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    PEDIATRICS

    GASTROENTEROLOGY

    Atan Baas SinuhajiSub Division of Pediatrics Gastroentero-Hepatology

    Department of ChildHealthSchool of Medicine

    University of North Sumatera

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    PEDIATRICSGASTROENTEROLOGY

    SYSTEMATIC PROBLEM

    BASED

    FUNCTION

    DIGESTIVESYSTEM

    MAJOR SIGNS

    &SYMPTOMS

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    DIGESTIVE SYSTEM

    PERITONEUM

    - ORAL CAVITY- GI TRACT (ESOPHAGUS ANAL)

    DIGESTIVE GLANDS SAL IVA RY GLA NDS LIVER & B ILE DUCT PANCREAS

    DIGESTIVE TRACT

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    MAJOR SIGNS SYMPTOMS

    1. DIARRHOEA2. VOMITING

    3. FAILURE TOTHRIVE4. JAUNDICE5. ENCEPHALOPATHY6. DISORDERS OF

    INGESTION

    7. ABDOMINAL PAIN8. ABDOMINAL

    DISTENSION9. CONSTIPATION10. GASTROINTESTINAL

    HEMORRHAGE

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    FUNCTION

    1. EATING & DRINKING2. TRANSPORT3. DIGESTION &

    ABSORPTION4. DEFENSE5. ENDOCRINE

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    HOST EFENSE

    IMMUNOLOGIC

    NON IMMUNOLOGIC

    GALT

    -MUCOSE-GASTRIC ACID-MUCUS

    -MOTILITY-MICROFLORA

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    GALT(GUT ASSOCIATED LYMPHOID TISSUE)

    SCATTERED AGGREGATES

    PEYERS PATCHES

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    MOTILITY

    CONTRACTION MOVEMENT

    RESTING NON RESTING MIXING PROPULSION

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    MOTILITY

    DISORDERS

    ESOPH.DYSMOTILITY

    CHESTPAIN

    DD :1.GER *2.ANGINA3.MUSKULOSCLETAL

    GASTROPARESIS

    - DELAYED GASTRIC EMPTYING- DYSPEPTIC- ABSENCE OF PERISTALSIS

    CHRONIC INT. PSEUDOOBSTRUCTION-NAUSEA & VOMITING-DISTENTION-ABDOMINAL PAIN-CONSTIPATION

    * GER = Gastro Esophageal Reflux

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    FEEDING

    EATING DRINKING -TO CARRY

    -TO BRING-TO SUCK-TO TASTE-TO MASTICATE-TO SWALLOW

    LIQUID

    SOLID

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    FEEDING

    ENTERAL PARENTERAL( I . V )

    ORAL TUBE

    OSTOMY NON OSTOMY

    - GASTROSTOMY

    - ILEOSTOMY

    NASOGASTRIC TUBE

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    PARENTERAL FEEDING

    ENTERAL STARVATION

    CHOLESTASISINTESTINAL ATROPHY

    COLON

    70 %INTRALUMINAL

    30 %INTRAVASAL

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    FLORA

    SMALL INTESTINE COLON

    AEROB > ANAEROB

    1. HOST DEFENSE2. MATURATION OF GUT IMMUNE3. NUTRITION

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    1. DIET2. ANTIMICROBIAL3. IMPAIRED OF GASTRIC

    ACIDITY4. MOTILITY DISORDER5. ILEOCAECAL SPHINCTER

    6. PCM7. ANATOMICAL

    CHANGING OFINTESTINAL FLORA

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    BIOTIC

    ANTI PRO PRE SYN (EU)

