GAWAT ABDOMEN

GAWAT ABDOMEN

Gawat abdomen menggambarkan keadaan klinik akibat kegawatan di rongga perut yang biasanya timbul mendadak dengan nyeri sebagai keluhan utama. Keadaan ini memerlukan penanggulangan segera yang sering berupa tindakan bedah, misalnya pada perforasi, perdarahan intraabdomen, infeksi, obstruksi dan strangulasi jalan cerna dapat menyebabkan perforasi yang mengakibatkan kontaminasi rongga perut oleh isi saluran cerna sehingga terjadilah peritonitis.1.7
Peradangan peritoneum merupakan komplikasi berbahaya yang sering terjadi akibat penyebaran infeksi dari organ-organ abdomen (misalnya apendisitis, salpingitis, perforasi ulkus gastroduodenal), ruptura saluran cerna, komplikasi post operasi, iritasi kimiawi, atau dari luka tembus abdomen.1.2
Pada keadaan normal, peritoneum resisten terhadap infeksi bakteri (secara inokulasi kecil-kecilan); kontaminasi yang terus menerus, bakteri yang virulen, resistensi yang menurun, dan adanya benda asing atau enzim pencerna aktif, merupakan faktor-faktor yang memudahkan terjadinya peritonitis.3
Keputusan untuk melakukan tindakan bedah harus segera diambil karena setiap keterlambatan akan menimbulkan penyakit yang berakibat meningkatkan morbiditas dan mortalitas. Ketepatan diagnosis dan penanggulangannya tergantung dari kemampuan melakukan analisis pada data anamnesis, pemeriksaan fisik dan pemeriksaan penunjang.3.7

Peritonitis selain disebabkan oleh kelainan di dalam abdomen yang berupa inflamasi dan penyulitnya, juga oleh ileus obstruktif, iskemia dan perdarahan. Sebagian kelainan disebabkan oleh cidera langsung atau tidak langsung yang mengakibatkan perforasi saluran cerna atau perdarahan.2

I. DEFINISI
Peritonitis adalah peradangan pada peritonium yang merupakan pembungkus visera dalam rongga perut.
Peritonitis adalah suatu respon inflamasi atau supuratif dari peritoneum yang disebabkan oleh iritasi kimiawi atau invasi bakteri.
Peritoneum adalah mesoderm lamina lateralis yang tetap bersifat epitelial. Pada permulaan, mesoderm merupakan dinding dari sepasang rongga yaitu coelom. Di antara kedua rongga terdapat entoderm yang merupakan dinding enteron. Enteron didaerah abdomen menjadi usus. Kedua rongga mesoderm, dorsal dan ventral usus saling mendekat, sehingga mesoderm tersebut kemudian menjadi peritonium.2.8
Lapisan peritonium dibagi menjadi 3 yaitu:
1. Lembaran yang menutupi dinding usus, disebut lamina visceralis (tunika serosa).
2. Lembaran yang melapisi dinding dalam abdomen disebut lamina parietalis.
3. Lembaran yang menghubungkan lamina visceralis dan lamina parietalis
kanan kiri saling menempel dan membentuk suatu lembar rangkap yang disebut duplikatura.
Dengan demikian baik di ventral maupun dorsal usus terdapat suatu duplikatura. Duplikatura ini menghubungkan usus dengan dinding ventral dan dinding dorsal perut dan dapat dipandang sebagai suatu alat penggantung usus yang disebut mesenterium. Mesenterium dibedakan menjadi mesenterium ventrale dan mesenterium dorsale. Mesenterium ventrale yang terdapat pada sebelah kaudal pars superior duodeni kemudian menghilang. Lembaran kiri dan kanan mesenterium ventrale yang masih tetap ada, bersatu pada tepi kaudalnya. Mesenterium setinggi ventrikulus disebut mesogastrium ventrale dan mesogastrium dorsale. Pada waktu perkambangan dan pertumbuhan, ventriculus dan usus mengalami pemutaran. Usus atau enteron pada suatu tempat berhubungan dengan umbilicus dan saccus vitellinus. Hubungan ini membentuk pipa yang disebut ductus omphaloentericus.
Usus tumbuh lebih cepat dari rongga sehingga usus terpaksa berbelok-belok dan terjadi jirat-jirat. Jirat usus akibat usus berputar ke kanan sebesar 270 ° dengan aksis ductus omphaloentericus dan a. mesenterica superior masing-masing pada dinding ventral dan dinding dorsal perut. Setelah ductus omphaloentericus menghilang, jirat usus ini jatuh kebawah dan bersama mesenterium dorsale mendekati peritonium parietale. Karena jirat usus berputar, bagian usus disebelah oral (kranial) jirat berpindah ke kanan dan bagian disebelah anal (kaudal) berpindah ke kiri dan keduanya mendekati peritoneum parietale.
Pada tempat-tempat peritoneum viscerale dan mesenterium dorsale mendekati peritoneum dorsale, terjadi perlekatan. Tetapi, tidak semua tempat terjadi perlekatan. Akibat perlekatan ini, ada bagian-bagian usus yang tidak mempunyai alat-alat penggantung lagi, dan terletak sekarang dorsal peritonium sehingga disebut retroperitoneal. Bagian-bagian yang masih mempunyai alat penggantung terletak di dalam rongga yang dindingnya dibentuk oleh peritoneum parietale, disebut terletak intraperitoneal. Rongga tersebut disebut cavum peritonei, dengan demikian: Duodenum terletak retroperitoneal; Jejenum dan ileum terletak intraperitoneal dengan alat penggantung mesenterium; Colon ascendens dan colon descendens terletak retroperitoneal; Colon transversum terletak intraperitoneal dan mempunyai alat penggantung disebut mesocolon transversum; Colon sigmoideum terletak intraperitoneal dengan alat penggatung mesosigmoideum; cecum terletak intraperitoneal karena pada permulaan merupakan suatu tonjolan dinding usus dan tidak mempunyai alat pengantung; Processus vermiformis terletak intraperitoneal dengan alat penggantung mesenterium, lipatan peritoneum akibat adanya arteria yang menuju ke ujung processus vermiformis. Ia sebenarnya lanjutan dari cecum.
Di berbagai tempat, perlekatan peritoneum viscerale atau mesenterium pada peritoneum parietale tidak sempurna, sehingga terjadi cekungan-cekungan di antara usus (yang diliputi oleh peritoneum viscerale) dan peritoneum parietale atau diantara mesenterium dan peritoneum parietale yang dibatasi lipatan-lipatan. Lipatan-lipatan dapat juga terjadfi karena di dalamnya berjalan pembuluh darah. Dengan demikian di flexura duodenojejenalis terdapat plica duodenalis superior yang membatasi recessus duodenalis superior dan plica duodenalis inferior yang membatasi resesus duodenalis inferior.
Pada colon descendens terdapat recessus paracolici. Pada colon sigmoideum terdapat recessus intersigmoideum di antara peritoneum parietale dan mesosigmoideum. Stratum circulare coli melipat-lipat sehingga terjadi plica semilunaris. Peritoneum yang menutupi colon melipat-lipat keluar diisi oleh lemak sehingga terjadi bangunan yang disebut appendices epiploicae.
Ventriculus memutar terhadap sumbu longitudinal, sehingga curvatura mayor di sebelah kiri dan curvatura minor di sebelah kanan. Kemudian ventriculus memutar terhadap sumbu sagital, sehingga cardia berpindah ke kiri dan pilorus ke kanan. Kerena ventriculus berputar, sebagian mesogastrium dorsale mendekati peritoneum perietale dan tumbuh melekat. Dengan demikian tempat perlekatan mesogastrium dorsale merupakan suatu lengkung dari kiri kranial ke kanan kaudal. Bagian yang terkaudal mendekati perlekatan mesocolon transversum yang berjalan trasversal. Dibagian kaudal juga terjadi perlekatan mesogastrium dorsale dengan mesocolon transversum dan disebut sebagai omentum majus. Kantong yang dibentuk olehnya disebut bursa omentalis.
Mesogastrium ventrale melekat pada peritoneum parietale dinding ventral perut dan pada diaphragma. Di dalam mesogastrium ventrale hepar terbentuk dan berkembang. Hepar berkembang ke kaudal sampai tepi batas mesogastrium yang disebut omentum minus atau ligamentum hepatogastricum dengan tepi bebasnya di sebelah kaudal disebut ligamentum hepatoduodenale. Ligamentum falciforme melekat pada batas antara lobus dexter dan lobus sinister. Omentum minus melekat pada fosa sagittalis sinistra bagian dorsokranial dan mengelilingi portae hepatis. Ligamentum teres hepatis yaitu sisa vena umbilikalis sinistra, terbentang dari umbilicus ke hepar di dalam tepi bebas ligamentum falciforme hepatis, masuk di dalam fossa sagittalis sinistra hepatis dan berakhir pada ramus sinistra vena portae.
Di dalam tepi bebas omentum minus atau ligamentum hepatoduodenale terdapat: Vena portae; Arteria hepatica propria; Ductus choledochus; Serabut-serabut saraf otonom; Pembuluh-pembuluh lympha.
Di sebelah kiri berjalan a. hepatica propria di sebelah dorsal kedua bangunan ini ditengah-tengah berjalan v. portae. Ductus choledocus dibentuk oleh oleh ductus cysticus dan ductus hepaticus communis, berjalan melalui ligamentum tersebut ke kaudomedial, menyilangi disebelah dorsal pars superior duodeni sampai di dalam sulcus diantara pars descendens duodeni dan caput pancreatis bermuara di papillae duodeni major.
Di dalam mesenterium dan duodenum (mesoduodenum) dan mesogastrium dorsale terjadi dan tumbuh pankreas. Karena mesoduodenum dan sebagian mesogastrium dorsale tumbuh melekat dengan peritoneum parietale, caput dan corpus pancreatis letaknya menjadi retroperitoneal, tetapi cauda pancreatis masih tetap didalam omentum majus.
Didalam omentum majus disebelah ventral cauda pancreatis lien terbentuk dan berkembang kearah kiri sehingga ia ditutupi sebagian besar oleh lembaran kiri omentum majus. Omentum majus dibagi dua oleh lien menjadi ligamentum precholienale, bagian antara lien dan peritoneum parietale yang menutupi diaphragma, ligamentum gastrolienale bagian antara lien dan ventriculus. Karena lien tumbuh terutama ke kiri, lembaran kanan kedua ligamentumtidak sampai melekat pada lien, sedangkan lembaran kiri mulai melekat pada lien dikelilingi hilus.
Karena perubahan letak ventriculus terjadilah bursa omentalis. Lubang masuk kedalam bursa omentalis disebut foramen epiploicum (Winslowi) dibatasi:
Dibagian cranial oleh processus caudatus
Dibagian ventral oleh lig.hepatoduodenale Dibagian kaudal oleh pars superior duodeni. Dibagian dorsal oleh peritoneum parietale yang menutupi vena cava inferior.
Bursa omentalis sendiri dibatasi: Dibagian cranial oleh lobus caudatus hepatis Dibagian ventral oleh omentum minus dan ventriculus
Dibagian kaudal oleh mesocolontransversum serta colon transversum
Dibagian dorsal oleh peritoneum parietale yang menutupi caput dan corpus pancreatic.
Dibagian kiri oleh omentum majus dengan cauda pancreatic dan lien
Omentum majus yang melekat pada colon tansversum ke kaudal menutupi usus dari sebelah vental sebagai suatu tirai untuk kemudian melipat ke arah cranial dan melekat pada curvatura major ventriculi. Kedua lembaran dari lipatan itu dibagian kaudal tumbuh melekat. Bagian yang tidak tumbuh merupakan lanjutan bursae omentalis yang disebut recessus inferior bursae omentalis. Bagian bursae omentalis terkranial disebut recessus superior bursae omentalis.
Dataran peritoneum yang dilapisis mesotelium, licin dan bertambah licin karena peritoneum mengeluiarkan sedikit cairan. Dengan demikian peritoneum dapat disamakan dengan stratum synoviale di persendian. Peritoneum yang licin ini memudahkan pergerakan alat-alat intra peritoneal satu terhadap yang lain. Kadang-kadang , pemuntaran ventriculus dan jirat usus berlangsung ke arah yang lain. Akibatnya alat-alat yang seharusnya disebelah kanan terletak disebelah kiri atau sebaliknya. Keadaan demikian disebut situs inversus.
Peritoneum adalah lapisan tunggal dari sel-sel mesoepitelial diatas dasar fibroelastik. Terbagi menjadi bagian viseral, yang menutupi usus dan mesenterium; dan bagian parietal yang melapisi dinding abdomen dan berhubungan dengan fasia muskularis.5
Peritoneum viserale yang menyelimuti organ perut dipersarafi oleh sistem saraf autonom dan tidak peka terhadap rabaan atau pemotongan. Dengan demikian sayatan atau penjahitan pada usus dapat dilakukan tanpa dirasakan oleh pasien. Akan tetapi bila dilakukan tarikan atau regangan organ, atau terjadi kontraksi yang berlebihan pada otot yang menyebabkan iskemia misalnya pada kolik atau radang seperti apendisitis, maka akan timbul nyeri. Pasien yang merasaka nyeri viseral biasanya tidak dapat menunjuk dengan tepat letak nyeri sehingga biasanya ia menggunakan seluruh telapak tangannya untuk menujuk daerah yang nyeri.4
Peritoneum parietale dipersarafi oleh saraf tepi, sehingga nyeri dapat timbul karena adanya rangsang yang berupa rabaan, tekanan, atau proses radang. Nyeri dirasakan seperti seperti ditusuk atau disayat, dan pasien dapat menunjukkan dengan tepat lokasi nyeri.4
Total peritoneum sekitar 2 meter, dan aktivitasnya konsisten dengan suatu membran semi permeabel. Cairan dan elektrolit kecil dapat bergerak kedua arah. Molekul-molekul yang lebih besar dibersihkan kedalam mesotelium diafragma dan limfatik melalui stomata kecil.5
Organ-organ yang terdapat di cavum peritoneum yaitu gaster, hepar, vesica fellea, lien, ileum, jejenum, kolon transversum, kolon sigmoid, sekum, dan appendix (intraperitoneum); pankreas, duodenum, kolon ascenden & descenden, ginjal dan ureter (retroperitoneum).6.7

II. ANATOMI
Dinding perut mengandung struktur muskulo-aponeurosis yang kompleks. Dibagian belakang struktur ini melekat pada tulang belakang sebelah atas pada iga, dan di bagian bawah pada tulang panggul. Dinding perut ini terdiri dari berbagai lapis, yaitu dari luar ke dalam, lapis kulit yang terdiri dari kuitis dan sub kutis, lemak sub kutan dan facies superfisial ( facies skarpa ), kemudian ketiga otot dinding perut m. obliquus abdominis eksterna, m. obliquus abdominis internus dan m. transversum abdominis, dan akhirnya lapis preperitonium dan peritonium, yaitu fascia transversalis, lemak preperitonial dan peritonium. Otot di bagian depan tengah terdiri dari sepasang otot rektus abdominis dengan fascianya yang di garis tengah dipisahkan oleh linea alba.6
Dinding perut membentuk rongga perut yang melindungi isi rongga perut. Integritas lapisan muskulo-aponeurosis dinding perut sangat penting untuk mencegah terjadilah hernia bawaan, dapatan, maupun iatrogenik. Fungsi lain otot dinding perut adalah pada pernafasan juga pada proses berkemih dan buang air besar dengan meninggikan tekanan intra abdominal.
Perdarahan dinding perut berasal dari beberapa arah. Dari kraniodorsal diperoleh perdarahan dari cabang aa. Intercostalis VI – XII dan a. epigastrika superior. Dari kaudal terdapat a. iliaca a. sircumfleksa superfisialis, a. pudenda eksterna dan a. epigastrika inferior. Kekayaan vaskularisasi ini memungkinkan sayatan perut horizontal maupun vertikal tanpa menimbulkan gangguan perdarahan.6
Persarafan dinding perut dipersyarafi secara segmental oleh n.thorakalis VI – XII dan n. lumbalis I.6

