Achalasia Esofagus: I. Pendahuluan

ACHALASIA ESOFAGUS I.

PENDAHULUAN

Achalasia esofagus adalah gangguan motorik pada otot polos esofagus, yang memiliki

karakteristik

berupa

kegagalan

spinchter

esofagus

berelaksasi dan tidak adanya gerakan peristaltik pada esofagus.

bawah

untuk 

1,2

Achalasia dideskripsikan pertama kali pada tahun 1672 oleh Sir Thomas Willis. Pada tahun 1881, von Mikulicz mendeskripsikan penyakit ini sebagai suatu kardiospasme, di mana gejalanya lebih disebabkan oleh suatu gangguan fungsional daripada suatu gangguan mekanik. Pada tahun 1929, Hurt dan Rake menyatakan bahwa penyakit tersebut disebabkan oleh kegagalan spinchter esofagus bawah untuk   berelaksasi. Mereka lalu menyebutnya sebagai “achalasia”, sebuah kata dari bahasa Yunani yang berarti gagal untuk berelaksasi.

2,3

Gambar 1. Achalasia esofagus dilihat secara anatomis (dikutip dari kepustakaan 4)

1

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II.

ETIOLOGI

Achalasia esofagus dapat terjadi secara primer (idiopatik) atau secara sekunder. Achalasia esofagus primer diduga terjadi akibat tidak adanya seluruh atau sebagian sel s el ganglion inhibitor pada pleksus Mienterikus (Auerbach’s) pada esofagus. Hal ini mengakibatkan ketidakseimbangan antara neuron eksitatorik dan neuron inhibitorik yang menyebabkan spinchter esofagus bawah tidak dapat berelaksasi. Beberapa penelitian telah mencatat sejumlah ganglion mienterik pada spesimen-spesimen penyakit esofagus dan menemukan adanya infiltrat limfositik  dan deposisi kolagen di dalam ganglion. Berdasarkan penemuan ini, agen-agen yang dapat menyebabkan penyakit infeksi, seperti virus, dan beberapa mediator radang akibat respon imunnya, diduga sebagai penyebab dari kehilangan ganglion, tetapi etiologi pastinya belum diketahui. Penelitian mengenai neurotransmisi dan penghantaran sinyal yang terjadi pada esofagus distal dan spinchter esofagus bawah pada achalasia esofagus telah berkembang pesat. Nitrit oksida diduga telah menjadi neurotransmitter inhibitori yang terbesar, yang mengontrol proses relaksasi dari otot polos esofagus. Hipotesis yang timbul, bahwa pada proses achalasia esofagus, terjadi kehilangan yang lebih besar pada neuron inhibitori nitrogenik daripada neuron kolinergik.

3

Penyebab sekunder achalasia esofagus yang paling sering adalah penyakit Chagas, suatu penyakit sistemik yang disebabkan oleh infestasi spesies protozoa, yaitu Trypanosoma cruzi, yang ditansmisikan oleh seekor serangga, menginfeksi neuron intramural, dan menyebabkan disfungsi otonom. Penyakit Chagas paling sering terjadi di Amerika Tengah dan Selatan, dan diduga penyakit ini menjadi penyebab sekunder terbanyak dari achalasia esofagus. Selain itu, penyebab sekunder dari achalasia esofagus dapat berupa malignansi (karsinoma lambung, esofagus), postvagotomi, pseudo-obstruksi intestinal kronik tipe neuropatik, amiloidosis, sarkoidosis, dan penyakit Anderson-Fabrey.

3,4

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III.

EPIDEMIOLOGI

Insiden achalasia esofagus di Amerika Serikat sekitar 1 per 100.000 orang per tahun, dengan rasio antara pria dan wanita adalah 1:1. Achalasia esofagus lebih sering terjadi pada orang dewasa, terbanyak sekitar usia 25-60 tahun. Pada anakanak, penyakit ini juga sangat jarang ditemukan, dan secara genetik tidak ditemukan hubungan. Kurang dari 5% dari kasus terjadi pada anak-anak, di mana mengenai anak laki-laki lebih banyak daripada anak perempuan, dengan rasio 6:1.

IV.

