Pemicu 6

Keracunan pada anak
Curigai keracunan pada anak sehat

yang mendadak sakit dan tidak
dapat dijelaskan penyebabnya.
WHO pocket book
Diagnosis
Carilah informasi:
- bahan penyebab keracunan
-jumlah racun yang terpajan
-waktu pajanan ke dalam tubuh
secara lengkap.
Periksalah tanda terbakar di dalam
atau sekitar mulut, atau apakah ada
stridor (kerusakan laring) yang
menunjukkan racun bersifat korosif.
WHO pocket book
Anak yang kemasukan bahan korosif atau

bahan hidrokarbon jangan dipulangkan
sebelum observasi selama 6 jam.
Bahan korosif luka bakar pada esofagus
yang mungkin tidak dapat segera
terlihat .
Bahan hidrokarbon jika terhirup edema
paru yang mungkin membutuhkan waktu
beberapa jam sebelum timbul gejala.
WHO pocket book
Prinsip tatalaksana racun yg

tertelan
Dekontaminasi Lambung
Dekontaminasi lambung
(menghilangkan racun dari lambung)
efektif bila dilakukan sebelum masa
pengosongan lambung terlewati.
tidak rutin dilakukan pada kasus
keracunan.
WHO pocket book
KI dekontaminasi lambung
~ Keracunan bahan korosif atau
senyawa hidrokarbon (minyak tanah,
dll) karena mempunyai risiko terjadi
gejala keracunan yang lebih serius .
~ Penurunan kesadaran (bila jalan
napas tidak terlindungi).
WHO pocket book

tertelan
Jika anak tertelan minyak tanah,
premium atau jika mulut dan
tenggorokan mengalami luka bakar
(misalnya karena bahan pemutih,
pembersih toilet atau asam kuat dari
aki), jangan rangsang muntah
tetapi beri minum air.
WHO pocket book

tertelan
Jika anak tertelan racun
lainnyaBerikan arang aktif
(activated charcoal) jika tersedia,
jangan rangsang muntah.
Jika arang aktif tidak tersedia,
rangsang muntah (hanya pada anak
sadar).
WHO pocket book
Prinsip tatalaksana keracunan

melalui kontak mata
Bilas mata selama 10-15 menit
dengan air bersih yang mengalir atau
garam normal, jaga curahannya tidak
masuk ke mata lainnya.
Jika ada kerusakan konjungtiva atau
kornea, anak harus diperiksa segera
oleh dokter mata.
WHO pocket book
Prinsip tatalaksana keracunan

melalui kontak kulit
Lepaskan semua pakaian dan barang
pribadi dan cuci menyeluruh seluruh
daerah yang terkontaminasi dengan
air hangat yang banyak.
Gunakan sabun dan air untuk bahan
berminyak.
WHO pocket book

terhirup
Keluarkan anak dari sumber pajanan
Berikan oksigen dan intubasi, jika
diperlukan
WHO pocket book
Keracunan
Akibat masuknya bahan kimia tertentu ke dalam
tubuh yang menyebabkan timbulnya kelainan pada
tubuh
Jenis jenis racun :
Padat : racun tikus, obat-obatan
Cair : bahan peluntur, cuka getah
Gas : karbon monoksida, ammonia, nitrogen dioksida
Sifat racun :
Korosif : merusak rongga mulut dan saluran

pencernaan (asid dan alkali)
Non korosif : obat-obatan, racun serangga, makanan
tercemar dan lain-lain
Cara racun masuk ke dalam tubuh : sentuhan kulit,

pernapasan, saluran makanan/mulut dan suntikan
Keracunan
Manifestasi klinik : pucat, muntah, sakit perut,
sesak napas, renjatan (shock), kesan terbakar di
mulut jika terminum racun membakar,
penurunan kesadaran
Penanganan :
Kenali racun
Jika pasien tidak sadarkan diri dan tidak bernafas
serta tiada denyutan nadi, lakukan CPR
Rawatan renjatan
Tanda keracunan :
Membakar : mulut hangus/berdarah, susah