    FRUCTO-OLIGOSACCHARIDE

    LACTOBACILLUS BIFIDOBACTERIUM

    DYS

    IMBALANCE

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    DYSBIOTIC

    IMBALANCE

    M.O PATHOGEN M.O NON PATHOGEN

    DISEASES

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    PROBIOTIC

    LIVE MICROORGANISMS

    SUPPLEMENTAL FOOD

    BENEFICIALLY AFFECT THE HOST

    MICROBIAL BALANCE

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    DIGESTION

    BREAK DOWN

    DIETARY FOOD

    - PHYSIS- CHEMICAL - MECHANICAL

    SMALLER PARTICLES&

    CAN BE ABSORBED

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    DIGESTION

    INTRALUMINAL-PANCREAS

    -LIVER-STOMACH

    INTRACELLULAR- PEPTIDASE

    - LIPASE

    MEMBRANE- SUCRASE- MALTASE- LACTASE- GLUCOAMYLASE

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    ABSORPTION

    TRANSPORT OF WATEROR

    DIGESTIVE PRODUCTS

    LUMEN

    MUCOSA

    VESSELS BLOOD

    LYMPH

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    MUCOSA

    TRANSCELLULAR PARACELLULAR

    LUMINALMEMBRANE

    TIGHT JUNCTION

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    DIGESTION - ABSORPTION

    INTRALUMINAL DIGESTION

    PARACELLULAR

    INTERCELLULAR

    SPACE

    TRANSCELLULAR

    MEMBR. DIGESTION

    CELLULAR UPTAKE

    INTRACELL. DIGESTION

    BASOLAT. MEMBRANE

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    INTERCELLULAR SPACE

    BASEMENT MEMBRANE

    INTERSTITIAL SPACE

    (LAMINA PROPIA)

    VESSELS - BLOOD

    - LYMPH

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    TRANSCELLULAR PARACELLULAR

    1

    2

    4 3 5

    6 7

    1. LUMINAL MEMBRANE2. TIGHT JUNCTION3. BASOLATERAL

    MEMBRANE

    4. INTERCELLULAR SPACE5. BASEMENT MEMBRANE6. LAMINA PROPRIA7. VESSELS (BLOOD /

    LYMPH)

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    DIARE AKUTPADA BAYI DAN ANAK

    ATAN BAAS SINUHAJI

    BAGIAN ILMU KESEHATAN ANAK

    FAKULTAS KEDOKTERAN UNIVERSITAS SUMATERA UTARARS H ADAM MALIK MEDAN

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    DIARE

    VOLUME AIR TINJA

    LEMBEK CAIR

    (WATERY) (LOOSE)

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    AIR

    HIPERSEKRESI

    MALABSORBSIMALDIGESTI

    HIPEROSMOLARPERISTALSISAREA OBSORBSI

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    DIARE

    - FREK. 3X /HARI - PERUB. KONSISTENSI- DGN / TANPA MUNTAH- DGN/TANPA DARAH

    DIARE CAIRAKUT

    (ACUTEWATERY

    DIARRHOEA)

    DISENTERI(DYSENTERY

    FORM)PERSISTEN

    < 14 HARI MENCRETBERDARAH > 14 HARI

    MALNUTRISIBERAT

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    BAYI YANG HANYA MINUM ASI SERINGKALI FREKUENSI B.A.B. 5-6x/HARI

    TETAPI KONSISTENSI TINJANYA BAIK

    BUKAN DIARE

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    DIARE

    RADANG

    NON RADANG

    INFEKSI - VIRUS- JAMUR

    - BAKTERI- PARASIT

    NON INFEKSI - ALLERGI- DLL

    - HORMONAL- ANATOMI- DLL

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    VIRUS PENYEBAB DIARE

    1. ROTAVIRUS 6 BLN s/d 2.5 TAHUN2. NORWALK VIRUS3. ENTERIC ADENOVIRUS4. ASTROVIRUS5. CALICI VIRUS6. CORONA VIRUS7. SMALL ROUND VIRUS

    - PARVOVIRUS LIKE AGENT- MINI ROTAVIRUS- MINI REOVIRUS

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    DALAM PRAKTEK SEHARI-HARI

    - SETIAP MENCRET CAIR 3x/HR,

    DGN/TANPA MUNTAH,

    DGN/TANPA LENDIR/DARAH

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    KLASIFIKASI

    1. USIA2. LAMA DIARE3. PENYEBAB4. BERAT - RINGAN5. PATOGENESIS6. DAYA TAHAN TUBUH7. PEROLEHAN8. KEJADIAN9. LOKALISASI KELAINAN10. WHO (2005)

    1 USIA

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    1.USIA

    -NEONATAL DIARRHOEA : DIARE PD NEONATUS

    -INFANTILE DIARRHOEA : DIARE PD INFANT

    -CHILDHOOD DIARRHOEA : DIARE PD ANAK

    2. LAMA DIARE

    -DIARE AKUT : < 7 HR (90-95%)