III. ETIOLOGI
Peritonitis dapat disebabkan oleh kelainan di dalam abdomen berupa inflamasi dan penyulitnya misalnya perforasi appendisitis, perforasi tukak lambung, perforasi tifus abdominalis. Ileus obstruktif dan perdarahan oleh karena perforasi organ berongga karena trauma abdomen.
a.Bakterial : Bacteroides, E.Coli, Streptococus, Pneumococus, proteus, kelompok Enterobacter-Klebsiella, Mycobacterium Tuberculosa.
b.Kimiawi : getah lambung,dan pankreas, empedu, darah, urin, benda asing (talk, tepung).2.3.9

IV. PATOFISOLOGI
Reaksi awal peritoneum terhadap invasi oleh bakteri adalah keluarnya eksudat fibrinosa. Kantong-kantong nanah (abses) terbentuk di antara perlekatan fibrinosa, yang menempel menjadi satu dengan permukaan sekitarnya sehingga membatasi infeksi. Perlekatan biasanya menghilang bila infeksi menghilang, tetapi dapat menetap sebagai pita-pita fibrosa, yang kelak dapat mengakibatkan obstuksi usus.1
Peradangan menimbulkan akumulasi cairan karena kapiler dan membran mengalami kebocoran. Jika defisit cairan tidak dikoreksi secara cepat dan agresif, maka dapat menimbulkan kematian sel. Pelepasan berbagai mediator, seperti misalnya interleukin, dapat memulai respon hiperinflamatorius, sehingga membawa ke perkembangan selanjutnya dari kegagalan banyak organ. Karena tubuh mencoba untuk mengkompensasi dengan cara retensi cairan dan elektrolit oleh ginjal, produk buangan juga ikut menumpuk. Takikardi awalnya meningkatkan curah jantung, tapi ini segera gagal begitu terjadi hipovolemia.5
Organ-organ didalam cavum peritoneum termasuk dinding abdomen mengalami oedem. Oedem disebabkan oleh permeabilitas pembuluh darah kapiler organ-organ tersebut meninggi. Pengumpulan cairan didalam rongga peritoneum dan lumen-lumen usus serta oedem seluruh organ intra peritoneal dan oedem dinding abdomen termasuk jaringan retroperitoneal menyebabkan hipovolemia. Hipovolemia bertambah dengan adanya kenaikan suhu, masukan yang tidak ada, serta muntah.10
Terjebaknya cairan di cavum peritoneum dan lumen usus, lebih lanjut meningkatkan tekana intra abdomen, membuat usaha pernapasan penuh menjadi sulit dan menimbulkan penurunan perfusi.5
Bila bahan yang menginfeksi tersebar luas pada permukaan peritoneum atau bila infeksi menyebar, dapat timbul peritonitis umum. Dengan perkembangan peritonitis umum, aktivitas peristaltik berkurang sampai timbul ileus paralitik; usus kemudian menjadi atoni dan meregang. Cairan dan elektrolit hilang kedalam lumen usus, mengakibatkan dehidrasi, syok, gangguan sirkulasi dan oliguria. Perlekatan dapat terbentuk antara lengkung-lengkung usus yang meregang dan dapat mengganggu pulihnya pergerakan usus dan mengakibatkan obstruksi usus.1
Sumbatan yang lama pada usus atau obstruksi usus dapat menimbulkan ileus karena adanya gangguan mekanik (sumbatan) maka terjadi peningkatan peristaltik usus sebagai usaha untuk mengatasi hambatan. Ileus ini dapat berupa ileus sederhana yaitu obstruksi usus yang tidak disertai terjepitnya pembuluh darah dan dapat bersifat total atau parsial, pada ileus stangulasi obstruksi disertai terjepitnya pembuluh darah sehingga terjadi iskemi yang akan berakhir dengan nekrosis atau ganggren dan akhirnya terjadi perforasi usus dan karena penyebaran bakteri pada rongga abdomen sehingga dapat terjadi peritonitis.7
Tifus abdominalis adalah penyakit infeksi akut usus halus yang disebabkan kuman S. Typhi yang masuk tubuh manusia melalui mulut dari makan dan air yang tercemar. Sebagian kuman dimusnahkan oleh asam lambung, sebagian lagi masuk keusus halus dan mencapai jaringan limfoid plaque peyeri di ileum terminalis yang mengalami hipertropi ditempat ini komplikasi perdarahan dan perforasi intestinal dapat terjadi, perforasi ileum pada tifus biasanya terjadi pada penderita yang demam selama kurang lebih 2 minggu yang disertai nyeri kepala, batuk dan malaise yang disusul oleh nyeri perut, nyeri tekan, defans muskuler, dan keadaan umum yang merosot karena toksemia.4
Perforasi tukak peptik khas ditandai oleh perangsangan peritonium yang mulai di epigastrium dan meluas keseluruh peritonium akibat peritonitis generalisata. Perforasi lambung dan duodenum bagian depan menyebabkan peritonitis akut. Penderita yang mengalami perforasi ini tampak kesakitan hebat seperti ditikam di perut. Nyeri ini timbul mendadak terutama dirasakan di daerah epigastrium karena rangsangan peritonium oleh asam lambung, empedu dan atau enzim pankreas. Kemudian menyebar keseluruh perut menimbulkan nyeri seluruh perut pada awal perforasi, belum ada infeksi bakteria, kadang fase ini disebut fase peritonitis kimia, adanya nyeri di bahu menunjukkan rangsangan peritonium berupa mengenceran zat asam garam yang merangsang, ini akan mengurangi keluhan untuk sementara sampai kemudian terjadi peritonitis bakteria.1
Pada apendisitis biasanya biasanya disebabkan oleh penyumbatan lumen apendiks oleh hiperplasi folikel limfoid, fekalit, benda asing, striktur karena fibrosis dan neoplasma. Obstruksi tersebut menyebabkan mukus yang diproduksi mukosa mengalami bendungan,makin lama mukus tersebut makin banyak, namun elastisitas dinding apendiks mempunyai keterbatasan sehingga menyebabkan peningkatan tekanan intralumen dan menghambat aliran limfe yang mengakibatkan oedem, diapedesis bakteri, ulserasi mukosa, dan obstruksi vena sehingga udem bertambah kemudian aliran arteri terganggu akan terjadi infark dinding apendiks yang diikuti dengan nekrosis atau ganggren dinding apendiks sehingga menimbulkan perforasi dan akhirnya mengakibatkan peritonitis baik lokal maupun general.7
Pada trauma abdomen baik trauma tembus abdomen dan trauma tumpul abdomen dapat mengakibatkan peritonitis sampai dengan sepsis bila mengenai organ yang berongga intra peritonial. Rangsangan peritonial yang timbul sesuai dengan isi dari organ berongga tersebut, mulai dari gaster yang bersifat kimia sampai dengan kolon yang berisi feses. Rangsangan kimia onsetnya paling cepat dan feses paling lambat. Bila perforasi terjadi dibagian atas, misalnya didaerah lambung maka akan terjadi perangsangan segera sesudah trauma dan akan terjadi gejala peritonitis hebat sedangkan bila bagian bawah seperti kolon, mula-mula tidak terjadi gejala karena mikroorganisme membutuhkan waktu untuk berkembang biak baru setelah 24 jam timbul gejala akut abdomen karena perangsangan peritonium.1.7

V. KLASIFIKASI
Berdasarkan patogenesis peritonitis dapat diklasifikasikan sebagai berikut: 2.3.5.9
a. Peritonitis bakterial primer
Merupakan peritonitis akibat kontaminasi bakterial secara hematogen pada cavum peritoneum dan tidak ditemukan fokus infeksi dalam abdomen. Penyebabnya bersifat monomikrobial, biasanya E. Coli, Sreptococus atau Pneumococus.

Peritonitis bakterial primer dibagi menjadi dua, yaitu:
1. Spesifik : misalnya Tuberculosis
2. Non spesifik: misalnya pneumonia non tuberculosis an Tonsilitis.
Faktor resiko yang berperan pada peritonitis ini adalah adanya malnutrisi, keganasan intraabdomen, imunosupresi dan splenektomi.
Kelompok resiko tinggi adalah pasien dengan sindrom nefrotik, gagal ginjal kronik, lupus eritematosus sistemik, dan sirosis hepatis dengan asites.

b. Peritonitis bakterial akut sekunder (supurativa) Peritonitis yang mengikuti suatu infeksi akut atau perforasi tractusi gastrointestinal atau tractus urinarius. Pada umumnya organisme tunggal tidak akan menyebabkan peritonitis yang fatal. Sinergisme dari multipel organisme dapat memperberat terjadinya infeksi ini. Bakterii anaerob, khususnya spesies Bacteroides, dapat memperbesar pengaruh bakteri aerob dalam menimbulkan infeksi. Selain itu luas dan lama kontaminasi suatu bakteri juga dapat memperberat suatu peritonitis. Kuman dapat berasal dari:
- Luka/trauma penetrasi, yang membawa kuman dari luar masuk ke dalam cavum peritoneal.
– Perforasi organ-organ dalam perut, contohnya peritonitis yang disebabkan oleh bahan kimia, perforasi usus sehingga feces keluar dari usus.
- Komplikasi dari proses inflamasi organ-organ intra abdominal, misalnya appendisitis.
c. Peritonitis tersier, misalnya:
- Peritonitis yang disebabkan oleh jamur
- Peritonitis yang sumber kumannya tidak dapat ditemukan.
- Peritonitis yang disebabkan oleh iritan langsung, sepertii misalnya empedu, getah lambung, getah pankreas, dan urine.

VI. MANIFESTASI KLINIS
Adanya darah atau cairan dalam rongga peritonium akan memberikan tanda – tanda rangsangan peritonium. Rangsangan peritonium menimbulkan nyeri tekan dan defans muskular, pekak hati bisa menghilang akibat udara bebas di bawah diafragma. Peristaltik usus menurun sampai hilang akibat kelumpuhan sementara usus.1
Bila telah terjadi peritonitis bakterial, suhu badan penderita akan naik dan terjadi takikardia, hipotensi dan penderita tampak letargik dan syok.1
Rangsangan ini menimbulkan nyeri pada setiap gerakan yang menyebabkan pergeseran peritonium dengan peritonium. Nyeri subjektif berupa nyeri waktu penderita bergerak seperti jalan, bernafas, batuk, atau mengejan. Nyeri objektif berupa nyeri jika digerakkan seperti palpasi, nyeri tekan lepas, tes psoas, atau tes lainnya.1.7

VII. DIAGNOSIS
Diagnosis dari peritonitis dapat ditegakkan dengan adanya gambaran klinis, pemeriksaan laboratorium dan X-Ray.
a. Gambaran klinis
Gambaran klinisnya tergantung pada luas peritonitis, berat peritonitis dan jenis organisme yang bertanggung jawab. Peritonitis dapat lokal, menyebar, atau umum. Gambaran klinis yang biasa terjadi pada peritonitis bakterial primer yaitu adanya nyeri abdomen, demam, nyeri lepas tekan dan bising usus yang menurun atau menghilang. Sedangkan gambaran klinis pada peritonitis bakterial sekunder yaitu adanya nyeri abdominal yang akut. Nyeri ini tiba-tiba, hebat, dan pada penderita perforasi (misal perforasi ulkus), nyerinya menjadi menyebar keseluruh bagian abdomen. Pada keadaan lain (misal apendisitis), nyerinya mula-mula dikarenakan penyebab utamanya, dan kemudian menyebar secara gradual dari fokus infeksi. Selain nyeri, pasien biasanya menunjukkan gejala dan tanda lain yaitu nausea, vomitus, syok (hipovolemik, septik, dan neurogenik), demam, distensi abdominal, nyeri tekan abdomen dan rigiditas yang lokal, difus atau umum, dan secara klasik bising usus melemah atau menghilang. Gambaran klinis untuk peritonitis non bakterial akut sama dengan peritonitis bakterial.1.3
Peritonitis bakterial kronik (tuberculous) memberikan gambaran klinis adanya keringat malam, kelemahan, penurunan berat badan, dan distensi abdominal; sedang peritonitis granulomatosa menunjukkan gambaran klinis nyeri abdomen yang hebat, demam dan adanya tanda-tanda peritonitis lain yang muncul 2 minggu pasca bedah.3
b. Pemeriksaan laboratorium
Pada pemeriksaan laboratorium ditemukan adanya lekositosis, hematokrit yang meningkat dan asidosis metabolik. Pada peritonitis tuberculosa cairan peritoneal mengandung banyak protein (lebih dari 3 gram/100 ml) dan banyak limfosit; basil tuberkel diidentifikasi dengan kultur. Biopsi peritoneum per kutan atau secara laparoskopi memperlihatkan granuloma tuberkuloma yang khas, dan merupakan dasar diagnosa sebelum hasil pembiakan didapat.3
c. Pemeriksaan X-Ray
Ileus merupakan penemuan yang tidak khas pada peritonitis; usus halus dan usus besar berdilatasi. Udara bebas dapat terlihat pada kasus-kasus perforasi.3

VIII. TERAPI
Prinsip umum terapi adalah penggantian cairan dan elektrolit yang hilang yang dilakukan secara intravena, pemberian antibiotika yang sesuai, dekompresi saluran cerna dengan penghisapan nasogastrik dan intestinal, pembuangan fokus septik (apendiks, dsb) atau penyebab radang lainnya, bila mungkin mengalirkan nanah keluar dan tindakan-tindakan menghilangkan nyeri.1.8

Resusitasi hebat dengan larutan saline isotonik adalah penting. Pengembalian volume intravaskular memperbaiki perfusi jaringan dan pengantaran oksigen, nutrisi, dan mekanisme pertahanan. Keluaran urine tekanan vena sentral, dan tekanan darah harus dipantau untuk menilai keadekuatan resusitasi.5.11
Terapi antibiotika harus diberikan sesegera diagnosis peritonitis bakteri dibuat. Antibiotik berspektrum luas diberikan secara empirik, dan kemudian dirubah jenisnya setelah hasil kultur keluar. Pilihan antibiotika didasarkan pada organisme mana yang dicurigai menjadi penyebab. Antibiotika berspektrum luas juga merupakan tambahan drainase bedah. Harus tersedia dosis yang cukup pada saat pembedahan, karena bakteremia akan berkembang selama operasi.5.11
Pembuangan fokus septik atau penyebab radang lain dilakukan dengan operasi laparotomi. Insisi yang dipilih adalah insisi vertikal digaris tengah yang menghasilkan jalan masuk ke seluruh abdomen dan mudah dibuka serta ditutup. Jika peritonitis terlokalisasi, insisi ditujukan diatas tempat inflamasi. Tehnik operasi yang digunakan untuk mengendalikan kontaminasi tergantung pada lokasi dan sifat patologis dari saluran gastrointestinal. Pada umumnya, kontaminasi peritoneum yang terus menerus dapat dicegah dengan menutup, mengeksklusi, atau mereseksi viskus yang perforasi.11
Lavase peritoneum dilakukan pada peritonitis yang difus, yaitu dengan menggunakan larutan kristaloid (saline). Agar tidak terjadi penyebaran infeksi ketempat yang tidak terkontaminasi maka dapat diberikan antibiotika ( misal sefalosporin ) atau antiseptik (misal povidon iodine) pada cairan irigasi. Bila peritonitisnya terlokalisasi, sebaiknya tidak dilakukan lavase peritoneum, karena tindakan ini akan dapat menyebabkan bakteria menyebar ketempat lain.2.3
Drainase (pengaliran) pada peritonitis umum tidak dianjurkan, karena pipa drain itu dengan segera akan terisolasi/terpisah dari cavum peritoneum, dan dapat menjadi tempat masuk bagi kontaminan eksogen. Drainase berguna pada keadaan dimana terjadi kontaminasi yang terus-menerus (misal fistula) dan diindikasikan untuk peritonitis terlokalisasi yang tidak dapat direseksi.2.3

IX. KOMPLIKASI
Komplikasi dapat terjadi pada peritonitis bakterial akut sekunder, dimana komplikasi tersebut dapat dibagi menjadi komplikasi dini dan lanjut, yaitu :9
a. Komplikasi dini Septikemia dan syok septik Syok hipovolemik Sepsis intra abdomen rekuren yang tidak dapat dikontrol dengan kegagalan multi sistem Abses residual intraperitoneal Portal Pyemia (misal abses hepar)
b. Komplikasi lanjut Adhesi Obstruksi intestinal rekuren

X. PROGNOSIS
Prognosis untuk peritonitis lokal dan ringan adalah baik, sedangkan pada peritonitis umum prognosisnya mematikan akibat organisme virulen.1

PENATALAKSANAAN PERIOPERATIF BAYI DAN ANAK DENGAN OBSTRUKSI USUS

ABSTRAK

 

Keberhasilan penatalaksanaan kasus obstruksi usus pada bayi dan anak, tergantung dari pengetahuan dasar dan penentuan diagnosis dini, persiapan praoperasi, tindakan anestesi dan pembedahan serta perawatan pasca operasi. Penatalaksanaan perioperatif yang baik akan meningkatkan keberhasilan penanganan obstruksi usus pada bayi dan anak .

