GERD (Reflux Esophagitis)

Gejala kronik atau kerusakan mukosa karena aliran reflux abnormal di dalam esophagus. Dengan berbagai gejala yang timbul akibat keterlibatan esofagus, faring, laring, dan saluran nafas. Epidemiologi Di RSCM didapat kasus esofagitis 22,8% dari semua pasien yang menjalani pemeriksaan endoskopi atas indikasi dispepsia. Di negara barat diduga karena faktor diet dan meningkatnya obesitas. Faal Esofagus dan gaster dipisahkan oleh zona tekanan tinggi (dihasilkan oleh kontraksi lower esophageal spincter (LES). Normalnya zona tekanan tinggi dipertahankan kecuali, saat tjd aliran antegard yg terjadi saat menelan atau aliran retrogard saat sendawa atau muntah. Aliran retrogard dari gaster ke esofagus mll LES hanya tjd jika tekanan/ tonus LES tdk ada / < 3mmHg. Mekanisme GERD 1. Refluks spontan pd saat relaksasi LES yg tdk adekuat 2. Aliran retrogard yg mendahului kembalinya tonus LES stlh menelan 3. Meningkatnya tekanan intra abdomen Ketahanan epitel esofagus Beda dgn gaster dan duodenum, esofagus tdk punya lapisan mukus yg melindung mukosa esofagus, mekanisme ketahanan epitel esofagus terdiri dari : 1. Membran sel
2. Batas intraseluler (intraseluler junction) yg membatasi difusi H+ ke jaringan esofagus

3. Aliran darah esofagus yg mensuplai nutrien, O2 dan bikarbonat, serta mengeluarkan ion

H+ dan CO2 4. Sel2 esofagus punya kemampuan untuk mentransport ion H dan Cl intraseluler dgn Na dan bikarbonat ekstraseluler Etiologi

Hiatus hernia Panjang LES (makin pendek LES, makin rendah tonusnya) Obat antikolinergik, beta adrenergik, theofilin, opiat lainnya Faktor hormonal (saat kehamilan, progesteron meningkat dpt menurunkan tonus LES Transient LES relaxation (TLESR) relaksasi LES spontan < dari 5 detik tanpa didahului proses menelan diduga krn pengosongan lambung lambat (delayed gastric emtying) dan dilatasi lambung

Nikotin dpt menghambat transport ion Na mll epitel esofagus sdgkan alkohol dan aspirin meningkatkan permeabilitas epitel terhadap ion H

Faktor ofensif (faktor potensi daya rusak bahan refluksat dari dlm gaster) HCl, pepsin, garam empedu, enzim pankreas

Derajat kerusakan mukosa esofagus meningkat jika pH <2 (Asam)

Patogenesis dapat menyebabkan esofagitis bila : 1. terjadi kontak dlm waktu yg cukup lama antara bahan refluksat dgn mukosa esofagus 2. terjadi penurunan resistensi jaringan mukosa esofagus, walau keadaan 1) tdk terjadi dlm waktu cukup lama
3. Pengaruh infeksi Helicobacter pylori kemungkinan kecil menyebabkan esofagitis,

berbanding terbalik dgn esofagitis krn strain yg virulens (Cag A+)

Gejala tipikal a. Gejala mayor Heartburn Regurgitation/reflux Susah menelan (dysphagia)

b. Gejala minor Nyeri saat menelan (odynophagia) Salivasi berlebihan mual Nyeri dada

Gejala atipikal Batuk kronik Laryngitis (hoarseness, throat clearing) Asthma Erosion of dental enamel Dentine hypersensitivity Sinusitis and damaged teeth

Kerusakan esofagus yang terjadi diakibatkan GERD

Reflux esophagitisNekrosis epitel esofagus dikarenakan ulserasi di pertemuan perut dan esofagus. Peradangan mukosa karena reflux asam lambung ke dalam esophagus. Jika semakin memburuk kemungkinan tjd erosi, ulceration and stricture formation mjd lebih tinggi.

Esophageal stricturesPenyempitan esofagus terus-menerus dikarenakan reflux shg menyebabkan inflamasi

Barrett's esophagusmetaplasia (perubahan sel epitel squamosa mjd epitel columnar) di bagian distal esophagus.

Esophageal adenocarcinomabentuk yang jarang pd kanker.

