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/hari
4.Bersifat mendadak
5.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 PERSISTEN
DIARE 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 lamamalnutrisi
*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 minimalVirus 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 minum
Masa “oral” 6 bulan-12 bulan (24 bulan)
Perilaku tidak higienis:
Makanan-minuman kotor/dihinggapi lalat
Makanan-air minum tidak dimasak
Alergi, sistim kekebalan minimal
Penggunakan 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 :

rus : Bakteri :
Parasit :
otavirus -E. coli ALERGI
-Entamoeb
erbanyak)-Salmonella
a malabsorpsi
nterovirus -Shigella
-Cryptospor
c -Staphyllococus,etc idium
-etc
 ETIOLOGI DIARE
Causative agent of gastroenteritis VIRUS
BACTERIA Astrovirus
Calciviruses
Aeromonas Norovirus **
Bacillus cereus Enteric Adenovirus
Campylobacter jejuni Rotavirus
Clostridium perfringens Cytomegalovirus *
Herpes Simplex Virus *
Clostridium difficile PARASITER
Escheria coli Balantidium Coli
Pleisomonas Shigellosis Blastocystis hominis
Salmonella Cryptosporodium Parvum
Cyclospora Cayetanensis
Shigella
Encephalitozoon Intestinalis *
Staphylococcus aureus Entamoboeba histolytica
Vibriocholerae 01 and 0139 Enterocutazoon biemeasi
Vibrio parahaemolyticus Giardia Lamblia
Yersinia enterocolitica Isospora belli
* Generally Associated with disease, only among Strongiloides Stercoralis
Trichuris Trichuria
immunocompromised person
** Norvalk like viruses
Other Causes of Diarrhea
FEEDING DIFFICULTY FOOD POISONING
ANATOMIC DEFECT Heavy Metal
Malrotation Scombroid
Intestinal duplication Ciguatera
Hirschprung Disease Mudhrooms
Fecal Impaction NEOPLASMA
Short Bowel Syndrome Neuroblastoma
Microvillus Atrophy Ganglioneuroma
Strictures Phaechromocytomas
MALABSORPTION Carcinoid
Disacharidase Deficiencies Zolinger-Ellison Syndrome
Glucose-Galactose Malabsorption Vasoactive Intestinal Peptide Syndrome
Pancreatic Insufficiency
MISCELLANEUS
- Cystic Fibrosis
Nongastrointestinal Infection
- Schwachmann Syndrome
Milk Allergy
Reduced Intraluminal bile Salts
Crohn Disease ( Regional enteritis)
- Cholestasis
Familial dysautonomia
Hartnup Disease
Abetalipoproteinemia
Protein-losing enteropathy
Celiac Disease Ulcerative Colitis
ENDOCRINOPATHIES Acrodermatitis enteropathy
Thyrotoxicosis Laxative abuse
Addison disease Motility disorders
Adrenogenital Syndrome Pellagra
 Differential Diagnosis of Osmotic
versus secretory Diarrhea
Osmotic Diarr Secretoric Diarr
Vol of Stool < 200 ml/24 hrs > 200 ml/24 hrs
Response to fasting
diarrhea stop diarrhea continue
Stool Na+ < 70 mEq/L >70mEq/L
Reducing substances
positif negative
Stool 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 bakterialtoksin.
Osmotic : malabsorpsi, infeksi
virus bakterial/virus dan ggn digesti
Allergi (CMA)
(peristaltik)
Causes of Secretory Diarrhea
Activation of Cyclic Adenosine Monophosphate
Bacterial toxins : enterotoxin of cholera, Escherichia Coli (heat-labile),
Shigella, Salmonella, Campylobacter jejuni, Pseudomonas
aeruginosa
Hormones : Vasoactive intestinal peptide, gastrin, Secretin
Anion Surfactans : Bile acids, Ricinolic acid

Activation of Cyclic Guanosine Monophosphate

Bacterial Toxins : E Coli (heat Stable) Enterotoxin, Yersinia
enterocolitica toxin

Calcium – Dependent
Bacterial toxins : Clostridium difficile enterotoxin
Neurotransmitters : Acethylcholine, Serotonin
Paracrine Agent : Bradykinin
Causes of Osmotic Diarrhea
Malabsorption 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 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
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 Hyperplasia

Irradiation
Autoimmune Enteropathy
Small Bowel Ischemia
Eosinophilic 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

