Minggu, 30 November 2008

factors that influence subfertility

Conception is most likely to occur in the first month of trying (about a 30% conception rate). The chance then falls steadily to about 5% by the end of the first year. Cumulative conception rates are around 75% after six months, 90% after a year, and 95% at two years. Subfertility is defined as a failure to conceive after one year of unprotected regular sexual intercourse. It is usually investigated after a year, although for some couples it may be appropriate to start investigations sooner. The likelihood of spontaneous conception is affected by age, previous pregnancy, duration of subfertility, timing of intercourse during the natural cycle, extremes of body mass, and pathology present. A reasonably high spontaneous pregnancy rate still occurs even after the first year of trying.

Subfertility is a failure to conceive after one year of unprotected regular sexual intercourse. Subfertility can be primary or secondary Primary subfertility—a delay for a couple who have had no previous pregnancies.
Secondary subfertility—a delay for a couple who have conceived
previously, although the pregancy may not have been successful (for
example, miscarriage, ectopic pregnancy)

Age
A strong association exists between subfertility and increasing female age. The reduction in fertility is greatest in women in their late 30s and early 40s. For women aged 35-39 years the chance of conceiving spontaneously is about half that of women aged 19-26 years. The natural cumulative conception rate in the 35-39 age group is around 60% at one year and 85% at two years.

This marked, age related decline in spontaneous conception is also mirrored in the outcome of assisted conception treatment. Recent evidence shows that male fertility also declines with age. Genetic defects in sperm and oocytes that are likely to contribute to impaired gamete function and embryonic development increase with age. The age related decline in female fecundity is caused by a steadily reducing pool of competent oocytes in the ovaries.

It has been estimated that smokers are 3 times more likely to take more than a year to conceive than non-smokers, and in each cycle smokers have two thirds the chance of conceiving compared with non-smokers

Duration of subfertility
The longer a couple has to try to conceive, the smaller the chance of spontaneous conception. If the duration of subfertility is less than three years, a couple is 1.7 times more likely to conceive than couples who have been trying for longer. With unexplained subfertility of more than three years, the chances of conception occurring are about 1-3% each cycle.

Previous pregnancy
When a delay in conception has no obvious cause the likelihood of conception is increased 1.8-fold if the couple has secondary rather than primary subfertility. Timing of intercourse during ovulatory cycle The chance of conception in an ovulatory cycle is related to the day in the cycle on which intercourse takes place.

The window of opportunity lasts six days, ending on the day of ovulation. A study by Dunson et al (2002) showed that the probability of conception rose from six days before ovulation, peaked two days before ovulation, then fell markedly by the day of
ovulation. This shows that sperm need to be deposited in the female genital tract before ovulation to maximise chances of conception. This is consistent with the progesterone induced changes in cervical mucus that occur immediately after ovulation and impede the penetration of sperm.

Weight
Pregnancy is less likely if the woman’s body mass index (BMI) (weight (kg)/(height (m)2)) is > 30 or <> 30 need advice about modifying their diet and doing more exercise to lose weight and they should aim for a BMI < style="font-weight: bold;">

Other factors affecting fertility
The chance of conception may be reduced by smoking, caffeine, and use of recreational drugs. The effect of some of these factors may be attributed in part to an association with other factors that affect fertility, such as an increased risk of sexually transmitted infection.

Obesity is also associated with an increased risk of miscarriage and obstetric complications such as hypertension, gestational diabetes, thromboembolism, and complicated delivery.

The effect of alcohol on fertility is not clear as the results of studies are conflicting. Some studies have found impaired fertility in women drinking more than five units of alcohol a week, whereas others have found that low to moderate alcohol consumption may be associated with a higher conception rate than in non-drinkers. Excess alcohol consumption in men can contribute to impotence and difficulties with ejaculation and may impair spermatogenesis.

Kamis, 27 November 2008

Hidrokel

Adalah adanya cairan disekitar testis (zakar) sehingga menyebabkan skrotum (kantong zakar) menjadi bengkak. Sekitar 10% bayi baru lahir mengalami ini, dan umunya akan hilang sendiri dalam tahun pertama kehidupan. Biasanya tidak terasa nyeri dan jarang membahayakan sehingga tidak membutuhkan pengobatan. Namun jika yang mengalaminya orang dewasa segera temui dokter untuk memastikan penyebabnya.

Pada bayi laki2 hidrokel dapat terjadi mulai dari dalam rahim. Pada usia kehamilan 28 minggu , testis turun dari rongga perut bayi kedalam skrotum, dimana setiap testis ada kantong yang mengikutinya sehingga terisi cairan yang mengelilingi testis tersebut.

Umumnya kantong ini akan menutup dengan sendirinya dan cairan akan diserap. Jika setelah kantong tadi tertutup dan cairan tetap ada, kedaan ini dinamakan hidrokel non-communicating. Cairan terkurung dan tidak bisa kembali ke rongga abdomen. Cairan akhirnya akan terserap habis dalam jangka waktu lebih kurang setahun. Kasus lainnya adalah hidrokel-communicating, dimana kantongnya berhubungan dengan rongga perut.

Pada laki-laki yang lebih tua, hidrokel bisa berasal dari proses radang atau cedera pada skrotum. Radang yang terjadi bisa berupa epididimitis (radang epididimis) atau orchitis (radang testis). Pada laki2 dewasa segera temui dokter jika mengalami pembengkakan scrotum guna menyingkirkan kemungkinan tumor atau hernia guna mendapatkan penanganan yang tepat. Sedangkan pada bayi hidrokel akan hilang dengan sendirinya. Namun jika dalam setahun tidak hilang, maka perlu diperiksakan ulang kembali, guna dilakukan proses pembedahan.

Hidrokelektomi

Tindakan pembedahan berupa hidrokelektomi. Pengangkatan hidrokel bisa dlakukan anestesi umum ataupun regional (spinal). Tindakan lain adalah dengan aspirasi jarum (disedot pakai jarum). Cara ini nggak begitu digunakan karena cairan hidrokelnya akan terisi kembali. Namun jika setelah diaspirasi kemudian dimasukkan bahan pengerut (sclerosing drug) mungkin bisa menolong.(Mayo Cliinic)

Selasa, 25 November 2008

Diarrhea : between myths and facts

You and me will agree if there is a wrong view or wrong opinion about a problem, it will cause wrong action to solve the problem as well. And so do the things with diarrhea problem. In reality,especially in my country (Indonesia) still many moms believe in myths, as the consequence, they give wrong handling when the child experiences diarrhea. While, Otherwise get handling quickly and correct action, diarrhea can cause child (especially infant) experience dehydration or Liquid deficit that have further consequence as death.


Between myth and Fact
Here are some myths that still many moms in my country (especially those who live in rural area) believe:
1. Breast-feed Mom who eat hot (chili) food or contain many cooking spices will causes the baby be attacked by diarrhea.
2. Diarrhea is such kind of sign that their child is going to be smarter.
3. Child who suffered diarrhea is preferable not being given food or Drink so the diarrhea will quickly stop.


While the true facts seems to be different :
1. A New kind of Formula Milk or Solid food that given to a child can causes diarrhea.
2. Baby and child under five has habit to put his finger into mouth that cause the germ easily enter the body and causing many diseases including diarrhea.
3. Consumption of snack that not well guaranteed it’s cleanliness causes diarrhea.
4. Milk bottle using or Spoon or Plate that not well washed can causes diarrhea in child.
5. Child has lower level of body stamina compared with adult. So, they easier to be infected by diarrhea caused germ.
6. Late to be fed is another factor causing a child easier experience diarrhea.
7. Diarrhea that caused by germ sometimes as consequence from environment and Not always come from food, if child suffered diarrhea doesn't eat or drink will make him weaker and tend to experience liquid deficit (dehydration) that can be fatal.


Diarrhea causes
There are some factors that cause diarrhea:
1. Bacteria, virus and or parasite (e.g., worm) infection in digestive track.
2. Bacteria, virus and or parasite that causing infection outside the digestive track, for example the infection in ear channel, throat infection, and measles.
3. Allergy towards certain medicine or food.
4. Psychiatric disorders like fear, stress or worried .
Diarrhea general symptoms
Diarrhea evokes physical and mental symptoms.

Physical symptoms :
• Frequency of defecates more than four times (in infants) and more than thrice in one month or elder babies
• Liquid feces and Can be espoused with mucus or blood
• Diminish of appetite or absolutely gone
• The child looks weak and pale
• Feel pain in stomach
• Vomit
• Fever

Mental symptoms :
• The child is restless and whine
• More spoiled from usually, inclined to be hugged or carried.


How to overcome it?

Basic diarrhea therapy :
1. Liquid therapy
- Oral rehydration liquid, Like:
  • Oralit
  • Household liquid, For example: Salt sugar solution (is made from two teaspoon of refined sugar mixed with one teaspoon of salt and mixed with 200 cc warm water, starch water, Vegetable sauce (gravy).
- Parenteral liquid (given through intravenous drips)

2. Diet (Feeding)
E.g : Breast feeding, low lactose formula milk, milk porridge and Rice porridge.

3. Diarrhea medicines
These days widely available diarrhea medicines that contain Kaolin and Pectin that can neutralize poison or bacteria that caused Diarrhea. That medicine can be use as therapy for non specific diarrhea (not caused by germ) e.g., diarrhea that caused by food allergy. But if the diarrhea is not going abate after two days of this medicine usage or the condition is getting worst, Best call your doctor for further help.

4. Antibiotic
Antibiotic is usually not widely used to cure diarrhea except the cause has been clearly known (for example in cholera) or If found co-exist disease (for example middle ear and throat infection).


