• DIARE AKUT PADA ANAK

• B.SUBAGYO

DEFINISI DIARE AKUT:1. Peningkatan Frekuensi buang air 1. Peningkatan Frekuensi buang air besar besar 2.Perubahan konsistensi & frekuensi 2.Perubahan konsistensi & frekuensi 3.Neonatus: BAB > 4 kali/hari3.Neonatus: BAB > 4 kali/hari BAB > 10 BAB > 10 gr/kg bb/hari gr/kg bb/hari.. Anak > 3 th; bab > Anak > 3 th; bab > 200 gr/hari 200 gr/hari ((Neonatus minum Neonatus minum ASI: > 4 kali,ASI: > 4 kali,normal bisa > 1normal bisa > 122 x, BB naik) x, BB naik) 4.Bersifat mendadak4.Bersifat mendadak5.Berlangsung < 1 minggu5.Berlangsung < 1 minggu (S/D < 14 HARI) Pada anak yang sebelumnya (S/D < 14 HARI) Pada anak yang sebelumnya sehat sehat (J.M.Rhoads & D.W.Powel, 1991)(J.M.Rhoads & D.W.Powel, 1991)

DEFINISI DIARE AKUT

• DIARE BERLANGSUNG < 14 HARI • Umumnya kurang dari 7 HARI)• BAB lunak-cair, darah +/-, lendir +/-• Muntah +/-, panas +/-

• ASI +/-• PASI +/-

• DIARE PERSISTENDIARE PERSISTEN• DIARE BERLANGSUNG LEBIH DARI 14 HARI

• DIARE KRONIKDIARE KRONIK,, • DIARE YG BERLANGSUNG LEBIH DARI 14 HARI

BERLANGSUNG INTERMITEN (HILANG TIMBUL (PMPD. 1999)

• ETIOLOGI:• *INFEKSI; Amoeba , • *NONINFEKSI MISALNYA • ALERGI SUSU SAPI (CMA) s/d 1-2-3 th• *AIDS• *dari infeksi akut sembuh lamamalnutrisi• *Malabsorpsi : KH, Lemak, Pretein

EPIDEMIOLOGI PPrevalensi diare tinggi : revalensi diare tinggi :

*Usia 6 bulan - 3 tahun: +PASI *Usia 6 bulan - 3 tahun: +PASI **mulai mulai mendapat mendapat PASIPASI **masamasa/fase /fase oral,oral, *sistim imun mukosa*sistim imun mukosa-mukus-mukus usus belum sempurna, usus belum sempurna, *antibodi (SIgA) *antibodi (SIgA) << << terhadap virus minimalterhadap virus minimalVirus Virus RotaRota, , *CMA*CMA

**Hygiene dan sanitasi burukHygiene dan sanitasi buruk *Terjadi pd*Terjadi pd bulan-bulan tertentu bulan-bulan tertentu

**Kadang terjadi KLBKadang terjadi KLB*Di Indonesia terdapat 60 juta / tahun, dimana 1 – 5 % *Di Indonesia terdapat 60 juta / tahun, dimana 1 – 5 % menjadi diare kronik menjadi diare kronik

CARA PENULARAN ANTIGEN:FEKAL-ORAL:

*air minum-makanan yg tercemar*bakteri-virus: PER-FEKAL-ORAL

dapat melalui-vektor: spt lalat-atau serangga lainnya

*atau langsung seperti-mandi (di sungai), tangan kotor,

cuci pakaian kotor, membersihkan tinja, cuci sayuran dengan air kotor.

CARA PENULARAN• 4 F: FINGERS• FESES-FLUID ORAL

• FOODS• • FLIES•

• FINGERSFINGERS• •

FEKALKUMAN / VIRUS

AIR/ MAKANAN/VEKTOR

bau, penampilan makanan, barier; asam lambung, lps mukus, SIgA

,ENTEROSIT SEHAT

ORAL-GASTROINTESTINAL & proses inflamasi, atrofi,toksin, “alergi”

DIARE

ROTAVIRUS

VILLI ATROFI=MUKUS < SIgA

LAKTASE DEFF

LAKTOSE INTRA.LUMINAL

OSMOL menyerap “air” jar usus

DIARE

• CMA/FOOD ALLERGY

• proses imunologi’~IgE (I) & • (III,IV)• ~Non IgE mediated

• efektor; m.g.i

• DIARE

SIKAP PERILAKU & WAHAM PENYEBAB MEMBURUKNYA DIARE

• Waham: anak njalaki-anakWaham: anak njalaki-anak,, mau tambah pintar mau tambah pintar• Anak diare cairAnak diare cair,ibu melarang b,ibu melarang banyak minumanyak minum• Masa “oral” 6 bulan-12 bulanMasa “oral” 6 bulan-12 bulan (24 bulan) (24 bulan)• Perilaku tidak higienis: Perilaku tidak higienis: • Makanan-minuman kotor/dihinggapi lalatMakanan-minuman kotor/dihinggapi lalat• Makanan-air minum tidak dimasakMakanan-air minum tidak dimasak• Alergi, sistim kekebalan minimalAlergi, sistim kekebalan minimal• Penggunakan PASI yg tidak benar(Penggunakan PASI yg tidak benar(susu formula:susu formula: takaran, takaran,

kebersihan, termasuk kebersihan alat2 minum)kebersihan, termasuk kebersihan alat2 minum)• Gencarnya Promosi promosi PASIGencarnya Promosi promosi PASI~pendidikan & sosioekonomi ~pendidikan & sosioekonomi

masyarakatmasyarakat.. (susu formula)