Sangat penting mempertahankan tiga stabilitas yaitu suhu, cairan dan elektrolit serta keseimbangan asam basa sebelum melakukan tindakan operasi. Penatalaksanaan nyeri dan pemberiaan nutrisi perenteral telah berubah secara radikal. Disamping itu penatakasanaan nyeri bermanfaat untuk mempersingkat periode pulih sadar, dan meningkatkan angka keberhasilan pembedahan. Mencegah timbulnya nyeri adalah tindakan pasca bedah yang perlu diperhatikan.

Pemberian nutrisi enteral dini dapat memperkuat anastomosis usus karena komsumsi asam amino dan protein dapat diberikan lebih awal sehingga dapat mengurangi kejadian kebocoran usus.

 

Kata kunci : Perioperatif , obstruksi usus , bayi dan anak

 

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PENATALAKSANAAN PERIOPERATIF

BAYI DAN ANAK DENGAN OBSTRUKSI USUS

 

PENDAHULUAN

Keberhasilan penatalaksanaan kasus obstruksi usus bayi dan anak tergantung dari pengetahuan dasar dan penentuan diagnosis dini, persiapan praoperasi, tindakan anestesi dan pembedahan serta perawatan pasca operasi. Penatalaksanaan perioperatif yang baik akan meningkatkan keberhasilan penanganan obstruksi usus bayi dan anak .

Tujuan penulisan makalah ini untuk mengingatkan kita kembali, untuk semaksimal mungkin melakukan penatalaksanaan perioperatif pada obstuksi usus untuk menurunkan morbiditas dan mortalitas pada bayi dan anak.

Beberapa kasus obstruksi yang sering dijumpai pada bayi dan anak adalah :

1. Obstruksi setinggi gaster misalnya volvulus gaster, stenosis pilorik hipertrofi, atresia pilorik, antral web dan prolap mukosa lambung
2. Obstruksi setinggi duodenum misalnya atresia duodenum, stenosis duodenum, duodenal web dan pankreas anulare
3. Obstruksi setinggi yeyunoileal seperti atresia yeyunum/ileum, duplikasi usus, sisa duktus omfalo-mesenterikus, mekonium ileus, intususepsi, sepsis akibat necrotizing enterocolitis
4. Obstruksi setinggi kolorektal seperti atresia kolon dan rektum, penyakit Hirschsprung, malformasi anorektal, ileus mekonium, sindroma sumbatan mekonium.

 

Akibat Obstruksi Usus.

Obstruksi usus akan menimbulkan kontraksi berlebihan pada usus di proksimal sumbatan, akan menimbulkan kolik sesuai dengan peristaltik. Usus proksimal sumbatan akan mengalami dilatasi dan sedemikian besarnya hingga terjadi penekanan terhadap diafragma, akibatnya akan timbul gangguan pernafasan dan hipoksia jaringan.

 

____________________

Dipresentasikan pada Pertemuan Ilmiah Tahunan (PIT) IKABI 2005

di Jakarta

Fungsi absorbsi usus akan terganggu, sehingga cairan akan berada di dalam lumen usus dan tidak dapat diabsorbsi. Penderita akan mengalami dehidrasi sesuai dengan derajat kehilangan cairan.

Distensi usus yang bertambah hebat akan menyebabkan terjadinya translokasi kuman ke rongga peritoneum dan sistem sirkulasi yang mengakibatkan sepsis. Disamping itu akibat distensi usus timbul gangguan vaskularisasi yang akhirnya terjadi perforasi.

 

TERMOREGULASI

Hampir 80% kasus bedah anak yang dirujuk, mengalami hipotermia ketika sampai ditempat rujukan. Hipotermia pada bayi yang baru lahir akan bersifat fatal terutama bila disertai kelainan saluran pencernaan.¹

Suhu kulit bayi normal adalah 36,5° – 37,5 ° C, hipotermi terjadi bila suhu tubuh turun dibawah 36,5° C (WHO, 1993). Bayi baru lahir dengan suhu tubuh antara 36 – 36,4 ° C berada dalam hipotermia ringan, pada suhu 32 – 35,9 ° C berada dalam hipotermia sedang dan pada suhu < 32 ° C disebut hipotermia berat.¹

Bayi yang baru lahir lebih mudah terjadi hipotermia karena :

1. Jaringan lemak subkutan tipis
2. Luas permukaan tubuh relatif lebih besar
3. Cadangan glikogen sedikit dan hepar belum berfungsi sempurna
4. Tidak ada respon mengigil pada bayi ²

Hipotermia akan mengakibatkan vasokonstriksi perifer, hal ini akan menyebabkan metabolisme anaerob sehingga terjadi asidosis metabolik yang akan memperburuk keadaan bayi. Juga akan terjadi efek sentral dengan terjadinya vasokonstriksi pembuluh pulmonal yang akan menyebabkan hipoksia jaringan.¹

Suhu lingkungan (inkubator) ideal untuk bayi baru lahir adalah 32 – 34  C, untuk bayi dengan berat badan lahir rendah (BBLR) adalah 34 – 35  C. ^1,3 Bayi dapat kehilangan panas dengan mekanisme konveksi, konduksi, evaporasi dan radiasi. Sebaiknya mencegah terjadinya hipotermia , beberapa cara yang dapat dilakukan adalah :Menggunakan inkubator waktu transportasi bayi

1. Gunakan topi dan selimut untuk mencegah kehilangan panas
2. Keringkan tubuh bayi untuk mencegah evaporasi
3. Setelah desinfeksi dengan cairan harus dikeringkan kembali
4. Bila menggunakan penghangat, peningkatan suhu tidak boleh mendadak

( 0,5 – 1 ° C/jam)

 

CAIRAN DAN ELEKTROLIT

Tatalaksana cairan dan elektrolit merupakan salah satu hal yang penting pada perawatan bayi dan anak sebelum, selama dan sesudah tindakan bedah. Untuk mencapai keseimbangan cairan, elektrolit, dan asam-basa diperlukan pengetahuan fisiologi dasar tentang cairan dan elektrolit. Tatalaksana cairan meliputi tiga hal pokok, yaitu terhadap defisit cairan, kebutuhan rumatan (maintenance), dan penggantian akibat kehilangan cairan (replacement).

Kekurangan cairan sebelum pembedahan terjadi akibat proses penyakit primer dan puasa. Kehilangan cairan selama puasa dapat dihitung dari jumlah kebutuhan cairan per jam dikalikan dengan lama puasa. Pemberian cairan rumatan selama tindakan pembedahan ditujukan untuk mengganti kehilangan cairan akibat penguapan (insensible water loss) sebesar 30-35 % pada keadaan biasa) dan urin. Insensible water loss tergantung pada suhu, kelembaban, maturitas bayi, pola pernapasan, dan luas permukaan tubuh yang terbuka. Penggunaan ventilasi mekanik dan pelembab udara tertutup (humidifier) memperkecil jumlah Insensible water loss. ^1,4

Bayi baru lahir mengalami masa transisi dari dalam kandungan ke dunia luar dimana harus mandiri. Komposisi cairan dan elektrolit pada bayi selalu berubah tergantung pada :

1. Maturitas bayi
2. Defisit saat preoperasi
3. Kehilangan saat durante operasi
4. Respon antidiuretik post operasi

Usia	CES	CIS	Total
Fetus Trisemester I			94% BB
Fetus 32 minggu	60%	25%	78% BB
Aterm	45%	33%	78% BB
Anak	30%	45%	75% BB
Dewasa	20%	40%	60% B

Air susu ibu (ASI) sedapat mungkin diberikan segera bila tidak ada kontraindikasi, pemberian ASI diberikan secara bertahap yaitu

1. hari I : 30 cc/kgBB/24jam ditingkatkan secara bertahap hingga mencapai
2. hari V: 150 cc/kgBB/24jam hingga diberikan 200 cc/kgBB/24 jam ¹

Sebagai pendekatan untuk mengetahui kebutuhan cairan rumatan banyak rumus yang kita kenal. Untuk mempermudah menghitung kebutuhan cairan kita mengenal rumus Holiday-Segar yang mudah diingat dan dipahami.³

 

10 kg I	100 ml/kgBB/hari	4 ml/kgBB/jam
10 kg II	1000 + 50 ml/kgBB/hari	40 + 2 ml/kgBB/jam
10 kg III	1500 + 20 ml/kgBB/hari	60 + 1 ml/kgBB/jam
	Rule 100/50/20	Rule 4/2/1

 

Sebelum pembedahan perlu dilakukan identifikasi masalah dan evaluasi dengan cermat. Gangguan cairan dan elektrolit segera dilakukan koreksi, misalnya hiperkalemia sebagai faktor predisposisi terjadinya aritmia jantung.⁵

Penderita yang akan dilakukan pembedahan perlu dilakukan pengosongan lambung untuk mencegah aspirasi saat pembedahan. Bayi seharusnya tidak diberi ASI 4 jam dan air putih 2 jam menjelang operasi. Gangguan cairan dan elektrolit menjelang operasi perlu dinilai kembali.¹ Defisit cairan (dehidrasi) harus segera dideteksi dan dikoreksi sebelum induksi anestesi, karena bila dikerjakan durante operasi akan lebih sulit dilakukan.

Jenis dan kecepatan cairan ditentukan oleh berat dan tipe gangguan yang terjadi⁶

Dehidrasi Isotonik ( Na : 135 – 150 mmol/L)

 

Dehidrasi ringan	Dehidrasi Sedang	Dehidrasi berat
5% EBV	10% EBV	15% atau lebih EBV
6% BB	8% BB	10% BB
Klinis : mukosa kering Nadi cepat	Klinis : turgor turun	Syok
Resusitasi 24 jam		Syok 20ml/kgBB/jam (25% cairan tubuh)

 

Dehidrasi Hipertonik (Na :> 150 mmol/L)

Perlu dipehatikan dengan cermat karena gejala lebih ringan dibanding dengan dehidrasi isotonik walaupun dalam derajat dehidrasi yang sama.

 

Dehidrasi Hipotonik (Na : < 130 mmol/L)

Dehidrasi hipotonik mempunyai gejala yang lebih berat dibanding dehidrasi isotonik pada derajat yang sama.

Kehilangan cairan dapat dibagi menjadi :

1. Kehilangan cairan yang dapat diukur yaitu kehilangan melalui NGT, muntahan, fistel serta urine
2. Kehilangan cairan yang tidak dapat diukur secara tepat yang disebut Insensible Water Loss (IWL), IWL terjadi melalui kulit : 70% dan pernafasan : 30%. IWL akan lebih besar pada bayi kecil dan premature, kelainan seperti omfalokel dan gastroskisis.

 

ELEKTROLIT

Gangguan elektrolit harus diketahui secara dini dan dilakukan koreksi. Bila tidak terdiagnosa sebelum operasi akan berakibat fatal karena akan menjadi lebih berat selama pembiusan. Gangguan elektrolit akan mengakibatkan gangguan metabolisme intra sel dan dapat mengakibatkan keadaan yang fatal yaitu kematian tingkat seluler.^1,4

 

Hiponatremia ( Na : < 130 mmol/l )

Hiponatremia dapat diakibatkan beberapa keadaan seperti berikut :

1. Retensi cairan, kehilangan natrium yang berlebihan akibat fungsi tubulus renalis yang belum sempurna.
2. Asupan cairan dan elektrolit yang tidak adekuat

Terapi disesuaikan dengan penyebabnya, bila diakibatkan sekunder oleh karena retensi cairan maka dilakukan restriksi cairan dengan observasi yag sangat ketat. Bila disebabkan asupan yang tidak adekuat, dilakukan koreksi natrium dengan rumus sebagai berikut :

Koreksi Na = defisit Na X BB X 0,6

 

Hipernatremia ( Na > 150 mmol/L )

Hipernatremia dapat terjadi pada:

1. Kehilangan air melebihi natrium, misalnya pada bayi dengan berat badan lahir rendah mempunyai IWL yang besar.
2. Evaporasi yang berlebihan pada perawatan yang menggunakan radiant-heater
3. Pemberian natrium yang berlebihan. Pemberian natrium tanpa memperhitungkan jumlah cairan akan mengakibatkan hipernatremia.

Hipernatremia dapat diatasi dengan cara retriksi natrium dan evaluasi ulang pemberian cairan dengan ketat.

 

Hipokalemia ( K < 3,0 mmol/L )

Hipokalemia dapat disebabkan karena asupan kalium yang kurang atau kehilangan yang berlebihan baik melalui ginjal atau saluran cerna. Hipokalemia yang disebabkan oleh keadaan alkalosis tanpa disertai perubahan total kalium, tidak memerlukan tambahaan kalium cukup dilakukan koreksi alkalosisnya saja. Pada kekurangan kalium dapat dikoreksi dengan mempergunakan rumus :

 

Koreksi K = defisit K X BB X 0,3

 

Kecepatan pemberian kalium adalah 0,5 mmol/kgBB/hari dengan konsentrasi maksimal intravena 40 mmol/L dan urine out put minimal 1 ml/kgBB/jam

 

Hiperkalemia ( K > 7 mmol/L )

Hiperkalemia sering dijumpai pada neonatus dengan asidosis metabolik, hemolisis pada bayi yang prematur. Pengelolaan hiperkalemia cukup rumit dan memerlukan observasi yang sangat ketat. Pengelolaannya adalah sebagai berikut :

1. Hentikan pemberian kalium melalui intravena.
2. Koreksi kelainan penyerta misalnya asidosis.
3. Berikan natrium bikarbonat 1 – 2 mmol/kg BB dalam waktu lebih dari 10 menit ( pelan-pelan)
4. Berikan 10% calsium glukonas 0,1 -0,2 ml/kgBB melalui cairan intravena
5. Jika tindakan di atas belum berhasil dapat diberikan ion exchange resin yaitu: sodium polystyrene sulfonat per rektal (kayexalate^®) dengan dosis 0,5–1 gr/kgBB
6. Penggunaan insulin infus glukosa untuk membantu uptake kalium oleh sel, dengan dosis glukosa 0,5 gr/kg BB selama 1 – 2 jam dengan 0,2 unit insulin. Metode di atas perlu pengawasan yang ketat dan kerjasama dengan Dokter Spesialis Anak.