Diarrhea without dehydration

Marking :
• Defecates liquid less than four times a day
• There is no vomit or Only a little
• Child doesn’t feel thirsty
• Urine volume and color is still normal
• The child looks well
• The eye is normal with tear
• Lip and tongue are wet
• The skin is still elastic
• Normal fontanel in infant

Handling:
• Give household liquid, like : Keep Breastfeeding or formula milk .
• Keep feeding the child with appropriate food for their age.


Diarrhea with light or medium dehydration

Marking:
• Defecates liquid 4-10 time a day
• Vomit many times
• Child felts thirst
• Decrease in Total urine volume and Rust colored
• The child looks weak and Restless
• Concave eye, Dry Tear
• Dry Lip and Tongue
• The skin less elastic (slow returns after pinched)
• The infant fontanel is concave

Handling
• Give Oralit
• Give household liquid
• Keep on breast-feeding
• Give appropriate food for age. Choose soft food, easy to digest and doesn't stimulate the digestive track.
• Give diarrhea medicine when needed (suitable with doctor instruction)
• When diarrhea persistent or goes heavier, Bring the child to hospital or clinic that equipped well for advance treatment.


Diarrhea with heavy dehydration

Marking:
• Defecates liquid more than 10 time a day
• Vomit repeatedly
• Child felts very thirsty or Can not drink
• The total urine volume is very small and Rust colored
• Pale child, Unconscious
• The eye very concave, Dry tear (not exist) .
• Very Dry Lip and Tongue.
• The skin is very less elastic (slow returns after pinched)
• The fontanel in infant is very concave

Handling:
• Bring the child soon to hospital or clinic with treatment facilities.
• Keep on gift Breastfeeding or Household liquid if child or Baby is still can drink.

Multivitamin meningkatkan risiko kanker ?

Sudah kah Anda Minum Multivitamin hari ini….Itu slogan yang sering kita dengar. Banyak diantara masyarakat awam bahkan kalangan medis sendiri mempunyai pikiran bahwa dengan multivitamin tubuh akan bertambah sehat.

Tetapi baru-baru ini suatu penelitian dari Christopher G. Slatore, MD, dari University of Washington in Seattle, Washington, and colleagues yang dimuat di American Journal of Respiratory and Critical Care Medicine memperlihatkan minum suplemen multivitamin jangka panjang tidak menurunkan risiko untuk terjadi kanker paru malah pemakaian dosis tinggi dapat meningkatkan risiko.

Baca full artikel disini...bukan di baca selengkapnya

Minggu, 23 November 2008

Disfungsi Ereksi

Disfungsi ereksi (ED) adalah jika seorang co tidak bisa ereksi saat akan ML atau tidak dapat mempertahankannya sampai akhir ML. Dulu dipakai istilah impotensia.

Penyebab ED adalah: kelainan jantung, arterosklrosis (penyumbatan pembuluh darah), tekanan darah tinggi, diabetes, obesitas dan gangguan metabolik. Penyebab lainnya : obat2an, merokok, alkohol dan beberapa penyakit degenerartif seperti Parkinson,
Multiple sclerosis dll.

Selain fisik, ED juga disebabkan oleh gangguan psikologis seperti: depressi, ansietas (gelisah), stres, kelelahan (fatigue), dan komunikasi dengan pasangan yang tidak bagus.

Pengobatan untuk ED diantaranya dengan memakai obat2an seperti: Sildenafil (Viagra), Tadalafil (Cialis) serta Vardenafil (Levitra). Cuma obat-obatan ini tidak secara otomatis menghasilkan ereksi. Tetap dibutuhkan stimulasi untuk memulainya, selanjutnya obat2an ini yang akan mempertahankan ereksi yang timbul.

Obat tersebut dilaporkan dapat mengatasi masalah ED tanpa memandang penyebabnya. Namun demikian ada keadaan dimana obat2 ini dilarang untuk dimakan: yaitu jika seseorang sedang makan obat2an untuk jantung seperti nitroglycerin, ISMN (Imdur) dan ISDN (Isordil) dan obat2 antikoagulan. Obat2 untuk ED juga tidak boleh dimakan jika menderita: kelainan jantung yang berat, stroke, tensi rendah, tensi tinggi dan diabetes

Diasamping dengan obat2an diatas, ada juga obat golongan prostaglandin yang di injeksikan (tembakkan) lewat kulit. Nama obatnya alprostadil. Obat ini merelaksasi otot daerah P, sehingga melancarkan aliran darah yang dibutuhkan untuk ereksi. Ada 2 cara pemakaiannya yaitu dengan injeksi jarum (nama dagangnya: caverject atau edex)yang disuntikkan pada kluit samping P. Jarumnya sangat kecil seperti jarum insulin sehingga nggak bakalan terasa sakit. Ereksi akan timbul dalam 5-20 menit serta berlangsung 1 jam. Bentuk obat lainnya adalah supositoria (Muse), yang dimasukkan kedalam liang pipis co dengan alat khusus (aplikator). Metode ini kurang nyaman bagi co yang memakainya.

Pengobatan hormon lainnya adalah pemberian testosteron pada kasus ED akibat defesiensi hormon ini. Pengobatan yang tergolong aneh adalah dengan pompa P. P disedot dengan vakum, sehingga darah masuk kedalamnya, kemudian diikat panggkalnya dengan karet penahan, selesai ML karet ini dilepas kembali.

Bedah vaskuler biasanya dikerjakan jika aliran darah P terganggu akibat cedera atau trauma. Pembedahan hanya mebebaskan sumbatan, ereksi diharapkan terjadi secara alamiah. Terapi lainnya adalah implan yag ditanamkan kedalam batang P dari bahan yang terbuat dari silikon. Implant ini bisa ditiup mejadi besar sehingga ereksi bisa dimunculkan sesering dan selama munkin. Cuma biayanya mahal sekali dan sepertinya kurang praktis.

Terakhir pengobatan yang bersifat konseling dan psikoterapi, terutama yang disebabkan oleh ansietas atau depresi. Kadang walaupun penyebabnya bukan karena stress atau ansietas ED bisa menimbulkan perasaan ansietas dan depressi terkait hubungan dengan pasangan, sehingga dibutuhkan juga terapi psikis dan konseling.(mayo clinic)

Bra for man

Bra hanya untuk ce ? ntar dulu, sebuah toko OL Jepang baru2 ini berhasil menjual 300 bra untuk co hanya dalam waktu 2 minggu sejak diluncurkannya. Suatu pencapaian yang luar biasa. Bra ini bukan buat co yang berdada besar, melainkan buat co yang sisi kewanitaannya kuat. Lihat sendiri video promosinya dibawah ini. Ada perasaan nyaman menurut para pemakainya.

Sabtu, 22 November 2008

Kembung Saat Hamil

Ada yang nanya via email, lagi hamil dan perutnya kembung. Setiap orang tanpa memandang gender atau hamil/nggak hamil sering mengalami kembung (banyak gas dalam lambung dan usus). Penyebab utamanya pasti saja banyak nelan udara, yang kedua udara tersebut muncul akibat dari proses pencernaan makanan kita.

Udara dapat tertelan terutama jika makan atau minum dengan cepat, merokok dan makan permen karet. Sedangkan makanan yang merupakan sumber udara yang utama adalah karbohidrat.

Makanan berikut dapat menyebabkan kembung :
o Sayuran seperti broccoli, kol, bawang, asparagus
o Buah-buahan seperti pear, apel, dan buah persik
o Semua biji-bijian
o Soft drink dan fruit drink
o Susu dan produk susu seperti keju, es krim, roti dan sereal
o Makanan yang mengandung sorbitol seperti makan diet dan makan bebas gula seperti permen bebas gula, syrup bebas gula dll.

Kembung dapat diatasi dengan mengkonsumsi obat yang mengandung simetichon atau obat2 yang mengandung enzym2 pencernaan. Sedangkan untuk mencegahnya tentu saja dengan menghindari tertelan udara dan menghindari/mengurangi memakan makanan-makanan yang disebutkan diatas.

Jumat, 21 November 2008

Mengenal Endometriosis

Endometriosis merupakan salah satu penyakit jinak ginekologi yang saat ini paling banyak mendapat perhatian para ahli. Di negara maju maupun negara berkembang, telah banyak penelitian yang dilakukan terhadap endometriosis, namun hingga kini penyebab dan patogenesisnya belum diketahui secara pasti. Namun dalam satu hal para ahli sepakat, bahwa pertumbuhan endometriosis sangat dipengaruhi oleh hormon steroid, terutama estrogen.


Definisi
Kata endometriosis berasal dari kata endometrium. Arti endometriosis secara klinis adalah kelenjar dan stroma endometrium yang terdapat di luar kavum uteri, seperti di organ-organ genitalia interna, vesika urinaria, usus, peritoneum, paru, umbilikus, mata dan otak. Di tempat ini, lesi endometriosis tetap dipengaruhi oleh hormon estrogen dan progesteron sehingga dapat mengalami perubahan siklik.


Endometriosis_ovarium_dengan_perlengketan_antara_ovarium_dan_kolon_sigmoidTempat umum terjadinya implantasi adalah pada ovarium, cavum Douglasi, ligamentum latum posterior, ligamentum uterosacral, uterus, tuba fallopi, kolon sigmoid, appendiks dan ligamentum rotundum.