PEMBAGIAN DIARE

Berdasarkan Berdasarkan EtiologiEtiologi : :

VirusVirus : :- Rotavirus Rotavirus

(terbanyak)(terbanyak)- EnterovirusEnterovirus-etcetc

Bakteri :Bakteri :-E. coliE. coli-SalmonellaSalmonella-ShigellaShigella-Staphyllococus,etcStaphyllococus,etc

Parasit :Parasit :-EntamoebEntamoebaa-CryptosporCryptosporidiumidium-etcetc

ALERGI

malabsorpsi

ETIOLOGI DIARE• Causative agent of gastroenteritis

BACTERIA• Aeromonas• Bacillus cereus• Campylobacter jejuni• Clostridium perfringens• Clostridium difficile• Escheria coli• Pleisomonas Shigellosis• Salmonella• Shigella• Staphylococcus aureus• Vibriocholerae 01 and 0139• Vibrio parahaemolyticus• Yersinia enterocolitica

VIRUS• Astrovirus• Calciviruses• Norovirus **• Enteric Adenovirus• RotavirusRotavirus• Cytomegalovirus *• Herpes Simplex Virus *

PARASITER• Balantidium Coli• Blastocystis hominis• Cryptosporodium Parvum• Cyclospora Cayetanensis• Encephalitozoon Intestinalis *• Entamoboeba histolytica• Enterocutazoon biemeasi• Giardia Lamblia• Isospora belli• Strongiloides Stercoralis• Trichuris Trichuria

* Generally Associated with disease, only among immunocompromised person

** Norvalk like viruses

Other Causes of Diarrhea• FEEDING DIFFICULTY• ANATOMIC DEFECT

MalrotationIntestinal duplicationHirschprung DiseaseFecal ImpactionShort Bowel SyndromeMicrovillus AtrophyStrictures

• MALABSORPTIONDisacharidase DeficienciesGlucose-Galactose MalabsorptionPancreatic Insufficiency

- Cystic Fibrosis- Schwachmann Syndrome

Reduced Intraluminal bile Salts- Cholestasis

Hartnup DiseaseAbetalipoproteinemiaCeliac Disease

• ENDOCRINOPATHIESThyrotoxicosisAddison diseaseAdrenogenital Syndrome

• FOOD POISONINGHeavy MetalScombroidCiguateraMudhrooms

• NEOPLASMANeuroblastomaGanglioneuromaPhaechromocytomasCarcinoidZolinger-Ellison SyndromeVasoactive Intestinal Peptide Syndrome

• MISCELLANEUSNongastrointestinal InfectionMilk AllergyCrohn Disease ( Regional enteritis)Familial dysautonomiaProtein-losing enteropathyUlcerative ColitisAcrodermatitis enteropathyLaxative abuseMotility disordersPellagra

Differential Diagnosis of Osmotic versus secretory Diarrhea

• Osmotic Diarr Secretoric DiarrVol of Stool < 200 ml/24 hrs > 200 ml/24 hrsResponse to fasting diarrhea stop diarrhea continueStool Na+ < 70 mEq/L >70mEq/LReducing substances positif negativeStool pH <5 >6

Sucrase is not a reducing agent. Add 5 drops of 0,1 HCl to stool sample before adding reducing agent (clinitest tablet)

(J.D.Snyder: Nelson T.P, 2004)

PATHOMEKANISME of Diarrhea

• Secretoric: infeksi bakterialtoksin. • Osmotic : malabsorpsi, infeksi virus

bakterial/virus dan ggn digesti• Inflamatorik (mukosa usus)• Allergi (CMA)• (peristaltik)-hiperperistaltik• -hipoperistaltik

Causes of Secretory Diarrhea• Activation of Cyclic Adenosine Monophosphate

Bacterial toxins : enterotoxin of cholera, Escherichia Coli (heat-labile), Shigella, Salmonella, Campylobacter jejuni, Pseudomonas aeruginosaHormones : Vasoactive intestinal peptide, gastrin, SecretinAnion Surfactans : Bile acids, Ricinolic acid

• Activation of Cyclic Guanosine MonophosphateBacterial Toxins : E Coli (heat Stable) Enterotoxin, Yersinia enterocolitica toxin

• Calcium – DependentBacterial toxins : Clostridium difficile enterotoxinNeurotransmitters : Acethylcholine, SerotoninParacrine Agent : Bradykinin

Causes of Osmotic DiarrheaMalabsorption of Water-Soluble Nutrients• Glucose-Galactose Malabsorption

- Congenital- Acquired

• Disaccharidase Deficiencies ( Lactase & Sucrase Isomaltase)- Congenital- Acquired

• Excessive intake of Carbonates fluids• Excessive intake of nonabsorbable soluts

