Dysentery comes from the Greek, namely dys (= interference) and enteron (= intestine), which means that the intestinal inflammation that cause widespread symptoms, blood mixed with feces mucus symptoms dysentery include:
• Dispose of water with bloody feces
• Diarrhea with a thin little volume
• Dispose of water mixed with feces lenders (mucus)
• pain when defecate (tenesmus)
Causes
1. Bacteria (dysentery basiler)
o Shigella, the most important cause of dysentery and tersering (± 60% of cases of dysentery, and almost all referred cases of dysentery and threaten the lives caused by Shigella Escherichia coli enteroinvasif (EIEC)
o Salmonella
o Campylobacter jejuni, especially in infants
2. Amoeba (amoeba dysentery), caused by Entamoeba hystolitica, most often in children aged> 5 years
Patofisiologi
Transmission: fecal-oral, through food / water terkontaminasi, person-to-person contact.
Dysentery basiler
Shigella and EIEC
MO -> colonization in the ileum terminalis / kolon, especially kolon invasion to intestinal cells epitel mukosa - distal> multiplikasi -> intrasel and dissemination intersel -> production enterotoksin -> ↑ camp -> hipersekresi intestine (diarrhea liquid , diarrhea sekresi). -> Production eksotoksin (Shiga toxin) -> sitotoksik -> inflammation cell infiltration -> nekrosis cells epitel mukosa -> ulkus-ulkus small -> eritrosit out to plasma and intestinal lumen -> blood mixed with feces. -> Invasion to the lamina propia? -> Bakteremia (especially in the infection S.dysenteriae serotype 1)
Salmonella
MO -> colonization in the jejunum / ileum / kolon -> invasion to intestinal cells epitel mukosa -> invasion to the lamina propia -> infiltration cellular inflammation -> Prostaglandin synthesis -> production of heat-labile cholera-like enterotoksin
invasion to plaque Peyeri -> dissemination to KGB mesenterium -> hipertrofi -> decrease in blood flow to mukosa -> nekrosis mukosa -> ulkus echo -> eritrosit and plasma to lumen exit -> blood mixed with feces.
Compylobacter
MO -> colonization in the jejunum / ileum / kolon -> invasion to intestinal cells epitel mukosa -> invasion to the lamina propia -> infiltration cellular inflammation -> Prostaglandin -> heat-stabile production of cholera-like enterotoksin -> sitotoksin production? -> Nekrosis mukosa -> ulkus -> eritrosit and plasma to lumen exit -> blood mixed with feces. -> Entrance to the circulation (bakteremia).
Dysentery amoeba
Histolitika form (trofozoit) -> invasion to intestinal cells epitel mukosa -> nekrosis network mukosa intestinal enzyme production histolisin -> invasion to the network submukosa -> ulkus amoeba -> ulkus out each other and form a sinus-related sinus submukosa -> malabsorpsi - damage the surface absorpsi> ↑ intraluminal mass -> osmotik intraluminal pressure -> osmotik diarrhea.
Symptoms-Symptoms
Dysentery basiler
• Diarrhea is accompanied by sudden blood and mucus in the feces. On dysentery shigellosis, at the beginning of pain, watery diarrhea can be found in the blood without first 6-24 hours, and after 12-72 hours after the beginning of pain, blood and mucus was found in the feces.
• Summer High (39.50 - 400 C), appear toxic.
• Vomiting, vomiting.
• Anoreksia.
• Pain Management in the stomach cramps and pain in the anus while CHAPTER.
• Sometimes accompanied with symptoms resembling encephalitis and sepsis (cramps, headache, letargi, rigid cervix, halusinasi).
Dysentery amoeba
• Diarrhea with blood and mucus in the feces.
• Frequency CHAPTER generally less than dysentery basiler (≤ 10x/hari)
• severe stomach Pain Management (kolik)
• constitutional symptoms usually do not have (only found in the hot 1 / 3 cases).