Epidemiologi
Endometriosis paling sering terjadi pada usia reproduksi. Insidennya yang pasti belum diketahui, namun prevalensinya pada kelompok tertentu cukup tinggi. Misalnya, pada wanita yang dilakukan laparoskopi diagnostik, ditemukan endometriosis sebanyak 0-53%; pada kelompok wanita dengan infertilitas yang belum diketahui penyebabnya ditemukan endometriosis sebanyak 70-80%; sedangkan pada kelompok wanita dengan infertilitas primer ditemukan endometriosis sebanyak 25%. Meskipun endometriosis dikatakan penyakit wanita usia reproduksi, namun telah ditemukan pula endometriosis pada usia remaja dan pascamenopause.


Patogenesis
Hingga kini penyebab endometriosis belum diketahui secara pasti. Banyak teori yang disebut ikut berperan dalam patogenesis endometriosis, sehingga penyakit ini disebut juga ‘penyakit penuh teori. Tetapi tidak satupun dari teori-teori tersebut yang benar-benar dapat menjelaskan kenapa jaringan endometrium sampai berada di luar kavum uteri.


1. Teori Regurgitasi dan Implantasi Haid
Teori ini pertama kali dikemukakan oleh Sampson pada tahun 1927. Biasanya darah haid keluar dari kavum uteri melalui vagina, namun kadang-kadang darah haid mengalir dari kavum uteri melalui tuba fallopi ke kavum peritoneum, dan berimplantasi pada permukaan peritoneum.


Meskipun tidak ada satu mekanisme tunggal yang dapat menerangkan semua kasus endometriosis, beberapa bukti mendukung teori ini sebagai teori utama dalam patogenesis endometriosis :

· Ketika laparoskopi dilakukan saat haid, darah dapat ditemukan dalam cairan peritoneal pada 75-90% wanita dengan tuba fallopi paten.
· Sel endometrium hidup yang diperoleh dari cairan peritoneal saat haid dapat tumbuh dalam kultur sel dan dapat melekat dan melakukan penetrasi ke permukaan mesothelial peritoneum.
· Endometriosis ditemukan lebih sering pada wanita dengan kelainan duktus mulleri obstruktif daripada wanita dengan malformasi dimana tidak terjadi obstrusi aliran keluar menstruasi.
· Insidensi endometriosis meningkat pada wanita dengan menarkhe awal, siklus menstruasi yang pendek, atau menorrhagi.
· Endometriosis ditemukan umumnya pada daerah pelvis, paling sering di ovarium, lalu daerah cul-de-sac anterior dan posterior, ligamentum uterosacralis, uterus posterior, dan ligamentum latum posterior.
· Endometriosis eksperimental dapat diinduksi pada primata setelah menstruasi peritoneal yang diinduksi melalui pembedahan atau injeksi retroperitoneal endometrium menstruasi, dan pada wanita yang menerima injeksi peritoneal jaringan menstruasi mereka.


Sayangnya teori ini tidak dapat menerangkan kejadian endometriosis di luar pelvis, seperti di paru, umbilikus, atau di tempat lain. Sebenarnya regurgitasi darah haid merupakan suatu hal yang fisiologik, namun yang masih menjadi bahan diskusi adalah faktor-faktor apa saja yang menyebabkan jaringan endometrium yang terdapat dalam darah haid tersebut dapat terus tumbuh dengan cepat.


2. Teori Metaplasia (Meier - 1919)
Teori ini mengemukakan bahwa lesi endometriosis terbentuk akibat metaplasia dari sel-sel epitel coelom yang berasal dari saluran Muller. Sel-sel ini berdiferensiasi menjadi sel-sel peritoneal, pleura dan sel-sel pada permukaan ovarium. Teori ini sampai kini masih dianut oleh para ahli patologi.


Beberapa fakta yang mendukung :

· Endometriosis ditemukan pada gadis premenarkhe, pada wanita yang tidak pernah menstruasi, dan juga pada gadis remaja yang mempunyai siklus menstruasi yang jarang.
· Karena sel endometrium intak tidak mempunyai akses ke thoraks pada keadaan tidak terdapatnya defek anatomi, teori implantasi tidak dapat menjelaskan kasus endometriosis di pleura dan pulmo. Metaplasia pada pleura (yang berasal dari epitelium coelom, seperti pada peritoneum dan duktus mulleri) diinduksi oleh hormon steroid atau rangsangan kimiawi yang dilepaskan sel endometrium yang berdegenerasi ke dalam cairan peritoneum (yang dapat berhubungan dengan kavum thoraks melalui hemidiafragma kanan), adalah mekanisme yang mungkin terjadi.
· Metaplasia pada epitelium coelom yang misintegrasi (yang berdekatan dengan bakal ekstremitas selama embriogenesis awal) adalah satu-satunya mekanisme yang dapat menerangkan endometriosis pada tempat perifer yang tidak umum seperti di ekstremitas (jari, kaki, lutut).
· Kasus endometriosis yang jarang ditemukan pada pria yang diterapi dengan estrogen dosis tinggi (vesika urinaria, dinding abdomen).
· Sel stroma dan epitelium permukaan ovarium, dikultur bersama dengan estrogen, membentuk stroma dan kelenjar endometrium.
· Endometrium eutopik (dalam uterus) dan ektopik (di luar uterus) jauh berbeda, baik dari morfologi dan fungsional, suatu fakta yang sulit digabungkan dengan pendapat bahwa implan endometriosis merupakan autotransplantasi dari jaringan endometrium normal.


3. Teori Induksi
Teori ini merupakan variasi teori metaplasia bahwa darah haid atau rangsangan atau paparan lain memicu sel-sel peritoneum sehingga terjadi perubahan sel-sel asal yang tidak berdiferensiasi menjadi sel-sel endometrium yang berdiferensiasi dan memiliki kemampuan untuk berimplantasi.


4. Teori Aliran Limfe (Halban-1924)
Halban berusaha menerangkan kemungkinan kejadian endometriosis jarak jauh berdasarkan aliran limfe yang membawa dan akhirnya dapat tumbuh di tempat yang baru.


5. Teori Iatrogenik
Teori iatrogenik menyatakan terjadinya endometriosis pada dinding abdomen adalah karena pemindahan desidua saat operasi sesarea.


6. Teori Neurologik
Teori ini merupakan konsep baru dalam patogenesis endometriosis: dimana lesi tampaknya menginfiltrasi dinding usus besar sepanjang nervus, pada jarak yang jauh dari lesi primer. Tentu saja, faktor lain seperti imunologi, genetik dan familial, juga dapat terlibat.8 Anaf et al, yang mempertimbangkan endometriosis usus besar sebagai fenomena invasi atau infiltrasi, menemukan bahwa terdapat kontinuitas histologis antara lesi superfisial dan dalam dibawahnya pada dinding usus besar, menunjukkan bahwa lesi berasal dari serosa yang secara progresif menginvasi muskulus propria. Mukosa jarang terlibat karena innervasi yang kurang.


7. Faktor Genetik dan Imunologik
Dmowski dan teman-temannya menduga faktor genetik dan imunologik sangat berperan terhadap timbulnya endometriosis. Ditemukan penurunan imunitas seluler pada jaringan endometrium wanita yang menderita endometriosis. Pada cairan peritoneum wanita dengan endometriosis ditemukan aktivitas sel makrofag yang meningkat, penurunan aktivitas natural killer cells dan penurunan aktivitas sel-sel limfosit. Makrofag akan mengaktifkan jaringan endometriosis dan penurunan sistem imunologik tubuh akan menyebabkan jaringan endometriosis terus tumbuh tanpa hambatan. Makin banyak regurgitasi darah haid, makin banyak pula sistem pertahanan tubuh yang terpakai. Pada wanita dengan darah haid yang sedikit, atau yang jarang haid, sedikit sekali ditemukan endometriosis. Bila salah satu orang tua (ibu) menderita endometriosis, maka anak dari orang tua tersebut lebih mungkin menderita endometriosis. Wanita Asia lebih banyak menderita endometriosis dibandingkan wanita Negro.


Genetika Endometriosis
Baik pada manusia maupun primata bukan manusia, endometriosis cenderung untuk mengelompok dalam keluarga. Penyakit ini seringkali ditemukan pada pasangan kembar monozigot dan dizigot dan timbul pada onset usia yang serupa pada saudara perempuan dari kembar tersebut. Endometriosis 6-7 kali lebih sering pada hubungan keluarga derajat satu dari wanita yang terkena. Semua ini menyatakan bahwa endometriosis mempunyai dasar genetik dan predisposisi dari penyakit ini adalah diturunkan. Penelitian oleh Treloar, dkk mengidentifikasi area yang berhubungan bermakna pada kromosom 10q26 pada saudara perempuan kembar.


Gen yang merupakan predisposisi perkembangan endometriosis mungkin saja termasuk mereka yang mengatur proses molekular yang mengontrol kelangsungan sel endometrium yang melekat, perlekatan dan invasinya ke permukaan peritoneum, proliferasi neovaskularisasi, atau respons inflamasi. Sel endometrium eutopik dari wanita dengan endometriosis bersifat resisten terhadap apoptosis. Endometrium ektopik tampaknya bahkan lebih resisten; protein Bcl-2 dan sistem ekspresi ligan, keduanya terlibat. Resistensi terhadap apoptosis meningkatkan kelangsungan sel endometrium yang memasuki cavum peritoneum dan juga membantu menjelaskan mengapa endometrium ektopik lebih resisten terhadap imunitas yang dimediasi makrofag.


Metaloproteinase matriks adalah enzim yang mendegradasi matriks ekstraseluler dan membantu memediasi breakdown endometrium normal dan pertumbuhan baru yang distimulasi estrogen. Ekspresi metaloproteinase matriks meningkat pada awal siklus dan biasanya disupresi oleh progesteron selama fase sekretori. Pada wanita dengan endometriosis, ekspresi metaloproteinase matriks endometrium sekretori bersifat resisten terhadap supresi progesteron. Ekspresi metaloproteinase matriks persisten pada sel endometrium yang terlepas dapat memberikan kemampuan invasif pada endometrium yang refluks yang memfasilitasi invasi ke permukaan peritoneum dan proliferasi sel berikutnya.