 

Hipertermi Maligna

Hipertermi dapat terjadi akibat obat-obat anestesi, dimana kelainan ini merupakan suatu keadaan hipermetabolik dari otot rangka ( otot rangka tubuh anak 40 % total berat badan ) yang menyebabkan peningkatan konsumsi oksigen, penumpukan asam laktat dan produksi panas.⁷ Yang dapat menyebabkan hipertermi maligna :

1. Obat anestesi : Halothan, succinylcholine, isoflurane, sevoflurane

2. Non anestesi : Kecemasan, stress dan kelelahan

Gejala klinik :

1. Kardiovaskuler : takikardia, hemodinamik tidak stabil

2. Respirasi : hipoksia, hiperkapnea dan edema paru

3. Saraf otot : spasme otot masseter, kekakuan otot rangka

4. Suhu tubuh : hiperpireksi

5. Kulit : Kemerahan dan diaforesis

6. Kegagalan organ: Saraf pusat, ginjal dan hemopoitik

Penatalaksanaan ⁷

1. Resusitasi
2. Hiperventilasi dengan oksigen 100 % menggunakan masker ventilasi
   1. 1. karena biasanya terjadi trismus
3. Bila terjadi durante operasi maka pembedahan segera diakhiri
4. Pemberian Dantrolene sodium i.v
5. Analisa gas darah dan elektrolit
6. Pendinginan dengan:
   1. Infus larutan fiologis (NaCl 0,9 %) dingin
   2. Pendinginan permukaan kulit dengan es dan alkohol
   3. Irigasi lambung, rektum, peritoneum dan rongga dada dengan larutan fisiologis dingin
7. Pertahankan produksi urine 2 cc/kg/jam
8. Rawat diruang intensif (NICU/PICU)

 

GANGGUAN KESEIMBANGAN ASAM BASA

 

Gangguan keseimbangan asam-basa perioperatif dapat terjadi akibat penyakit primer maupun didapat. Asidosis dan alkalosis respiratorik adalah gangguan keseimbangan asam-basa yang sering dijumpai. Hal ini disebabkan karena penggunaan ventilasi mekanik yang tidak dipantau secara seksama, pembiusan, pemulihan tidak sempurna dari obat pelumpuh otot. ^1,3,5

Koreksi terhadap gangguan keseimbangan asam basa dilakukan bila tubuh sudah tidak mampu lagi melakukan kompensasi untuk melakukan koreksi terhadap kelainan di atas. Koreksi dilakukan dengan rumus :

 

Koreksi asam basa = BE X BB X 1/3

 

Defisit diberikan setengahnya dulu dengan observasi yang sangat ketat.

 

PERAWATAN PASCA OPERASI

Setelah tindakan operasi mayor perlu dilakukan pengaturan homeostasis, terapi nyeri, pencegahan dan deteksi dini kemungkinan komplikasi akibat operasi. ⁴

 

Cairan

Pada pasca pembedahan dibutuhkan tambahan cairan dan natrium, disamping cairan rumatan untuk mempertahankan homeostasis akibat pergeseran cairan ke ruang ketiga yang keluar dari intravaskuler. Jumlah cairan yang bergeser ini tidak dapat diperhitungkan besar volumenya. Salah satu pendekatan yang dilakukan adalah dengan meningkatkan kecepatan infus 1,5 – 2 kali cairan rumatan dalam 24 jam pasca bedah, dan dapat disesuaikan dengan besar kecilnya operasi. ⁸

Filston et al 1996 menggunakan skema kwadran untuk memperkirakan pergeseran cairan internal pasca laparotomi. Tiap kwadran abdomen yang terlibat dengan penyakit obstruktif atau inflamasi ditambah ¼ kali cairan rumatan dan diberikan cairan rumatan. Satu hal yang lebih penting adalan observasi ketat keadaan klinis dan respon penderita setelah terapi cairan. ⁸

Pemberian nutrisi enteral pada penderita pasca anastomosis usus, masih merupakan perdebatan oleh banyak ahli bedah. Dahulu pemberian nutrisi enteral pasca anastomosis usus diberikan setelah diperkirakan anastomosis sudah menjadi kuat dan aman untuk dilalui makanan^. Namun sekarang nutrisi enteral diberikan lebih dini tanpa memperhatikan peristaltik usus. ^8,12 Dengan pertimbangan bahwa pada penderita anastomosis usus, sekresi cairan usus telah diproduksi dan telah melalui anastomosis usus. Maka penulis mencoba melakukan nutrisi enteral secara dini tanpa takut akan komplikasi kebocoran usus, dengan formula seperti dibawah ini :

 

Waktu	Jenis Nutrisi enteral
- Sadar penuh dari anastesi - Tiap 2 jam - 3 jam - 3 jam - 3 jam - 3 jam - 3 jam - selanjutnya	- 10 ml cairan jernih - 10 ml cairan jernih , sampai tercapai 30 ml - 30 ml ½ Streng formula - 45 ml ½ Streng formula - 60 ml ½ Streng formula - 60 ml Full Streng formula - 75 ml Full Streng formula - ad libitum Full streng formula/ air susu ibu / diet cair sesuai umur anak

 

Pemberian nutrisi enteral dini tidak dijumpai komplikasi seperti : kebocoran usus, aspirasi pneumonia karena kembung. Bahkan nutrisi enteral dini memperkuat anastomosis usus karena komsumsi asam amino dan protein dapat diberikan lebih awal⁸

 

Penatalaksanaan nyeri

 

Penatalaksanaan nyeri pasca operasi pada bayi dan anak telah berubah secara radikal. Tujuan dari penatakasanaan nyeri bermanfaat untuk mengurangi periode pulih sadar, dan meningkatkan angka keberhasilan pembedahan. Mencegah timbulnya nyeri adalah tindakan pasca bedah yang penting. Penggunaan ketorolac menggantikan opioid mempunyai manfaat yang sangat besar, karena ada beberapa keuntungan yaitu Ketorolac tidak mendepresi SSP, tidak pengaruhi pusat napas, berefek antinosiseptif di neuron perifer maupun di spinal dan supraspinal. Efek analgetik Ketorolac setara dengan morfin, lebih kuat dari kodein atau petidin. Lama pemberian yang direkomendasikan tidak melebihi 7 hari.^9,10,11

Dosis dan waktu pemberian ketorolac

Intravenous/intramuscular	Dosis
Initial dosage	0.5 mg/kg
Subsequent dosage	mg/kg q6h (or, by IV infusion 0.17 mg/kg/h)
Maximum daily dosage	90 mg
Maximum duration	2 days
Oral
Oral dosage	0.25 mg/kg q6h
Maximum daily dosage	1 mg/kg
Maximum duration	7 days

 

Pemberian

 

Pada obstruksi usus telah terjadi translokasi kuman atau perforasi, sehingga kasus obstruksi usus digolongkan sebagai luka operasi terkontaminasi. Infeksi disebabkan flora usus yaitu kuman gram positif, gram negatif dan anaerob. Cloud, 1993 merekomendasikan pemberian tripel antibiotik yang terdiri dari ampisilin ,gentamisin dan clindamisin. Dimana ampisilin ditujukan untuk bakteri gram positif aerob, gentamisin untuk bakteri gram negatif aerob, sedangkan clindamisin ditujukan untuk bakteri anaerob. Metronidasol dapat dipakai untuk menggantikan clindamisin. Efektivitas pemberian antibiotik ditandai dengan hilangnya demam dan perbaikkan kondisi penderita⁸

 

 

KEPUSTAKAAN

 

 

1. Damanik SM, Sarwono E; Cara rujukan kasus darurat bedah saluran cerna pada neonatus dalam Pertemuan bedah anak 1996, Surabaya
2. Taylor R: The general management of surgical neonate dalam Surgery of the newborn 1994, Churchil Livingstone editor, hal 15 – 22.
3. Rowe MI : The newborn as a surgical patient dalam O’ Neill editor. Pediatric Surgery ed 3. 1998. hlm 48-49. St Louis : Mosby.
4. Deliana E: Pengelolahan cairan pra dan pasca bedah pada neonatus dan anak dalam Basic Science in Pediatric Surgery 2003, Semarang.
5. Abdul Latief: Tatalaksana cairan, elektrolit, dan asam basa perioperatif dalam Manajemen komprehensif pembedahan pada bayi dan anak, pada Pertemuan Ilmiah Terpadu Bedah Anak Indonesia. 2005. Jakarta
6. Tuggle DW : Fluid and electrolyte management dalam Zieger MM editor Operative pediatric surgery. 2003. hlm 55-56. New York : Mac Graw Hill.
7. Bell C :: Malignant hyperthermia dalam The anesthesia handbook. 2000. hlm 485-493. St Louis : Mosby.
8. Surasak S : Early enteral feeding after closure of colostomy in pediatric patients. J Pediatric Surgery. 2003 : 1416-1519.
9. Bartle EJ : Post operative monitoring of unstable patients dalam Norton editor Surgical decision making ed.3. 1993. hlm 8-9. Philadelphia : WB Saunders Co
10. Redjeki IS: Ketorolac for postoperative pain management in Paediatric patient dalam Manajemen komprehensif pembedahan pada bayi dan anak, pada Pertemuan Ilmiah Terpadu Bedah Anak Indonesia. 2005. Jakarta
11. Pellegrini CA : Post operative complication dalam Lawrence WW editor. Current surgical diagnosis and treatment ed 9. 1995 . hlm. 40 . London : Appleton & Lange.
12. Win Shwe. 2002. The Benefit of bowel rest for healing processed. Melalui http://www.thai-otsuka.co.th/pxnews/0102nl.html.

Penyakit Paru Obstruktif Menahun (PPOM)

DEFINISI Penyakit Paru Obstruktif Menahun /PPOM (Chronic Obstructive Pulmonary Disease/COPD) adalah suatu penyumbatan menetap pada saluran pernafasan yang disebabkan oleh emfisema atau bronkitis kronis. PPOM lebih sering menyerang laki-laki dan sering berakibat fatal. PPOM juga lebih sering terjadi pada suatu keluarga, sehingga diduga ada faktor yang dirurunkan. Bekerja di lingkungan yang tercemar oleh asap kimia atau debu yang tidak berbahaya, bisa meningkatkan resiko terjadinya PPOM. Tetapi kebiasaan merokok pengaruhnya lebih besar dibandingkan dengan pekerjaan seseorang, dimana sekitar 10-15% perokok menderita PPOM. Angka kematian karena emfisema dan bronkitis kronis pada perokok sigaret lebih tinggi dibandingkan dengan angka kematian karena PPOM pada bukan perokok. Sejalan dengan pertambahan usia, perokok sigaret akan mengalami penurunan fungsi paru-paru yang lebih cepat daripada bukan perokok. Semakin banyak sigaret yang dihisap, semakin besar kemungkinan terjadinya penurunan fungsi paru-paru.

PENYEBAB Ada 2 (dua) penyebab dari penyumbatan aliran udara pada penyakit ini, yaitu emfisema dan bronkitis kronis. Emfisema adalah suatu pelebaran kantung udara kecil (alveoli) di paru-paru, yang disertai dengan kerusakan pada dindingnya. Dalam keadaan normal, sekumpulan alveoli yang berhubungan ke saluran nafas kecil (bronkioli), membentuk struktur yang kuat dan menjaga saluran pernafasan tetap terbuka. Pada emfisema, dinding alveoli mengalami kerusakan, sehingga bronkioli kehilangan struktur penyangganya. Dengan demikian, pada saat udara dikeluarkan, bronkioli akan mengkerut. Struktur saluran udara menyempit dan sifatnya menetap. Bronkitis kronis adalah batuk menahun yang menetap, yang disertai dengan pembentukan dahak dan bukan merupakan akibat dari penyebab yang secara medis diketahui (misalnya kanker paru-paru). Pada saluran udara kecil terjadi pembentukan jaringan parut, pembengkakan lapisan, penyumbatan parsial oleh lendir dan kejang pada otot polosnya. Penyempitan ini bersifat sementara. Adanya bahan-bahan iritan menyebabkan peradangan pada alveoli. Jika suatu peradangan berlangsung lama, bisa terjadi kerusakan yang menetap. Pada alveoli yang meradang, akan terkumpul sel-sel darah putih yang akan menghasilkan enzim-enzim (terutama neutrofil elastase), yang akan merusak jaringan penghubung di dalam dinding alveoli. Merokok akan mengakibatkan kerusakan lebih lanjut pada pertahanan paru-paru, yaitu dengan cara merusak sel-sel seperti rambut (silia) yang secara normal membawa lendir ke mulut dan membantu mengeluarkan bahan-bahan beracun. Tubuh menghasilkan protein alfa-1-antitripsin, yang memegang peranan penting dalam mencegah kerusakan alveoli oleh neutrofil estalase. Ada suatu penyakit keturunan yang sangat jarang terjadi, dimana seseorang tidak memiliki atau hanya memiliki sedikit alfa-1-antitripsin, sehingga emfisema terjadi pada awal usia pertengahan (terutama pada perokok).

GEJALA Gejala-gejala awal dari PPOM, yang bisa muncul setelah 5-10 tahun merokok, adalah batuk dan adanya lendir. Batuk biasanya ringan dan sering disalah-artikan sebagai batuk normal perokok, walaupun sebetulnya tidak normal. Sering terjadi nyeri kepala dan pilek. Selama pilek, dahak menjadi kuning atau hijau karena adanya nanah. Lama-lama gejala tersebut akan semakin sering dirasakan. Bisa juga disertai mengi/bengek. Pada umur sekitar 60 tahun, sering timbul sesak nafas waktu bekerja dan bertambah parah secara perlahan. Akhirnya sesak nafas akan dirasakan pada saat melakukan kegiatan rutin sehari-hari, seperti di kamar mandi, mencuci baju, berpakaian dan menyiapkan makanan. Sepertiga penderita mengalami penurunan berat badan, karena setelah selesai makan mereka sering mengalami sesak yang berat sehingga penderita menjadi malas makan. Pembengkakan pada kaki sering terjadi karena adanya gagal jantung. Pada stadium akhir dari penyakit, sesak nafas yang berat timbul bahkan pada saat istirahat, yang merupakan petunjuk adanya kegagalan pernafasan akut.

DIAGNOSA Pada PPOM yang ringan, mungkin tidak ditemukan kelainan selama pemeriksaan fisik, kecuali terdengarnya beberapa mengi pada pemeriksaan dengan menggunakan <>I>stetoskop. Suara pernafasan pada stetoskop juga terdengar lebih keras. Biasanya foto dada juga normal. Untuk menunjukkan adanya sumbatan aliran udara dan untuk menegakkan diagnosis, dilakukan pengukuran volume penghembusan nafas dalam 1 detik dengan menggunakan spirometri. Pada penderita PPOM akan terjadi penurunan aliran udara selama penghembusan nafas. Jika PPOM terjadi pada usia muda, dicurigai adanya kekurangan alfa-1-antitripsin, sehingga perlu dilakukan pemeriksaan darah untuk mengetahui kadar afa-1-antitripsin dalam darah.