    -DIARE BERKEPANJANGAN (PROLONGED) : 7-14 HR

    -DIARE KRONIK : > 14 HR

    3. PENYEBAB-RADANG : INFEKSI / NON INFEKSI

    -NON RADANG

    4 BERAT RINGAN ( WHO 1984)

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    4. BERAT RINGAN ( WHO, 1984)

    -DIARE RINGAN : < 1x / 2 JAM atau < 5cc / KgBB / JAM

    -DIARE BERAT : > 1x / 2 JAM atau > 5 cc/KgBB/JAM

    5.DAYA TAHAN TUBUH

    -IMMUNOCOMPETENT : DAYA TAHAN TUBUH BAIK

    -IMMUNOCOMPROMISED : DAYA TAHAN TUBUH

    TERGANGGU ( MIS. AIDS )

    6. PEROLEHAN

    -NOSOCOMIAL : INFEKSI DI DAPAT DI RUMAH SAKIT

    -COMMUNITY : INFEKSI DI DAPAT DI MASYARAKAT

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    8. KEJADIAN

    -ENDEMIC : SEPANJANG THN DIJUMPAI

    -EPIDEMIC : ADA LETUSAN-LETUSAN

    -CAMPURAN : SEPANJANG THN DIJUMPAIDISERTAI LETUSAN-LETUSAN

    9. LOKALISASI KELAINAN

    -USUS HALUS : CHOLERA, ETEC, ROTAVIRUS &G. LAMBLIA DIARRHOEA

    -USUS BESAR : SHIGELLOSIS, AMOEBIASIS-KEDUANYA : CAMPYLOBACTERIOSIS,

    SALMONELLOSIS

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    10. WHO (2005)

    -DIARE CAIR AKUT-DIARE PERSISTEN

    -DIARE DISENTERI

    -DIARE DENGAN MALNUTRISI BERAT

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    MIKRO ORGANISME

    GASTRIC BARRIER

    MULTIPLIKASI

    KOLONISASIADHEREN

    - INVASI- DAMAGE

    ENTEROTOXIN

    MALABSORPSIHIPERSEKRESI

    HIPERPERISTALIS

    DIARE

    PATOGENESIS DIARE INFEKSI AKUT

    COLONIC SALVAGE

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    DIARE

    Membersihkan Bahan Patogen

    Pertahanan

    Self Limited

    Kehilangan Air dan Elektrolit Makanan

    Air dan Elektrolit Makanan

    Dehidrasi HipoglikemiaStarvationMalnutrisi

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    DI

    ARE

    AIR DEHIDRASI

    BASA ASIDOSIS METAB

    MAKANAN - HIPOGLIKEMIA- STARVATION- PCM

    RUSAKMUKOSA

    - MALABSORPSI- ENTEROPATI

    HILANG PROT.- SENSITISASI

    - NEC

    ELEKTROLIT Na+ ==> atau

    K+ ==> Ca2+ ==> Mg2+ ==> Zn ==> ACRODERMATITIS ENTEROPATHICA

    ELEKTROLIT Na+ atau

    K+ Ca2+ ==> TETANIMg2+ ==> TETANIZn ==>ACRODERMATITIS ENTEROPATHICA

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    TETANY

    HYPOCALCEMIC

    HYPOMAGNESEMIC

    ALKALOTIC

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    KEHILANGAN AIR VIA TINJA

    DEHIDRASI

    AIR PLASMA

    DEMAM HEMOKONSENTRASI HIPOVOLEMIA

    RENJATAN RBF SYMPATH. DISCHARGE

    - HEART RATE- VASOKONSTRIKSI

    KOMA ARF

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    TANDA DEHIDRASI

    1. GELISAH S/DKOMA

    2. UUB CEKUNG

    3. MATA CEKUNG4. AIR MATA KERING5. BIBIR KERING6. HR

    7. HIPOTENSI8. POLS HALUS9. OLIGURIA/ANURIA

    10. TURGOR11. UJUNG JARI

    DINGIN12. BB

    DEHIDRASI

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    DEHIDRASI

    VOLUME NATRIUM PLASMA

    DEHIDRASI RINGAN- SEDANG

    = 5 - 10 % BB DEHIDRASI BERAT

    > 10% BB

    ISONATREMIA= 135 - 150 mEq/L

    HIPO/HIPER NATREMIA

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    TUJUAN PENGOBATAN PENDERITA DIARE

