4. Ge Dan Demam Tifoid

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BAHANKULIAHGASTROENTERITIS

TYPHOID FEVER

Dr. H. Syafruddin A.R. LelosutanSubGastroenterologi-Hepatologi Dep. Peny. Dalam

RSPAD Gatot Soebroto Jakarta.___________________________________________


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(Lambung)

(Usus halus)

(Usus besar)


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( TOPIK I )


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MUNCULAN KLINIS :

DIARRHOEA (mencret)

VOMITING (muntah)

ABDOMINAL PAIN (nyeri perut)

Mengikuti konsumsi makanan atau

minuman yang terkontaminasi :


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PENYEBAB

Penyebab Gastroenteritis :

BACTERIA

VIRUSES

PROTOZOA

Salmonella typhimurium/paratyphi A & BSalmonella enteritidis/choleraesuis

Shigella dysenteriae, flexneri, sonnei, boydiiClostridia perfringens, botulinumStaphylococcus aureus, Helicobacter sp.E. coli, Bacillus cereus, Y. enterocoliticaVibrio cholerae

Rotavirus,AdenovirusNorwalk agent

CryptosporidiosisGiardia lamblia

Entamoeba histolytica


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GAMBARAN KLINIS

RINGAN :

mencret-mencret untuk beberapa hari

BERAT :

mencret, muntah nyeri perut

dehidrasi

(gastroenteritis dehidrasi)


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SALMONELLOSIS

Taxonomy :

SALMONELLAE sp. : 2000 serotypes

Human infection :

S. entericasubspesies 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,34thEdition. A Lange medicalbook Intl Ed. 1995;1173-9.

(Infections caused by Gram-negative bacteria)


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Clinical Patterns of Infection

1. Enteric fever (typhoid fever), due toserotype typhi.

2. Acute enterocolitis, caused by serotypetyphimurium.

3. Septicemic type, due to serotypecholeraesuis, characterized by :

- bacteremia

- focal lesionsThis is responsible for 75% of reported cases of food poisoning in UK

How in INDONESIA ?


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( ENTERIC FEVER )

HAYES, et al. Churchills Pocketbook of Medicine 3rdEdition.Churchill Livingstone. China, 2002.

( TOPIK II )


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Science basics

____________________________

ETIOLOGY :

Gram-negative bacilli :

Salmonella typhi


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Science basics

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EPIDEMIOLOGY :

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.

Often there is a history of recent travel to endemic areas.


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Science basics

____________________________

PATHOGENESIS :

INGESTIONTHE ORGANISMSWith foodstuffs(contaminated)

Intestinal wall or MUCOSA OFTHE GI TRACT

penetrating

RETICULOENDOTHELIALCELLS, invade mesentericLymphnodes and the spleen.Principally in the lymphoid tissueof the small intestine.

to be taken up~

ORGANISMS

MULTIPLY, dis-seminate to theLungs, GB, Kid-eys, CNS

Incubation period 5-14 up to 18 days.

Peyers patches

become inflamed andulcerate.


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Science basics

____________________________

CLINICAL CLASSIFICATIONS :

1. Septicaemic spread then occurs

throughout the body

2. Enteritis typhus abdominalis

3. Carriers the Gall bladder may act

as a reservoir forongoing infections


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GAMBARAN KLINIS

____________________________

SUBJECTIVES :

1. Headache (nonspecific)

2. Dry cough, sore throat

3. Lethargy, malaise

4. Abdominal pain

5. Pyrexia stepwise fashion fever

6. Confusion

Prodromal stage :


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GAMBARAN KLINIS

____________________________ OBJECTIVES :

1. Macular rose spots (the trunk rash or pink papule)2. Relative bradycardia, dicrotic pulse

3. Meningismus4. Splenomegaly, abdominal distension5. Constipation, or pea soup diarrhea6. If untreated, deteriorates with :

- dehydration- doughy abdomen- GI bleeding- possible perforation


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GAMBARAN KLINIS

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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 largelysuperceded by ELISA

4. Bone marrow culture


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TIPE KLINIS TANDA VITAL

Incubationperiode Week1

Week2 Week3 Week4 Chronicperiode

--- Blood pressure --- Temperature

--- Pulse

Tripple Cross

Normal

High

PATHOGENESIS :

10-12 daysS. Typhi MouthPeyers patch

Blood stream V.VeleaIntestinePeyers patch

Small intestine :Plaque Peyeri Necrosis separation of slough Perforation

or healing ( ulceration, hemorrhagesup to perforation ) or healed

Relaps or

Carrier

(Stepwise fashion fever)


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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, Pea-soup 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


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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)


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Widal Test

INTERPRETATION :

Titer O (somatic) :

(+) 1/160 or more : INFEKSI AKTIF

Titer H (flagella) :

(+) 1/160 or more : PERNAH DI VAKSINASIATAU PASCA INFEKSI

Titer Vi (+) : Carriers (+)

Kaniawati M. Panel Pemeriksaan Laboratorium untuk Demam.Forum Dignosticum No. 4/1996. LK Prodia, 2002.


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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, Meningitisand Psychosis.


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PROGNOSIS

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Mortality rate : about 2% in treated cases

With complications : poorly

Relapses occur in up to 15% of cases

Elderly or debilitated persons : poorly


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PENCEGAHAN

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Immunization is not always effective

Adequate waste disposal and protection offood and water supplies fromcontamination

Carriers must not be permitted to work asfood handlers


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PENATALAKSANAAN

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DIAGNOSTICS (Pemeriksaan diagnostik):

1. Base data : clinically and laboratory investigations

2. Ultrasound

3. GI Endoscopies

DIFFERENTIAL DIAGNOSIS :

1. Other GI illnesses,like : ileitis, colitis ulserative, gastroduodenitis,

pancreatitis2. Other infections that have few localizing findings,

like : Tbc, endocarditis, viral hepatitis, malaria, amebiasis,brucellosis, lymphoma, Q fever.


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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 needcholecystectomy.

PENATALAKSANAAN

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


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PENATALAKSANAAN

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EDUCATIONAL (penyuluhan) :

- Cost benefit and effectiveness

- Pathogenesis- Prevention

- On step management

- Prognosis

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