Perkembangan dan pertumbuhan endometriosis bersifat estrogen-dependent, dan terdapat bukti kuat bahwa baik produksi dan metabolisme estrogen berubah pada endometriosis ke arah yang mendukung penyakit tersebut. Aromatase, enzim yang mengubah androgen menjadi estrogen, diekspresikan secara abnormal pada endometrium eutopik wanita dengan endometriosis sedang dan berat; pada wanita yang tidak menderita penyakit ini, aktivitas aromatase endometrium umumnya tidak terdeteksi. Lebih jauh, endometrioma dan implan endometriosis peritoneal menampilkan aktivitas aromatase yang sangat tinggi. Faktor transkripsi yang menstimulasi aromatase diekspresikan berlebihan pada jaringan endometriosis dan yang menghambat enzim tersebut kurang diekspresikan, menghasilkan aktivitas aromatase dan sintesis estrogen abnormal. Enzim ini memungkinkan keberadaan endometriosis setelah menopause dan histerektomi.


Estrone dan estradiol dikonversi oleh 17βHSD, yang terdiri dari dua bentuk, 17βHSD tipe 1 yang mengkonversi estrone menjadi estradiol dan 17βHSD tipe 2 mengkatalisasi konversi estradiol menjadi estrone (estrogen yang lebih lemah). Pada endometrium eutopik normal, progesteron menginduksi aktivitas 17βHSD tipe 2 pada epitel kelenjar; enzim ini banyak diekspresikan pada kelenjar endometrium sekretori. Pada jaringan endometriosis, 17βHSD tipe 1 diekspresikan normal tetapi ekspresi 17βHSD tipe 2 tidak ada. Progesteron tidak menginduksi aktivitas 17βHSD tipe 2 pada implan endometriosis karena ekspresi reseptor progesteron (PR) juga tidak normal. Aksi progesteron pada gen target dimediasi terutama oleh PR-B; PR-A bertindak sebagai repressor fungsi PR-B. Pada endometrium eutopik normal, PR-A dan PR-B diekspresikan. Pada jaringan endometrium, PR-A diekspresikan, tetapi PR-B tidak.


Imunologi Endometriosis
Endometriosis dihubungkan dengan perubahan pada imunitas humoral dan seluler, dimana penurunan respon imun yang mengakibatkan penghilangan debris menstruasi refluks yang inefektif mungkin faktor penyebab perkembangan penyakit ini. Meskipun cairan peritoneum wanita dengan endometriosis mengandung sel imun dengan jumlah yang meningkat, bukti menyatakan bahwa aksi mereka lebih ke arah mendukung penyakit daripada mencegahnya. Apakah abnormalitas imunologis ini merupakan penyebab atau konsekuensi dari endometriosis masih belum jelas.


Makrofag melindungi host dengan pengenalan, fagositosis, dan destruksi mikroorganisme yang menyerang dan juga bertindak sebagai pembersih, menolong membersihkan sel apoptosis dan debris seluler. Makrofag mensekresi berbagai sitokin, faktor pertumbuhan, enzim, dan protaglandin yang membantu memediasi fungsi mereka saat menstimulasi pertumbuhan dan proliferasi sel lain. Makrofag ditemukan normal pada cairan peritoneal dan jumlah dan aktivitas mereka meningkat pada wanita dengan endometriosis. Bukannya bertindak sebagai pembersih untuk menghilangkan sel endometrium ektopik, makrofag peritoneal yang efektif dan monosit sirkulasi pada wanita dengan endometriosis malah menyokong penyakit dengan mensekresi faktor pertumbuhan dan sitokin yang menstimuli proliferasi endometrium ektopik dan menghambat fungsi pembersih mereka.


Estrogen terlibat dalam sistem imun, dan makrofag mengekspresikan reseptor estrogen (ER). Penelitian Capellino, dkk menyatakan bahwa mereka menemukan reseptor estrogen α dan β diekspresikan berlebihan pada makrofag wanita dengan endometriosis dibandingkan kontrol. Hasil ini menyarankan bahwa estrogen, melalui reseptor fungsional mereka, mungkin mengatur respon imun setidaknya pada makrofag. Dengan demikian, estrogen mempunyai peran penting dalam respon imun, terlepas dari patologinya.


Interleukin-1 adalah sitokin yang terlibat dalam respon imun dan inflamasi dan disekresi oleh makrofag dan monosit yang teraktivasi, limfosit T dan B, dan sel natural killer. Interleukin-1 teridentifikasi dalam cairan peritoneal wanita dengan endometriosis dan ekspresi reseptor interleukin-1 meningkat pada sel stroma endometriosis. Interleukin-1 menyokong perkembangan endometriosis dengan merangsang pelepasan faktor angiogenik dan dengan membantu sel endometrium yang memasuki cavum peritoneum untuk meloloskan diri dari immunosurveillance dengan menginduksi pelepasan bentuk terlarut dari intercellular adhesion molecule-1 (ICAM-1) dari sel endometriosis yang berkompetisi dengan sel natural killer dan sel imun lain untuk tempat pengenalan imunitas.


Interleukin-8 adalah sitokin angiogenik kuat yang diproduksi oleh sel mesotelial, makrofag, sel endometrium dan sel lain. Level interleukin-8 cairan peritoneum meningkat pada wanita dengan endometriosis dan berhubungan dengan beratnya derajat penyakit. Interleukin-8 diekspresikan pada implan endometriosis dan diregulasi oleh interleukin-1. Interleukin-8 merangsang perlekatan sel stroma endometrium pada protein matriks ekstraseluler, aktivitas metaloproteinase matriks, dan proliferasi stroma endometrium, yang keseluruhannya menyokong implantasi dan pertumbuhan endometrium ektopik.


Patologi Endometriosis
Gambaran mikroskopik dari endometriosis sangat beragam. Lokasi yang sering terdapat adalah pada ovarium, dan biasanya didapati pada kedua ovarium. Pada ovarium tampak kista-kista biru kecil sampai kista besar (kadang-kadang sebesar tinju) berisi darah tua menyerupai coklat (kista coklat atau endometrioma).


Darah tua dapat keluar sedikit-sedikit karena luka pada dinding kista dan dapat menyebabkan perlekatan antara permukaan ovarium dengan uterus, sigmoid dan dinding pelvis. Kista coklat kadang-kadang dapat mengalir dalam jumlah banyak ke dalam rongga peritoneum karena robekan dinding kista dan menyebabkan acute abdomen. Tuba pada endometiosis biasanya normal. Pada salah satu atau kedua ligamentum sakrouterina, pada kavum Douglasi, dan pada permukaan uterus sebelah belakang dapat ditemukan satu atau beberapa permukaan sigmoid atau rektum seringkali ditemukan benjolan yang berwarna kebiru-biruan ini. Sebagai akibat dari timbulnya perdarahan pada waktu haid dari jaringan endometriosis, mudah sekali timbul perlekatan antara alat-alat di sekitar kavum Douglasi.


Pada pemeriksaan mikroskopik ditemukan ciri-ciri khas bagi endometriosis, yakni kelenjar-kelenjar dan stroma endometrium, dan perdarahan bekas dan baru berupa eritrosit, pigmen hemosiderin, dan sel-sel makrofag berisi hemosiderin. Di sekitarnya tampak sel-sel radang dan jaringan ikat, sebagai reaksi dari jaringan normal disekelilingnya. Jaringan endometriosis seperti juga jaringan endometrium di dalam uterus, dapat dipengaruhi oleh estrogen dan progesteron. Akan tetapi besarnya pengaruh tidak selalu sama, dan tergantung dari beberapa faktor, antara lain komposisi endometriosis yang bersangkutan (apakah jaringan kelenjar atau jaringan stroma yang lebih banyak), dari reaksi jaringan normal di sekitarnya, dan sebagainya. Sebagai akibat dari pengaruh hormon-hormon tersebut, sebagian besar sarang-sarang endometriosis berdarah secara periodik. Perdarahan yang periodik ini menyebabkan reaksi jaringan sekelilingnya berupa radang dan perlekatan.


Pada kehamilan, dapat ditemukan reaksi desidual jaringan endometriosis. Apabila kehamilannya berakhir, reaksi desidual menghilang disertai dengan regresi sarang endometriosis, dan dengan membaiknya keadaan. Pengaruh baik dari kehamilan kini menjadi dasar pengobatan endometriosis dengan hormon untuk mengadakan apa yang dinamakan kehamilan semu (pseudopregnancy).


Secara mikroskopik, endometriosis merupakan suatu kelainan yang jinak, akan tetapi kadang-kadang sifatnya seperti tumor ganas. Antara lain, bisa terjadi penyebaran endometriosis ke paru-paru dan lengan, selain itu bisa terdapat infiltrasi ke bawah kavum Douglasi ke fasia rektovaginal, ke sigmoid, dan sebagainya.