PENGOBATAN Karena merokok sigaret merupakan penyebab paling penting dari PPOM, maka pengobatan utama adalah berhenti merokok. Menghentikan kebiasaan merokok pada saat penyumbatan airan udara masih ringan atau sedang, akan memperlambat timbulnya sesak nafas. Tetapi, berhenti merokok pada stadium manapun dari penyakit ini, pasti akan memberikan banyak keuntungan. Penderita juga harus mencoba untuk menghindari pemaparan terhadap bahan iritan lainnnya di udara. Unsur-unsur dari penyumbatan aliran udara yang bisa diperbaiki adalah kejang otot, peradangan dan peningkatan jumlah lendir. Perbaikan dari unsur-unsur tersebut akan mengurangi gejala-gejala. Kejang otot bisa dikurangi dengan memberikan bronkodilator, termasuk agonis reseptor beta-adrenergik (albuterol inhaler) dan theophylline per-oral (melalui mulut) yang diserap lambat. Peradangan bisa dikurangi dengan memberikan corticosteroid, tetapi hanya 20% penderita yang memberikan respon terhadap corticosteroid. Tidak ada pengobatan terpercaya yang dapat mengurangi kekentalan lendir sehingga mudah dikeluarkan melalui batuk. Tetapi menghindari dehidrasi bisa mencegah pengentalan lendir. Minum cairan yang cukup untuk menjaga air kemih tetap encer dan bening. Pada PPOM yang berat, terapi pernafasan bisa membantu menghilangkan lendir di dada. Terapi oksigen jangka panjang akan memperpanjang hidup penderita PPOM yang berat dan penderita dengan kadar oksigen darah yang sangat rendah. Oksigen diberikan 12 jam/hari. Hal ini akan mengurangi kelebihan sel darah merah yang disebabkan menurunnya kadar oksigen dalam darah, memperbaiki fungsi mental dan memperbaiki gagal jantung akibat PPOM. Terapi oksigen juga bisa memperbaiki sesak nafas selama beraktivitas. Program latihan bisa dilakukan di rumah. Program ini bisa meningkatkan kualitas hidup dan kemandirian penderita, menurunkan frekuensi dan lamanya perawatan di rumah sakit dan meningkatkan kemampuan berlatih meskipun fungsi paru-parunya belum pulih sempurna. Untuk melatih kaki bisa dilakukan latihan sepeda statis, naik-turun tangga dan berjalan. Untuk melatih lengan bisa dilakukan latihan angkat beban. Untuk penderita dengan kekurangan alfa-1-antitripsin yang berat, bisa diberikan protein pengganti melalui pemberian protein melalui infus setiap minggu. Pencangkokan paru-paru bisa dilakukan pada penderita dibawah usia 50 tahun. Pada penderita dengan emfisema yang berat, bisa dilakukan pembedahan yang disebut operasi reduksi volume paru-paru. Prosedurnya rumit dan penderita harus berhenti merokok setidaknya 6 bulan sebelum pembedahan dan menjalani program latihan intensif. Pembedahan akan memperbaiki fungsi paru-paru dan kemampuan berlatih. PROGNOSIS 30% penderita PPOM dengan sumbatan yang berat akan meninggal dalam waktu 1 tahun, dan 95% meninggal dalam waktu 10 tahun. Kematian bisa disebabkan oleh kegagalan pernafasan, pneumonia, pneumotoraks (masuknya udara ke dalam rongga paru), aritmia jantung atau emboli paru (penyumbatan arteri yang menuju ke paru-paru). Penderita PPOM juga memiliki resiko tinggi terhadap terjadinya kanker paru.

PENCEGAHAN Jika penderita mengalami influenza atau pneumonia, PPOM akan semakin memburuk dengan jelas. Karena itu, penderita PPOM harus mendapatkan vaksinasi influenza setiap tahun dan vaksinasi pneumokokus setiap 6 tahun atau lebih.

Ectopic Pregnancy 2

TREATMENT FOR ECTOPIC PREGNANCY (Ectopic Pregnancy 2)

Medical Management

Methotrexate therapy of ectopic pregnancy has been used successfully over the last 2 decades. The folic acid antagonist, methotrexate, inhibits de novo synthesis of purines and pyrimidines, interfering with DNA synthesis and cell multiplication. Rapidly proliferating trophoblasts are very dependent on folic acid and thus differentially vulnerable to the cytotoxic effect of methotrexate, and this differential sensitivity forms the basis of the therapy. When methotrexate is administered to pregnant women undergoing planned termination, a single dose of 50 mg/m² significantly blunts the β-hCG increment over the following 7 days and has been associated with a drop in circulating progesterone and 17-α-hydroxyprogesterone concentrations prior to abortion. It appears that methotrexate directly impairs trophoblastic production of hCG with a secondary decrement of corpus luteum progestin secretion. Hemodynamically stable patients with unruptured ectopic pregnancy measuring less than or equal to 4 cm by ultrasonography are eligible for methotrexate therapy. Patients with larger masses or evidence of acute intra-abdominal bleeding should undergo immediate surgical treatment. Methotrexate treatment regimens are shown in Table 2 and include the multiple dose, single dose, and the newly introduced two-dose protocol.

TABLE 2 Comparison of Methotrexate Regimens

Single-Dose Regimen Multiple-Dose Regimen Two-Dose Regimen Methotrexate dose 50 mg/m2 1 mg/kg 50 mg/m2 Leucovorin dose NONE 0.1 mg/kg NONE Dose frequency Day 0 Potential dose on day 7 Alternating-day dosing of methotrexate and leucovorin, maximum of four doses of each Day 0 and day 4 Potential doses on day 7 and day 11 β-hCG monitoring Day 0, day 4, day 7 Day 11 and day 14 if additional doses given Day 0, and then odd-numbered days until success Day 0, day 4, day 7 Day 11 and day 14 if additional doses given Success determined by 15% drop in β-hCG day 4 to day 7 15% drop in β-hCG day 11 to day 14 if second dose given 15% drop in β-hCG between any two blood draws 15% drop in β-hCG day 4 to day 7 15% drop in hCG day 7 to day 11 or day 11 to day 14 if third and fourth dose given

Multiple-Dose Methotrexate

Multiple-dose methotrexate therapy is tailored to the patient’s weight and ectopic pregnancy responsiveness. Outcomes of 12 studies comparing multiple-dose systemic methotrexate with laparoscopic salpingostomy are presented in Table 3. Between 1982 and 1997, this tabulation shows 338 cases of ectopic pregnancy treated with variable-dose methotrexate (number of medication administrations varies according to response). Of these cases, 93% were treated successfully with multiple-dose systemic methotrexate (no subsequent therapy was required), and 75% of the women tested had patent fallopian tubes; in addition, of the women desiring pregnancy, 58% had a subsequent intrauterine pregnancy and 7% developed a repeat ectopic pregnancy. These rates all compare favorably with conservative surgical management.

There is one randomized clinical trial comparing laparoscopic salpingostomy with systemic multiple dose methotrexate. In it, 100 patients with laparoscopy-confirmed ectopic pregnancy were randomly treated with systemic methotrexate or laparoscopic salpingostomy. In the 51 patients treated with methotrexate, seven (14%) required surgical intervention for active bleeding or tubal rupture. An additional course of methotrexate was required in two patients (4%) for persistent trophoblast, based on continued β-hCG secretion. Of the 49 patients in the salpingostomy group, four patients (8%) failed and required salpingectomies, and ten patients (20%) required treatment with methotrexate for persistent trophoblast. Homolateral tubal patency was present in 23/42 (55%) of the patients assessed in the methotrexate group and in 23/39 (59%) of those assessed in the salpingostomy group. This randomized study and previous meta-analysis have demonstrated the effectiveness of systemic methotrexate therapy as equal to laparoscopic salpingostomy.

TABLE 3 Outcome of Different Treatments for Ectopic Pregnancy

Subsequent Fertility Rate Method Number of Studiesa Number of Patients Number with Successful Resolution Tubal Patency Rate Intrauterine Pregnancy Ectopic Pregnancy Conservative laparoscopic surgery 32 1,626 1,516 (93%) 170/223 (76%) 366/647 (57%) 87/647 (13%) Variable-dose methotrexate 12 338 314 (93%) 136/182 (75%) 55/95 (58%) 7/95 (7%) Single-dose methotrexate 7 393 340 (87%) 61/75 (81%) 39/64 (61%) 5/64 (8%) Direct-injection methotrexate 21 660 502 (76%) 130/162 (80%) 87/152 (57%) 9/152 (6%) Expectant management 14 628 425 (68%) 60/79 (76%) 12/14 (86%) 1/14 (7%) aReferences available on the Lancet Web site (http://www.thelancet.com) or from the journal’s London office. Accessed December 6, 2002. From Pisarska MD, Carson SA, Buster JE, et al. Ectopic pregnancy. Lancet 1998;351:1115-1120.

Single-Dose Methotrexate

Single-dose methotrexate, although more convenient, is not as efficacious as multiple-dose methotrexate. The high success rates in the initial studies using single-dose methotrexate were most likely due to the inclusion of spontaneously aborting intrauterine pregnancies. Subsequent studies of single-dose methotrexate therapy involving 393 patients are presented in Table 3. Although overall success of treatment, measured as no surgical intervention, is 87%, 8% of patients required more than one dose of methotrexate. Of the patients considered successfully treated (with one or more doses), tubal patency was found in 81% of the women evaluated. The subsequent intrauterine pregnancy rate was 61%, and for ectopic pregnancies 8%, in the patients desiring future fertility in the same group (those treated with either one or more doses of methotrexate). Based on the clinical evidence presently available, the routine use of methotrexate as a single-dose intramuscular regimen is probably not as effective as multiple doses. However, single-dose therapy remains a standard according to publications of the American College of Obstetricians and Gynecologists.

With this background, a recent meta-analysis of 26 studies evaluating methotrexate dosing for ectopic pregnancy by Barnhart and colleagues showed an odds ratio of 1.96 higher likelihood of rupture with use of single-dose methotrexate over multidose therapy. Controlling for initial β-hCG value and the presence of cardiac activity, the failure rate with single-dose therapy was almost five times greater (odds ratio 4.75). What makes direct comparisons of these protocols even harder is that based on the data from this meta-analysis, 15% of patients under a single-dose protocol actually receive more than one dose, while 10%, 23%, and 14% of those under a multidose protocol actually need only 1, 2, or 3 doses of methotrexate, respectively.

Two-Dose Methotrexate Protocol

In recognition that the single-dose protocol has fewer visits and fewer injections but may have a higher failure rate, a two-dose protocol was introduced. This protocol uses the dosing and monitoring parameters of the single-dose protocol but gives a second dose of 50 mg/m² on day 4, when only a serum β-hCG would have been drawn according to the single-dose protocol. No leucovorin rescue is used in this protocol. The same logic is used to determine if more methotrexate is needed based on the difference between the serum β-hCG on day 4 and day 7. In the single-dose protocol, a second dose would be given on day 7 if the β-hCG did not decline by at least 15% between day 4 and day 7 (Table 2). In the two-dose protocol, a second dose is given on day 4, and a third dose can be given on day 7 if the β-hCG did not decline by a least 15% between days 4 and 7. Thus, the two-dose protocol gives two doses in the first week and has provisions to give up to two more. In this way, the number of visits and surveillance laboratories are the same as the single dose, but more methotrexate is given sooner in hopes of maximizing success rate (without increasing complexity or the number of visits). This regimen was demonstrated to be safe in a three-center trial; the overall success rate will be determined as it is used more widely.

TABLE 4 Treatment with Multiple-dose Methotrexate

Indications for systemic methotrexate for uncomplicated ectopic pregnancy: No rupture (hemodynamic stability) UTZ size >4 cm Β-hCG >10,000 mIU/mL Positive fetal heartbeat: proceed with caution Willingness of patient to comply with subsequent treatment monitoring UTZ, ultrasound; hCG, human chorionic gonadotropin.

Safeguards and Counseling

Prior to instituting methotrexate therapy, physicians should evaluate baseline laboratory values. The patient should be screened with a complete blood count, liver function tests, and serum creatinine. A chest x-ray should be considered in women reporting a history of prior pulmonary disease due to their risk of developing methotrexate-related interstitial pneumonitis.

During methotrexate therapy, a woman should be examined by a single examiner only once, to diminish the risk of causing mechanical trauma and tubal rupture. The physician and the patient must recognize that transient pain (“separating” or “tearing pain”) is common. Transient pelvic pain from tubal bleeding or hematoma formation at the ectopic site frequently occurs 3 to 7 days after the start of therapy, lasts 4 to 12 hours, and is presumably due to tubal abortion. Perhaps the most difficult aspect of methotrexate therapy is learning to distinguish the transient abdominal pain of successful therapy from that of a rupturing ectopic pregnancy. Physicians must therefore carefully observe for clinical indications that an operation is necessary (Tables 4, 5). Thus, surgical intervention is required when pain is worsening and persistent beyond 12 hours. Orthostatic hypotension or a falling hematocrit should lead to immediate surgery. Sometimes, it is necessary to hospitalize the patient with pain for observation (usually about 24 hours) to insure a correct diagnosis. In addition, colicky abdominal pain is common during the first 2 or 3 days of methotrexate therapy, and the woman should avoid gas-producing foods such as leeks and cabbage. Women receiving methotrexate should discontinue prenatal vitamins, as they contain folic acid, and should especially avoid any additional folic acid supplementation. Finally, the patient should avoid exposure to the sun because photosensitivity can be a complication of methotrexate.

TABLE 5 Dealing with Methotrexate Failure

Operate when high suspicion of rupture: Pain is severe and persistent, regardless of β-hCG levels Falling hematocrit Orthostatic hypotension Consider operating when signs of treatment failure: Levels of β-hCG do not decline by at least 15% between days 4 and 7 of treatment Levels of β-hCG increase or plateau after first week of treatment

Methotrexate by Direct Injection

In 1987, Feichtinger and Kemeter instilled 10 mg (1 mL) of methotrexate into an ectopic gestational sac under transvaginal ultrasonography, and resolution occurred within 2 weeks. Direct injection delivers concentrations of methotrexate to the site of implantation at higher concentrations than those achieved with systemic administration. Less systemic distribution of the drug should decrease the overall toxicity. However, this approach has the substantial disadvantage of requiring laparoscopic or ultrasound needle guidance.

Outcomes in 21 studies involving direct injection of methotrexate with either laparoscopic or transvaginal ultrasound guidance are presented in Table 3. Between 1989 and 1997, 75.1% of 668 cases of ectopic pregnancy were treated successfully with methotrexate by direct injection, and some patients required more than one injection. Tubal patency and subsequent pregnancy rates were comparable to conservative laparoscopic surgery and systemic methotrexate: 80.2% of the women tested had patent oviducts, and of the women desiring pregnancy, 57.2% had a subsequent intrauterine pregnancy and 5.9% developed a recurrent ectopic pregnancy.

Randomized, controlled trials have demonstrated successful treatment with methotrexate by direct injection in 86.2% of the patients. Again, successful therapy included some patients who received more than one injection. Tubal patency was present in 85.1% of the women evaluated, and intrauterine pregnancy occurred in 73.1% of the women desiring subsequent fertility. One of the earlier randomized, controlled trials was discontinued because three of seven patients assigned to laparoscopic injection of methotrexate required additional laparoscopic surgery. Even with the higher success rate in the randomized trials, this technique is more cumbersome than systemic methotrexate. Given the overall tolerability and high success rate of systemic methotrexate, it continues to be the most accepted nonsurgical treatment modality.

Side Effects

High doses of methotrexate can cause bone marrow suppression, hepatotoxicity, stomatitis, pulmonary fibrosis, alopecia, and photosensitivity. These side effects are infrequent in the short treatment schedules used in ectopic pregnancy and can be attenuated by the administration of leucovorin (citrovorum factor). The side effects of methotrexate resolve within 3 to 4 days after the therapy is discontinued. Impaired liver function is the most common side effect. Other side effects include stomatitis, gastritis and enteritis, and bone marrow suppression. Local therapy by direct injection of methotrexate into the ectopic gestation resulted in fewer side effects, likely because of less systemic absorption. Even with local injection, impaired liver function tests, gastritis and enteritis, and bone marrow suppression can occur. Additional case reports exist in the literature. Cases of life-threatening neutropenia and febrile morbidity can occur after single or multidose intramuscular methotrexate, requiring hospitalization. Cases of transient interstitial pneumonitis from methotrexate therapy for ectopic pregnancy have been observed. Reversible alopecia (a loss of 33% to 50% of the scalp hair) on two separate occasions following single-dose therapy for an ectopic pregnancy has also been reported. Rarely, hematosalpinx and pelvic hematoceles have been noted as late sequelae of methotrexate following the normalization of β-hCG levels. These patients have pelvic pain, abnormal bleeding, and a pelvic mass, requiring surgical intervention, 3 to 5 months after therapy.

