Diarrhea is defined as a change in bowel habit, with an increase in stool frequency or fluidity or both, more than 3 times daily

or stool weight > 200 g/day. Acute diarrhoe if it is less than 2 weeks of duration, persistent if between 2-4 weeks in duration, and Chronic if it is more than 4 weeks in duration. Berdasarkan mekanisme patofisiologi yang mendasari terjadinya diare kronis, maka penyebab utama diare kronis adalah sebagai berikut : a. Diare cair (watery diarrhea): Diare osmotik: osmotik laxative, malabsorpsi karbohidrat Diare sekretorik: Sindrom kongenital, misalnya congenital chloridorhea. Toksin bakterial, ileal malabsorpsi asam empedu ileum. Inflamatory bowel disease (IBD) terdiri dari kolotis ulseratif, dan penyakit Chrons, kolitis mikroskopis, dan divertikulitis. Vaskulitis, keracunan dan obat. Penyalahgunaan laxative (stimulant laxative). Gangguan motilitas atau regulasi berupa diare postvagotomy, postsympathectomy, diabetes autonomik neuropati, irritable bowel syndrome. Tumor lain: karsinoma kolon, limfoma, villous adenoma. Diare sekretorik idiopatik: diare sekretorik epidemik (Brained), idiopatik diare sekretorik sporadik. b. Diare inflamasi Inflamatory bowel disease: colitis ulserative, penyakit Chrons, diverticulitis, ulcerative jejunoileitis. Penyakit infeksi: Kolitis pseudomembranosa. Infeksi bakteri invasive seperti TBC, yersinosis. Infeksi viral ulceratif: citomegalo, herpes simplek Iinfeksi parasit invasif: amebiasis, strongiloides. Kolitis iskemik, kolitis radiasi, keganasan (karsinoma kolon, limfoma). c. Diare berlemak (fatty diarrhea) Sindrom malabsorpsi Penyakit mukosa (celiac sprue, whipple disease). Sindrom usus pendek, pertumbuhan bakteri berlebih diusus halus (SIBO), iskemik mesenterik. Maldigesti: insufisiensi eksokrin pankreas, konsentrasi asam empedu liminal inadequat Pendekatan diagnostic Bila dg puasa diare berkurang, biasanya disebabkan diare osmotic Adanya penurunan berat badan yg bermakna hrs diwaspadai suatu tumor kolon Anamnesis yg akurat sgt diperlukan Pemeriksaan feses: mulai dari kemungkinan telur cacing, parasit, leukosit feses, sampai analisis lemak feses 24 jam dan osmolalitas feses

Pemeriksaan darah: elektrolit ( kemungkinan hipokalemi, hiponatremi), adanya anemia krn malabsorbsi ( vit. B12, folat dan besi ), adanya hipoalbuminemia Kolonoskopi dan biopsy Penatalaksanaan Scr umum dibagi atas terapi umum / supportif dan terapi farmakologik Pentalaksanaan umum atau supportif yg dpt dilakukan yaitu: Rehidrasi : pertahankan keseimbangan cairan dan elektrolit pasien Perbaiki keadaan umum dan tanda vital : infus dan lain lain Nutrisi Penyuluhan / edukasi Penatalaksanaan farmakologik yg diberikan yaitu: 1. Antibiotik / antiparasit / anti jamur : Infeksi salmonella : chlorampenicol, kotrimoksazole, quinolon, cephalosporin. Infeksi giardiasis: metronidazole Infeksi campylobacter: kotrimoksazole, makrolide Infeksi cholera: tetracyclin Infeksi entamoeba histolitica : metronidazole 2. Obat anti diare : kaolin, diphenoxylate, codein, loperamide dll. Amebiasis is a parasitic infection caused by the protozoon Entamoeba histolytica. The parasite has 2 forms: a motile form, called the trophozoite, and a cyst form, responsible for the person-to-person transmission of infection. The trophozoite of E histolytica inhabits the large intestine to produce lesions of amebic colitis. Invasion of the colonic mucosa leads to dissemination of the organism to extracolonic sites, predominantly the liver. E. histolytica has a two-part life cycle. The protozoa enter the gastrointestinal (GI) tract as cysts during the first part of the cycle. These cysts have a cell wall made of chitin, making them resistant to gastric 6 acid in the stomach ( ). The cysts are quadrinucleated, and released four ameboid trophozoites once in the small intestine, which travel to and inhabit the colon. The trophozoite of E histolytica averages 25 mm, ranging from 10-60 mm (see following image). It has a clear ectoplasm and a somewhat granular endoplasm that contains several vacuoles. The trophozoite has a single 3-mm to 5-mm nucleus with fine peripheral

chromatin and a central nucleolus. Ingested RBCs may be present within the trophozoite.

