmosphere (atm) and 24% oxygen ("treatment group", n = 33) or slightly pressurized room air at 1.03 atm and 21% oxygen ("control group", n = 29). Outcome measures included Clinical Global Impression (CGI) scale, Aberrant Behavior Checklist (ABC), and Autism Treatment Evaluation Checklist (ATEC). Results After 40 sessions, mean physician CGI scores significantly improved in the treatment group compared to controls in overall functioning (p = 0.0008), receptive language (p < 0.0001), social interaction (p = 0.0473), and eye contact (p = 0.0102); 9/30 children (30%) in the treatment group were rated as "very much improved" or "much improved" compared to 2/26 (8%) of controls (p = 0.0471); 24/30 (80%) in the treatment group improved compared to 10/26 (38%) of controls (p = 0.0024). Mean parental CGI scores significantly improved in the treatment group compared to controls in overall functioning (p = 0.0336), receptive language (p = 0.0168), and eye contact (p = 0.0322). On the ABC, significant improvements were observed in the treatment group in total score, irritability, stereotypy, hyperactivity, and speech (p < 0.03 for each), but not in the control group. In the treatment group compared to the control group, mean changes on the ABC total score and subscales were similar except a greater number of children improved in irritability (p = 0.0311). On the ATEC, sensory/cognitive awareness significantly improved (p = 0.0367) in the treatment group compared to the control group. Post-hoc analysis indicated that children over age 5 and children with lower initial autism severity had the most robust improvements. Hyperbaric treatment was safe and well-tolerated. Conclusion Children with autism who received hyperbaric treatment at 1.3 atm and 24% oxygen for 40 hourly sessions had significant improvements in overall functioning, receptive language, social interaction, eye contact, and sensory/cognitive awareness compared to children who received slightly pressurized room air.