Reflux esophagitis

Esophageal strictures

Barrett's esophagus

Esophageal adenocarcinoma

Diagnosa x-rays endoscopy, a procedure in which a thin flexible tube with a tiny camera is placed in your mouth and down into your stomach so your provider can see your esophagus and stomach Esofagografi dgn barium Pemantauan pH 24 jam Tes bernstein esophageal manometry (a test to measure pressure in the esophagus) Sintigrafi esofagus Tes pompa proton (proton pump inhibitor/ PPI test/ tes supresi asam/acid supression

Pengobatan A number of drugs are registered for GERD treatment, and they are among the most-oftenprescribed forms of medication in most Western countries. They can be used in combination with other drugs, although some antacids can interfere with the function of other drugs:

Proton pump inhibitors (such as omeprazole, pantoprazole, lansoprazole, and rabeprazole) are the most effective in reducing gastric acid secretion. These drugs stop acid secretion at the source of acid production, i.e., the proton pump.

Gastric H2 receptor blockers (such as ranitidine, famotidine and cimetidine) can reduce gastric secretion of acid. These drugs are technically antihistamines. They relieve complaints in about 50% of all GERD patients. Compared to placebo (which also is associated with symptom improvement), they have a number needed to treat of eight (8).

Antacids before meals or symptomatically after symptoms begin can reduce gastric acidity (increase pH).

Alginic acid (Gaviscon) may coat the mucosa as well as increase pH and decrease reflux. A meta-analysis of randomized controlled trials suggests alginic acid may be the most effective of non-prescription treatments with a number needed to treat of 4.

Prokinetics strengthen the lower esophageal sphincter (LES) and speed up gastric emptying. Cisapride, a member of this class, was withdrawn from the market for causing Long QT syndrome.

Sucralfate (Carafate) is also useful as an adjunct in helping to heal and prevent esophageal damage caused by GERD, however it must be taken several times daily and at least two (2) hours apart from meals and medications.

Mosapride citrate is a 5-HT4 receptor agonist used outside the United States largely as a therapy for GERD and dyspepsia.

Surgical treatment The standard surgical treatment, sometimes preferred over longtime use of medication, is the Nissen fundoplication. The upper part of the stomach is wrapped around the LES to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia. The procedure is often done laparoscopically. An obsolete treatment is vagotomy ("highly selective vagotomy"), the surgical removal of vagus nerve branches that innervate the stomach lining. This treatment has been largely replaced by medication. Another treatment is transoral incisionless fundoplication (TIF) with the use of a device called Esophyx, which allows doctors to rebuild the valve between the stomach and the diaphragm by going through the esophagus. Repeated inflammation and scarring may make your esophagus become narrower. If this happens, your health care provider may: dilate (widen) your esophagus use surgery to repair a hiatal hernia if you have one use surgery to create a new segment of esophagus.

Perawatan antacids to take after meals and at bedtime medicine that decreases the amount of acid your stomach makes medicine that helps food and acid move forward through your digestive tract weight loss to decrease the pressure on your stomach eating smaller meals avoiding late-evening snacks or meals before bedtime raising the head of your bed about 6 inches to help the acid stay in your stomach.

Pencegahan Take medicines with plenty of liquid. Swallowing medicine without enough liquid can irritate the esophagus. Avoid smoking. Avoid drinking alcohol. Avoid eating chocolate, peppermint, fatty foods, citrus foods, caffeine, or tomato products. These foods make reflux worse. Wear loose fitting clothing without belts. Avoid heavy meals. Avoid lying down right after you eat. Sleep with your head elevated at least 6 inches. Maintain your proper weight. Keep your follow-up appointments with your health care provider.

Tell your health care provider if your symptoms get worse.

Referensi
1. DeVault KR, Castell DO (1999). "Updated guidelines for the diagnosis and treatment of

gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology". Am. J. Gastroenterol. 94 (6): 143442. doi:10.1111/j.1572-0241.1999.1123_a.x. PMID 10364004. 2. http://www.healingdaily.com/conditions/saliva-ph-test.htm
3. Kahrilas, PJ (2008). "Gastroesophageal Reflux Disease". New England Journal of

Medicine. 359 (16): 17001707. doi:10.1056/NEJMcp0804684. http://content.nejm.org/cgi/content/short/359/16/1700.

4. Tran T, Lowry A, El-Serag H (2007). "Meta-analysis: the efficacy of over-the-counter

gastro-oesophageal reflux disease drugs". Aliment Pharmacol Ther 25 (2): 14353. doi:10.1111/j.1365-2036.2006.03135.x. PMID 17229239. 5. "www.medscape.com". http://www.medscape.com/viewarticle/518324_4.
6. Abbas A, Deschamps C, Cassivi SD, et al. (2004). "The role of laparoscopic

fundoplication in Barretts esophagus". Annals of Thoracic Surgery 77 (2): 393396. doi:10.1016/S0003-4975(03)01352-3. PMID 14759403. 7. New Surgery For Acid Reflux Sufferers. Retrieved on 2009-01-16. 8. Buku ajar ilmu penyakit dalam. Jakarta: Departemen Ilmu Penyakit Dalam Fakultas Kedokteran Universitas Indonesia; 2006. Hal 315-19.