 GANGGUAN DIGESTI MALNUTRISI

KUMAN-VIRUS MASUK
KERUSAKN VILI KEDALAM MULUT:
MANDI,MINUM, MAKAN

DIARE
Susu sapi Susu formula
Susu sapi Susu formula
Bayi Minum
ASI
CRO
SIKLUS DIARE AKUT-DIARE
KRONIK-MALNUTRISI-INFEKSI

GNG
DIARE
AKUT ABSORPSI

INFEKSI
DIARE KRONIK

MALNUTRISI
 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
Enterotoxigenic
Escherichia coli
160 53 37 24 18 110
Rotavirus 130-160 37 38 22 6 140
Normal 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 DARAH
1.DIARE HIPOTONIK:
KADAR NA< 130 meq/L
2.DIARE ISOTONIK: KADAR NA
131-145 meq/L
3.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 : CT
enterotoksin, tumor kripta, hormon
dan- neurotransmiter
3. Reaksi imun-allergi
4. Meningitis/encephalitis
(5. Peristaltik usus)
“”””
KOMPLIKASI DIARE:
KEHILANGAN H2O: DEHIDRASI
 RINGAN-SEDANG-BERAT
SYOK, GAGAL GINJAL (LIHAT:BAK, UREUM
CREATININ), ENSEFALOPATI
Na+, (Na TINGGIKEJANG, RENDAH
DEHIDRASI BERAT)
K+,(ILEUS PARALYTICUS, FIBRILASI
JANTUNG)
Cl-, (@ Na)
HCO3-, (ASIDOSIS, RR CEPAT DAN DALAM,
KUSSMAUL)
HIPOGLIKEMI: KEJANG, ENSEFALOPATI
 DIAGNOSTIK
1. 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?
Endemik
B.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 Nilai 1 Nilai 2 Nilai 3
yg diperiksa

eadaan umum Sehat Gelisah, ngantuk Mengigau, koma

cengeng, apatis syok
HAUS *)
ekenyalan kulit Normal Sedikit kurang Sangat kurang
BERKURANG*)
ata Normal Sedikit cekung Sangat cekung
CEKUNG *)
bun-ubun besar Normal Sedikit cekung Sangat cekung
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
 PENILAIAN DERAJAT
DEHIDRASI
A. Berdasarkan Kehilangan Berat
Badan
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 %
KEBUTUHAN CAIRAN
MAINTENAN 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 KALIUM
PERHATIAN: DILARANG MEMBERIKAN SECARA BOLUS
Paling 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/hari
HIPERKALEMIA:
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
jam
RUMATAN: 100 ML/KG BB/sisa waktu 24 jam 1
24 jam -3-4 jam 10 menit atau 3-4 jam 30 menit
Pada 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
jam
KP: pasang NGT/OGT

DEHIDRASI RINGAN/TANPA
DEHIDRASI:CAIRAN PER-ORAL (HF)
DEFISIT: 30-50 ML/KG BB/CRT/ORS/3-4jam
RUMATAN: 100 ML/KG BB
TETESAN CAIRAN INFUS
1 ML=15 TETES,
Kalau 1 TETES PERMENIT, maka dalam
1 JAM= 4 MLL, dalam
24 JAM= 96 ML
1 ML=20 TETES,
Kalau 1 TETES PERMENIT, maka dalam
1 JAM= 3 MLL , dalam
24 JAM= 72 ML
1 ML=60 TETES,
1 TETES PERMENIT, maka dalam
1 JAM= 1 MLL , dalam
 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 DIARE
Tidak cukup tanda2 untuk diklasifikasikan
sebagai dehidrasi 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:
Gelisah, rewel/mudah marah
Mata cekung
Haus, minum dengan lahap
Cubitan kulit perut kembalinya lambat
DEHIDRASI 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 oralit 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:
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)
 C. Berdasarkan Gejala
Klinis
Gejala klinis Ringan Sedang Berat

K.U, kesadaran C.M Gelisah Apatis-koma

Rasa haus + ++ Tak bisa
minum
Nadi Normal cepat Cepat sekali
(120)
Pernafasan Biasa Agak cepat kusmaull
Ubun ubun Agak cekung Cekung sekali
cekung
Mata Agak cekung Cekung sekali
cekung
Turgor biasa Agak kurang Kurang sekali
 PRINSIP TERAPI
1. 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 mau
3. 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 spasmolitika
7. 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