corticosteroids, which inhibit the inflammatory process and allow E. histolytica to continue attacking the now 2 further compromised host ( ). Trophozoites in the mucosa may be able to escape the intestinal mucosa and invade the liver and brain. Entering the liver through the venous portal system, E. histolytica attacks hepatocytes and neutrophils, producing liver abscesses and causing further liver damage due to the release of 2 cytokines from the damaged neutrophils ( ). Maintenance of the airway, breathing, and circulation must be monitored at all times while in the ED. Treatment of amebic colitis involves the prescription or administration of several drugs. Patients with mild colitis (not needing intravenous [IV] fluid therapy) may be treated on an outpatient basis with metronidazole 3 (Flagyl) 750 mg orally three times daily for 10 days ( ). This treatment should be a followed by luminal agent such as the aminoglycoside paromomycin (Humatin) to destroy the cysts in the intralumen. Dosing of paromomycin is 25-35 mg/kg orally three times daily for 3 seven days ( ). Taking these two medicines at the same time is not recommended, as paromomycin may cause diarrhea and may become difficult distinguish from the 11 signs of amebic colitis ( ). The use of loperamide (Imodium) is discouraged. Loperamide slows the ability of the intestinal smooth muscles to move, allowing increased water uptake in 14 the colon for the typical diarrhea case ( ). However, decreased smooth muscle activity increases the time the luminal wall is exposed to E. histolytica, increasing the 15 chance of further amebic invasion ( ). The use of corticosteroids is discouraged as well, as these agents 1 may result in toxic megacolon ( ). Patients with severe colitis should be admitted to the 3 hospital and given intravenous (IV) hydration ( ). Normal saline with 5% dextrose may be useful for severe volume depletion as well as providing glucose lost to diarrhea. Potassium should be replaced if the patient is found to be hypokalemic because of the diarrhea. Admitted patients should receive metronidazole 500 mg 11 IV every six hours for ten days ( ). In the case of fulminant amebic colitis, broad-spectrum antibiotics should be given in addition to metronidazole, 16 particularly if intestinal perforation is suspected ( ). Ciprofloxacin (Cipro) may be given IV at 400 mg every 17 eight hours ( ).

Trophozoites begin to attach to the epithelial cells of the colon by releasing D-galactose/N-acetyl-Dglactosamine (Gal/GalNAc), which allows adherence to the epithelial 7 surface of the colon ( ). Cysteine proteinases from the trophozoite causes the mucus lining of the colon to disperse and the affected epithelial cells quickly begin to 7 lose their structure ( ). The trophozoite uses structures called amebapores to puncture the epithelial cell's 2 phospholipid bilayer, causing cytolysis ( ). Lysed cells release pre-Interleukin 1, which is degraded by amebic cysteine protease to form Interleukin-1 (IL-1), a 8 cytokine ( ). IL-1 then attaches to adjacent epithelial cells, causing them to release the cytokines 2 cycloexegenase-2 (COX-2) and Interleukin-8 (IL-8) ( ). These substances attract neutrophils, which squeeze into the intestinal lumen from the mucosa by creating a passage between the epithelial cells, providing an entryway for the amebae to enter the colonic mucosa. Neutrophils, killed when exposed to E. histolytica, release their own destructive contents and cause 2 further injury to nearby epithelial cells ( ). Trophozoites are also able to cause host cell death by causing the cell to enter apoptosis, or programmed cell death. This process adds to the ability of the ameba to invade the mucosa via channels created by macrophages called to destroy the dying epithelial cell 6 ( ). Once in the host's mucosa, the trophozoite is able to continue its tissue destruction in a lateral direction. This destruction results in an ulcer that is characteristically flask-shaped, with a wide base and a thin neck that 6 extends to the intestinal lumen ( ). This ulcer produces 2 bloody stools that are a hallmark of amebic colitis ( ). The host is at risk of developing paralytic ileus, sloughing of colonic mucosa, and perforation of the GI tract, causing fulminant amebic colitis, which has a mortality 2 rate of greater than 40% ( ). Toxic megacolon may also develop, particularly if the patient has been treated with