Diagnosis
Diagnosis di buat berdasarkan atas :

○ Anamnesis
Nyeri pelvik siklik atau dismenorea adalah khas untuk endometriosis. Nyeri haid ini muncul beberapa hari menjelang haid, dan mencapai puncaknya saat haid, dan menghilang setelah berhenti haid. Pasien tidak dapat melakukan kegiatan sehari-hari dan memerlukan pengobatan untuk menghilangkan nyeri. Nyeri pelvik dapat juga terjadi asiklik. Nyeri pelvik siklik maupun asiklik ditemukan hampir pada 70-80% penderita endometriosis. Tempat nyeri yang dirasakan pasien dapat diduga sebagai perkiraan lesi endometriosis berada. Endometriosis di peritoneum biasanya menimbulkan nyeri di perut bagian bawah. Endometriosis di vagina atau cavum Douglasi mengakibatkan nyeri saat sanggama atau saat dilakukan pemeriksaan ginekologi. Endometriosis di vesika urinaria mengakibatkan nyeri suprapubik dan air seni bercampur darah.


Pada 50% pasutri yang mengalami infertilitas ditemukan endometriosis dan 70-80% wanita dengan infertilitas yang tidak dapat dijelaskan ditemukan endometriosis. Pada 15% wanita dengan infertilitas sekunder ditemukan endometriosis. Endometriosis yang ditemukan ini belum tentu merupakan penyebab infertilitas. Banyak wanita hamil yang atas indikasi tertentu dilakukan seksio sesarea ditemukan secara kebetulan endometriosis di rongga pelvis. 1


○ Pemeriksaan Klinis
Pada pemeriksaan dalam atau colok dubur, kadang teraba adanya nodul-nodul di daerah kavum Douglasi dan daerah ligamentum sakrouterina yang sangat nyeri. Uterus biasanya teraba retrofleksi dan sulit digerakkan. Di parametrium terba massa kistik yang nyeri pada penekanan. Selalu harus dilakukan pemeriksaan kombinasi retrovaginal.

Dengan USG atau Ctscan terlihat adanya massa kistik di satu atau dua ovarium yang mengarah ke kista coklat, atau terlihat adanya bercak-bercak endometriosis dalam miometrium (adenomiosis). Nyeri yang disertai darah saat berkemih atau saat buang air besar perlu dilakukan tindakan endoskopi.

Pemeriksaan petanda seperti Ca125 memiliki sensitivitas 60% dan spesifisitas 90%.


Pengobatan
Tidak ada terapi tunggal terbaik bagi wanita dengan endometriosis. Terapi harus diberikan per individu. Faktor-faktor utama yang dipertimbangkan adalah kebutuhan untuk mempertahankan reproduksi, derajat gejala endometriosis, ada tidaknya infertilitas dan usia wanita tersebut.

1. Pil Kontrasepsi
Pil kontrasepsi memiliki sejumlah keuntungan, terutama pada endometriosis ringan atau sedang, yaitu:
· Menurunkan beratnya menstruasi dan lama menstruasi, sehingga menurunkan jumlah produk menstruasi yang retrograd.
· Memberikan efek desidual pada implan-implan endometriosis yang menghambat pertumbuhan implan lebih lanjut.
· Menurunkan level estrogen sirkulasi, terutama estradiol. Dengan menghambat fungsi ovarium dan memberikan estrogen tambahan, level estradiol darah umumnya lebih rendah daripada sebelum mengkonsumsi pil kontrasepsi. Level estrogen yang lebih rendah akan menurunkan stimulasi hormonal pada implan.
· Bila dikonsumsi terus, pil kontrasepsi akan menghentikan perdarahan withdrawal episodik yang terjadi baik pada endometrium normal maupun implan endometrium.
Pil kontrasepsi dapat diberikan 3-6 bulan.

2. Danazol
Danazol merupakan turunan testosteron dan mempunyai efek langsung maupun tak langsung pada endometriosis. Danazol: 1
· Menghambat pertumbuhan implan melalui efek desidualisasinya.
· Menekan sekresi gonadotropin hipofisis, yang mengakibatkan inhibisi fungsi ovarium dan menurunkan level estrogen.
· Memblok enzim steroidogenik.
Kerugian penggunaan Danazol adalah harganya yang mahal dan efek sampingnya yang bermakna (pertambahan berat badan, maskulinisasi dan depresi). Tetapi, Danazol sangat efektif dalam terapi endometriosis dan sedikit pasien yang menghentikan terapi meskipun mengalami efek samping tersebut.

3. Progestin
Progestin menghambat pelepasan gonadotropin hipofisis, memblokade fungsi ovarium dan mempunyai efek desidualisasi pada implan endometrium, yang menghambat pertumbuhannya. Progestin sama efektifnya dengan pil kontrasepsi dalam terapi endometriosis, tetapi lebih banyak efek samping terutama pertambahan berat badan dan perdarahan breakthrough.

4. Pembedahan konservatif
Pembedahan konservatif berarti mengambil sebanyak mungkin lesi endometriosis, tetapi dengan batasan untuk mempertahankan fungsi reproduksi. Ini berarti mempertahankan uterus, tuba Fallopi dan ovarium. Pembedahan konservatif adalah pilihan terbaik untuk pasien infertil karena tidak ada terapi tanpa pembedahan yang dapat memperbaiki fertilitas pasien. Sebaliknya, pembedahan konservatif mencapai 40-60% angka kehamilan post-pembedahan, tergantung dari derajat endometriosisnya.

5. Pembedahan Definitif
Pembedahan definitif melibatkan histerektomi, dengan atau tanpa mengambil tuba, ovarium dan tempat lain endometriosis. Pembedahan definitif memberikan kemungkinan terbesar untuk secara permanen menghilangkan nyeri endometriosis, tetapi menghilangkan fungsi reproduksinya.

Pengangkatan ovarium bersifat kontroversial. Bila diangkat, tingkat kesembuhan menjadi lebih besar, tetapi akan menimbulkan keadaan menopause. Untuk menghilangkan gejala menopause tersebut, dapat diberikan terapi pengganti hormon estrogen segera setelah pembedahan. Pemberian estrogen ini tampaknya tidak cukup untuk menumbuhkan kembali endometriosis.

Di tulis oleh dr. Miranty Firmansyah, PPDS OBGYN Unhas, Makassar

Pain Treatment with anti pain drugs

ACUTE PAIN
Sometimes treating the underlying condition doesn't immediately relieve pain even though the ideal treatment for any pain is to remove the cause, thus diagnosis should always precede treatment planning. Furthermore, some conditions are so painful that rapid and effective analgesia is essential (for example, the postoperative state, burns, trauma, cancer, sickle cell crisis). Analgesic medications are a first line of treatment in these cases, and all practitioners should be familiar with their use.


Aspirin, Acetaminophen, and Nonsteroidal Anti-Inflammatory Agents (NSAIDS) are drugs that considered together because they are used for similar problems and may have a similar mechanism of action . All these compounds inhibit cyclooxygenase (COX), and, except for acetaminophen, all have anti-inflammatory actions, especially at higher dosages. They are particularly effective for mild to moderate headache and for pain of musculoskeletal origin. Since they are effective for these common types of pain and are available without prescription, COX inhibitors are by far the most commonly used analgesics. They are absorbed well from the gastrointestinal tract and, with occasional use, side effects are minimal. With chronic use, gastric irritation is a common side effect of aspirin and NSAIDs and is the problem that most frequently limits the dose that can be given. Gastric irritation is most severe with aspirin, which may cause erosion of the gastric mucosa, and because aspirin irreversibly acetylates platelets and thereby interferes with coagulation of the blood, gastrointestinal bleeding is a risk. The NSAIDs are less prob lematic, but their risk in this regard is still significant. In addition to their well known gastrointestinal toxicity, nephrotoxicity is a significant problem for patients using NSAIDs on a chronic basis, and patients at risk for renal insufficiency should be monitored closely. NSAIDs also cause an increase in blood pressure in a significant number of individuals.


Treatment with NSAIDs in long-term therapy requires regular blood pressure monitoring and treatment if necessary. Although toxic to the liver when taken in a high dose, acetaminophen rarely produces gastric irritation and does not interfere with platelet function. The introduction of a parenteral form of NSAID, ketorolac, extends the usefulness of this class of compounds in the management of acute severe pain. Ketorolac is sufficiently potent and rapid in onset to supplant opioids for many patients with acute severe headache and musculoskeletal pain.


There are two major classes of COX: COX-1 is constitutively expressed and COX-2 is induced in the inflammatory state. COX-2-selective drugs have moderate analgesic potency and produce less gastric irritation than the nonselective COX inhibitors. It is not yet clear whether the use of COX-2 selective drugs is associated with a lower risk of nephrotoxicity compared to nonselective NSAIDs. On the other hand, COX-2-selective drugs offer a significant benefit in the management of acute postoperative pain because they do not affect blood coagulation. This is a situation in which the nonselective COX inhibitors would be contraindicated because they impair platelet-mediated blood clotting and are thus associated with increased bleeding at the operative site. A corollary of this is that COX-2 drugs do not provide the same degree of protection from thromboembolic cardiovascular adverse events such as myocardial infarction. In fact, in patients treated for arthritis, those treated with naproxen had significantly fewer adverse thromboembolic events than those treated with rofecoxib, a selective COX-2 inhibitor.


Opioid Analgesics Opioids are the most potent pain-relieving drugs currently available. Furthermore, of all analgesics, they have the broadest range of efficacy, providing the most reliable and effective method for rapid pain relief. Although side effects are common, they are usually not serious except for respiratory depression and can be reversed rapidly with the narcotic antagonist naloxone. The physician should not hesitate to use opioid analgesics in patients with acute severe pain. Table 11-1 lists the most commonly used opioid analgesics. Opioids produce analgesia by actions in the central nervous system. They activate pain-inhibitory neurons and directly inhibit pain-transmission neurons. Most of the commercially available opioid analgesics act at the same opioid receptor (mu receptor), differing mainly in potency, speed of onset, duration of action, and optimal route of administration. Although the dose-related side effects (sedation, respiratory depression, pruritus, constipation) are similar among the different opioids, some side effects are due to accumulation of nonopioid metabolites that are unique to individual drugs. One striking example of this is normeperidine, a metabolite of meperidine. Normeperidine produces hyperexcitability and seizures that are not reversible with naloxone. Normeperidine accumulation is increased in patients with renal failure. The most rapid relief with opioids is obtained by intravenous administration; relief with oral administration is significantly slower.