- Sorbitol- Lactulose- Magnesium hydroxide

F.K Ghisham 2004

BACTERIAL ENTEROTOXINS THAT AFFECT INTESTINAL ELECTROLYTE TRANSPORT TROUGH

STIMULATION OF ADENYLATE OR GUANYLATE CYCLASE

• Adenylate cyclase-cyclic AMPAdenylate cyclase-cyclic AMP *Cholera toxin*Cholera toxin *Heat-labile Escherichia coli enterotoxin*Heat-labile Escherichia coli enterotoxin *Salmonella enterotoxin*Salmonella enterotoxin *Campylobacter jejuni enterotoxin*Campylobacter jejuni enterotoxin *Pseudomonas auruginosa enterotoxin*Pseudomonas auruginosa enterotoxin *Shigella enterotoxin*Shigella enterotoxin• Guanylate cyclase-cyclic GMPGuanylate cyclase-cyclic GMP *Heat-stable Escherichia coli enterotoxin*Heat-stable Escherichia coli enterotoxin *Yersinia enterocolitica enterotoxin*Yersinia enterocolitica enterotoxin *Klebsiella pneumoniae enterotoxin*Klebsiella pneumoniae enterotoxin (J.M.Rhoads, D,W.Powell, 1994)(J.M.Rhoads, D,W.Powell, 1994)

Cause of Small Bowel Villous Damage & Crypt Hyperplasia

• Infectious Agent - Rotavirus - Norwalk agent - Other viruses, adenovirus, mini-reovirus,

calcivirus, astrovirus - Giardia lamblia - Cryptosporodium - Enteroadherent Escheriachia coli - Yersinia - Campylobacter jejuni - Strongyloides• Food Intolerance - Celiac disease - Cow ’s milk or soy milk protein intolerance

Cause of Small Bowel Villous Damage & Crypt Hyperplasia

• Drugs *Chemotheurapeutic agent (e,g..cytosine arabinose, methotrexate) *Ipecac *Neomycin *Para-amino salicylic acid• Crohn’s Disease

• Cause of Small Bowel Villous Damage & Crypt Cause of Small Bowel Villous Damage & Crypt HyperplasiaHyperplasia

• Irradiation• Autoimmune Enteropathy• Small Bowel Ischemia• Eosinophilic Gastroenteropathy

• H2O• Na+,Cl-,K+,HCO3- 311 oam/lNa+,Cl-,K+,HCO3- 311 oam/l• A.A-AL-MS 245 osm/lA.A-AL-MS 245 osm/l• 285-295 osm/l285-295 osm/l

• H2O, Na+,Cl-,K+ dllH2O, Na+,Cl-,K+ dll

MALNUTRISI

KUMAN-VIRUS MASUK KEDALAM MULUT:

MANDI,MINUM, MAKANKERUSAKN VILI

DIARE

GANGGUAN DIGESTI

Susu sapi Susu formula

Susu sapi Susu formula

Bayi Minum ASI

CRO

SIKLUS DIARE AKUT-DIARE KRONIK-MALNUTRISI-INFEKSI

GNG ABSORPSI

DIARE KRONIK

DIAREAKUT

INFEKSI

MALNUTRISI

KOMPOSISI TINJA PD PDT DIARE Selain H2O:

PEAK STOOL VOL ELEKTROLIT OSMOTIC GAP ml/kg/day mMol/L mOsm/L 290-2[(Na)+(K)]

Na+ K+ Cl- HCO3-Cholera 180 80 30 86 32 7

EnterotoxigenicEscherichia coli

160 53 37 24 18 110Rotavirus 130-160 37 38 22 6 140Normal stool 5-10 22 54 21 ND 140

(Jon Marc Rhoads.M.D Don W.Powell,M.D, in Walker Durie, Hamilton, Walker-Smith, Watkins

Pediatric Gastrointestinal disease1991)

MEKANISME TERJADI DIARE :1.1. Peningkatan osmolaritas intraluminal:Peningkatan osmolaritas intraluminal: zat yg tdk diserap, reseksi usus, obat,zat yg tdk diserap, reseksi usus, obat,

kerusakan mukosa- villi, metabolit kerusakan mukosa- villi, metabolit intraluminal, chloridorhea intraluminal, chloridorhea

2. Peningkatan sekresi : 2. Peningkatan sekresi : CTCTenterotoksin, tumor kripta, hormon dan-enterotoksin, tumor kripta, hormon dan-

neurotransmiterneurotransmiter3. Inflamatorik3. Inflamatorik4. Reaksi imun-allergi4. Reaksi imun-allergi5. Peristaltik usus5. Peristaltik usus

“”””• KOMPLIKASI DIAREKOMPLIKASI DIARE::

• KEHILANGAN H2O: DEHIDRASI KEHILANGAN H2O: DEHIDRASI • RINGAN-SEDANG-BERATRINGAN-SEDANG-BERAT• SYOK, GAGAL GINJAL (LIHAT:BAK, UREUM SYOK, GAGAL GINJAL (LIHAT:BAK, UREUM