2,4,5

ANATOMI ESOFAGUS

Esofagus merupakan saluran yang menghubungkan dan menyalurkan makanan dari rongga mulut ke lambung. Dalam perjalanannya dari faring menuju gaster, esofagus melalui tiga kompartemen, yaitu leher, toraks dan abdomen. Esofagus yang berada di leher adalah sepanjang lima sentimeter dan berjalan di antara trakea dan kolumna vertebralis, serta selanjutnya memasuki rongga toraks setinggi manubrium sterni.

6

Di dalam rongga dada, esofagus berada di mediastinum posterior mulai di belakang lengkung aorta dan membelok ke kiri dari trakea di belakang bronkus cabang utama kiri, kemudian agak membelok ke kanan beberapa sentimeter pada area subcarinal dan kembali membelok ke kiri dan depan aorta torakalis, dan masuk  ke dalam rongga perut melalui hiatus esofagus dari diafragma dan berakhir di kardia lambung. Panjang esofagus yang berada di rongga perut berkisar dua sampai empat sentimeter. Diameter rata-rata esofagus pada orang dewasa sekitar 2,5 sentimeter.

6,7

Otot esofagus sepertiga bagian atas adalah otot serat lintang yang berhubungan erat dengan otot-otot faring, sedangkan dua pertiga bagian bawah adalah otot polos yang terdiri atas otot sirkular dan otot longitudinal seperti ditemukan pada saluran cerna lainnya.

6,7

Esofagus menyempit pada tiga tempat. Penyempitan pertama yang bersifat

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kedua terletak di rongga dada bagian tengah, akibat tertekan lengkung aorta dan bronkus utama kiri. Penyempitan ini tidak bersifat spinchter.

6,7

Gambar 2. Struktur esofagus (dikutip dari kepustakaan 8)

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Gambar 3. Daerah penyempitan esofagus (dikutip dari kepustakaan 8)

Esofagus mendapat darahnya dari banyak arteri kecil. Bagian atas dari esofagus yang berada di leher dan rongga dada mendapat darah dari arteri tiroidea inferior, beberapa cabang arteri bronkialis dan beberapa arteri kecil dari aorta. Esofagus di hiatus esofagus dan rongga perut mendapat darah dari arteri frenika inferior kiri dan cabang arteri gastrika kiri.

6,7

Pembuluh vena dimulai sebagai pleksus di submukosa esofagus. Di esofagus bagian atas dan tengah, aliran vena dari pleksus esofagus berjalan melalui vena esofagus ke vena azygos dan vena hemiazygos untuk kemudian masuk ke vena cava superior. Di esofagus bagian bawah, semua pembuluh vena masuk ke dalam vena

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lambung tersebut. Hubungan ini yang menyebabkan timbulnya varises esofagus bila terjadi bendungan vena porta.

6,7

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Pembuluh limfe esofagus membentuk pleksus di dalam mukosa, submukosa, lapisan otot, dan tunika adventisia. Di bagian sepertiga cranial, pembuluh ini berjalan secara longitudinal bersama dengan pembuluh limfe dari laring ke kelenjar di leher, sedangkan dari bagian dua pertiga kaudal dialirkan ke kelenjar seliakus, seperti pembuluh limfe dari lambung.

6

Metastasis dari keganasan esofagus dapat ditemukan antara kelenjar limfe leher dan kelenjar limfe seliakus di perut, bergantung pada letaknya, stadium dan tingkat keganasan tersebut.

6

Ductus torachicus berjalan di depan tulang belakang toraks di sebelah dorsal kanan esofagus, kemudian menjelang setinggi vertebra thorakal VI atau VII ke sebelah kiri belakang esofagus untuk turun kembali dan masuk ke dalam vena subklavia kiri.

V.

6

FISIOLOGI ESOFAGUS

Motilitas yang berkaitan dengan esofagus adalah menelan. Menelan dimulai ketika suatu bolus secara sengaja didorong oleh lidah ke bagian belakang mulut menuju faring. Tekanan bolus di faring merangsang reseptor tekanan di faring yang kemudian mengirim impuls aferen ke pusat menelan di medula. Pusat menelan kemudian secara refleks mengaktifkan serangkaian otot yang terlibat dalam proses menelan. Menelan adalah suatu contoh refleks all-or-none yang terprogram secara

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masuk ke trakea. Semua ini dilaksanakan melalui berbagai aktivitas terkoordinasi berikut ini: 

9

Makanan dicegah kembali ke mulut selama menelan oleh posisi lidah menekan langit-langit



Uvula terangkat dan tersangkut di bagian belakang tenggorokan, sehingga saluran hidung tertutup dari faring dan makanan tidak masuk hidung.



