4. Ge Dan Demam Tifoid

Dr. H. Syafruddin A.R. Lelosutan SubGastroenterologi-Hepatologi Dep. Peny. Dalam RSPAD Gatot Soebroto – Jakarta. ___________________________________________

BAHAN KULIAH GASTROENTERITIS TYPHOID FEVER

(Lambung)

(Usus halus)

(Usus besar)

( TOPIK I )

MUNCULAN KLINIS :  DIARRHOEA (mencret)  VOMITING (muntah)  ABDOMINAL PAIN (nyeri perut) Mengikuti konsumsi makanan atau minuman yang terkontaminasi :

PENYEBAB  Penyebab Gastroenteritis : BACTERIA

VIRUSES

PROTOZOA

Salmonella typhimurium/paratyphi A & B Salmonella enteritidis/choleraesuis Shigella dysenteriae, flexneri, sonnei, boydii Clostridia perfringens, botulinum Staphylococcus aureus, Helicobacter sp. E. coli, Bacillus cereus, Y. enterocolitica Vibrio cholerae Rotavirus, Adenovirus Norwalk agent Cryptosporidiosis Giardia lamblia Entamoeba histolytica

GAMBARAN KLINIS  RINGAN : mencret-mencret untuk beberapa hari

 BERAT : mencret, muntah nyeri perut  dehidrasi

(gastroenteritis dehidrasi)

SALMONELLOSIS (Infections caused by Gram-negative bacteria)

 Taxonomy :  SALMONELLAE sp. : 2000 serotypes  Human infection :  S. enterica subspesies enterica  which three serotypes : 1. S. typhi 2. S. typhimurium (S. paratyphi A and B), now called : S. schottmulleri 3. S. choleraesuis CHAMBERS. Infectious Diseases. In: Lawrence, et al. Current MD&T, 34th Edition. A Lange medicalbook Int’l Ed. 1995;1173-9.

Clinical Patterns of Infection 1. Enteric fever (typhoid fever), due to serotype typhi. 2. Acute enterocolitis, caused by serotype typhimurium. 3. Septicemic type, due to serotype choleraesuis, characterized by : bacteremia focal lesions This is responsible for 75% of reported cases of food poisoning in UK How in INDONESIA ?

( ENTERIC FEVER ) ( TOPIK II )

HAYES, et al. Churchill’s Pocketbook of Medicine 3rd Edition. Churchill Livingstone. China, 2002.

Science basics ____________________________  ETIOLOGY :  Gram-negative bacilli : Salmonella typhi

Science basics ____________________________  EPIDEMIOLOGY : Often there is a history of recent travel to endemic areas.

 Penyebaran dari manusia ke manusia khususnya pada kondisi : 1. Higiene – sanitasi buruk 2. Makanan dan atau minuman terkontaminasi salmonela (contaminated food or drink)  Occurs sporadically or in epidemics.

Science basics ____________________________  PATHOGENESIS : 

INGESTION THE ORGANISMS With foodstuffs (contaminated)

Intestinal wall or MUCOSA OF THE GI TRACT penetrating

ORGANISMS MULTIPLY, disseminate to the Lungs, GB, Kideys, CNS



Peyer’s patches become inflamed and ulcerate.

~

to be taken up

RETICULOENDOTHELIAL CELLS, invade mesenteric Lymphnodes and the spleen. Principally in the lymphoid tissue of the small intestine.

Incubation period 5-14 up to 18 days.

Science basics ____________________________  CLINICAL CLASSIFICATIONS : 1. Septicaemic 2. Enteritis 3. Carriers

 



spread then occurs throughout the body typhus abdominalis the Gall bladder may act as a reservoir for ongoing infections

GAMBARAN KLINIS ____________________________  SUBJECTIVES : 

1. 2. 3. 4. 5. 6.

Prodromal stage :

Headache (nonspecific) Dry cough, sore throat Lethargy, malaise Abdominal pain Pyrexia  stepwise fashion fever Confusion

GAMBARAN KLINIS ____________________________  OBJECTIVES : 1. 2. 3. 4. 5. 6.