CREATININ), ENSEFALOPATI CREATININ), ENSEFALOPATI • Na+, (Na TINGGINa+, (Na TINGGIKEJANG, RENDAH KEJANG, RENDAH

DEHIDRASI BERAT)DEHIDRASI BERAT)• K+,(ILEUS PARALYTICUS, FIBRILASI JANTUNG)K+,(ILEUS PARALYTICUS, FIBRILASI JANTUNG)• Cl-, (@ Na) Cl-, (@ Na) • HCO3-, (ASIDOSIS, RR CEPAT DAN DALAM, HCO3-, (ASIDOSIS, RR CEPAT DAN DALAM,

KUSSMAUL)KUSSMAUL)• HIPOGLIKEMI: KEJANG, ENSEFALOPATIHIPOGLIKEMI: KEJANG, ENSEFALOPATI

DIAGNOSTIK1.1. Anamnesis:Anamnesis: Lama,frekuensi,konsistensi, lendir? Darah?, Lama,frekuensi,konsistensi, lendir? Darah?,

panas, muntah (freq,jumlah) panas, muntah (freq,jumlah) masukan yg dicurigai, minum, endemik? masukan yg dicurigai, minum, endemik?

ASI/PASI?riwayat atopi dalam keluarga,UmurASI/PASI?riwayat atopi dalam keluarga,Umur (DD, derajad dehidrasi, etiologi & perjalanan(DD, derajad dehidrasi, etiologi & perjalanan

2.2. Pemeriksaan fisik:Pemeriksaan fisik: ( penilaian derajat dehidrasi, ( penilaian derajat dehidrasi, TV, KESADARAN, CRT,TURGOR,TENESMUS ? TV, KESADARAN, CRT,TURGOR,TENESMUS ? ; ; etiologi & komplikasi)etiologi & komplikasi)3. Pemeriksaan penunjang :3. Pemeriksaan penunjang :

- darah- darah - ELISA -urine- ELISA -urine- tinja - tinja - Klinitest-pH- Klinitest-pH -BGA -BGA- biakan - biakan - Sudan III- Sudan III

PEMERIKSAAN FISIK:*KESADARAN,NADI, UUB CEKUNG +/-, AIR MATA +/-,

MATA CEKUNG +/-,MUKOSA MULUT BASAH +/-, NAFAS CUPING HIDUNG +/-, RETRAKSI INTERKOSTAL

INTERKOSTAL +/-, TURGOR KULIT </> 2’’, CRT > 2’’ ,

AKRAL DINGIN +/- , *TENESMUS, LASERASI PERIANAL, JAMUR ORAL

Dehidrasi berat vs Syok(askanatt)

APATIS, SOMNOLEN,KOMA, ASIDOSIS,NADI, AKRAL DINGIN, TENSI TURUN, TURGOR JELEK

LABORATORIUM:Darah: JL, Hemogram, elektrolit, PCO2,PO2.

Tinja: Konsistensi, lekosit, eritrosit, amoeba,parasit lainnya

pH, klinitest, Sudan III, Serologi (virus Rota)INGAT Kuman komensal =flora usus (COLON= 1012-13/ml TINJA=kuman dlm tinja selalu (+) .

Urine: makroskopis, mikroskopis

KEBUTUHAN CAIRANMAINTENAN per hari mnrt berat

badan• -s/d 10 kg: 100 ml/kg.bb/24 jam• >10-20 kg pertama: 50 ml/kg.bb/24 jam• >20 kg: 20 ml/kg.bb/24 jam• INGAT keperluan MAKSIMIUM:• anak2: sekitar 2.000-3000 ml/hari • (formula Darrow,)

KOREKSI DEFISIT KALIUMPERHATIANPERHATIAN: : DILARANG MEMBERIKAN SECARA BOLUSDILARANG MEMBERIKAN SECARA BOLUSPaling aman diberikan per-oral=75 mg/kg bb/dayPaling aman diberikan per-oral=75 mg/kg bb/day 3,5-Kcl pdt x BB X 0,4 + 2 meq/kgBB/ dalam 4jam

3,5-Kcl x BB x 0,4 + 1/6 x 2 meq/kgBB/ dalam 20jam Oral: 75 mg/kg BB/hariHIPERKALEMIA:HIPERKALEMIA:Calcium glukonas=0,1-1 ml/kg bb, bolus pelan

• DEHIDRASI SEDANG: CAIRAN PER-ORAL (ORS)DEHIDRASI SEDANG: CAIRAN PER-ORAL (ORS) (WHO/PMPD :ringan sedang) (WHO/PMPD :ringan sedang)DEFISIT: 70 ML/KG BB:3-4 jam 9 (ORS/IV)DEFISIT: 70 ML/KG BB:3-4 jam 9 (ORS/IV)RUMATAN: 100 ML/KG BB/sisa waktu RUMATAN: 100 ML/KG BB/sisa waktu 24 jam- 3jam/4 jam 24 jam- 3jam/4 jamKP: pasang NGT/OGTKP: pasang NGT/OGT

• DEHIDRASI RINGANDEHIDRASI RINGAN/TANPA DEHIDRASI/TANPA DEHIDRASI:CAIRAN :CAIRAN PER-ORAL (HF)PER-ORAL (HF)DEFISIT: 30-50 ML/KG BB/CRT/ORS/3-4jamDEFISIT: 30-50 ML/KG BB/CRT/ORS/3-4jamRUMATAN: 100 ML/KG BBRUMATAN: 100 ML/KG BB