Makanan dicegah masuk ke trakea terutama oleh elevasi laring dan penutupan erat pita suara melintasi lubang faring, atau glotis. Bagian awal trakea adalah laring, tempat pita suara terentang di dalamnya. Selama menelan, pita suara melaksanakan fungsi yang tidak berkaitan dengan berbicara. Kontraksi otot-otot laring menyebabkan pita suara merapat erat satu sama lain, sehingga pintu masuk glotis tertutup. Selain itu, bolus menyebabkan suatu lembaran kecil  jaringan ikat, epiglotis, tertekan ke belakang menutupi glotis yang menambah proteksi untuk mencegah makanan masuk ke saluran pernapasan.



Karena saluran pernapasan tertutup sementara saat menelan, pernapasan terhambat secara singkat sehingga individu tidak mencoba melakukan usaha yang sia-sia untuk bernapas.



Dengan laring dan trakea tertutup, otot-otot faring berkontraksi untuk  mendorong bolus ke dalam esofagus. Esofagus dijaga di kedua ujungnya oleh spinchter. Spinchter adalah struktur

esofagus ke lambung, berotot berbentuk cincin yang jika tertutup mencegah

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tekanan di dalam dinding esofagus, menimbulkan gelombang peristaltik kedua yang lebih kuat yang diperantarai oleh pleksus saraf intrinsik di tempat peregangan. Spinchter esofagus melemas secara refleks saat gelombang peristaltik mencapai bagian bawah esofagus sehingga bolus dapat masuk ke dalam lambung. Setelah bolus masuk ke lambung, spinchter gastroesofagus kembali berkontraksi.

VI.

9

PATOFISIOLOGI

Teori utama yang dapat menjelaskan penyakit ini, antara lain: 

Terjadi

abnormalitas

neurogenik

primer

yang

disertai

5

dengan

tidak 

berfungsinya neuron inhibitorik dan terjadi degenerasi progresif dari ganglion sel 

Terjadi defisiensi dari ganglion sel pleksus mienterik, dapat juga disebabkan oleh Gastro-Esophageal Reflux Disease (GERD), penyakit Chagas, dan infeksi virus. Abnormalitas motorik pada achalasia esofagus merupakan hasil dari

penurunan fungsi pada motor neuron yang terletak pada pleksus mienterikus intramural. Secara fungsional, kontraksi spinchter esofagus diatur oleh pelepasan neurotransmitter eksitatorik (asetilkolin dan substansi P) dan relaksasi spinchter esofagus diatur oleh pelepasan neurotransmitter inhibitorik (nitrit oksida dan vasoactive intestinal peptide). Seseorang yang menderita achalasia esofagus

kehilangan ganglion sel inhibitori yang menyebabkan ketidakseimbangan dalam

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terjadi karena terdapat retensi sejumlah besar makanan pada esofagus yang berdilatasi. Regurgitasi ini sering terjadi pada malam hari karena posisi pasien yang telentang ketika tidur, dan hal ini berpotensi menyebabkan suatu pneumonia aspirasi. Kadang-kadang, makanan dapat tertinggal pada esofagus (sebelum bagian yang menyempit) dan biasanya pasien mengatasi hal ini dengan minum air dalam  jumlah yang besar agar meningkatkan meningkatkan tekanan pada esofagus dan memaksa makanan untuk melaluinya dan masuk ke lambung. Nyeri dada retrosternal yang berat dapat terjadi karena adanya tekanan yang tinggi pada esofagus, dan para dokter sering mendiagnosis nyeri ini sebagai nyeri yang berasal dari jantung. Gejala heartburn-like chest pain juga ditemukan pada beberapa penderita achalasia

esofagus, mungkin disebabkan karena adanya asam laktat yang terbentuk dari fermentasi sisa-sisa makanan pada lumen esofagus. Pada penderita achalasia esofagus, kehilangan berat badan mungkin saja terjadi karena pasien berusaha mengurangi makannya untuk mencegah terjadinya regurgitasi dan perasaan nyeri di daerah retrosternal. Jika kehilangan berat badan terjadi dengan cepat, dapat dipikirkan suatu keganasan sebagai penyebab achalasia esofagus.

VIII.