    DEHIDRASI KURANG KALORIPROTEIN

    AIR & ELEKTROLIT PEMBERIANMAKANAN

    PENCEGAHAN PENGOBATAN

    LAMA, BERAT,EPISODE

    ZINK

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    TATA LAKSANA

    PEMERIKSAAN PENGOBATAN

    1. Derajat Dehidrasi2. Problem Lain :

    Malnutrisi Pneumonia dll

    1. Air & elektrolit2. Makanan3. Obat-obatan

    - Zink- anti mikroba- Simptomatis-

    DERAJAT DEHIDRASI (WHO 2005)

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    TANPADEHIDRASI

    DEHIDRASIRINGAN -SEDANG

    DEHIDRASIBERAT

    KEADAANUMUM

    BAIK GELISAH /REWEL

    LESU, LUNGLAI,KOMA

    MATA NORMAL CEKUNG CEKUNG

    HAUS NORMAL HAUS TIDAK BISAMINUM

    TURGOR NORMAL KURANG JELEK

    NB : 1. PEMBACAAN DARI KANAN KE KIRI2. DISEBUT DEH. BERAT ATAU RINGAN SEDANG BILA DIJUMPAI

    MINIMAL 2 TANDA.

    DERAJAT DEHIDRASI (WHO, 2005)

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    TERAPI CAIRAN

    REHIDRASI PEMELIHARAAN

    INISIAL REPLETION NORMAL

    HOLLIDAY SEGAR

    TAMPUNG

    ABNORMAL+

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    REHIDRASI

    ORAL

    ORALIT

    I.V.

    RINGER LAKTAT

    RINGER ASETAT

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    KH

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    Na +

    2K +

    LAMINAPROPRIA

    BASEMENTMEMBRANE

    3Na +

    ENTEROSIT

    LUMEN KH Peptida A.Amino

    Na + air

    PEMBULUH DARAH

    MEKANISME KERJA ORALIT

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    ORALIT (WHO)

    LAMA(mmol/L)

    BARU(mmol/L)

    Na 90 75K 20 20Cl 80 65Sitrat 10 10

    Glukosa 111 75311 245

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    KEUNTUNGAN ORALIT (WHO, BARU)

    STOOL OUTPUT = 20%

    MUNTAH = 30%KEBUTUHAN CAIRAN IV = 33%

    L U P D

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    LUMEN USUS P. D ARAH

    DIARE

    LARUTAN GULA

    LARUTAN GARAM

    LARUTAN GARAM-GULA

    INDIKASI I V

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    INDIKASI I.V1. DEHIDRASI BERAT DGN/TANPA

    RENJATAN2. MENCRET HEBAT

    3. MASUKAN PER ORAL4. MALABSORPSI GLUKOSA5. DISTENSI ABDOMEN / OBSTR.

    PARALITIK6. OLIGURIA / ANURIA YANG

    BERLARUT-LARUT

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    DEHIDRASI

    TANPA RINGAN - SEDANG BERAT

    < 5% 5 - 10% > 10%

    A B C

    A TANPA DEHIDRASI

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    A. TANPA DEHIDRASI

    1. ORALIT

    1 Thn = 50 - 100 CC / X Mencret > 1 Th = 100 - 200 CC/ X Mencret

    2. MINUM/MAKAN LBH BANYAK DARI BIASA

    MENCEGAH JANGAN

    TIMBUL DEHIDRASI

    3. ZINK 10 20 mg/hari10 - 14 hari

    B DEHIDRASI RINGAN SDG

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    B. DEHIDRASI RINGAN -SDG

    ORALIT 75 CC/kg BB /3 a 4 jam

    INDIKASI

    Ringer Laktat Ringer Asetat

    C DEHIDRASI BERAT

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    C. DEHIDRASI BERAT

    100 CC/ kgBB/3-6 jam

    < 1 Thn * initial = 30 CC/kgBB/ 1 jam* repletion= 70 cc/kgBB/5 jam

    > 1 Thn * initial = 30 cc/kgBB/ jam* repletion = 70 cc/kgBB/2

    jam

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    ORALIT

    PREVENTION

    TREATMENT MAINTENANCE

    DEHIDRASI DIARE

    DIARE

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    REHIDRASI

    ANURIA/OLIGURIA URINCUKUP *

    RENALFAILURE

    PHYSIOLOGICOLIGURIA

    TIDAKPERSOALAN

    CAIRAN CAIRAN

    NB : 1. * 1 cc / kg BB / jam2. Oliguria : < 400 cc / m 2 / hari

    R l Ph i l i

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    Fractionalexcretion

    of Na+

    %100

    plasmaurin/Cr..Cr

    plasmaurin/Na Na

    RenalFailure

    PhysiologicOliguria

    Lasix diuresis (-) diuresis (+)