TETESAN CAIRAN INFUS• 1 ML=15 TETES1 ML=15 TETES,,• Kalau 1 TETES PERMENIT, maka dalam• 1 JAM= 4 MLL, dalam• 24 JAM= 96 ML

• 1 ML=20 TETES1 ML=20 TETES,,• Kalau 1 TETES PERMENIT, maka dalam• 1 JAM= 3 MLL , dalam• 24 JAM= 72 ML

• 1 ML=60 TETES1 ML=60 TETES,,• 1 TETES PERMENIT, maka dalam• 1 JAM= 1 MLL , dalam• 24 JAM= 24 ML

TERAPI CAIRAN DEHIDRASI BERAT

• Berat : cairan yang hilang 100cc/kg• Di bawah 1th diberi 30 cc/kg dalam 1 jam• Diteruskan 70 cc/kg dalam waktu 5 jam• Diatas 1 th diberi 30 cc/kg dalam 0,5 jam• Diteruskan 70 cc/kg dalam waktu 2,5 jam• Sisa Maintenance diberikan sesuai dosis

dalam sisa waktu 18 jam untuk yang 1th, jika lebih 1 th sisa 21 jam.

KLASIFIKASI DIARE• Tidak cukup tanda2 untuk diklasifikasikan sebagai Tidak cukup tanda2 untuk diklasifikasikan sebagai

dehidrasi berat atau ringan/sedangdehidrasi berat atau ringan/sedang• *TANPA DEHIDRASI• Beri cairan & makanan sesuai Rencana Terapi A. • Nasehati ibu tentang kapan harus kembali

segera*kunjungan ulang setelah 5 hari bila tidak ada perbaikan

• Terdapat dua atau lebih dari tanda2 berikut:Terdapat dua atau lebih dari tanda2 berikut:• Gelisah, rewel/mudah marahGelisah, rewel/mudah marah• Mata cekung• Haus, minum dengan lahap• Cubitan kulit perut kembalinya lambat• DEHIDRASI RINGAN/SEDANGDEHIDRASI RINGAN/SEDANG• Beri cairan & makanan sesuai Rencana Terapi B.• Jika anak juga mempunyai klasifikasi berat lainnya:• Rujuk segera ke RS & selama dalam perjalanan mintalah

agar ibu memberikan larutan oralitoralit sedikit demi sedikit• Nasehati ibu kapan harus kembali• Kunjungan ulang setelah 5 hari bila tidak ada perbaikan

• Terdapat 2 atau lebih dari tanda2 berikut ini:Terdapat 2 atau lebih dari tanda2 berikut ini:• Letargis atau tidak sadar• Mata cekung• Tidak bisa minum atau malas minum• Cubitan kulit perut kembalinya lambat• DEHIDRASI BERAT:• Jika tidak ada klasifikasi berat lainnya:• Beri cairan untuk dehidrasi berat (Rencana Terapi C)• Jika anak juga mempunyai klasifikasi berat lainnya:• Rujuk segera & selama dalam perjalanan agar mintalah ibu

terus memberikan larutan oralit sedikit demi sedikit• Anjuran agar ibu tetap memberikan ASI• Jika ada kolera didaerah tersebut, beri antibiotika untuk

kolera (MTBS, 1997)

Role of probiotics in diarrhea;

• In clinical settings, these "biotherapeutic" agents have repeatedly been helpful in the resolution of antibiotic-associated diarrhea, and preventing clostridium difficule associated diarrhea.

(J of american association 2004,J gastrol enterol hepatol 2002, cochrane 2004, peds inf disease 2004, british med j 2002, JAMP 1994,).

• (di salin dari: )

TERAPI CAIRANTERAPI CAIRAN

1.1.20 ml/kg BB/10’ 20 ml/kg BB/10’ 1x 1x 80ml/kgBB/3 jam 80ml/kgBB/3 jam2.2.20 ml/kg BB/10’ 20 ml/kg BB/10’ 2x 2x 60/ml/kgBB/3jam 60/ml/kgBB/3jam3.3.20 ml/kg BB/10’ 20 ml/kg BB/10’ 1x 1x koloid (kalau perlu) koloid (kalau perlu)sisa 100 ml-(20 ml) (40 ml) (60 ml) : 3 jam sisa 100 ml-(20 ml) (40 ml) (60 ml) : 3 jam Rumatan 100 ml dibagi sisa waktu(24 jam -3 jam Rumatan 100 ml dibagi sisa waktu(24 jam -3 jam

10,20,30mnt): RL, D1/2S, D1/4S,NaCl, ORS)10,20,30mnt): RL, D1/2S, D1/4S,NaCl, ORS)

))

880 ml/kgBB/7 jam 0 ml/kgBB/7 jam tetesan minimal tetesan minimalOralitOralit

Rumatan=100 ml/sisa waktu (CRT/ORS)Rumatan=100 ml/sisa waktu (CRT/ORS)

