DIARE AKUT

DIARE AKUT

B. Subagyo

ACUTE DIAORHHEA

Diarrhea, its come from Greek= to flow through,penyakit gangguan transport air dan elektrolit intestinal

Defekasi normal : *Bayi minum ASI, 2-3-4 wks:4-12 x/hari-lebih berat badan meningkat/ tidak menurun *Infant: formula feeding, defekasi 1-3 X/hari* normal 4 tahun atau lebih: < 3 x / hari*Normal infant, daef: 5-10 g/kg bb weight/day.*Adult: 100-200 gr/day

(J.M.Rhoads & D.W.Powel, 1991)

DEFINISI DIARE AKUT:1. Peningkatan Frekuensi buang air besar 2.Perubahan konsistensi & frekuensi 3.Neonatus: BAB > 4 kali/hari (ASI: > 4 kali,normal bisa > 12 x) BAB > 10 gr/kg bb/hari. Anak > 3 th; bab > 200 gr/hari4.Bersifat mendadak5.Berlangsung < 1 minggu (S/D < 14 HARI) Pada anak yang sebelumnya sehat (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 BERLANGSUNG LEBIH DARI 14 HARI

DIARE KRONIK, DIARE YG BERLANGSUNG LEBIH DARI 14 HARI BERLANGSUNG INTERMITEN (HILANG TIMBUL (PMPD. 1999)ETIOLOGI:*INFEKSI; Amoeba , Cholera, E. coli

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

EPIDEMIOLOGI Prevalensi diare tinggi :

*Usia 6 bulan - 2 tahun: +PASI *masa/fase oral, *sistim imun mukosa usus belum sempurna, *antibodi (SIgA) terhadap virus minimalVirus

Rota, *mulai PASI *CMA

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

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

FINGERS

FEKAL KUMAN / VIRUS

AIR/ MAKANAN/VEKTOR

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-anak, mau tambah pintar Anak diare cair,ibu melarang banyak minumMasa “oral” 6 bulan-12 bulan (24 bulan)Perilaku tidak higienis: Makanan-minuman kotor/dihinggapi lalatMakanan-air minum tidak dimasakAlergi, sistim kekebalan minimalPenggunakan PASI yg tidak benar(susu formula: takaran, kebersihan, termasuk kebersihan alat2 minum)Gencarnya Promosi promosi PASI~pendidikan & sosioekonomi masyarakat. (susu formula)

PEMBAGIAN DIARE

Berdasarkan Etiologi :

Virus :- Rotavirus (terbanyak)- Enterovirus-etc

Bakteri :-E. coli-Salmonella-Shigella-Staphyllococus,etc

Parasit :-Entamoeba-Cryptosporidium-etc

ALERGI

malabsorpsi

ETIOLOGI DIARE

Causative agent of gastroenteritis

BACTERIAAeromonasBacillus cereusCampylobacter jejuniClostridium perfringensClostridium difficileEscheria coliPleisomonas ShigellosisSalmonellaShigellaStaphylococcus aureusVibriocholerae 01 and 0139Vibrio parahaemolyticusYersinia enterocolitica

VIRUSAstrovirusCalcivirusesNorovirus **Enteric AdenovirusRotavirusCytomegalovirus *Herpes Simplex Virus *

PARASITERBalantidium ColiBlastocystis hominisCryptosporodium ParvumCyclospora CayetanensisEncephalitozoon Intestinalis *Entamoboeba histolyticaEnterocutazoon biemeasiGiardia LambliaIsospora belliStrongiloides StercoralisTrichuris Trichuria

* Generally Associated with disease, only among immunocompromised person

** Norvalk like viruses

FEEDING DIFFICULTYANATOMIC DEFECTMalrotationIntestinal duplicationHirschprung DiseaseFecal ImpactionShort Bowel SyndromeMicrovillus AtrophyStricturesMALABSORPTIONDisacharidase DeficienciesGlucose-Galactose MalabsorptionPancreatic Insufficiency

- Cystic Fibrosis- Schwachmann Syndrome

Reduced Intraluminal bile Salts- Cholestasis

Hartnup DiseaseAbetalipoproteinemiaCeliac DiseaseENDOCRINOPATHIESThyrotoxicosisAddison diseaseAdrenogenital Syndrome