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 jam

Dehidras 2.20 ml/kg BB/10’  2x  60/ml/kgBB/3jam

3.20 ml/kg BB/10’  1x  koloid (kalau perlu)

i berat
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)

) Dehidras
i sedang 80 ml/kgBB/7 jam tetesan minimal
V (RL)
Oralit
Rumatan=100 ml/sisa waktu (CRT/ORS)

ORS
Dehidras Rumatan=100 ml dibagi sisa waktu
i ringan CRT
30-50 ml/kgBB/3-4 jam tetesan minimal
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 jelek
2.20ml/kg BB/10’-30 ml/kgbb 30-60 menit –
RL,kalau masih jelek
3.20 ml/kg BB/10 menit-plasma ekspander
4.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
Prof Iqbal Memon
Pakistan
In Malnourished Children the RISK of
DEATH from Diarrhea is:

4 fold
 Management of Dehydration
(WHO)
SIGNS No signs of Some (mod.) Severe
dehydration dehydration 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 Plan A Plan B Plan C

of dehydration at Home At OR Center At Hospital
SHOCK
SHOCK 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 WEIGHT
I.V. RINGER’S WITH 5% DEXTROSE OR
HALF NORMAL WTH 5% DEXTROSE OR
HALF STRENGTH DARROW’S WITH 5% DEXTROSE
15 CC/Kg OVER ONE HOUR
PULSE & Resp Rate q 5-10MIN
GOOD CHANGE: REPEAT; SWITCH TO RESOMAL PER
NG@ 10ml/kg/HRX10 HRS; AND THEN REFEEDING
WITH F-75
NO CHANGE ….after first load …septic shock
 ELECTROLYTE COMPOSITION

Diarrheal Stool WHO oral Rehydration

Solution (ORS) Non
WHO
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
rehydratio
n therapy
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
DEHIDRASI SEDANG
Defisit cairan: 80 ml kg BB/7 jam (oral
atau IV)
Diteruskan rumatan 100 ml/sisa waktu
(Oral atau IV)

DEHIDRASI RINGAN
Diberikan CRT; 30-50 ml/kg BB/ atau
tetesan minimal
KOMPOSISI CAIRAN TUBUH
C.Intraselule
r 40%
Cairan
tubuh C.Intersti
60% sial 15 %
C.Ekstraselule
r 20 %

Plasma
Lemak,
darah
protein,
5%
mineral
40 %
 KOMPOSISI CAIRAN
Cairan Na Cl K Ca Asetat laktat Dekst Kal Osm

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

D½S 77 77 - - - - 50 200 428

D¼S 38.5 38.5 - - - - 50 200 353

B.SOEBAGYO
 Etiology of Chronic Diarrhea
INTRALUMINAL FACTORS
Pancreatic Disorders
Cystic Fibrosis
Schwachmann-Diamond Syndrome
Johannson-Blizzard Syndrome
Isolated-Pancreatic enzyme
deficiencies
Chronic Pancreatitis
Pearson Syndrome
MUCOSAL FACTORS
Altered 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 Diarrhea
Bile acid Disorders *Altered immune function
Chronic cholestasis Autoimmune enteropathy
Terminal ileum resection Eosinophilie gastroenteropathy
Bacterial overgrowth AIDS
Chronic use of bile acid Combined immunodeficiency
squestrant Immunoglobulin A & G
Primary bile acid deficiency
malabsoprtion
Intestinal disorder
Etiology of Chronic Diarrhea
*Internal Disorder Altered Function
Intraluminal osmolarity Defect in Cl-/HCO3-
Carbohidratemalabsoprtion Na+/H+,bile acids
Congenital & acquired Acrodermatitis enteropathie
sucrase, lactase deficiencies Sekretoric lactase deficient
Congenital & acquired
monosacharide Abetta lipoproteinemia
malabsorption
Excessive carbonated fluid
intake
Excessive intake of sorbitol,
Mg (OH)2 & lactase
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
 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 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 10 8-1010
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
Tetrasiklinin-klroramfenicol-kotrimoxasol
Amoeba
Anak >3 tahun (?)=pola makan
bermacam2kontaminasi kuman>>
Berak lembek, berdarah, berlendir,
frekuensi kadang >10 x/hari
Tenesmus
Tanpa panas
T/metronidazole-tetrasiklin