Rumatan=100 ml dibagi sisa waktu Rumatan=100 ml dibagi sisa waktu CRTCRT 30-50 ml/kgBB/3-4 jam tetesan minimal30-50 ml/kgBB/3-4 jam tetesan minimal

DehidraDehidrasi beratsi berat

DehidraDehidrasi si

sedangsedang

DehidraDehidrasi ringansi ringan

V (RL)V (RL)

ORSORS

Dehidrasi berat

shok dehidrasi berat

20 ml/kg(10’)-atau 30 ml/kg dalam 30’-60’

BAIK JELEK

80/70 ml/ 2,5 -5 jam(RL) 20 ml/10’(RL)/30 ml/30-

BAIK JELEK

60 ml/3-4JAM(RL) 10-20 ml/10’ 10-20 ml/10’ 40 ml/3-4 jam (KOLLOID;HES.DEXTRAN.L,PLASMA)

Prof Iqbal MemonPakistan

In Malnourished ChildrenIn Malnourished Children the RISK of DEATH from Diarrhea is:

• 4 fold4 fold

Management of Dehydration (WHO)

SIGNS No signs of dehydration

Some (mod.) dehydration

Severe dehydration

G General condition

well, alert

restless, irritable

lethargic, unconscious

E Eyes normal sunken sunken

M Mouth & Drinking

normal thirsty, drink eagerly

poor or una-ble to drink

S Skin pinch returns rapidly returns slowly very slowly

Management of dehydration

Plan A at Home

Plan B At OR Center

Plan C At Hospital

SHOCK• SHOCK WITH SEVERE DEHYDRATIONSHOCK WITH SEVERE DEHYDRATION:

– HISTORY OF PROFUSE DIARRHEA; – KNOWN CHOLERA OUTBREAKS

• SEPTIC SHOCKSEPTIC SHOCK: – Hx OF FEBRILE ILLNESS; – VERY ILL CHILD; – KNOWN OUTBREAK OF MENINGOCOCCAL INFECTION

• BLEEDING SHOCK:BLEEDING SHOCK: – Hx OF TRAUMA, – HISTORY OF HIGH FEVER PURPURE– BLEEDING SITE

• CARDIAC SHOCKCARDIAC SHOCK: – Hx OF HEART DISEASE; ENLARGED NECK VEINS AND LIVER

• DENGUE SHOCK SYNDROMEDENGUE SHOCK SYNDROME: – KNOWN DENGUE OUTBREAK OR SEASONHipoglikemic shockHipoglikemic shock

SHOCK IN CHILD WITH DIARRHEA [with SEVERE MALNUTRITION]

• WEIGH THE CHILD OR OR ESTIMATE WEIGHT• I.V. RINGER’S WITH 5% DEXTROSE OROR• HALF NORMAL WTH 5% DEXTROSE OROR• HALF STRENGTH DARROW’S WITH 5% DEXTROSE• 15 CC/Kg OVER ONE HOUR15 CC/Kg OVER ONE HOUR• PULSE & Resp Rate q 5-10MIN• GOOD CHANGEGOOD CHANGE: REPEAT; SWITCH TO RESOMAL PER NG@

10ml/kg/HRX10 HRS; AND THEN REFEEDING WITH F-75 • NO CHANGE ….after first load …septic shock

STOOL AND REHYDRATION SOLUTION ELECTROLYTE COMPOSITION

Diarrheal StoolDiarrheal Stool WHO oral RehydrationWHO oral Rehydration

Solution (ORS)Solution (ORS) NonNonWHOWHO ORSORS Cereal-based ORSCereal-based ORS Soft Drinks, Soft Drinks, Cola etc.Cola etc. Sodium Sodium 50-10050-100 90 90 45 45 60-90 60-90 02 02 ChlorineChlorine1 1 75-9075-90 80 80 35 35 Variable Variable ( - ) ( - )44

PotassiumPotassium1 1 25-3525-35 20 20 20 20 Variable Variable 0.1 0.1 BASE BASE Type Type HCOHCO33 Citrate Citrate CitrateCitrate VariableVariable HCOHCO33 ConcentrationConcentration11 25-4025-40 30 30 30 30 Variable Variable 13 13 CARBOHYDRATECARBOHYDRATE Type --Type -- Glucose Glucose Glucose Glucose Starch Starch33 F/G F/G55

Concentration -- Concentration -- (g/L)(g/L) 20g 20g 25 25 50g 50g 50-150g 50-150g Osmolality Osmolality 250-300250-300 300 300 264 264 200-225200-225 550 550

For Breast-fed

• Continue Continue breast breast feeding feeding as usual as usual during and during and after after rehydration rehydration therapytherapy

Children on Mixed Diet

• Continue normal feeding as usual

• Give repeated small frequent feeds (every 3-4 hours)

• Avoid sweetened foods• Avoid foods containing a lot

of fibers• Avoid foods known to have

a laxative effect

KOMPOSISI CAIRAN TUBUHKOMPOSISI CAIRAN TUBUH

Cairan Cairan tubuh tubuh 60%60%

C.IntraseluleC.Intraseluler 40%r 40%

Lemak, Lemak, protein, protein, mineral mineral 40 %40 %

C.EkstraseluleC.Ekstraseluler 20 %r 20 %

C.InterstiC.Interstisial 15 %sial 15 %

Plasma Plasma darah darah 5%5%

KOMPOSISI CAIRANKOMPOSISI CAIRAN CairanCairan NaNa ClCl KK CaCa AsetatAsetat laktatlaktat DekstDekst KalKal OsmOsm