FOOD POISONINGHeavy MetalScombroidCiguateraMudhroomsNEOPLASMANeuroblastomaGanglioneuromaPhaechromocytomasCarcinoidZolinger-Ellison SyndromeVasoactive Intestinal Peptide SyndromeMISCELLANEUSNongastrointestinal InfectionMilk AllergyCrohn Disease ( Regional enteritis)Familial dysautonomiaProtein-losing enteropathyUlcerative ColitisAcrodermatitis enteropathyLaxative abuseMotility disordersPellagra

Other Causes of Diarrhea

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 digestiAllergi (CMA)(peristaltik)

Causes of Secretory Diarrhea

Activation of Cyclic Adenosine MonophosphateBacterial 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 Diarrhea

Malabsorption of Water-Soluble NutrientsGlucose-Galactose Malabsorption

- Congenital- Acquired

Disaccharidase Deficiencies ( Lactase & Sucrase Isomaltase)

- Congenital- Acquired

Excessive intake of Carbonates fluidsExcessive 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 AMP *Cholera toxin *Heat-labile Escherichia coli enterotoxin *Salmonella enterotoxin *Campylobacter jejuni enterotoxin *Pseudomonas auruginosa enterotoxin *Shigella enterotoxin

Guanylate cyclase-cyclic GMP *Heat-stable Escherichia coli enterotoxin *Yersinia enterocolitica enterotoxin *Klebsiella pneumoniae enterotoxin (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


Drugs *Chemotheurapeutic agent

(e,g..cytosine arabinose, methotrexate) *Ipecac *Neomycin *Para-amino salicylic acid

Crohn’s Disease


IrradiationAutoimmune EnteropathySmall Bowel IschemiaEosinophilic Gastroenteropathy

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

H2O, Na+,Cl-,K+ dll

MALNUTRISI

KUMAN-VIRUS MASUK KEDALAM MULUT:

MANDI,MINUM, MAKANKERUSAKN VILI

DIARE

GANGGUAN DIGESTI

Bayi Minum ASI

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 7EnterotoxigenicEscherichia 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)

PEMBAGIAN DIARE MENURUT TONISITAS DARAH1.DIARE HIPOTONIK: KADAR NA< 130 meq/L2.DIARE ISOTONIK: KADAR NA 131-145 meq/L3.DIARE HIPERTONIK:KADAR NA > 145> /150 meq/l

MEKANISME TERJADI DIARE :

1. Peningkatan osmolaritas intraluminal: zat yg tdk diserap, reseksi usus, obat,

kerusakan mukosa- villi, metabolit intraluminal, chloridorhea

2. Peningkatan sekresi : CTenterotoksin, tumor kripta, hormon dan-

neurotransmiter3. Reaksi imun-allergi4. Meningitis/encephalitis(5. Peristaltik usus)

“”””KOMPLIKASI DIARE:

KEHILANGAN H2O: DEHIDRASI RINGAN-SEDANG-BERAT SYOK, GAGAL GINJAL (LIHAT:BAK, UREUM CREATININ), ENSEFALOPATI Na+, (Na TINGGIKEJANG, RENDAH DEHIDRASI BERAT)K+,(ILEUS PARALYTICUS, FIBRILASI JANTUNG)Cl-, (@ Na) HCO3-, (ASIDOSIS, RR CEPAT DAN DALAM, KUSSMAUL)HIPOGLIKEMI: KEJANG, ENSEFALOPATI

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

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

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

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

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

Anamnesis:Derajat dehidrasi:*cair-jumlah, muntah, lendir,darah?, Diare: *lama, frekuensi, jumlah, muntah+/-, minum +/-, L(+), D(+), tenesmus +/-,BAK +/-terakir-kapan(berapa jam yll, nafas cepat, kesadaran, wabah, *panas ? +/-,tinggi/subfebril ?pergantian susu ?, ASI +/-?, Makanan yg dicurigai?EndemikB.B SEKARANG: naik/turun brp %?