    Laboratorium

    Urine osmolality(mOsm/kgH 2O)500

    Na + urin (mEq/l) > 40 1%

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    PEMBERIAN MAKANAN

    SETELAH REHIDRASI

    TIDAK MEMPERBERAT /

    MENIMBULKAN DIARE

    UJI TOLERANSI

    ASI SUB BAGIAN GE BIKA FKUSU: SUSU FORMULA DISTOP USIA 4 -6 BLN : MAKANAN PENDAMPING ASI PROBLEM: USIA < 4 BLN & ASI ( -)

    MTBS : SUSU FORMULA ( -)

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    BUKU MANAJEMEN TERPADU BALITA SAKIT (MTBS) WHO

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    ANTIMIKROBA

    1. Kolera

    2. Disenteri Sigella3. Amubiasis4. Giardiasis

    Diare Akut(WHO)

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    ANTIMIKROBA (WHO)

    1. KOLERA TETRASIKLIN 12,5 mg/Kg BB - 4 x sehari

    3 hari

    2. DISENTERI BASILLER 5 mg TMP + 25 mg SMX/Kg BB - 2 x sehari

    5 hari

    3. AMUBIASIS METRONIDAZOLE 10mg/Kg BB - 3 x sehari

    5 hari

    4. GIARDIASIS METRONIDAZOLE 5 mg / Kg BB - 3 x sehari5 hari

    EFEK SAMPING ANTIMIKROBA

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    EFEK SAMPING ANTIMIKROBA

    1. PERUBAHAN FLORA USUS2. OVERGROWTH:

    - MONILIA- ENTEROCOCCUS

    - ANAEROB- PSEUDOMONAS

    3. KERUSAKAN MUKOSA USUS4. IRITASI5. PSEUDOMEMBRANOUS ENTEROCOLITIS6. BLOOD DYSCRASIA7. MUNTAH

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    ANTIDIARRHOEAL (United States F.D.A)

    1. Bowel Movement2. Stool Consistency3. Cramps

    A drug that can be shown by objective

    measurement to treat or control the symptomsof diarrhea

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    1.ANTI MIKROBA YG SEDIKIT /TIDAK DISERAP :

    -Streptomisin-Neomisin-Hidroksikuinolin-Sulfa yang tidak diserap

    2. ANTI MOTILITAS :-- Loperamid-- Difenoksilat

    3. ADSORBEN :-Kaolin/pektin-Carkoal-Atapulgit / smektit

    4. ANTI SEKRESI :-Asam salisilat-Klorpromazin

    5. PENELITIAN :-Laktobasillus-Fruktooligosakarida

    Obat Antidiare

    NB : Gol 1 s/d 4 TIDAK DIANJURKAN

    KAOLIN

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    KAOLIN

    1. Mempermudah penetrasi jar. oleh virus

    2. Tidak terbukti bermanfaat dlm mengurangi/merubah komposisi tinja

    3. Mengganggu kerja antibiotik4. Efek kosmetik5. Malabsorpsi

    IODOHIDROXY QUINOLINE

    1. Tidak berguna2. Di Jepang ==> Subacute Myelo Optic Neuropathy

    ( SMON)