AseringAsering 130130 109109 44 33 2828 -- -- -- 273273

RLRL 130130 109109 44 33 -- 2828 -- -- 273273

RDRD 147147 155155 44 4.54.5 -- -- 5050 200200 589589

NaCl NaCl 0,0,9%9% 154154 154154 -- -- -- -- -- -- 300300

KaEN 3BKaEN 3B 5050 5050 2020 -- -- 2020 2727 108108 290290

KaEN 3AKaEN 3A 6060 5050 1010 -- -- 2020 2727 108108 290290

KaEN 1BKaEN 1B 38.538.5 38.538.5 -- -- -- -- 37.537.5 150150 285285

D ½ SD ½ S 7777 7777 -- -- -- -- 5050 200200 428428

D ¼ SD ¼ S 38.538.5 38.538.5 -- -- -- -- 5050 200200 353353

Prinsip terapi diare

• 1. Cairan: a.ringan->HF• b.SedangORS• c.Beratresusitasi • Asering, RL, NaCl 0,9%• 2. Early feeding• 3.Zn: < 1 th10 mg,10-12 hari• > 1 th20 mg,10-12 hari• 4. Antibiotika: amoeba, shigella, cholera, • giardia, infeksi ditempat lain• 5. Tidak boleh diberikan spasmolitika• 6. Promosi

Prinsip terapi diare

• 6. Promosi:• a. Promosi ASI exclucive• b. Penyapihan yg benar• c. Penggunaan air bersih• d. Pemakaian jamban untuk bayi & • anak• e. Cuci tangan kapan saja• f. Vaksinasi campak

B.SOEBAGYO

Etiology of Chronic Diarrhea

INTRALUMINAL FACTORSINTRALUMINAL FACTORSPancreatic DisordersPancreatic Disorders

Cystic FibrosisCystic Fibrosis

Schwachmann-Diamond SyndromeSchwachmann-Diamond Syndrome

Johannson-Blizzard SyndromeJohannson-Blizzard Syndrome

Isolated-Pancreatic enzyme Isolated-Pancreatic enzyme deficienciesdeficiencies

Chronic PancreatitisChronic Pancreatitis

Pearson SyndromePearson Syndrome

MUCOSAL FACTORSMUCOSAL FACTORSAltered IntegrityAltered Integrity

Infections : bacterial, viral,fungalInfections : bacterial, viral,fungal

Infestations : parasitic Cow’s and soy Infestations : parasitic Cow’s and soy protein intoleranceprotein intolerance

Inflammatory bowel disease Inflammatory bowel disease ( Ulcerative Colitis, microscopic ( Ulcerative Colitis, microscopic colitis, Crohn’s)colitis, Crohn’s)

Etiology of Chronic Diarrhea• Bile acid Disorders• Chronic cholestasis• Terminal ileum resection• Bacterial overgrowth• Chronic use of bile acid• squestrant• Primary bile acid

malabsoprtion• Intestinal disorder

*Altered immune functionAutoimmune enteropathyEosinophilie gastroenteropathyAIDSCombined immunodeficiencyImmunoglobulin A & G deficiency

Etiology of Chronic Diarrhea• *Internal Disorder• Intraluminal osmolarity• Carbohidratemalabsoprtion• Congenital & acquired sucrase,

lactase deficiencies• Congenital & acquired

monosacharide malabsorption• Excessive carbonated fluid intake• Excessive intake of sorbitol, Mg

(OH)2 & lactase

• Altered Function• Defect in Cl-/HCO3-Na+/H+,bile

acids• Acrodermatitis enteropathie• Sekretoric lactase deficient• Abetta lipoproteinemia

Etiology of Chronic Diarrhea

• Altered Digestive Function

• Enterokinase deficiency• Glucoamylase deficiency

• Altered Surface Area• Celiac disease• Postgastroenteritis syndrome• Microvillus inclusion disease• Short bowel syndrome

Etiology of Chronic Diarrhea• Altered Secretory Function• Enterotoxin producing

bacteria• Tumors secreting vasoactive

peptides• Altered Anatomic

Structure• Hirsprung’s diasease• Partial small bowel

obstruction• Malrotation

GENGEN

ASAH-ASIH-ASUH:ASAH-ASIH-ASUH: NUTRISINUTRISI:pendidikan OTU:pendidikan OTU PENYAKIT:PENYAKIT:

PJB,DARAH,GINJAL PARU,HATI, SAL.CERNA SAL.URINE, SSM TLG,OTAK MATA,HIDUNG,TELINGA DLL HORMONAL (hipotiroid,pubertas precock),sakit jiwa

TUMBUH KEMBANGTUMBUH KEMBANG

Shigella(Thomas G.Cleary. T.B in Nelson;Textbook of Pediatrics, 2004)

• Shigella species:• S.dysentriae (serogroup A); 13 serotype• S.flexneri (serogroup B); 15 serotype• S.boydii (serogroup C); 18 sertype• S.Sonnei (serogroup D); 1 serotype• Invasif• Shiga toxin=s.dysentriae serotype 1 & Shet-1

Transmisi

• Contaminated food & water• Person to person transmission is the probably the

major mechanism of infection in the most areas of the world.