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

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

.B. Berdasarkan Skor Maurice King

Bagian tubuh yg diperiksa

Nilai 1 Nilai 2 Nilai 3

Keadaan umum Sehat Gelisah, ngantuk cengeng, apatisHAUS *)

Mengigau, koma, syok

Kekenyalan kulit Normal Sedikit kurangBERKURANG*)

Sangat kurang

Mata Normal Sedikit cekungCEKUNG *)

Sangat cekung

Ubun-ubun besar

Normal Sedikit cekung Sangat cekung

Mulut Normal Kering Kering,sianosis

Denyut nadi/mnt

Kuat<120 Sedang(120-140)

Lemah>140*) PEN

LABORATORIUM:Darah: JL, Hemogram, elektrolit, PCO2,PO2.Tinja: Konsistensi, lekosit, eritrosit, amoeba,parasit lainnyapH, klinitest, Sudan III, Serologi (virus Rota)INGAT Kuman komensal =flora usus (COLON= 1012-13/ml TINJA=kuman dlm tinja selalu (+) .Urine: makroskopis, mikroskopis

PENILAIAN DERAJAT DEHIDRASI

1.Tidak ada dehidrasi, penurunan BB < 2,5%2.Dehidrasi ringan, penurunan BB 2,5 – 5 % 3.Dehidrasi sedang, penurunan BB 5 –10 %4.Dehidrasi berat, (sampai syok) penurunan BB > 10 %

A. Berdasarkan Kehilangan Berat Badan

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 jamINGAT keperluan MAKSIMIUM: anak2: sekitar 2.000-3000 ml/hari (formula Darrow,)

KOREKSI DEFISIT KALIUM

PERHATIAN: DILARANG MEMBERIKAN SECARA BOLUSPaling 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:Calcium glukonas=0,1-1 ml/kg bb, bolus pelan

DEHIDRASI BERAT:I.V.DEFISIT: 100 ML/KG BB-koreksi 20ml/kg.bb/10menit-(shok)atau 30 ml/kg.BB/ 30-60 menit-sisanya diberikan 3-4 jamRUMATAN: 100 ML/KG BB/sisa waktu 24 jam 124 jam -3-4 jam 10 menit atau 3-4 jam 30 menitPada anak dgn bb < 6 kg, pakailah mikro drip

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

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

TETESAN CAIRAN INFUS1 ML=15 TETES,Kalau 1 TETES PERMENIT, maka dalam1 JAM= 4 MLL, dalam24 JAM= 96 ML

1 ML=20 TETES,Kalau 1 TETES PERMENIT, maka dalam1 JAM= 3 MLL , dalam24 JAM= 72 ML

1 ML=60 TETES,1 TETES PERMENIT, maka dalam1 JAM= 1 MLL , dalam24 JAM= 24 ML

APAKAH ANAK DIARE(MTBS)

JIKA YA, TANYAKAN:SUDAH BERAPA LAMA?APAKAH BERAKNYA BERDARAH (APAKAH ADA DARAH DALAM TINJA?)LIHAT & RABA:LIHAT KEADAAN UMUM ANAK:APAKAH ANAK: LETARGIS ATAU SADAR?GELISAH & REWEL/MUDAH MARAH?LIHAT APAKAH MATANYA CEKUNG?BERI ANAK MINUM, APAKAH ANAK:TIDAK BISA MINUM ATAU MALAS MINUM. HAUS, MINUM DENGAN LAHAP?CUBIT KULIT PERUT UNTUK MENGETAHUI TURGOR. APAKAH KEMBALINYA: SANGAT LAMBAT(LEBIH DARI 2 DETIK)? LAMBAT

KLASIFIKASI DIARETidak cukup tanda2 untuk diklasifikasikan sebagai dehidrasi berat atau ringan/sedang*TANPA DEHIDRASIBeri 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:Gelisah, rewel/mudah marahMata cekungHaus, minum dengan lahapCubitan kulit perut kembalinya lambatDEHIDRASI RINGAN/SEDANGBeri 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 oralit sedikit demi sedikitNasehati ibu kapan harus kembaliKunjungan ulang setelah 5 hari bila tidak ada perbaikan

Terdapat 2 atau lebih dari tanda2 berikut ini:Letargis atau tidak sadarMata cekungTidak bisa minum atau malas minumCubitan kulit perut kembalinya lambatDEHIDRASI 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 sedikitAnjuran agar ibu tetap memberikan ASIJika ada kolera didaerah tersebut, beri antibiotika untuk kolera (MTBS, 1997)