Common acute side effects include nausea, vomiting, and sedation. The most serious side effect is respiratory depression. Patients with any form of respiratory compromise must be kept under close observation following opioid administration; an oxygen saturation monitor may be useful. The opioid antagonist, naloxone, should be readily available. Opioid effects are dose-related, and there is great variability among patients in the doses that relieve pain and produce side effects.
Because of this, initiation of therapy requires titration to optimal dose and interval. The most important principle is to provide adequate pain relief. This requires determining whether the drug has adequately relieved the pain and the duration of the relief. The most common error made by physicians in managing severe pain with opioids is to prescribe an inadequate dose. Since many patients are reluctant to complain, this practice leads to needless suffering. In the absence of sedation at the expected time of peak effect, a physician should not hesitate to repeat the initial dose to achieve satisfactory pain relief. An innovative approach to the problem of achieving adequate pain relief is the use of patient-controlled analgesia (PCA). PCA requires a device that delivers a baseline continuous dose of an opioid drug, and preprogrammed additional doses whenever the patient pushes a button. The device can be programmed to limit the total hourly dose so that overdosing is impossible. The patient can then titrate the dose to the optimal level. This approach is used most extensively for the management of postoperative pain, but there is no reason why it should not be used for any hospitalized patient with persistent severe pain. PCA is also used for short-term home care of patients with intractable pain, such as is caused by metastatic cancer. Many physicians, nurses, and patients have a certain trepidation about using opioids that is based on an exaggerated fear of addiction. In fact, there is a vanishingly small chance of patients becoming addicted to narcotics as a result of their appropriate medical use.


The availability of new routes of administration has extended the usefulness of opioid analgesics. Most important is the availability of spinal administration. Opioids can be infused through a spinal catheter placed either intrathecally or epidurally. By applying opioids directly to the spinal cord, regional analgesia can be obtained using a relatively low total dose. In this way, such side effects as sedation, nausea, and respiratory depression can be minimized. This approach has been used extensively in obstetric procedures and for lower-body postoperative pain. Opioids can also be given intranasally (butorphanol), rectally, and transdermally (fentanyl), thus avoiding the discomfort of frequent injections in patients who cannot be given oral medication. The fentanyl transdermal patch has the advantage of providing fairly steady plasma levels, which maximizes patient comfort.

OPIOID AND CYCLOOXYGENASE INHIBITOR COMBINATIONS
When used in combination, opioids and COX inhibitors have additive effects. Because a lower dose of each can be used to achieve the same degree of pain relief and their side effects are nonadditive, such combinations can be used to lower the severity of dose-related side effects. Fixed-ratio combinations of an opioid with acetaminophen carry a special risk. Dose escalation as a result of increased severity of pain or decreased opioid effect as a result of tolerance may lead to levels of acetaminophen that are toxic to the liver.

CHRONIC PAIN
Managing patients with chronic pain is intellectually and emotionally challenging. The patient’s problem is often difficult to diagnose; such patients are demanding of the physician’s time and often appear emotionally distraught. The traditional medical approach of seeking an obscure organic pathology is usually unhelpful. On the other hand, psychological evaluation and behaviorally based treatment paradigms are frequently helpful, particularly in the setting of a multidisciplinary pain-management center.

There are several factors that can cause, perpetuate, or exacerbate chronic pain. First, of course, the patient may simply have a disease that is characteristically painful for which there is presently no cure. Arthritis, cancer, migraine headaches, fibromyalgia, and diabetic neuropathy are examples of this. Second, there may be secondary perpetuating factors that are initiated by disease and persist after that disease has resolved. Examples include damaged sensory nerves, sympathetic efferent activity, and painful reflex muscle contraction. Finally, a variety of psychological conditions can exacerbate or even cause pain.


There are certain areas to which special attention should be paid in the medical history. Because depression is the most common emotional disturbance in patients with chronic pain, patients should be questioned about their mood, appetite, sleep patterns, and daily activity. A simple standardized questionnaire, such as the Beck Depression Inventory, can be a useful screening device. It is important to remember that major depression is a common, treatable, and potentially fatal illness.


Other clues that a significant emotional disturbance is contributing to a patient’s chronic pain complaint include: pain that occurs in multiple unrelated sites; a pattern of recurrent, but separate, pain problems beginning in childhood or adolescence; pain beginning at a time of emotional trauma, such as the loss of a parent or spouse; a history of physical or sexual abuse; and past or present substance abuse. On examination, special attention should be paid to whether the patient guards the painful area and whether certain movements or postures are avoided because of pain. Discovering a mechanical component to the pain can be useful both diagnostically and therapeutically. Painful areas should be examined for deep tenderness, noting whether this is localized to muscle, ligamentous structures, or joints. Chronic myofascial pain is very common, and in these patients deep palpation may reveal highly localized trigger points that are firm bands or knots in muscle. Relief of the pain following injection of local anesthetic into these trigger points supports the diagnosis. A neuropathic component to the pain is indicated by evidence of nerve damage, such as sensory impairment, exquisitely sensitive skin, weakness and muscle atrophy, or loss of deep tendon reflexes. Evidence suggesting sympathetic nervous system involvement includes the presence of diffuse swelling, changes in skin color and temperature, and hypersensitive skin and joint tenderness compared with the normal side. Relief of the pain with a sympathetic block is diagnostic. A guiding principle in evaluating patients with chronic pain is to assess both emotional and organic factors before initiating therapy. Addressing these issues together, rather than waiting to address emotional issues after organic causes of pain have been ruled out, improves compliance in part because it assures patients that a psychological evaluation does not mean that the physician is questioning the validity of their complaint. Even when an organic cause for a patient’s pain can be found, it is still wise to look for other factors. For example, a cancer patient with painful bony metastases may have additional pain due to nerve damage and may also be depressed. Optimal therapy requires that each of these factors be looked for and treated.


TREATMENT of CHRONIC PAIN
Once the evaluation process has been completed and the likely causative and exacerbating factors identified, an explicit treatment plan should be developed. An important part of this process is to identify specific and realistic functional goals for therapy, such as getting a good night’s sleep, being able to go shopping, or returning to work. A multidisciplinary approach that utilizes medications, counseling, physical therapy, nerve blocks, and even surgery may be required to improve the patient’s quality of life. There are also some newer, relatively invasive procedures that can be helpful for some patients with intractable pain. These procedures include implanting intraspinal cannulae to deliver morphine or intraspinal electrodes for spinal stimulation. There are no set criteria for predicting which patients will respond to these procedures. They are generally reserved for patients who have not responded to conventional pharmacologic approaches. Referral to a multidisciplinary pain clinic for a full evaluation should precede any of these procedures. Such referrals are clearly not necessary for all chronic pain patients. For some, pharmacologic management alone can often provide adequate relief.


ANTIDEPRESSANT MEDICATIONS
The tricyclic antidepressants (TCAs) are extremely useful for the management of patients with chronic pain. Although developed for the treatment of depression, the tricyclics have a spectrum of dose-related biologic activities that include the production of analgesia in a variety of clinical conditions. Although the mechanism is unknown, the analgesic effect of TCAs has a more rapid onset and occurs at a lower dose than is typically required for the treatment of depression. Furthermore, patients with chronic pain who are not depressed obtain pain relief with antidepressants. There is evidence that tricyclic drugs potentiate opioid analgesia, so they are useful adjuncts for the treatment of severe persistent pain such as occurs with malignant tumors. TCAs are of particular value in the management of neuropathic pain such as occurs in diabetic neuropathy and postherpetic neuralgia, for which there are few other therapeutic options. The TCAs that have been shown to relieve pain have significant side effects . Some of these side effects, such as orthostatic hypotension, cardiac conduction delay, memory impairment, constipation, and urinary retention, are particularly problematic in elderly patients, and several are additive to the side effects of opioid analgesics.


The serotonin-selective reuptake inhibitors such as fluoxetine (Prozac) have fewer and less serious side effects than TCAs, but they are much less effective for relieving pain. It is of interest that venlafaxine (Effexor), a nontricyclic antidepressant that blocks both serotonin and norepinephrine reuptake, appears to retain most of the pain-relieving effect of TCAs with a side-effect profile more like that of the serotonin-selective reuptake inhibitors. The drug may be particularly useful in patients who cannot tolerate the side effects of tricyclics.

ANTICONVULSANTS AND ANTIARRHYTHMICS
These drugs are useful primarily for patients with neuropathic pain. Phenytoin (Dilantin) and carbamazepine (Tegretol) were first shown to relieve the pain of trigeminal neuralgia. This pain has a characteristic brief, shooting, electric shock–like quality. In fact, anticonvulsants seem to be helpful largely for pains that have such a lancinating quality. A newgeneration anticonvulsant, gabapentin (Neurontin), is effective for a broad range of neuropathic pains.


Antiarrhythmic drugs such as low-dose lidocaine and mexiletine (Mexitil) can also be effective for neuropathic pain. These drugs block the spontaneous activity of damaged primary afferent nociceptors.


CHRONIC OPIOID MEDICATION
The long-term use of opioids is accepted for patients with pain due to malignant disease. Although opioid use for chronic pain of nonmalignant origin is controversial, it is clear that for many such patients opioid analgesics are the best available option. This is understandable since opioids are the most potent and have the broadest range of efficacy of any analgesic medications.