Macular rose spots (the trunk rash or pink papule) Relative bradycardia, dicrotic pulse Meningismus Splenomegaly, abdominal distension Constipation, or “pea soup” diarrhea If untreated, deteriorates with : dehydration doughy abdomen GI bleeding possible perforation

GAMBARAN KLINIS ____________________________  INVESTIGATION : 1. Neutropenia 2. Blood, urine, rose spot and stool culture 3. Serological tests (Widal test)  to both the O and H antigens of the organism have been largely superceded by ELISA 4. Bone marrow culture

TIPE KLINIS TANDA VITAL (Stepwise fashion fever)

PATHOGENESIS : High

Small intestine : Plaque Peyeri  Necrosis Incubation Week1 periode 10-12 days S. Typhi  Mouth  Peyer’s patch  Blood stream  V.Velea  Intestine  Peyer’s patch

 separation of slough  Perforation or healing  ( ulceration, hemorrhages up to perforation )  or healed Week2 Week3 Week4 Chronic periode Relaps or Carrier Tripple Cross

Normal --- Blood pressure

--- Temperature --- Pulse

MANIFESTASI KLINIS  WEEK 1

: Pulse slow, smooth, lower. Postration, Diarrhea or Constipation, Abd. Distension, Bronchitis, Epistaxis, Rose Spots. Blood culture (+), O(-).

 WEEK 2

: Pulse increased, Blood pressure decreased, Toxemia, Delirium, Peasoup stool, typhoid tongue. Stool culture (+), O (+)

 WEEK 3

: Typhoid state, Stupor, Delirium, Muscular twitching, Meningismus, Hemorrhages, Perforation. Urine culture (+), O (++), H(+)  WEEK 4 : Healed or Die, or Sequellae (cholecystitis, periostitis, osteomyelitis, orchitis). Bone marrow culture (+), O (+++), H (++).

 CHRONIC PERIODE

: Sequellae

PEMERIKSAAN LABORATORIUM  HEMATOLOGY : Leukopenia : 3000-4000 Leukositosis : complication (+)  BLOOD CULTUR : Gall culture, Bismuth Sulphate W&B, Salmonella-Shigella Mc Conkey jelly  WIDAL TEST (Serologic methode)

Widal Test  INTERPRETATION : Titer O (somatic) : (+) 1/160 or more : INFEKSI AKTIF Titer H (flagella) : (+) 1/160 or more : PERNAH DI VAKSINASI ATAU PASCA INFEKSI Titer Vi (+) : Carriers (+) Kaniawati M. Panel Pemeriksaan Laboratorium untuk Demam. Forum Dignosticum No. 4/1996. LK Prodia, 2002.

KOMPLIKASI ____________________________  Occur in about 30% of untreated cases  Account for 75% of all deaths  Intestinal hemorrhage, manifested by : sudden drop in temperature signs of shock dark or fresh blood in the stool  Intestinal perforation, accompanied by : abdominal pain and tenderness  Urinary retention, Pneumonia, Myocarditis, Cholecystitis, Thrombophlebitis, Nephritis, Osteomyelitis, Meningitis and Psychosis.

PROGNOSIS ____________________________  Mortality rate : about 2% in treated cases  With complications : poorly  Relapses occur in up to 15% of cases  Elderly or debilitated persons : poorly

PENCEGAHAN ____________________________  Immunization is not always effective  Adequate waste disposal and protection of food and water supplies from contamination  Carriers must not be permitted to work as food handlers

PENATALAKSANAAN ____________________________  DIAGNOSTICS (Pemeriksaan diagnostik): 1.

Base data : clinically and laboratory investigations

2. 3.

Ultrasound GI Endoscopies

DIFFERENTIAL DIAGNOSIS : 1. Other GI illnesses, like : ileitis, colitis ulserative, gastroduodenitis, pancreatitis 2. Other infections that have few localizing findings, like : Tbc, endocarditis, viral hepatitis, malaria, amebiasis, brucellosis, lymphoma, Q fever.

PENATALAKSANAAN ____________________________  THERAPEUTICS (Pengobatan): 1.

Barrier nursing

2.

Rehydration

3.

Antibiotics : Drug of choice : Ciprofloxacin 200 mg bd iv, or 750 bd orally. Alternatives : - Chloramphenicol 500 mg 4-hourly, - Amoxicillin 500 mg 6-hourly - Cotrimoxazole 960 mg 12-hourly for two weeks (iv. initially) - Ceftriaxone 2 g once a day  Recommended duration of therapy are 2 – 4 weeks.

4.

Carriers can be treated with Ciprofloxacin 500 mg bd but may need cholecystectomy.

HAYES, et al. Churchill’s Pocketbook of Medicine 3rd Edition. Churchill Livingstone. China, 2002.

PENATALAKSANAAN ____________________________  EDUCATIONAL (penyuluhan) : -

Cost benefit and effectiveness Pathogenesis Prevention On step management Prognosis