C. Berdasarkan Gejala Klinis

Gejala klinis Ringan Sedang Berat

K.U, kesadaranRasa haus

C.M+

Gelisah++

Apatis-komaTak bisa minum

Nadi Normal (120)

cepat Cepat sekali

Pernafasan Biasa Agak cepat kusmaull

Ubun ubun Agak cekung

cekung Cekung sekali

Mata Agak cekung

cekung Cekung sekali

Turgor biasa Agak kurang Kurang sekali

Diuresis Normal Oliguri Anuri

Selaput lendir Normal Agak kering kering

PRINSIP TERAPI1. Cairan: RINGAN->HF, SEDANG-> ORS, BERAT->RL-ASR (NaCl 0,9%) Cairan RESUSITASI: RL, Asering, NaCl 0,9%2. Diit: harus segera deberikan, kl pdt mau3. Probiotika: 10 9-12 (~mikroflora usus)4. Zn (10 MG/ < 6 BULAN. > 6 BULAN;20 mg/hari-s/d 10 hari- 14 hari) (Revitalisasi PMPD, 2006)5. Antibiotik atas indikasi (Shigella,Amoeba,Cholera, Giardia)6.Jangan menggunakan spasmolitika7. Promotif Penggunaan air bersih Peningkatan penggunaan ASI Penggunaan jamban dan pembuangan tinja bayi di jamban Cuci tangan sebelum menyuapi/ makan/kapan saja Penyapihan yang benar Vaksinasi campak (PMPD, 1999)8.MENCEGAH KOMPLIKASI DIARE KRONIK

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 CAIRAN

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

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

)

80 ml/kgBB/7 jam tetesan minimalOralit

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

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

Dehidrasi

berat

Dehidrasi

sedang

Dehidrasi

ringan

V (RL) ORS

Dehidrasi berat

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

BAIK JELEK

80/70 ml/3-4 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)

TERAPI CAIRAN DEHIDRASI BERAT 1.20 ml/kg BB/10 menit-30 ml/kgbb /30 menit-60 menit RL, bila masih jelek2.20ml/kg BB/10’-30 ml/kgbb 30-60 menit – RL,kalau masih jelek3.20 ml/kg BB/10 menit-plasma ekspander4.Sisa defisit: *kalau no 1 sudah membaik: 80-70 ml/kg BB/3 jam *kalau no 2 sudah membaik:60-40 ml/kg BB/ 3-4 jam *kalau no 3 sudah membaik: 40-20 ml/kg BB/3-4 jam *Selanjutnya diteruskan rumatan 100 ml/sisa waktu

Prof Iqbal MemonPakistan

In Malnourished Children the RISK of DEATH from Diarrhea is:

4 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

SHOCKSHOCK WITH SEVERE DEHYDRATION:

HISTORY OF PROFUSE DIARRHEA; KNOWN CHOLERA OUTBREAKS

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

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

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

DENGUE SHOCK SYNDROME: KNOWN DENGUE OUTBREAK OR SEASON

SHOCK IN CHILD WITH DIARRHEA [with SEVERE MALNUTRITION]

WEIGH THE CHILD OR ESTIMATE WEIGHTI.V. RINGER’S WITH 5% DEXTROSE ORHALF NORMAL WTH 5% DEXTROSE ORHALF STRENGTH DARROW’S WITH 5% DEXTROSE15 CC/Kg OVER ONE HOURPULSE & Resp Rate q 5-10MINGOOD 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 Stool WHO oral Rehydration

Solution (ORS) NonWHO ORS Cereal-based ORS Soft Drinks,

Cola etc. Sodium 50-100 90 45 60-90 02 Chlorine1 75-90 80 35 Variable ( - )4

Potassium1 25-35 20 20 Variable 0.1 BASE Type HCO3 Citrate Citrate Variable HCO3 Concentration1 25-40 30 30 Variable 13 CARBOHYDRATE Type -- Glucose Glucose Starch3

F/G5

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

For Breast-fed

Continue breast feeding as usual during and after rehydration therapy

Children on Mixed Diet

Continue normal feeding as usualGive repeated small frequent feeds (every 3-4 hours)Avoid sweetened foodsAvoid foods containing a lot of fibersAvoid foods known to have a laxative effect

DEHIDRASI SEDANGDefisit cairan: 80 ml kg BB/7 jam (oral atau IV)Diteruskan rumatan 100 ml/sisa waktu (Oral atau IV)