Fortunately, the side effects reported with methotrexate used to treat ectopic pregnancy have mostly been minor. Out of 100 patients treated in one study, only two patients developed stomatitis and three had transient elevation of transaminases, all resolving spontaneously. Another study that used the single-dose regimen had only one patient reporting nausea and vomiting following methotrexate treatment. Thus, with its overall good tolerability, methotrexate remains the first choice before surgical therapy.

Direct Injection of Cytotoxic Agents

Prostaglandins, hyperosmolar glucose, potassium chloride, and saline by direct injection have been tried as therapeutic alternatives to methotrexate. The limited experience with these agents, poor success rates, and the need for laparoscopic or transvaginal aspiration makes these unattractive treatment alternatives.

Evidence-Based Recommendation

Multiple-dose systemic methotrexate is the first-line medical treatment for ectopic pregnancy. Nearly half of patients under a multidose protocol will require fewer doses for ectopic pregnancy resolution. (Strength of recommendation: A.)

Surgical Treatment

Since the first successful salpingectomy (resection of involved fallopian tube segment with implanted trophoblastic tissue) performed by Tait in 1884, ectopic pregnancies traditionally have been treated by salpingectomy, usually by laparotomy. Historically, ectopic pregnancies were diagnosed at the time of emergency surgery, when concern for the patient’s life superseded any concerns for her future fertility. It was not until 1953, when Stromme performed the first conservative procedure (salpingostomy, or removal of only the ectopic pregnancy with conservation of the tube) for ectopic pregnancy, that subsequent successful pregnancy outcomes were reported, confirming the potential for fertility preservation after salpingostomy. These surgical techniques have been modified for endoscopy. The laparoscopic approach is associated with less blood loss, less analgesia requirement, and a shorter duration of hospital stay. In addition, cost analysis has demonstrated significant savings in randomized trials. When evaluating subsequent fertility, intrauterine pregnancy rates are comparable for laparoscopy and laparotomy, as are rates of recurrent ectopic pregnancy.

Ruptured Ectopic Pregnancy

Early diagnosis and treatment of ectopic pregnancy avoids rupture in most cases. In the 1970s, 13.5% to 17.8% of patients with ectopic pregnancies arrived for treatment in hypovolemic shock, whereas in the early 1980s, only 4.4% of patients arrived in this condition. Today, either laparotomy or laparoscopy with salpingectomy is the first choice for rupture.

Once contraindicated over concern of decreased venous return from intraperitoneal insufflation, laparoscopic salpingectomy can be successful in patients in hypovolemic shock. Still, in critical instances when expeditious entry into the peritoneal cavity and tamponade of bleeding is necessary, rapid laparotomy to stem the bleeding is the preferred method. Nearly all patients in hypovolemic shock require blood transfusions; those with large red blood cell requirements also need fresh frozen plasma. In the hands of a highly skilled laparoscopist, with adequate cardiac monitoring and anesthesia, laparoscopic salpingectomy is an acceptable alternative to laparotomy even when there has been extensive intraperitoneal bleeding. At present, it is the surgeon’s choice of laparoscopy or laparotomy for ruptured ectopic pregnancy.

Stable Ectopic Pregnancy

If methotrexate is contraindicated, laparoscopic salpingostomy is the first surgical choice. Alternatively, salpingectomy can be performed either during laparotomy or laparoscopy by using cautery or sutures (laparoscopic or endoloops). A review of data from nine studies showed that subsequent to salpingostomy, 53% of patients have intrauterine pregnancies compared with 49.3% after salpingectomy. Recurrent ectopic pregnancy rates were slightly higher after conservative surgery, 14.8% compared with 9.9%. Other studies have suggested a higher intrauterine pregnancy rate in women after salpingostomy, but at the cost of a possible higher risk of recurrent ectopic after 3 years of follow-up. Laparoscopic salpingectomy is preferred over salpingostomy in cases of uncontrollable bleeding not resolving with conservative measures when extensive tubal damage is present, if the ectopic pregnancy has recurred in the same tube, if it is a large pregnancy (>5 cm), and if sterilization is desired.

The recommended conservative surgical procedure for an ampullary ectopic pregnancy is linear salpingostomy, because the ectopic nidation typically is located between the endosalpinx and serosa rather than in the tubal lumen. A linear salpingostomy is created through a longitudinal incision by electrocautery, scissors, or laser over the bulging antimesenteric border of the fallopian tube. The products of conception are removed with forceps or gentle flushing or suction. After maintaining hemostasis, the incision is left to heal by secondary intention or closed primarily. There appears to be no additional benefit to suturing the tubal defect closed, as studies have shown no difference in subsequent tubal patency rates, postoperative adhesion rates, or cumulative pregnancy rates.

Historically, isthmic segment pregnancies were routinely treated with segmental excision followed by intraoperative or delayed microsurgical anastomosis. The tubal lumen is narrower and the muscularis is thicker in the isthmus than in the ampulla, predisposing the isthmus to greater damage after salpingostomy and greater rates of proximal tubal obstruction. With today’s high success rates of in vitro fertilization (IVF), tubal anastomosis is rarely performed and the resected tubal segment is bypassed altogether by use of ART. Manual fimbrial expression, also known as milking, should not be used unless the trophoblastic tissue is already aborting spontaneously through the fimbriae.

Laparoscopic salpingostomy and fimbrial expression have been evaluated in 32 studies and are presented in Table 3. Of the 1,626 patients treated between 1980 and 1997, treatment was successful in 93.4% (defined as requiring no additional therapy). Of the patients evaluated for tubal patency by using either hysterosalpingography or laparoscopy, 76% had patent tubes. Of the women desiring subsequent fertility, 56.6% had an intrauterine pregnancy and 13.4% developed another ectopic pregnancy.

Persistent Ectopic Pregnancy Following Salpingostomy

Persistent ectopic pregnancy is diagnosed by a plateauing or rising β-hCG concentration following conservative surgical therapy. The β-hCG level should be checked on postoperative day 1, keeping in mind that a drop of <50%>

The increased rate of persistent ectopic pregnancies has been a criticism of conservative laparoscopic therapy when compared with laparotomy. A decision analysis that compared prophylactic methotrexate with linear salpingostomy against no methotrexate in a group of 1,000 women concluded that prophylactic methotrexate at the time of surgery was preferable if certain clinical conditions are met as follows: (a) the incidence of persistent ectopic pregnancy is greater than 9% with observation alone after salpingostomy, (b) the incidence of persistence is less than 5% when prophylactic methotrexate is given, (c) the probability of ectopic pregnancy rupture is greater than 7.3% with a persistent ectopic pregnancy, and (d) the complication rate associated with prophylactic methotrexate is less than 18%. Because the great majority of clinical circumstances meet these recommendations, prophylactic methotrexate administration is recommended.

Evidence-Based Recommendation

Due to lower morbidity and equal efficacy, laparoscopic surgery is preferable to laparotomy in the treatment of bleeding or complicated ectopic pregnancy. Salpingectomy by laparotomy is reserved for ectopic ruptures with a hemodynamically unstable patient. (Strength of recommendation: A.)

Ectopic Pregnancy and Assisted Reproductive Technology

Incidence

The risk of ectopic pregnancy is increased in patients undergoing an ART procedure. This increased risk has been attributed to the cause of infertility for which most patients seek treatment, that is, tubal factor infertility. Information on ectopic pregnancies resulting from ART comes from data obtained from institutions in the United States and Canada reporting to the Society for Assisted Reproductive Technology. The rate of pregnancies that resulted in ectopic pregnancies after IVF in 1999 was 3%, with newer figures from 2004 reporting the ectopic rate to be about 2%. The latter included outcome of ART cycles using fresh, nondonor eggs or embryos in approximately 76,000 embryo transfers. This lower percentage likely reflected the trend toward performing salpingectomies when hydrosalpinges are present to improve the success of ART.

Location

As in naturally occurring ectopic pregnancies, the fallopian tube is the most common site for ectopic pregnancies following IVF. Data obtained from three case-control studies reveal that 82.2% of ectopic pregnancies were tubal. When tubal location was specified, 92.7% were ampullary and 7.3% interstitial. Extratubal ectopic nidations were as follows: 4.6% ovarian or abdominal, 1.5% cervical, and 11.7% heterotopic pregnancies (Fig. 1).

Tubal Pathology

Tubal pathology is the most important predisposing factor for ectopic pregnancy in patients undergoing IVF. Ectopic pregnancies are four times higher in patients with tubal factor infertility compared with patients with normal tubes. Hydrosalpinges are associated more commonly with ectopic pregnancy than other types of tubal pathology. Prior tubal reconstructive surgery (salpingostomy) increases the risk of ectopic pregnancy by 10% above that in patients with tubal factor infertility without prior surgery.

Thus, it is not surprising that patients with previous pelvic inflammatory disease have a sixfold increase in ectopic pregnancy after IVF. However, a history of prior ectopic pregnancy does not seem as important a risk factor in IVF cycles as in natural cycles.

Salpingectomy, particularly with hydrosalpinx, has been shown to decrease risks of ectopic pregnancy while increasing pregnancy rates after IVF. Meta-analysis has demonstrated that the presence of hydrosalpinges decreases the chance for viable pregnancy by approximately 50% when compared with patients with tubal disease but without hydrosalpinges. The implantation rate was also noted to be 50% lower with a higher chance of miscarriage and ectopic gestation. The ultimate conclusion is that when a hydrosalpinx is present, there is a decreased pregnancy rate with resultant decreased delivery rate following IVF. In addition, patients who undergo salpingectomy or proximal tubal occlusion prior to oocyte retrieval and transfer are at decreased risk for pelvic infection as well as future ectopic pregnancy.

Ovulation Induction

Hormone alterations during ovulation induction theoretically alter tubal function. In animal models, estrogen administration results in functional tubal blockage and embryo arrest in the fallopian tube. In humans, steroid hormones alter tubal function and contractility, thus affecting tubal peristalsis. There remains controversy as to whether ovulation-inducing agents, including clomiphene citrate, increase ectopic pregnancy rates, but it will be difficult to separate out the impact of the therapeutic agent from occult tubal disease.

Embryo Transfer

Knutzen and associates injected 40 µL of radiopaque fluid in mock embryo transfers and found that the material entered the tubes either partially or totally in 44% of subjects, suggesting that misplacement of embryos into the fallopian tubes leads to ectopic pregnancy. Embryo catheter placement also was implicated in the increased risk of ectopic pregnancies, which occurred more frequently in patients who underwent deep fundal transfer versus midcavity placement. Although transfer techniques may increase the chances of embryos reaching the fallopian tubes, it is the tubal pathology preventing the embryos from moving back into the uterus and resulting in an ectopic pregnancy.

Heterotopic Pregnancy

Heterotopic pregnancies occur in 1% to 3% of pregnancies following ART procedures and are usually diagnosed incidentally on routine follow-up ultrasonographic studies. This increased prevalence of heterotopic pregnancies following ART may be related to ovarian hyperstimulation and multiple ovum development. Of 111 reported heterotopic pregnancies following ART, 88.3% were tubal, 6.3% cornual, 2.7% abdominal, 1.8% cervical, and 0.9% ovarian.

Evidence-Based Recommendation

Heterotopic and extratubal ectopic pregnancies are more frequent following ART than with natural cycles. Salpingectomy or proximal tubal occlusion of a preexisting hydrosalpinx prior to IVF helps to prevent tubal ectopic pregnancies while increasing pregnancy rates following ART. (Strength of recommendation: B.)

Expectant Management

Ectopic pregnancies may resolve spontaneously. In a cavalier experiment in 1955, Lund hospitalized 119 women with ectopic pregnancy for observation. All were at least 6 weeks gestation. Some required multiple blood transfusions, and many were hemodynamically unstable. However, 68 resolved without surgery being required. Twelve additional studies reported in the literature since Lund’s study found similar results (Table 3). Of the ectopic pregnancies, 67.2% resolved without surgery. Thus, both conservative medical and surgical therapy overtreats at least 50% of women with ectopic pregnancy. Falling β-hCG levels under 1,000 mIU/mL have been followed with conservative expectant management. Although patients with an equivocal diagnosis of ectopic pregnancy may be treated in this fashion, there are no data to support expectant management in clinical practice. In addition, despite close follow-up and even in the context of declining β-hCG levels, tubal rupture may still occur.

Evidence-Based Recommendation

Expectant management of ectopic pregnancy may be considered an appropriate conservative therapy for some patients with low initial (1,000 mIU/mL) and falling β-hCG levels. Both clinicians and patients need to be aware of the potential risks of choosing expectant management over proven therapies.

Cost Analysis

The last estimated U.S. costs for ectopic pregnancy are over 15 years old. In 1990, total costs for ectopic pregnancies were estimated to be $1.1 billion. Direct costs, expenditures for health care, accounted for 77% of the total costs, and the remainder were incurred as a result of lost wages or household responsibilities not performed due to illness (indirect costs). Direct costs from hospital charges were estimated at $6,079 per case, with hospital accommodations (mean length of stay, 3.47 days) and operating room charges accounting for the majority of the hospital expense, 36% and 40%, respectively. An additional $3,254 for professional fees increased inpatient charges to $9,333, and $149 for postoperative follow-up visits increased the total direct cost to $9,482 per case. Indirect costs for a 28-day disability were estimated at $250.5 million, 67% as a result of lost wages and the remainder from lost household duties. These costs are likely substantially higher today.

European studies by Mol and colleagues have attempted to evaluate costs, but it is important to remember that they figured in longer hospital stays and more sick days than are customary in the United States and that the costs they estimated are within a socialized medical system. A study undertaken to compare the costs of systemic methotrexate with surgery concluded that there would be a reduction in overall costs if patients were treated without confirmatory laparoscopy when β-hCG levels were below 3,000 mIU/mL; otherwise, there was not a substantial cost saving over surgery. Because a confirmatory laparoscopy is no longer required for diagnosis, the lower cost for medical therapy is more realistic. Compared with the cost of a laparoscopic salpingostomy, methotrexate results in an estimated 20% decrease in the cost of treatment.

A decision analysis by Morlock and associates created a model to estimate the costs incurred by treating ectopic pregnancy by methotrexate or by laparoscopic salpingostomy. They felt that such an analysis was important because although previous studies found cost advantages with methotrexate, they had not adequately considered failure of ectopic resolution after only one dose of methotrexate or the potential side effects and complications of methotrexate use. They also felt that several European studies had calculated the costs of inpatient laparoscopy, not currently standard care in the United States where treatment is routinely done in the outpatient setting. Incorporating all of the assumptions about failed methotrexate treatment and costs of surgery and hospitalization for medical failures, the authors found a $3,011 cost saving with methotrexate treatment compared with laparoscopy. Even when they altered the model by assuming the lowest resolution rate for methotrexate-treated ectopic pregnancy of 57% and highest complication rates, the model still supported the use of methotrexate with a saving of $760.