Although addiction is rare in patients who first use opioids for pain relief, some degree of tolerance and physical dependence are likely with long-term use. Therefore, before embarking on opioid therapy, other options should be explored, and the limitations and risks of opioids should be explained to the patient. It is also important to point out that some opioid analgesic medications have mixed agonist-antagonist properties (e.g., pentazocine and butorphanol). From a practical standpoint, this means that they may worsen pain by inducing an abstinence syndrome in patients who are physically dependent on other opioid analgesics.


With long-term outpatient use of orally administered opioids, it is desirable to use long-acting compounds such as levorphanol, methadone, or sustained-release morphine. Transdermal fentanyl is another excellent option. The pharmacokinetic profile of these drug preparations enables prolonged pain relief, minimizes side effects such as sedation that are associated with high peak plasma levels, and reduces the likelihood of rebound pain associated with a rapid fall in plasma opioid concentration. Constipation is a virtually universal side effect of opioid use and should be treated expectantly. It is worth emphasizing that many patients, especially those with chronic pain, seek medical attention primarily because they are suffering and because only physicians can provide the medications required for their relief. A primary responsibility of all physicians is to minimize the physical and emotional discomfort of their patients. Familiarity with pain mechanisms and analgesic medications is an important step toward accomplishing this aim.

Related article : Understanding Pain

Rabu, 19 November 2008

Understanding Pain

Because pain is universally understood as a signal of disease, it is the most common symptom that brings a patient to a physician's attention. Thus, understanding pain is very essential in order to preserve and restore health and to relieve suffering. The function of the pain sensory system is to protect the body and maintain homeostasis. It does this by detecting, localizing, and identifying tissue- damaging processes. Since different diseases produce characteristic patterns of tissue damage, the quality, time course, and location of a patient's pain complaint and the location of tenderness provide important diagnostic clues and are used to evaluate the response to treatment. Once this information is obtained, it is the obligation of the physician to provide rapid and effective pain relief.


THE PAIN SENSORY SYSTEM

Pain is an unpleasant sensation localized to a part of the body. It is often described in terms of a penetrating or tissue-destructive process (e.g., stabbing, burning, twisting, tearing, squeezing) and/or of a bodily or emotional reaction (e.g., terrifying, nauseating, sickening). Furthermore, any pain of moderate or higher intensity is accompanied by anxiety and the urge to escape or terminate the feeling.These properties illustrate the duality of pain: it is both sensation and emotion.


When acute, pain is characteristically associated with behavioral arousal and a stress response consisting of increased blood pressure, heart rate, pupil diameter, and plasma cortisol levels. In addition, local muscle contraction (e.g., limb flexion, abdominal wall rigidity) is often present.


nerv_system_on_pain

Fig.1. Pprimary afferents with cell bodies in the dorsal root ganglion, and sympathetic postganglionic fibers with cell Components of a typical cutaneous nerve. There are two distinct functional categories of axons: bodies in the sympathetic ganglion. Primary afferents include those with large-diameter myelinated (Aβ), smalldiameter myelinated (Aδ), and unmyelinated (C) axons. All sympathetic postganglionic fibers are unmyelinated


PERIPHERAL MECHANISMS The Primary Afferent Nociceptor A peripheral nerve consists of the axons of three different types of neurons: primary sensory afferents, motor neurons, and sympathetic postganglionic neurons. The cell bodies of primary afferents are located in the dorsal root ganglia in the vertebral foramina. The primary afferent axon bifurcates to send one process into the spinal cord and the other to innervate tissues.


Primary afferents are classified by their diameter, degree of myelination, and conduction velocity. The largest-diameter fibers, A-beta (Aβ), respond maximally to light touch and/or moving stimuli; they are present primarily in nerves that innervate the skin. In normal individuals, the activity of these fibers does not produce pain. There are two other classes of primary afferents: the small-diameter myelinated


A-delta (Aδ) and the unmyelinated (C fiber) axons . These fibers are present in nerves to the skin and to deep somatic and visceral structures. Some tissues, such as the cornea, are innervated only by Aδ and C afferents. Most Aδ and C afferents respond maximally only to intense (painful) stimuli and produce the subjective experience of pain when they are electrically stimulated; this defines them as primary afferent nociceptors (pain receptors).


The ability to detect painful stimuli is completely abolished when Aδ and C axons are blocked. Individual primary afferent nociceptors can respond to several different types of noxious stimuli. For example, most nociceptors respond to heating, intense mechanical stimuli such as a pinch, and application of irritating chemicals.


Sensitization When intense, repeated, or prolonged stimuli are applied to damaged or inflamed tissues the threshold for activating primary afferent nociceptors is lowered and the frequency of firing is higher for all stimulus intensities. Inflammatory mediators such as bradykinin, some prostaglandins, and leukotrienes contribute to this process, which is called sensitization. In sensitized tissues normally innocuous stimuli can produce pain. Sensitization is a clinically important process that contributes to tenderness, soreness, and hyperalgesia. A striking example of sensitization is sunburned skin, in which severe pain can be produced by a gentle slap on the back or a warm shower. Sensitization is of particular importance for pain and tenderness in deep tissues. Viscera are normally relatively insensitive to noxious mechanical and thermal stimuli, although hollow viscera do generate significant discomfort when distended. In contrast, when affected by a disease process with an inflammatory component, deep structures such as joints or hollow viscera characteristically become exquisitely sensitive to mechanical stimulation.

pain_modulation

Fig 2. Events leading to activation, sensitization, and spread of sensitization of primary afferent nociceptor terminals. A. Direct activation by intense pressure and consequent cell damage. Cell damage induces lower pH (H⁺)and leads to release of potassium (K⁺)and to synthesis of prostaglandins (PG) and bradykinin (BK). Prostaglandins increase the sensitivity of the terminal to bradykinin and other pain-producing substances. B. Secondary activation. Impulses generated in the stimulated terminal propagate not only to the spinal cord but also into other terminal branches where they induce the release of peptides, including substance P (SP).Substance P causes vasodilation and neurogenic edema with further accumulation of bradykinin. Substance P also causes the release of histamine (H) from mast cells and serotonin (5HT) from platelets.


A large proportion of Aδ and C afferents innervating viscera are completely insensitive in normal noninjured, noninflamed tissue. That is, they cannot be activated by known mechanical or thermal stimuli and are not spontaneously active. However, in the presence of inflammatory mediators, these afferents become sensitive to mechanical stimuli. Such afferents have been termed silent nociceptors, and their characteristic properties may explain how under pathologic conditions the relatively insensitive deep structures can become the source of severe and debilitating pain and tenderness. Low pH, prostaglandins, leukotrienes, and other inflammatory mediators such as bradykinin play a significant role in sensitization.


Nociceptor-Induced Inflammation One important concept to emerge in recent years is that afferent nociceptors also have a neuroeffector function. Most nociceptors contain polypeptide mediators that are released from their peripheral terminals when they are activated . An example is substance P, an 11-amino-acid peptide. Substance P is released from primary afferent nociceptors and has multiple biologic activities. It is a potent vasodilator, degranulates mast cells, is a chemoattractant for leukocytes, and increases the production and release of inflammatory mediators. Interestingly, depletion of substance P from joints reduces the severity of experimental arthritis. Primary afferent nociceptors are not simply passive messengers of threats to tissue injury but also play an active role in tissue protection through these neuroeffector functions.


CENTRAL MECHANISMS

The Spinal Cord and Referred Pain The axons of primary afferent nociceptors enter the spinal cord via the dorsal root. They terminate in the dorsal horn of the spinal gray matter . The terminals of primary afferent axons contact spinal neurons that transmit the pain signal to brain sites involved in pain perception. The axon of each primary afferent contacts many spinal neurons, and each spinal neuron receives convergent inputs from many primary afferents.


The convergence of sensory inputs to a single spinal pain-transmission neuron is of great importance because it underlies the phenomenon of referred pain. All spinal neurons that receive input from the viscera and deep musculoskeletal structures also receive input from the skin. The convergence patterns are determined by the spinal segment of the dorsal root ganglion that supplies the afferent innervation of a structure. For example, the afferents that supply the central diaphragm are derived from the third and fourth cervical dorsal root ganglia. Primary afferents with cell bodies in these same ganglia supply the skin of the shoulder and lower neck. Thus sensory inputs from both the shoulder skin and the central diaphragm converge on paintransmission neurons in the third and fourth cervical spinal segments.


Because of this convergence and the fact that the spinal neurons are most often activated by inputs from the skin, activity evoked in spinal neurons by input from deep structures is mislocalized by the patient to a place that is roughly coextensive with the region of skin innervated by the same spinal segment.


Thus inflammation near the central diaphragm is usually reported as discomfort near the shoulder. This spatial displacement of pain sensation from the site of the injury that produces it is known as referred pain.



Fig 3. The convergence-projection hypothesis of referred pain. According to this hypothesis, visceral afferent nociceptors converge on the same pain-projection neurons as the afferents from the somatic structures in which the pain is perceived. The brain has no way of knowing the actual source of input and mistakenly "projects" the sensation to the somatic structure.



Ascending Pathways for Pain A majority of spinal neurons contacted by primary afferent nociceptors send their axons to the contralateral thalamus. These axons form the contralateral spinothalamic tract, which lies in the anterolateral white matter of the spinal cord, the lateral edge of the medulla, and the lateral pons and midbrain. The spinothalamic pathway is crucial for pain sensation in humans. Interruption of this pathway produces permanent deficits in pain and temperature discrimination. Spinothalamic tract axons ascend to several regions of the thalamus.