DEHIDRASI RINGANDiberikan CRT; 30-50 ml/kg BB/ atau tetesan minimal

KOMPOSISI CAIRAN TUBUH

Cairan tubuh 60%

C.Intraseluler 40%

Lemak, protein, mineral 40 %

C.Ekstraseluler 20 %

C.Interstisial 15 %

Plasma darah 5%

KOMPOSISI CAIRAN Cairan Na Cl K Ca Asetat laktat Dekst Kal Os

m

Asering 130 109 4 3 28 - - - 273

RL 130 109 4 3 - 28 - - 273

RD 147 155 4 4.5 - - 50 200 589

NaCl 0,9%

154 154 - - - - - - 300

KaEN 3B 50 50 20 - - 20 27 108 290

KaEN 3A 60 50 10 - - 20 27 108 290

KaEN 1B 38.5

38.5 - - - - 37.5 150 285

D ½ S 77 77 - - - - 50 200 428

D ¼ S 38.5

38.5 - - - - 50 200 353

B.SOEBAGYO

Etiology of Chronic Diarrhea

INTRALUMINAL FACTORSPancreatic Disorders

Cystic Fibrosis Schwachmann-Diamond Syndrome Johannson-Blizzard Syndrome Isolated-Pancreatic enzyme deficiencies Chronic Pancreatitis Pearson Syndrome

MUCOSAL FACTORSAltered Integrity

Infections : bacterial, viral,fungal Infestations : parasitic Cow’s and soy protein intolerance Inflammatory bowel disease ( Ulcerative Colitis, microscopic colitis, Crohn’s)

Etiology of Chronic DiarrheaBile acid DisordersChronic cholestasisTerminal ileum resectionBacterial overgrowthChronic use of bile acid squestrantPrimary bile acid malabsoprtionIntestinal disorder

*Altered immune function

Autoimmune enteropathyEosinophilie

gastroenteropathyAIDSCombined

immunodeficiencyImmunoglobulin A & G

deficiency


*Internal DisorderIntraluminal osmolarityCarbohidratemalabsoprtionCongenital & acquired sucrase, lactase deficienciesCongenital & acquired monosacharide malabsorptionExcessive carbonated fluid intakeExcessive intake of sorbitol, Mg (OH)2 & lactase

Altered FunctionDefect in Cl-/HCO3-Na+/H+,bile acidsAcrodermatitis enteropathieSekretoric lactase deficientAbetta lipoproteinemia


Altered Digestive FunctionEnterokinase deficiencyGlucoamylase deficiency

Altered Surface AreaCeliac diseasePostgastroenteritis syndromeMicrovillus inclusion diseaseShort bowel syndrome


Altered Secretory FunctionEnterotoxin producing bacteriaTumors secreting vasoactive peptidesAltered Anatomic StructureHirsprung’s diaseasePartial small bowel obstructionMalrotation

GEN

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

PJB,DARAH,GINJAL PARU,HATI, SAL.CERNA SAL.URINE, SSM TLG,OTAK MATA,HIDUNG,TELINGA DLL HORMONAL

(hipotiroid,pubertas precock),sakit jiwa

TUMBUH KEMBANG

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

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

Transmisi

Contaminated food & waterPerson 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 illnesThe inoculum effect explains the ease of person to person transmission of shigella in contrast to V.cholerae

PathogenesisThe 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 toxinA 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


Incubation:12 hr’s-day’sSevere abdominal pain ( tenesmus )High fever Emesis, anoreksia, generalized toxicity, painful defecationShiga toxin ~ convultionFrekuentAbdominal distention, tenderness, hyperactive bowel sounds, tender rectum on digital examination.Berak diawali cair dalam jumlah besar, diikuti bab sedikit2


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.


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.


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 berasDiare frequent-disertai tumpah2Cepat mengalami dehidrasi beratTanpa panasEndemisT/cairan rehidrasi Tetrasiklinin-klroramfenicol-kotrimoxasol

Amoeba

Anak >3 tahun (?)=pola makan bermacam2kontaminasi kuman>>Berak lembek, berdarah, berlendir, frekuensi kadang >10 x/hariTenesmusTanpa panasT/metronidazole-tetrasiklin

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