Finally, it should be noted that Ailawadi and colleagues performed a decision analysis comparing the complicating rate and cost of diagnosis ectopic pregnancy with evaluation of the uterus prior to medical management versus presumptively treating women with a presumed ectopic pregnancy with methotrexate without confirming the diagnosis with a dilation and curettage (D&C). Surprisingly, the outcomes were quite similar. Thus, there is no advantage to taking the “shortcut”of treating women presumed to but not confirmed to have an ectopic pregnancy in terms of cost and/or complications. Data supporting the definitive diagnosis was that there were fewer visits required by patients after performance of an evacuation of the cavity, as fewer women needed medical management and evaluation of serial β-hCG concentration. Moreover, a more accurate prognosis can be given to a woman regarding recurrence of miscarriage, ectopic pregnancy, or overall fecundity if a miscarriage is accurately distinguished from an ectopic pregnancy.

Evidence-Based Recommendation

Systemic methotrexate for unruptured ectopic pregnancy is less expensive than surgery, and direct costs are decreased substantially with methotrexate therapy. In addition to its cost effectiveness, systemic methotrexate does not subject patients to the risks of surgery. This cost benefit, however, diminishes with higher β-hCG titers and even disappears with levels greater than 3,000 mIU/mL because of single-dose methotrexate treatment failures and increased complications. (Strength of recommendation: B.)

Rare Types of Ectopic Pregnancy

Abdominal Pregnancy

The incidence of abdominal pregnancy is estimated at 1 in 8,000 births and represents 1.4% of all ectopic pregnancies. The prognosis is poor, with an estimated maternal mortality rate of 5.1 per 1,000 cases. The risk of dying from an abdominal pregnancy is 7.7 times higher than from other forms of ectopic pregnancy. The high rate of morbidity and mortality from abdominal pregnancy often results from a delay in diagnosis.

Abdominal pregnancies can be categorized as primary or secondary. These ectopic pregnancies may become apparent anywhere throughout gestation, from the first trimester to fetal viability. Symptoms may vary from those considered normal for pregnancy to severe abdominal pain, intra-abdominal hemorrhage, and hemodynamic instability. Primary abdominal pregnancies are rare and are thought to occur as a result of primary peritoneal implantation. They usually abort early in the first trimester due to hemorrhagic disruption of the implantation site and hemoperitoneum. Secondary abdominal pregnancies occur with reimplantation after a partial tubal abortion or intraligamentary extension following tubal rupture. Historical criteria to distinguish between primary and secondary abdominal pregnancies are moot, because treatment is guided by the clinical picture.

Ultrasonography is the diagnostic tool of choice and usually can identify the empty uterus along with the extrauterine products of conception. If the fetus is near viability, hospitalization is recommended. If time permits, bowel preparation, administration of prophylactic antibiotics, and adequate blood replacement should be made available prior to an operative delivery. Unless the placenta is implanted on major vessels or vital structures, it should be removed. Although complications may occur, including sepsis, abscess formation, secondary hemorrhage, intestinal obstruction, wound dehiscence, amniotic fluid cyst formation, hypofibrinogenemia, and preeclampsia, the placenta can be left in place to prevent further hemorrhage at the time of surgery. In contrast to the typical tubal ectopic pregnancy, methotrexate is unlikely to accelerate retained placental absorption because the trophoblastic cells are no longer actively dividing.

Ovarian Pregnancy

Ovarian pregnancy, the most common form of abdominal pregnancy, is rare, accounting for less than 3% of all ectopic gestations. Clinical findings are similar to those of tubal ectopic gestations: abdominal pain, amenorrhea, and abnormal vaginal bleeding. In addition, hemodynamic instability as a result of rupture occurs in 30% of patients. Women with ovarian pregnancies are usually young and multiparous, but the factors leading to ovarian pregnancies are not clear.

The diagnosis usually is made by the pathologist because many ovarian pregnancies are mistaken for a ruptured corpus luteum or other ovarian tumors. Only 28% of cases were diagnosed correctly at time of laparotomy. The recommended treatment is cystectomy, wedge resection, or oophorectomy during laparotomy, although laparoscopic removal has been successful.

Cornual Pregnancy

Cornual or interstitial pregnancy accounts for 4.7% of ectopic gestations and carries a 2.2% maternal mortality. Clinically, a pregnancy implanted at this site where the fallopian tube is traversing the muscular wall of the uterus is seen as a swelling lateral to the round ligament. Almost all cases are diagnosed after the patient is symptomatic. The most frequent symptoms are menstrual aberration, abdominal pain, abnormal vaginal bleeding, and shock, resulting from the brisk hemorrhage associated with uterine rupture. Due to myometrial distensibility, rupture is usually delayed, occurring at 9 to 12 weeks gestation.

A unique risk factor for interstitial pregnancy is previous salpingectomy, present in about 25% of patients. Only a high index of suspicion and repeated ultrasonographic examination with Doppler flow studies allows early diagnosis. With a timely early diagnosis, alternatives to the traditional cornual resection during laparotomy have been performed successfully. These include laparoscopic cornual resection, systemic methotrexate administration, local injection of methotrexate, potassium chloride injection, and removal by hysteroscopy. Regardless of the initial treatment attempted, if uncontrolled hemorrhage occurs, immediate laparotomy with uterine repair or hysterectomy is warranted to stop the blood loss.

Cervical Pregnancy

The incidence of cervical pregnancy ranges from 1 in 2,500 to 1 in 12,422 pregnancies. The most common predisposing factor is a prior D&C, present in 68.6% of patients. Interestingly, 31% of these were performed for termination of pregnancy. Other predisposing factors implicated in cervical pregnancies are previous cesarean delivery and IVF.

The most common initial symptom of cervical pregnancy is painless vaginal bleeding. These extrauterine pregnancies are usually diagnosed incidentally during routine ultrasonography or at the time of surgery for a suspected abortion in progress. In reported cases, 91% of patients sought treatment for vaginal bleeding, and 29.2% had massive bleeding. Not surprisingly, abdominal pain occurred with vaginal bleeding in only 25.8% of cases. The cervix is usually enlarged, globular, or distended. On occasion, it appears cyanotic, hyperemic, and soft in consistency. Sonography and magnetic resonance imaging have improved diagnosis of cervical pregnancy. Up to 81.8% of patients have been diagnosed correctly with ultrasonographic identification of the gestational sac in the cervix below a closed internal cervical os, with trophoblastic invasion into the endocervical tissue.

When the patient is hemodynamically stable, conservative therapy commonly is employed. There are no large studies-only several case series for clinical guidance. These have shown that use of methotrexate, local prostaglanding or hyperosmolar glucose injection, curettage, or a combination of these methods have been successful. Prior to curettage, uterine artery embolization minimizes the substantial risk of postevacuation hemorrhage. Systemic and local treatment with various agents carries an overall success rate of 81.3%. Unfortunately, massive hemorrhage may occur despite conservative measures, and hysterectomy may be the only lifesaving option.

Heterotopic Pregnancy

Heterotopic pregnancy is the coexistence of an intrauterine and ectopic gestation. In 1948, the spontaneous heterotopic pregnancy rate was calculated as 1 in 30,000 pregnancies, based on an ectopic pregnancy incidence of 0.37% and dizygous twinning rate of 0.8%. In the 1980s, the calculation rose to 1 in 10,000 due to an increased ectopic pregnancy rate. Today, heterotopic pregnancies occur in 1 in 3,889 to 1 in 6,778 pregnancies in the general population. Out of almost 133,000 pregnancies reported in the U.S. ART Registry between 1999 and 2002, 207 heterotopic pregnancies were reported, an incidence of about 1:640. In a review of 66 heterotopic pregnancies by Reece and associates, 93.9% were tubal and 6.1% ovarian.

Simultaneous existence of intra- and extrauterine pregnancies poses several diagnostic pitfalls. Heterotopic pregnancies are diagnosed in most cases after clinical signs and symptoms develop, and 50% of patients are admitted for emergency surgery following rupture. The delay in diagnosis is secondary to the finding of an intrauterine pregnancy, which provides false reassurance of absence of pathology, with the assumption that any symptoms will be self-limited.

Similar to tubal ectopic pregnancies, the most common complaint is lower abdominal pain. Routine ultrasonography detects only about 50% of tubal heterotopic pregnancies, and the remainder are diagnosed during laparoscopy or laparotomy when patients become symptomatic. Serial levels of the β-hCG are not helpful due to the effect of the intrauterine pregnancy.

If patients are hemodynamically unstable, exploratory laparotomy is warranted. If the diagnosis is suspected or the patient is symptomatic but hemodynamically stable, laparoscopy can be performed. Expectant management is not recommended, because β-hCG levels cannot be monitored adequately and the course of the ectopic cannot be followed. Systemic methotrexate is contraindicated if a viable intrauterine pregnancy is present and desired. Local injection of methotrexate with potassium chloride has been noted as successful in a small case series.

Summary Points

• In most circumstances, ectopic pregnancy can be diagnosed before symptoms develop and treated definitively with few complications.
• Quantitative β-hCG testing, ultrasonography, and curettage allow early diagnosis of ectopic pregnancy and use of medical therapy as the initial therapy option.
• Conservative surgical therapy and medical therapy for ectopic pregnancy are comparable in terms of success rates and subsequent fertility. Medical therapy is the preferred choice because of the freedom from surgical complications and lower cost.
• Surgery is the treatment of choice for hemorrhage, medical failures, neglected cases, and when medical therapy is contraindicated.
• Multiple-dose methotrexate is preferable to single-dose methotrexate, direct injection, or tubal cannulation and is the first choice for unruptured, uncomplicated ectopic pregnancy.
• Laparoscopic salpingostomy or salpingectomy is favored for cases of intra-abdominal hemorrhage, medical failure, neglected cases, and complex cases when medical therapy is contraindicated.
• Prophylactic postoperative systemic methotrexate (a single dose) can prevent virtually all cases of persistent ectopic pregnancy following salpingostomy.
• Salpingectomy prior to IVF decreases ectopic pregnancy incidence while increasing pregnancy rates in select patients with preexisting tubal disease.

Ectopic Pregnancy (Part 1)

Beata E. Seeber
Kurt T. Barnhart
(Danforth’s Obstetrics and Gynecology, 10th Edition, Lippincott Williams & Wilkins.2008)

Ectopic pregnancy, the implantation of a fertilized ovum outside of the endometrial cavity, is a condition that is unique to primates. Although ectopic pregnancy remains a leading cause of life-threatening first-trimester morbidity, informed clinical suspicion and modern diagnostic procedures now routinely lead to diagnosis and treatment at the early signs of symptoms. Management of ectopic pregnancy has changed dramatically over the years. Medical therapy with systemic methotrexate, an intervention targeted specifically toward proliferating trophoblasts, is now often preferred to surgery as standard first-line treatment. However, surgery remains the first choice when rupture causes intraperitoneal hemorrhage, medical failures, neglected cases, and cases where medical therapy is contraindicated. In the wake of these changes, the United States has seen a considerable drop in maternal morbidity and mortality from this disease.

Early diagnosis and selection of optimal therapy are key to prevention of complications, preservation of fertility, control of costs, and elimination of mortality. The optimal dosing protocol for methotrexate therapy remains controversial. Similarly, the timing and technique for surgical intervention during medical failures are for the most part empirical. Using an evidence-based approach to the diagnosis of and treatment for ectopic pregnancy, this chapter provides a comprehensive examination of the standard of care for this serious gynecologic disease.

Incidence

The incidence of ectopic pregnancy in the United States is not known precisely. Recent attempts by the Centers for Disease Control and Prevention (CDC) to estimate the incidence of this disease have been thwarted, because there are no clear reporting standards and many cases are treated medically in outpatient facilities and are thus not recorded in hospital registries. The latest reported numbers date back to the mid 1990s. Where hospital records were used, a relentless increase in ectopic pregnancies from 4.5 per 1,000 in 1970 to 16.8 per 1,000 in 1989 to 19.7 per 1,000 (108,000 cases) in 1992 was reported. Several recent epidemiologic trends make it likely that the current incidence of ectopic pregnancy is even higher. First, there is a continued increase in the risk factors associated with ectopic pregnancy (Table 5.1). Second, there is increased ascertainment of ectopics from use of more sensitive and specific diagnostic methods that detect many cases that in the past may have resolved spontaneously without diagnosis or treatment (increase in prevalence due to lead-time bias). Third, with the increasing use of assisted reproductive technology (ART) for treatment of infertility, there is increased risk of ectopics, which comprise up to 5% of pregnancies achieved by using ART. Not surprisingly, heterotopics also are being reported with increasing frequency in ART pregnancies. Between 1979 and 1986, 13% of maternal deaths were secondary to ectopic pregnancy; by 1992, this dropped to 9%. However, ectopic pregnancies continue to be the leading cause of maternal death in the first trimester, accounting for 5% to 6% of all maternal deaths in the United States. Ninety percent of these deaths were due to hemorrhagic complications.

Pathogenesis

Any event that impairs the ability of the tube to transport gametes or embryos will predispose to ectopic implantation. The most common site of ectopic pregnancy is the fallopian tube, which accounts for 98.3% of all ectopic gestations. Of tubal implantation sites, the ampulla is observed in 79.6%, 12.3% are in the isthmus, 6.2% are in the fimbrial end, and the remaining 1.9% occur in the interstitial (cornual) region. Ectopic nidation outside the fallopian tubes is rare; only 1.4% of ectopic pregnancies are abdominal pregnancies, 0.15% ovarian, and 0.15% cervical (Fig. 5.1).

TABLE 5.1 Risk Factors Associated with Ectopic Pregnancy

Patients at increased risk need aggressive monitoring of their pregnancies immediately after first missed menses. Risk Factor Odds Ratioa High risk Tubal surgery 21.0 Tubal ligation 9.3 Previous ectopic pregnancy 8.3 In utero exposure to DES 5.6 Use of IUD 4.2 – 45.0 Tubal pathology 3.8 – 21.0 Assisted reproduction 4.0 Moderate risk Infertility 2.5 – 21.0 Previous genital infections 2.5 – 3.7 Multiple sexual partners 2.1 Salpingitis isthmica nodosa 1.5 Low risk Previous pelvic infection 0.9 – 3.8 Cigarette smoking 2.3 – 2.5 Vaginal douching 1.1 – 3.1 First intercourse <18> 1.6 DES, diethylstilbestrol; IUD, intrauterine device. aSingle values, common odds ratio from homogenous studies; point estimates, range of values from heterogenous studies.

In most tubal implantations, the proliferating trophoblast invades the tubal wall. Ectopic pregnancies in the ampullary portion of the tube are often within the tubal lumen and have not caused tubal rupture, while those in the isthmic portion are more likely to be found outside the lumen, having caused tubal rupture. The degree of trophoblastic invasion of maternal tissues, the age and viability of the pregnancy, and the site of implantation determine the sequence of clinical events. As the trophoblasts proliferate, the growth may extend from the luminal mucosa, into the muscularis and lamina propria, through to the serosa and, ultimately, full thickness even into large blood vessels in the broad ligament. With vascular disruption, bleeding takes place that distorts the tube, stretches the serosa, and causes pain. The embryo is abnormal and degenerates in about 80% of cases. If left untreated, spontaneous tubal abortion occurs in about 50% of tubal ectopic pregnancies and may often be clinically silent. Likewise, spontaneous tubal abortion with hemorrhage can occur with bleeding that is self-limited. However, the remaining cases of ectopic pregnancy will eventually cause tubal rupture and are associated with significant and possibly life-threatening hemorrhage. As noted previously, this complication is most likely to occur in the isthmic part of the tube, which has limited distensibility. Chronic tubal rupture with extension into the broad ligament can produce a pelvic hematoma that can last for several weeks. Unruptured ectopic pregnancies can produce a chronic course, with persistently elevated β-human chorionic gonadotropin (β-hCG) levels that may last for weeks.

Fig.1 Implantation sites for ectopic pregnancy following natural cycles and ART.