1,4,10,11

DIAGNOSIS

Diagnosis ditegakkan berdasarkan gejala klinis, pemeriksaan radiologi, pemeriksaan manometrik esofagus, dan pemeriksaan endoskopi. Pemeriksaan fisik  dan pemeriksaan laboratorium untuk menegakkan diagnosis achalasia esofagus,

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Gambar 6. Gambaran foto toraks pada achalasia esofagus. Tanda panah menunjukkan esofagus yang berdilatasi hebat (dikutip dari kepustakaan 13)

Pemeriksaan esofagografi dengan menggunakan barium, memiliki akurasi sekitar 95% dalam mendiagnosis achalasia esofagus, dan secara khas menunjukkan bagian esofagus yang berdilatasi dan terdapat juga bagian yang

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

Relaksasi spinchter esofagus bawah yang tidak sempurna



Tidak ada peristaltik yang ditandai dengan tidak adanya kontraksi esofagus secara simultan sebagai reaksi dari proses menelan.



Tanda klasik achalasia esofagus yang dapat terlihat adalah tekanan yang tinggi pada spinchter esofagus bawah (tekanan spinchter esofagus bawah saat istirahat lebih besar dari 45 mmHg), dan tekanan esofagus bagian proksimal dan media saat istirahat (relaksasi) melebihi tekanan di lambung saat istirahat (relaksasi)

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Gambar 10. Perbandingan achalasia esofagus jika dilihat secara: A. Anatomis, B. Endoskopi, C. Esofagografi (dikutip dari kepustakaan 16)

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progresifitas penyakit sudah lanjut 

Kehilangan

berat

badan

dengan cepat Pemeriksaan

endoskopi

Disfagia dapat terjadi akibat

menunjukkan

esofagitis

adanya

refluks, dengan atau tanpa





ataupun

pembengkakan striktur

peptikum, tanpa Esofagitis refluks

striktur

fibrosis

dengan kelainan

atau

Mungkin terdapat hernia

pada

hiatus yang terletak di bawah striktur.

endoskopi 

Pasien

biasanya

mengeluhkan



tambahan

dari

Pemeriksaan esofagografi memiliki sensitivitas yang

heartburn

rendah

dan/atau regurgitasi sebagai gejala

peptikum.



Terdapat

perbedaan

pH

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gambaran aperistaltik yang ditunjukkan pada achalasia esofagus. Gejala klinis berupa disfagia

Biopsi

Esofagitis

intermitten, lebih sering terjadi

menunjukkan

eosinofilik 

pada laki-laki muda dengan

eosinofil (>15 eosinofil per

riwayat atopi

lapangan pandang) 



Gejala klinis serupa dengan

pada

esofagus infiltrasi

Biopsi gastroskopik pada gastroesophageal junction

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X.

PENATALAKSANAAN

Sifat terapi pada achalasia hanyalah paliatif, karena fungsi peristaltik  esofagus tidak dapat dipulihkan kembali. Terapi dapat dilakukan dengan memberi diet tinggi kalori, medikamentosa, tindakan dilatasi, psikoterapi, dan operasi esofagokardiotomi (operasi Heller). 1)

11

Terapi Non-Bedah a.

Medikamentosa Pemberian

obat

yang

bersifat

merelaksasikan

otot

polos,

seperti

nitrogliserin 5 mg sublingual atau 10 mg per oral, dan juga methacholine,

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yang sama 1 bulan kemudian untuk mendapatkan hasil yang maksimal. Namun demikian, terapi ini mempunyai penilaian yang terbatas, di mana 60% pasien yang telah diterapi masih tidak merasakan disfagia 6 bulan setelah terapi; persentasi ini selanjutnya turun menjadi 30% walaupun setelah beberapa kali penyuntikan dua setengah tahun kemudian. Sebagai tambahan, terapi ini sering menyebabkan reaksi inflamasi pada bagian gastroesophageal junction, yang selanjutnya dapat membuat miotomi

menjadi lebih sulit. Terapi ini sebaiknya diaplikasikan pada pasien lanjut usia, yang mempunyai kontraindikasi terhadap  pneumatic dilation atau

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DAFTAR PUSTAKA

1.

Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin JB, Kasper DL, et al,

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13. Wikipedia. Achalasia [online]. 2012 [cited 2012 April 6]. Available from: URL: http://en.wikipedia.org/wiki/Achalasia 14. Kalloo A. Gastroesophageal reflux disease: diagnosis [online]. 2012 [cited 2012