    OPIAT & SPASMOLITIKA

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    OPIAT & SPASMOLITIKA

    1. MEMPERPANJANG MASA DEMAM2. MEMPERPANJANG MASA EKSKRESI

    BAHAN PATOGEN

    3. MENGGANGGU PERISTALTIK USUS4. MENAMBAH MASA UNTUK PROLIFERASI,

    PEMBENTUKAN TOKSIN & INVASI

    MIKROORGANISME

    5. PARALISIS USUS

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    ELEKTROLIT - ASAM BASA

    INISIAL

    DIAGNOSA

    REHIDRASI

    TREATMENT

    ELEKTROLIT ASAM BASA

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    ELEKTROLIT ASAM BASA

    INITIAL

    DEHIDRASIISONATREMIA

    REHIDRASI

    HIPONATREMIA

    DILUTIONAL

    DIARRHOEA

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    METABOLIC ACIDOSIS

    ANION GAP

    NORMAL

    LOSS OF HCO 3-

    INCREASED

    STARVATION

    RENALHYPOPERFUSION

    TISSUE HYPOXIA SALICYLATE

    INTOXICATION INBORN ERROR

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    ANION GAP = Na+

    - (Cl + HCO 3-

    )

    NILAI NORMAL = 8 16 mEq/L

    CLINICAL MANIFESTATIONS

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    CLINICAL MANIFESTATIONS

    AIR HUNGER : KUSSMAUL BREATHING ANOREXIA , NAUSEA & VOMITINGDEPRESSION OF CNS FUNCTIONS : COMA &CONVULSIONPERIPHERAL VASCULAR RESISTANCE :HYPOTENSIONCARDIAC CONTRACTILITY :

    A LOWERED THRESHOLD FOR VENTRICULARFIBRILATIONPREDISPOSES TO PULMONARY EDEMAK + INTRACELLULAR

    AFFINITY Hb TO O 2

    DEHIDRASI + ASIDOSIS METABOLIK

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    REHIDRASI

    pH , HCO 3- , pCO 2

    pH < 7.2 ATAU HCO 3- < 10 mEq/L

    HCO 3- = 1-2 mEq/Kg BB

    - FUNGSI PARU BAIK- TIDAK ADA HIPOKALEMIA

    pCO 2 (calculated) = (1.54 X HCO3-) + 8.36 + 1.11

    SESUAI TIDAK SESUAI

    ASIDOSIS METABOLIK

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    TIDAK SESUAI

    pCO 2 (c) > pCO 2 (lab) pCO 2 (c) < pCO 2 (lab)

    ASIDOSIS METABOLIK+

    ALKALOSIS RESPIRATORIK

    ASIDOSIS METABOLIK+

    ASIDOSIS RESPIRATORIK

    OVERSH OOT M ETABOLI C AL KAL OSI S ASIDOSIS PARADOKSAL

    HCO 3-

    DOSAGE OF HCO 3- ( m g)

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    HCO 3- = (HCO 3- desired - HCO 3- actual ) X 0,3 X BB(kg)

    HCO 3- d ?

    HCO 3- d H 2CO 3

    20

    HCO 3- d 20 x 0,03 pCO 2 = 0,6 pCO 2 ..(1)

    pCO 2 ( 1,54 X HCO 3-a ) + 8,36 1,11 (2)

    HCO 3-a pCO 2 - 8,36

    1,54 (O.6 pCO 2 - 5) HCO 3- =

    = 1,5 m g/kgBB=

    1 - 2 m g/kgBB

    =

    =

    =

    =

    0,6 pCO 2 - ( 0,6 pCO 2 - 5) X 0,3 BB(KG)

    PEMBERIAN HCO 3-

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    1. TIDAK BOLEH TERLALU CEPAT OVERSHOOT MET.ALKALOSIS ASIDOSIS INTRASEL

    2. HIPOKALEMIAPARALISIS OTOT PERNAFASAN

    3. GGN FUNGSI PARU-PARU

    4. INSUFF. SIRKULASI

    3

    NaHCO 3

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    I.V. ADMINISTRATION

    SERUM : HCO 3- + H +

    CORRECTION OF ACIDOSIS

    DECREASINGRESPIRATORYDRIVE

    H 2O + CO 2

    BLOOD BRAIN BARRIER

    BRAIN : HCO 3- + H +

    SLOW

    H 2O + CO 2 RAPID

    CEREBRAL ACIDOSIS AND DEPRESSION

    MECHANISM OF PARADOXAL ACIDOSIS

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    vasodilatasi ICP

    anoxia

    intracelluler acidosisHiperkarbia

    DEHIDRASI + HIPERNATREMIA

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    REHIDRASI

    HIPERNATREMIA( > 150 mEq/l)