Besides tubal disease, factors inherent to the embryo itself may theoretically lead to premature implantation in the tube, prior to its entry into the uterine cavity. However, studies have not supported the theory that genetic or other morphologic abnormalities of the embryo cause implantation at an ectopic site, as the rate of chromosomal abnormalities in surgically excised tubal pregnancies is comparable to that expected for gestational and age-related factors.Other molecular-level factors that may be responsible for the molecular dialog between embryo and implantation site, or cell-cell and cell-extracellular matrix interactions, are being studied for their possible role in aberrant implantations.

Risk Factors

Ectopic pregnancy most often is associated with risk factors leading to tubal epithelial damage, which alters gamete and embryo transport. Meta-analyses identify the risk factors listed in Table 1 as the most influential.

Tubal Damage and Infection

Documented tubal pathology carries a 3.5-fold common adjusted odds ratio for ectopic pregnancy. Patients with a previous ectopic pregnancy are six to eight times more likely to experience another ectopic pregnancy, and 8% to 14% of patients experience more than one ectopic pregnancy. The approximate recurrent ectopic pregnancy rate is 13% after a history of one ectopic and 28% after two previous ectopics. Patients with a history of tubal surgery have a 21-fold common adjusted odds ratio of ectopic pregnancy, but it is not clear if it is the tubal disease itself or the surgery required for the disease.

Tubal pathology frequently results from pelvic infections. Patients with a history of pelvic infections, including gonorrhea, serologically confirmed chlamydia, and nonspecific pelvic inflammatory disease, have a twofold to fourfold higher risk of developing an ectopic pregnancy. The ectopic pregnancy rate is 4% in women with laparoscopically documented salpingitis, compared with 0.7% in women with normal-appearing tubes. In evaluating histologic specimens of ectopic pregnancy, microscopic evidence of salpingitis is present in 38% of cases. Recurrent episodes of pelvic infections increase the likelihood of tubal occlusions: 12.8% after one infection, 35.5% after two infections, and 75% in women with three or more infections.

Salpingitis Isthmica Nodosa

Salpingitis isthmica nodosa is a disease defined by an anatomic thickening of the proximal portion of the fallopian tubes at the junction with the uterus and is histologically characterized by multiple luminal diverticula. The etiology of this disease is not known; however, this pattern of tubal pathology increases the incidence of ectopic pregnancy by 52% in age- and race-matched controls.

Diethylstilbestrol

Prenatal exposure to diethylstilbestrol (DES) alters fallopian tubal development, resulting in absent or minimal fimbrial tissue, a small tubal os, and decreased length and caliber of the tube. This abnormal tubal anatomy is associated with a fivefold increase in the risk for ectopic pregnancy.

Cigarette Smoking

Patients who smoke cigarettes are at a slightly increased risk for ectopic pregnancy. It is difficult to conceptualize the link between ectopic pregnancy and cigarettes. Theories include impaired immunity in smokers predisposing them to pelvic infections, alterations in tubal motility, or a representation of a lifestyle associated with an increased risk of tubal infection.

Contraception

Intrauterine devices (IUDs) have been associated with ectopic pregnancy. A multicenter case-controlled study conducted by the World Health Organization in ten countries found an odds ratio of 6.4 for ectopic pregnancy in current IUD users compared with pregnant controls, whereas the odds ratio was only 0.5 when the comparison was made with nonpregnant controls. Similarly, in the Oxford Study of 17,032 contraceptive users, the proportion of unplanned pregnancies that were ectopic was higher in women using IUDs compared with women taking oral contraceptives. Thus, IUDs effectively prevent pregnancy, but if pregnancy does occur in a woman using an IUD, there is increased likelihood that the pregnancy will be ectopic.

Tubal ligation carries a similar risk for ectopic pregnancy to what is observed with current IUD use. A meta-analysis using case-controlled studies found the odds ratio for tubal sterilization to be 9.3 when compared with pregnant controls and 0.52 when compared with nonpregnant controls, a finding confirmed by two additional multicenter case-controlled trials. As with the IUD, tubal ligations effectively prevent pregnancy, but if pregnancy does occur, the suspicion for an ectopic pregnancy should be high.

Tubal sterilization by using electrocoagulation procedures are associated with higher ectopic pregnancy risk than other methods of tubal sterilization, possibly resulting from tubal recanalization or uteroperitoneal fistula formation. Uteroperitoneal fistulas have been found in up to 75% of hysterectomy specimens from women with previous tubal ligations in which the tubes were cauterized flush with the uterus.

Oral contraceptives are associated with a reduced risk of ectopic pregnancy when compared with nonpregnant controls but with elevated risk when compared with pregnant controls. This protection is presumably due to the suppression of ovulation by oral contraceptives. It is therefore not surprising that patients who take emergency contraception, such as oral contraceptives after fertilization, are at substantial risk for an ectopic pregnancy. This has been attributed to altered tubal motility, but this etiology remains controversial.

Barrier contraception (condoms, spermicides, and diaphragms) also reduces the odds ratio of ectopic pregnancy. An additional advantage may be attributed to the decreased risk of sexually transmitted diseases in women using barrier methods.

Evidence-Based Recommendation

Women with a previous ectopic pregnancy, tubal surgery, tubal pathology, or with prenatal DES exposure are at high risk for ectopic pregnancy. Women who have experienced genital infections, infertility, or more than one sexual partner have a moderate risk of ectopic pregnancy. Previous pelvic or abdominal surgery, smoking, vaginal douching, or an early age of first sexual intercourse have only a slightly increased risk of ectopic pregnancy.

Contraception, if used properly, is an effective way of reducing pregnancy, both intrauterine and ectopic. If pregnancy occurs in women with an IUD, after tubal ligation, or following emergency contraception, suspicion for ectopic pregnancy should be high. (Strength of recommendation: A.)

Signs and Symptoms

The classic symptoms of an ectopic pregnancy are abdominal or pelvic pain and vaginal bleeding or spotting in the context of a positive pregnancy test. However, these symptoms may be variable, range from mild to severe, and are neither sensitive nor specific for the diagnosis of ectopic pregnancy. Today, many ectopic pregnancies never produce symptoms; rather, they are diagnosed and treated in a timely fashion because the patient is identified as high risk. Table 5.1 summarizes and weighs risk factors that should be examined in every woman who has just been identified as being pregnant. However, the medical and economic benefits of screening asymptomatic women, including those who are considered at high risk, are outweighed by the still overall low incidence of ectopic pregnancy and the high false-positive rate of doing so. Thus, universal screening of all women, including some considered at higher risk, is not recommended. Since at least 40% to 50% of patients with proven ectopic pregnancies have no risk factors, absence of these factors is not wholly reassuring and does not exclude an ectopic pregnancy. Unfortunately, early diagnosis is not always achievable, and fallopian tube rupture secondary to ectopic pregnancy remains a relatively frequent clinical occurrence.

The most common signs are detected on abdominal examination. Abdominal tenderness is present in 90% of patients and rebound tenderness in 70%. The pelvic examination is usually nonspecific; cervical motion tenderness is present in up to two thirds of patients, while a tender adnexal mass is present in 10% to 50%. Pain radiating to the shoulder, syncope, and shock, as a result of hemoperitoneum, occur in up to 20% of patients and are indications for immediate surgical intervention.

Diagnosis

Ectopic pregnancy can be diagnosed as early as 4.5 weeks gestation. Unfortunately, visualizing an ectopic pregnancy this early frequently is not possible. More importantly, traditional laparoscopic visualization (Figs. 5.2, 5.3, 5.5) is now rarely necessary. Routine diagnostic tests are serial measurements of β-hCG, ultrasonography, uterine sampling via manual vacuum extraction or curettage, and, in some instances, serum progesterone levels.

Outpatient diagnosis of ectopic pregnancy by using various algorithms has been shown to be safe and effective without need for hospitalization even when the diagnosis is equivocal. The clinical algorithm in Figure 5.4 is highly efficacious in diagnosing ectopic pregnancy.

The diagnosis of ectopic pregnancy begins by excluding a normal intrauterine pregnancy. Transvaginal ultrasound examination should identify an intrauterine pregnancy with nearly 100% accuracy for gestations greater that 5 weeks by identifying structures such as a gestational sac, a yolk sac, and fetal pole with later cardiac motion (usually seen around 6 weeks). Because of the inaccuracies inherent in pregnancy dating, β-hCG is often used as a surrogate marker for pregnancy dating. As will be further discussed below, an intrauterine pregnancy should be visualized at the “discriminatory cutoff” of β-hCG, a level corresponding to 1,500 to 2,500 IU/L (depending on operator and equipment used) with near 100% sensitivity. These β-hCG thresholds are not universal, and each institution must identify its own values to avoid terminating normal intrauterine pregnancies. The absence of such implies an abnormal gestation. If the pregnancy is earlier than the aforementioned 5 weeks and/or the β-hCG is below the “discriminatory cutoff”, then serial β-hCG measurements aid in the diagnosis and determine the need for intervention.

Figure 2 Laparoscopic visualization of an isthmic ectopic pregnancy.

Figure 3 Laparoscopic visualization of an ampullary ectopic pregnancy.

Serial β-Human Chorionic Gonadotropin Determinations

The advent of radioimmunoassay (RIA) and specific antiserum to the β-subunit of hCG has allowed for the accurate quantification of β-hCG and the ability to closely follow trends in the rise and fall of this hormone, detecting low β-hCG concentrations in urine and serum, 20 mIU/mL down to 1 mIU/mL, respectively. Currently, β-hCG is almost exclusively assayed using the third International Reference Preparation (IRP), a standard very similar to the original first IRP.

The β-hCG, produced by trophoblastic cells in normal pregnancy, has long been accepted to rise at least 66% and up to twofold every 2 days. Recent data has shown that the minimum rise for a potentially viable pregnancy that presents with pain and/or vaginal bleeding may be as low as 53% in 2 days, based on the 99th percentile confidence interval (CI) around the mean of the curve of normal β-hCG rise. Thus, intervention for a β-hCG rise of less than 66% over 2 days, a practice supported by previous data, may potentially interrupt a normally developing intrauterine pregnancy. This generally applies to β-hCG values below 10,000 mIU/mL.

Figure 4 Diagnostic algorithm for ectopic pregnancy. (From Seeber BE, Barnhart KT. Suspected ectopic pregnancy. Obstet Gynecol 2006;107:402)

Figure 5 Ultrasonogram of free fluid noted under the liver edge above the right kidney. Confirmed to be blood from a ruptured ectopic pregnancy at the time of surgery. (Courtesy of R. Mangal, M.D., Obstetrics/Gynecologic Associates, Houston, TX.)

Eight-five percent of abnormal pregnancies, whether intrauterine or ectopic, have impaired β-hCG production with an abnormal rate of β-hCG rise. β-hCG levels that plateau or fail to rise normally along with a low serum progesterone value should be considered nonviable. Rapidly declining β-hCG values (at least 21% to 35% in 2 days) are likely consistent with a miscarriage that may resolve spontaneously but could still represent a spontaneously resolving ectopic gestation. In such situations, β-hCG levels should be followed serially until no longer detectable, indicating complete resolution of the pregnancy, regardless of the implantation site.

If a viable intrauterine gestation is not visible by transvaginal ultrasonography when the β-hCG is above the “discriminatory cutoff” and no fetal heartbeat can be visualized in the adnexa, uterine curettage or manual vacuum extraction can be performed. This intervention is necessary to accurately differentiate between an abnormal intrauterine gestation (spontaneous abortion) and an ectopic pregnancy. Either treatment of a nonviable intrauterine pregnancy is performed or ectopic pregnancy is diagnosed when the uterine contents fail to demonstrate presence of chorionic villi on histologic examination or the β-hCG levels do not fall appropriately postuterine evacuation.

If histologic examination is not readily available, β-hCG determinations are further employed for diagnosis after uterine curettage. If the β-hCG fails to decline by 15% after 12 to 24 hours from a level drawn immediately before surgery, the pregnancy is presumed ectopic and treatment should be initiated. To definitively confirm resolution of the pregnancy in the absence of a tissue diagnosis, β-hCG levels should be followed weekly until undetectable.

Progesterone

The diagnostic algorithm presented here does not include the measurement of serum progesterone levels, a test whose results are not immediately available to aid in diagnosis in many clinical settings. Although progesterone levels are higher in intrauterine pregnancies than in ectopic pregnancies, there is no established cutoff to use to discriminate between these two entities. A meta-analysis has shown that although low progesterone levels can identify patients at risk for ectopic pregnancy, this test alone is insufficient to diagnose ectopic pregnancy with certainty. In addition, a low progesterone level of less than 5 ng/mL can rule out a normal pregnancy with almost 100% accuracy but does not differentiate whether that pregnancy is an abnormal one in the uterus or at an ectopic site.

Ultrasonography

Although the uterus and adnexa may be evaluated by an abdominal or pelvic examination, transvaginal ultrasonography reliably detects intrauterine gestations when the β-hCG levels are between 1,500 and 2,500 mIU/mL (third IRP), or as early as 1 week after missed menses. An intrauterine gestation should almost always be visualized when the β-hCG level is greater than 2,000 mIU/mL.

Diagnosis of an ectopic pregnancy can be made with 100% sensitivity but with low specificity (15% to 20%) if an extrauterine gestational sac containing a yolk sac or embryo is identified. A complex adnexal mass without an intrauterine pregnancy improves specificity to 21% to 84% at the expense of lower sensitivity (93.0% to 99.5%). In reviewing the literature, the presence of any noncystic, extraovarian adnexal mass in the absence of an intrauterine gestation was diagnostic of an ectopic pregnancy with 98.9% sensitivity, 96.3% positive predictive value, 84.4% specificity, and a 94.8% negative predictive value (Fig. 6). Despite the high resolution of transvaginal ultrasonography, an adnexal mass will not be found in 15% to 35% of patients with an ectopic pregnancy, particularly in early stages. Some sonographic images, such as the pseudogestational sac, may mislead even an experienced examiner to falsely diagnose a gestational sac. This is a collection of fluid within the endometrial cavity, usually in a central as opposed to eccentric location that occurs due to bleeding from the decidualized endometrium when an extrauterine gestation is present.

Figure 5.6 Transvaginal ultrasonographic illustration of tubal ectopic gestation.

Serial β-hCG concentrations and transvaginal ultrasonography predict ectopic pregnancy with a positive predictive value of 95%. Ultrasonography should be used to document the presence or absence of an intrauterine pregnancy when the β-hCG levels have risen above the designated discriminatory cutoff zone.

However, in those patients with an “indeterminate” ultrasound, 25% have an ectopic pregnancy. Therefore, serial β-hCG and ultrasonography alone cannot diagnose all ectopic pregnancies. In order to make the definitive diagnosis and differentiate an abnormal intrauterine from an ectopic pregnancy, uterine evacuation for tissue diagnosis is necessary. In order to minimize the inadvertent interruption of a desired intrauterine pregnancy, a high (not low) discriminatory zone should be used before uterine evacuation is considered.

Uterine Evacuation

Uterine curettage or manual vacuum extraction is necessary when a transvaginal ultrasonogram and a rising or plateauing β-hCG level below the cutoff value are not sufficient for diagnosis. With this procedure, tissue can be obtained to look for intrauterine products of conception. If present, the patient had an abnormal intrauterine pregnancy and now a completed abortion; if negative, the patient has an ectopic pregnancy needing further management. If histologic examination is not available, then a guideline of a decrease in the β-hCG level of 15% or more 12 hours after curettage is diagnostic of a complete abortion. If the β-hCG titer plateaus or rises and the trophoblast was not removed by curettage, an ectopic pregnancy is likely.

Evidence-Based Recommendation

Serial β-hCG determinations, transvaginal ultrasonography, and uterine sampling allow for definitive diagnosis of ectopic pregnancy. A confirmatory laparoscopy is rarely necessary. (Strength of recommendation: A.)