• Spread in the families, custodial instutions • & child care centers demonstrated the ability of low

numbers of organisms to cause disease on person-to-person basis.

Transmisi

• Shigella require very low inocula to cause illnes.• Ingestion of as low as 10 S.dysentriae serotype 1

organism can cause dysentery in some susceptible individuals.

• This is the contrast to organisms such Vibrio cholerae, which require ingestion of 108-1010 organisms to cause illnes

• The inoculum effect explains the ease of person to person transmission of shigella in contrast to V.cholerae

Pathogenesis

• The basic virulence trait shared by all shigellae is the ability to invade intestine.

• This characteristic is encoded on a large (120-140 megadalton) plasmid that is responsible for synthesis of group of polypeptide involved in cell invasion & killing. Shigellae that lose the virulence plasmid enteroinvasive. E.coli that harbor this plasmid (enteroinvasive E coli) be have) clinically like shigellae.

Pathogenesis

• Shiga toxin• A potent protein synthesis-inhibiting exotoxin, is

produced in significant amounts by S.dysentriae serotype 1, by certain E.coli, which are known as Shiga toxin-producing E.coli (STEC), and rarely by other organisms. The watery diarrhea fase of shigellosis may be caused by enterotoxins

Pathogenesis

• The pathologic changes of shigella take place primarily in the colon, the target organ of shigellae. The changes are most intense in the distal colon, although pancolitis may accur. Grossly, localized or difusse mucosal edema, ulceration, friable mucosal,bleeding & exudate may be seen. Microscopycally ulcerations, pseudomembranes, epithelial cell death, infiltration extending from mucosae by polymorphonuclear & mononuclear cells, & submucosal edema occur

Immunity

• SIgA & serum antibodies develop within days to weeks after ingestion with shigella.

• Both antipolysaccharide & antivirulence plasmid polypeptide antibodies have been described: protection is serotype specific.

• Induction of multiple cytikines & brisk inflammatory respones is followed by healing. Interferron-y produced by NK cells is critically important to resistence.

Clinical Manifestation of Shigella• Bacillary dysentery is clinically similar

regardless of whether the disease is caused by any of the four species of shigella or enteroinvasive E.coli; however, tehre are some clinical differences, particulary relating to the greater severity & risk of complications with S.dysenterae serotype 1 infection

•

Clinical Manifestation of Shigella• Incubation:12 hr’s-day’s• Severe abdominal pain ( tenesmus )• High fever • Emesis, anoreksia, generalized toxicity, painful defecation• Shiga toxin ~ convultion• Frekuent• Abdominal distention, tenderness, hyperactive bowel sounds,

tender rectum on digital examination.• Berak diawali cair dalam jumlah besar, diikuti bab sedikit2

Clinical Manifestation of Shigella• The diarrhea may be watery & large volume initialy, evolving

into frequent small-volume, bloody mucoid stools; however, some children never progress the stage of bloody diarrhea, whereas in others the firt stools are bloody. Significant dehydration related to the fluid & electrolyte losses in both feces & emesis can occur. Untreated diarrhea may last 1-2 wk; only about 10% of patients have diarrhea persisting for more than 10 days.

• Persistent diarrhea accurs in malnourihed infant, those with AIDS, and occasionally previously normal children. Even nondysenteryc disease can be complicated by persistent illness.

Clinical Manifestation of Shigella

• Neurologic findings are among the most common extraintestinal manifestations of bacillary dysentery, occuring in as many as 40% of hospitalized infected children. Enteroinvasive E coli can cause similar neurologic toxicity. Convultions, headache, lethargy, confusion, nuchal rigidity, or hallucinations may be present before or after the onset of diarrhea.

Clinical Manifestation of Shigella

• The cause of these neurologic findings is not understood. In the past, these symptoms were attributed to the neurotoxicity of Shiga toxin, but it is now clear that axplanation is wrong. Seizures sometimes occur when little fever is present, suggesting that simple febrile convultion do not explain their appearance.

• Hypocalcemia or hyponatremia may be associated with seuzures in small number patients. Althoug symptoms often suggest central nervous system infection, and cerebrospinal fluid pleocytosis with minimally elevated protein levels can occur, meningitis due to shigellae is rare.

• The most common complication of shigellosis is dehydration. Inappropriate secretion of antidiuretic hormone

Cholera (Vibrio Cholerae)

• Diare cair~cucian beras• Diare frequent-disertai tumpah2• Cepat mengalami dehidrasi berat• Tanpa panas• Endemis• T/cairan rehidrasi-Asering/Ringer lactate• Tetrasiklinin-klroramfenicol-kotrimoxasol

Amoeba

• Anak >3 tahun (?)=pola makan bermacam2kontaminasi kuman>>

• Berak lembek, berdarah, berlendir, frekuensi kadang >10 x/hari

• Tenesmus• Tanpa panas• T/metronidazole-tetrasiklin