    -INFUS STOP- AIR PUTIH

    DEHIDRASI + HIPONATREMIA

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    REHIDRASI

    HIPONATREMIA( < 135 mEq/L)

    HipoNasimpt

    SetelahRehidrasi

    HipoNaasimpt

    NaCl 3% Restriksi CairanRL

    Na (mEq) = (135 - NaSerum) x 0,6 x BB (kg) DEHIDRASI HIPO/ HIPERKALEMIA

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    REHIDRASI

    HIPOKALEMIA

    Mencret (+) Mencret

    HIPERKALEMIA

    Fungsi Ginjal

    ECGRL

    N abN

    K + oral K + drip(sampai 3 mEq / kgBB / hari)

    Gagal Ginjal Akut

    Restriksi Cairan

    DEMAM

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    TURUNKAN TEMP

    MENDINGINKANTUBUH

    OBAT

    - Buka Baju- Lap Keringat- Kipas

    - Kompres

    1. Paracetamol :30 mg/Kg/hari - 3 dosis

    2. - Acetyl Salicylic Acid

    - Mefenamic Acid

    Tidak dianjurkan

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    V. CHOLERAE

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    O1 Non O 1(Non Agglutinable)

    - Biotip - Eltor- Classic

    - Serotip - Ogawa- Inaba- Hikojima

    O2 - 138O140 - 142 O139

    Bengal Strain

    ENTERO TOXIN

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    Tidak MenggangguAbsorpsi Na + di Villus Cell

    Surface Receptor

    Sekresi Cl - di Crypt Cell

    Adenyl Cyclase

    C - AMP

    Absorpsi

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    Villi

    Crypt

    Lumen Usus

    Absorpsi

    Sekresi

    V. CHOLERAE

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    JEJUNUM

    - COPIOUS DIARRHOEA

    - FISHY RICE WATER STOOLS- DEMAM (-)- SAKIT PERUT (-)- RAPID DEHYDRATION & SHOCK

    - BIOKIMIA (+)- HISTOLOGI (-)

    DIAGNOSA

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    - KLINIS

    ANAK BESAR

    DEH. BERAT

    ANAK-ANAK LAIN (+)

    - LABDARK FIELD MICROSCOPEKULTUR

    Th C i l kt lit Ri g L t t I V

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    Th Cairan elektrolit Ringer Lactate I.V.

    MAKANAN

    AB Tetrasiklin atauDoksisiklin

    Rehidrasi & Pemeliharaan

    Kadar Na + tinja( 88 101 mEq/ L)

    SINDROMA DISENTRI

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    = DIARE + DARAH

    1. DISENTRI- BASILLER- AMUBA

    2. Enterocolitis- Cows milk allergy

    3. Trichuriasis

    4. Lain-lain - Entero invasive E coli

    - C. jejuni

    DISENTRI BASILLER

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    = SHIGELLOSIS

    KOLON

    S. DYSENTRIAE

    S. FLEXNERIS. BOYDIIS. SONNEI

    SHIGELA

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    SHIGELA

    INVASI SHIGA TOXIN

    INHIBISISINTESA PROTEIN

    SITOTOKSIK

    SHIGELA

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    - DIARE AIR- DIARE BERDARAH- TENESMUS- SAKIT PERUT- URGENSI

    - DEMAM- KEJANG- SEPSIS- HEMOLYTIC UREMIC

    SYNDROME- TOXIC MEGA COLON- PROLAPSUS RECTI

    Th

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    Th

    1. CAIRAN-ELEKTROLIT

    2. FEEDING

    3. - SELF LIMITED- BERAT TMP - SMX

    Cefixime: 8 mg/kg/hr

    2 dosis nalidixic acid ampisilin

    SALMONELLOSIS

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    TYPHOIDAL ENTERIC FEVER :-S. TYPHOID TYPHOID FEVER

    -S. PARATYPHOID PARATYPHOID FEVER

    NON TYPHOIDAL : SALMONELLA

    GASTROENTERITIS

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    INDIKASI PEMBERIAN AB PADASALMONELLA GASTROENTERITIS

    1. 3 MONTH OF AGE

    2. OLD DEBILITATED PATIENT

    3. DYSENTERY FORM ESPECIALLYILLNESS > 5 DAYS

    4. IMMUNOCOMPROMISED : STEROID,MALIGNANCY

    5. BACTERIAEMIA