There is tremendous divergence of the pain signal from these thalamic sites to broad areas of the cerebral cortex that subserve different aspects of the pain experience. One of the thalamic projections is to the somatosensory cortex. This projection mediates the purely sensory aspects of pain, i.e., its location, intensity, and quality.


Other thalamic neurons project to cortical regions that are linked to emotional responses, such as the cingulate gyrus and other areas of the frontal lobes. These pathways to the frontal cortex subserve the affective or unpleasant emotional dimension of pain. This affective dimension of pain produces suffering and exerts potent control of behavior. Because of this dimension, fear is a constant companion of pain.


PAIN MODULATION

The pain produced by similar injuries is remarkably variable in different situations and in different individuals. For example, athletes have been known to sustain serious fractures with only minor pain, and Beecher's classic World War II survey revealed that many soldiers in battle were unbothered by injuries that would have produced agonizing pain in civilian patients. Furthermore, even the suggestion of relief can have a significant analgesic effect (placebo).


Fig 4.

A. Transmission system for nociceptive messages. Noxious stimuli activate the sensitive peripheral ending of the primary afferent nociceptor by the process of transduction. The message is then transmitted over the peripheral nerve to the spinal cord, where it synapses with cells of origin of the major ascending pain pathway, the spinothalamic tract. The message is relayed in the thalamus to the anterior cingulate (C), frontal insular (F), and somatosensory cortex (SS).

B. Pain-modulation network. Inputs from frontal cortex and hypothalamus (Hyp.)activate cells in the midbrain that control spinal pain-transmission cells via cells in the medulla.



On the other hand, many patients find even minor injuries (such as venipuncture) frightening and unbearable, and the expectation of pain has been demonstrated to induce pain without a noxious stimulus. The powerful effect of expectation and other psychological variables on the perceived intensity of pain implies the existence of brain circuits that can modulate the activity of the pain-transmission pathways. One of these circuits has links in the hypothalamus, midbrain, and medulla, and it selectively controls spinal pain-transmission neurons through a descending pathway.


Human brain imaging studies have implicated this pain-modulating circuit in the pain-relieving effect of attention, suggestion, and opioid analgesic medications. Furthermore, each of the component structures of the pathway contains opioid receptors and is sensitive to the direct application of opioid drugs. In animals, lesions of the system reduce the analgesic effect of systemically administered opioids such as morphine.


Along with the opioid receptor, the component nuclei of this pain-modulating circuit contain endogenous opioid peptides such as the enkephalins and endorphin.

The most reliable way to activate this endogenous opioid-mediated modulating system is by prolonged pain and/or fear. There is evidence that pain-relieving endogenous opioids are released following surgical procedures and in patients given a placebo for pain relief.


Pain-modulating circuits can enhance as well as suppress pain. Both pain-inhibiting and pain-facilitating neurons in the medulla project to and control spinal pain-transmission neurons. Since pain-transmission neurons can be activated by modulatory neurons, it is theoretically possible to generate a pain signal with no peripheral noxious stimulus. In fact, functional imaging studies have demonstrated increased activity in this circuit during migraine headache. A central circuit that facilitates pain could account for the finding that pain can be induced by suggestion and could provide a framework for understanding how psychological factors can contribute to chronic pain.


NEUROPATHIC PAIN

Lesions of the peripheral or central nervous pathways for pain typically result in a loss or impairment of pain sensation.

Paradoxically, damage or dysfunction of these pathways can produce pain. For example, damage to peripheral nerves, as occurs in diabetic neuropathy, or to primary afferents, as in herpes zoster, can result in pain that is referred to the body region innervated by the damaged

nerves. Though rare, pain may also be produced by damage to the central nervous system, particularly the spinothalamic pathway or thalamus. Such neuropathic pains are often severe and are notoriously intractable to standard treatments for pain. Neuropathic pains typically have an unusual burning, tingling, or electric shock–like quality and may be triggered by very light touch.


These features are rare in other types of pain. On examination, a sensory deficit is characteristically present in the area of the patient's pain. Hyperpathia is also characteristic of neuropathic pain; patients often complain that the very lightest moving stimuli evoke exquisite pain (allodynia). In this regard it is of clinical interest that a topical preparation of 5% lidocaine in patch form is effective for patients with postherpetic neuralgia who have prominent allodynia.


A variety of mechanisms contribute to neuropathic pain. As with sensitized primary afferent nociceptors, damaged primary afferents, including nociceptors, become highly sensitive to mechanical stimulation and begin to generate impulses in the absence of stimulation. There is evidence that this increased sensitivity and spontaneous activity is due to an increased concentration of sodium channels.


Damaged primary afferents may also develop sensitivity to norepinephrine. Interestingly, spinal cord pain-transmission neurons cut off from their normal input may also become spontaneously active. Thus both central and peripheral nervous system hyperactivity contribute to neuropathic pain.


Sympathetically Maintained Pain Patients with peripheral nerve injury can develop a severe burning pain (causalgia) in the region innervated by the nerve. The pain typically begins after a delay of hours to days or even weeks. The pain is accompanied by swelling of the extremity, periarticular osteoporosis, and arthritic changes in the distal joints. The pain is dramatically and immediately relieved by blocking the sympathetic innervation of the affected extremity. Damaged primary afferent nociceptors acquire adrenergic sensitivity and can be activated by stimulation of the sympathetic outflow. A similar syndrome called reflex sympathetic dystrophy can be produced without obvious nerve damage by a variety of injuries, including fractures of bone, soft tissue trauma, myocardial infarction, and stroke .


Although the pathophysiology of this condition is poorly understood, the pain and the signs of inflammation are rapidly relieved by blocking the sympathetic nervous system. This implies that sympathetic activity can activate undamaged nociceptors when inflammation is present. Signs of sympathetic hyperactivity should be sought in patients with posttraumatic pain and inflammation and no other obvious explanation.

Straddle injury = cedera daerah selangkangan

Hari ini di IGD ada konsul dari GP, pasiennya anak perempuan usia 10 tahunan, mengalami perdarahan akibat terjatuh dari sepeda. Hasil pemeriksaan didapatkan hymen utuh, tetapi ada luka lebih kurang 1 cm vertikal tepat dibawah clit nya. Masih aktif berdarah serta ada timbunan darah (heamatoma). Injuri atau trauma didaearah selangkangan ini disebut strradle injury. Karena pasiennya msih kecil dan sangat tidak kooperatif, maka penjahitan dilakukan dalam general anestesia (bius umum).

Straddle injuries terjadi jika seseorang (bisa anak bisa dewasa) menunggang (straddle) sesuatu lalu terjatuh, menecederai daerah uro-genitalia oleh bobot tubuhnya sendiri. Luka atau cedera disebabkan oleh jaringan terjepiy antara tulang daearah pinggul (pelvis) dengan bobot tubuh. Straddle injury sering ditemukan pada anak2 dan sering terjadi saat bersepeda, jatuh atau bermain dengan palang monyet (monkey bar).

Pada anak kecil harus hati2, jika nggak diketahui pasti kejadinnya, maka harus dibedakan dengan injury akibat sex abbuse. Dengan anamnesa yang teliti. Gambar samping merupakan contoh straddle injury yang menyebabkan terjadinya hematom (penumpukan darah) pada bagain kiri bibir V. Untuk kasus seperti ini dilakukan insisi (dibeler) lalau darahnya dikeluarkan, sumber darahnya dihentikan, kemudian ditutup lagi dengan jahitan atau diberi saluran keluar jika darahnya masih ngalir dari pembuluh darah yg kecil2.


Senin, 17 November 2008

Waktu bersalin : Kenapa tidur miring kiri ?

Bagi yang sudah pernah melahirkan pervaginam (normal) pasti pernah mengalaminya, yaitu saat menunggu pembukaan lengkap disuruh tidur miring kiri (left lateral position) oleh dokter atau bu bidan yang mengawasi proses persalinan. Barusan juga ternyata ada yang nyari via google dengan keyword seperti diatas.

Sudah pernah baca posting tentang gerakan (jurus) bayi dalam proses persalinan? Hal ini berhubungan dengan hal tersebut. Yaitu gerakan kepala bayi saat didasar panggul (internal rotation).

Sebetulnya nggak selalu harus miring kiri, bisa juga miring kanan. Kok bisa? Tergantung posisi ubun2 kecilnya (pada letak belakang kepala) di kiri atau kanan, baca jenis2 letak kepala bayi. Kalau letak muka tergantung dimana dagunya dstnya.

Bagaimana bisa tahu letak penunjuknya? Tentunya dengan pemeriksaan dalam (Vaginal Toucher baca Vaginal Tuse) yang benar maka posisi bagian2 penunjuk ini bisa diketahui. Guna posisi miring ini agar internal rotasi ini bisa berlangsung lebih cepat dan sempurna.

Makanya ibu2 kudu patuh mengikuti arahan SpOG-nya kalau disuruh miring kesalah satu posisi. Banyak bulin yang karena rasa sakit persalinannya jadi nggak peduli jika disuruh untuk tidur miring. Apa akibatnya? Putaran paksi dalam (internal rotasi) tidak berlangsung sempurna dan cepat atau malah salah putar, selanjutnya terjadilah kemacetan persalinan.

Berapa lama harus miring ? Jika posisi penunjuk tadi sudah sesuai dengan yang diharapkan. Kalau posisi normal (letak belakang kepala) maka ubun-ubun kecil sudah berada di posisi jam 12 (depan), selanjutnya jika kepala sudah crowning (terlihat 3 cm dan nggak mundur lagi), baru kemudian bulin dipimpin untuk meneran.

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