Diagnosis
Clinical diagnosis can ditegakkan simply find excrement mixed with blood. Diagnosis is usually difficult ditegakkan etiology. Etiology of diagnosed through clinical picture alone is difficult, while the feces culture examination for the agency is often the cause need not be done because it takes a long time (at least 2 days) and symptoms generally improve with empirical antibiotic therapy.
Supplementary examination can be done:
• Vetting feces
o Makroskopis: a dysentery amoeba can ditegakkan when found in the feces of trofozoit
o Benzidin test
o microscopic: fecal leukosit (indication of kolitis), fecal blood.
• feces culture:
o Media: so MacConkey, xylose-lysine deoxycholate (XLD), to SS.
• Routine blood examination: leukositosis (5,000 - 15,000 sel/mm3), sometimes can be found leucopenia.
Complications
1. Dehydration
2. Electrolyte disturbances, especially hiponatremia
3. Strain
4. Protein Loosing enteropathy
5. Sepsis and DIC
6. Sindoma Hemolitik Uremik
7. Malnutrition / malabsorpsi
8. Hipoglikemia
9. Prolapsus rektum
10. Reactive arthritis
11. Guillain-Barre syndrome
12. Ameboma
13. Toxic megacolon
14. Local perforation
15. Peritonitis
Treatment
1. Note the general condition of children, if children appear toxic, less nutritional status, do the examination of blood (if possible accompanied by blood culture) to detect the existence of bakteremia. If there is suspected sepsis, provide appropriate therapy penatalaksanaan sepsis in children. Waspadai of sepsis shock. 2. Component therapy dysentery: a. Correction and maintenance fluid and electrolyte. b. C. Diet Antibiotics d. Sanitation
Ad. a. Correction and maintenance fluid and electrolyte
As in the cases of acute diarrhea in general, the first thing that must be considered in penatalaksanaan dysentery after assessment of the situation is stable and the corrections to the status hidrasi and electrolyte balance.
Ad. b. Diet
Children with dysentery should be the provision of food. Provide high-calorie soft diet and protein to prevent malnutrition. Single high dose of vitamin A (200,000 IU) can be given to lower levels of illness dysentery, especially in children suspected of having defisiensi. To shorten the illness, can be given sinbiotik preparation and zinc oral8, 9. In the provision of medicines, must be observed that drugs that slow the intestinal motilitas should not be because of the risk to extend the period of illness.
Ad. c. Antibiotics
• Children with dysentery should have suspected shigellosis and get the appropriate therapy. Treatment with appropriate antibiotics will reduce the pain and decrease the risk of complications and death. • Options for the main Shigelosis (according to the WHO recommendation): Kotrimokasazol (trimetoprim 10mg/kbBB/hari and sulfametoksazol 50mg/kgBB/hari) in 2 divided doses, for 5 days. • From the results of the research, the difference is not obtained the benefit of kotrimoksazol compared placebo10. • The alternatives can be provided: o Ampisilin 100mg/kgBB/hari divided in 4 doses o Cefixime 8mg/kgBB/hari divided in 2 doses 50mg/kgBB/hari o Ceftriaxone, single-dose IV or IM o acid nalidiksat 55mg/kgBB/hari divided in 4 doses. • Repairs should appear in 2 hours, for example, heat down, pain and blood in the feces decreased, CHAPTER reduced frequency, etc.. In 2 days if not improvement, antibiotics should be discontinued and replaced with alternatives. • Terapi antiamubik with the indications given: o Found trofozoit Entamoeba hystolistica in microscopic feces. o bloody feces settling after therapy with 2 antibiotics successively (each given for 2 days), which is usually effective for dysentery basiler. • Terapi selected as intestinal antiamubik on children is Metronidazol 30-50mg/kgBB/hari in 3 divided doses for 10 days. When the dysentery caused by E. hystolistica, akan situation improved in 2-3 days therapy.
Ad. d. Sanitation
Tell children to parents to always wash hands with clean postwar clean up feces to prevent children autoinfeksi.