Selasa, 08 September 2015

Hyperbaric hope for fibromyalgia sufferers

Hyperbaric hope for fibromyalgia sufferers MIKE WILLIAMS – JUNE 2, 2015 POSTED IN: CURRENT NEWS Rice University part of Israel study to test novel treatment for little-understood condition Women who suffer from fibromyalgia benefit from a treatment regimen in a hyperbaric oxygen chamber, according to researchers at Rice University and institutes in Israel. A clinical trial involving women diagnosed with fibromyalgia showed the painful condition improved in every one of the 48 who completed two months of hyperbaric oxygen therapy. Brain scans of the women before and after treatment gave credence to the theory that abnormal conditions in pain-related areas of the brain may be responsible for the syndrome. Results of the study appear in the open-access journal PLOS One. Fibromyalgia is a chronic pain syndrome that can be accompanied by – and perhaps related to – other physical and mental conditions that include fatigue, cognitive impairment, irritable bowel syndrome and sleep disturbance. More than 90 percent of those diagnosed with the syndrome are women, said Eshel Ben-Jacob, a lead author of the proof-of-concept study who developed the analytical method used to show the association between patients’ improvement and changes in their brains. He is an adjunct professor of biosciences at Rice University, a senior investigator at Rice’s Center for Theoretical Biological Physics and a professor of physics and member of the Sagol School of Neuroscience at Tel Aviv University. Editor’s note: After this story’s publication, Rice’s Eshel Ben-Jacob died suddenly at his home in Israel June 5. An obituary appears in the June 8 edition of Rice News. “Symptoms in about 70 percent of the women who took part have to do with the interpretation of pain in their brains,” Ben-Jacob said. “They’re the ones who showed the most improvement with hyperbaric oxygen treatment. We found significant changes in their brain activity.” Scientists have not pinned down the syndrome’s cause, although another recent PLOS One study identified a possible RNA-based biomarker for its diagnosis. A variety of treatments from drugs to lifestyle changes have been tried to relieve patients’ suffering, with limited success, Ben-Jacob said. “Most people have never heard of fibromyalgia,” he said. “And many who have, including some medical doctors, don’t admit that this is a real disorder. I learned from my M.D. friends that this is not the only case in which disorders that target mainly women raise skepticism in the medical community as to whether they’re real or not. However, these days there are increasing efforts to understand the effect of gender on body disorders.” Two 20-seat hyperbaric chambers at the Sagol Center for Hyperbaric Medicine and Research in Israel. Two 20-seat hyperbaric chambers at the Sagol Center for Hyperbaric Medicine and Research in Israel were used in a study to see if hyperbaric oxygen treatment could help patients with fibromyalgia. A new study by researchers at Rice University and institutes in Israel showed patients in a small trial experienced remarkable improvement after two months of treatment. Courtesy of the Sagol Center for Hyperbaric Medicine and Research Researchers at the Sagol Center for Hyperbaric Medicine and Research at the Assaf Harofeh Medical Center and Tel Aviv University were studying post-traumatic brain injury patients when they realized hyperbaric oxygen treatment (HBOT) could help patients with fibromyalgia. “Patients who had fibromyalgia in addition to their post-concussion symptoms had complete resolution of the symptoms,” said Dr. Shai Efrati, who noted his own mother suffers from the syndrome. Efrati is lead author of the study, head of the research and development unit at the Assaf Harofeh Medical Center and a member of the Sagol School of Neuroscience at Tel Aviv University. Hyperbaric oxygen chambers that expose patients to pure oxygen at higher-than-atmospheric pressures are commonly used to treat patients with embolisms, burns, carbon monoxide poisoning and decompression sickness (known to divers as “the bends”), among many other conditions. One effect of exposure is to push more oxygen into a patient’s bloodstream, which delivers it to the brain. Efrati’s earlier trials found HBOT induces neuroplasticity that leads to repair of chronically impaired brain functions and improved quality of life for post-stroke and mild traumatic brain injury patients, even years after the initial injury. Ben-Jacob said two patients spearheaded the push for the study. One was an Oxford graduate student who developed fibromyalgia after suffering a traumatic brain injury in a train crash. “By chance, the secretary of the department where she worked is the mother of the nurse in charge of the HBOT. She said you have to go and try to do it,” he recalled. The other, he said, is a professor of sociology who specializes in post-traumatic stress disorders due to child abuse. The professor had suffered from fibromyalgia for many years. Her symptoms got worse through the initial treatments – a common experience for other patients in the study who she said had suppressed memories due to child abuse – before they got better. But by the end of treatment both women showed remarkable improvement, Ben-Jacob said. The interior of a hyperbaric chamber at the Sagol Center for Hyperbaric Medicine and Research in Israel, used to treat patients with fibromyalgia in a recent trial. The interior of a hyperbaric chamber at the Sagol Center for Hyperbaric Medicine and Research in Israel, used to treat patients with fibromyalgia in a recent trial. Courtesy of the Sagol Center for Hyperbaric Medicine and Research Efrati said some patients will likely require follow-up sessions. “The abnormalities in brain regions responsible for the chronic pain sensation in fibromyalgia patients can be triggered by different events,” he said. “Accordingly, the long-term response may be different. “We have learned, for example, that when fibromyalgia is triggered by traumatic brain injury, we can expect complete resolution without any need for further treatment. However, when the trigger is attributed to other causes, such as fever-related diseases, patients will probably need periodic maintenance therapy.” The clinical trial involved 60 women who had been diagnosed with fibromyalgia at least two years earlier. A dozen left the trial for various reasons, but half of the 48 patients who completed it received 40 HBOT treatments five days a week over two months. The 90-minute treatments exposed patients to pure oxygen at two times the atmospheric pressure. The other half were part of what Ben-Jacob called a crossover-control group. They were evaluated before the trial and after a control period that saw no improvement in their conditions. After the two-month control, they were given the same HBOT treatment as the first group and experienced the same relief, according to the researchers. The researchers noted the successful treatment enabled patients to drastically reduce or even eliminate their use of pain medications. “The intake of the drugs eased the pain but did not reverse the condition, while HBOT did reverse the condition,” the researchers wrote. Efrati said the findings warrant further study. “The results are of significant importance since, unlike the current treatments offered for fibromyalgia patients, HBOT is not aiming for just symptomatic improvement,” he said. “HBOT is aiming for the actual cause — the brain pathology responsible for the syndrome. It means that brain repair, including even neuronal regeneration, is possible even for chronic, long-lasting pain syndromes, and we can and should aim for that in any future treatment development.” Co-authors of the paper are Ham Golan, Olga Volkov, Gregori Fishlev, Jacob Bergan and Mony Friedman of the Sackler School of Medicine at Tel Aviv University and the Assaf Harofeh Medical Center, Zerifin, Israel; Yair Bechor of the Institute of Hyperbaric Medicine at Assaf Harofeh; Yifat Faran of Ashkelon Academic College, Israel; Shir Daphna-Tekoah of Ashkelon Academic College and Kaplan Medical Center, Israel; Gal Sekler of Tel Aviv University; Jacob Ablin of the Tel Aviv Sourasky Medical Center and Tel Aviv University; and Dan Buskila of Ben-Gurion University of the Negev, Israel. - See more at: http://news.rice.edu/2015/06/02/hyperbaric-hope-for-fibromyalgia-sufferers-2/#sthash.F9sisw1m.dpuf