bernapas, sakit, renjatan, bibir menjadi putih
Tidak membakar : muntah, sakit perut, muka pucat,
demem, pusing
Pertolongan Segera pada Keracunan

yang Mengancam Nyawa (1st survey)
Pastikan jalan napas terbuka
Dapat diberikan tambahan oksigen, 12 L/mnt(non
rebreathing mask)
Intubasi apabila reflkes menelan
Ukur kadar gas darah arteri dan pH darah
Berikan akses IV
Cek kadar glukosa darah, tes darah lengkap, serum
elektrolit, dan cek fungsi ginjal dan hepar
Tatalaksana koma
Apabila respon pasien lemah/curiga overdosis
narkotik (pinpoint pupil, nafas lemah) naloxone
2mg setiap 1-2 mnt s/d dosis max 10-20mg
Pertolongan Segera pada Keracunan

yang Mengancam Nyawa (1st survey)
Jika diduga keracunan alkohol dan malnutrisi

thiamine, 100mg IM/IV dengan kontrol glukosa
Pertahankan sirkulasi kontrol sirkulasi dan
tatalaksana syok dengan mengembalikan
volume iv dengan infus/crystalloid sollution
Tatalaksana kejang
Monitor EKG
Lakukan bilas lambung
Dengan NGT/OGT dengan arang aktif (1g/kg)
dicampur dengan solutio 70% sorbitol
Cari etiologi
2nd survey
Lakukan anamnesa cepat dan tepat
Mengumpulkan informasi selengkaplengkapnya untuk mengetahui penyebab
Dekontaminasi etiologi penyebab toksisitas
Racun yang terhirup segera pindahkan
penderita dari sumber racun menuju tempat
terbuka dan berikan oksigen
Mata yang terkontaminasi
Segera bilas mata dengan air bersih atau
dengan saline normal
Jika zat asing bersifat asam/basa dapat
menggunakan pH untuk menentukan terapi
2nd survey
Kulit yang terkontaminasi
Segera bilas kulit yang terkontaminasi
dengan air mengalir dan dilute soap solution
Pada kulit yang mengalami luka bakar dapat
menggunakan kalsium glukonat 0.5 ml dari
solutio 10%
Bilas lambung apabila diduga keracunan
akibat tertelan
Bilas lambung dilakukan apabila keracunan
termasuk serius dengan tanda kesadaran
menurun
Terapi bilas lambung dengan obat emetik
sudah tidak dilakukan
Klasifikasi
Menurut cara terjadinya
Self poisoning
Pasien makan obat dengan dosis berlebihan

tetapi dengan pengetahuan dosis ini tidak akan
membahayakan, tidak bermaksud bunuh diri
hanya untuk menarik perhatian
Attempted
suicide
Pasien memang bermaksud bunuh diri
Accidental
poisoning
Faktor kecelakaan
Homicidal
Keracunan
poisoning
akut
Keracunan
kronik
Menurut mula waktu

Seseorang sengaja meracuni orang lain
Terjadi mendadak setelah memakan sesuatu, banyak
orang (makanan)
Gejala perlahan & lama setelah terpajan
Zat penyebabnya diekresi > 24 jam, T panjang
akumulasi
Manifestasi kronik pada organ zat kimia T pendek,
toksisitas terhadap organ kumulatif (nekrosis papilla
ginjal o.k analgesik bertahun)
Klasifikasi
Menurut organ yang terkena :
Racun SSP, hati, jantung, ginjal, dsb
Menurut bahan kimia :
Alkohol, fenol, logam berat, organoklorin
Diagnosis
Laboratorium toksikologi diagnosis pasti
penyebab keracunan
Membantu penegakan diagnosis:
Autoanamnesis & aloanamnesis
Pemeriksaan fisik dugaan tempat masuknya
racun inhalasi, peroral (dgn bau khas),
absorbi kulit & mukosa, atau parentral
berpengaruh pada efek kecepatan & lama
reaksi keracunan
Status kesadaran GCS
Penemuan klinis lain
Bau racun
Bau
Penyebab
Aseton
Isopropil alkohol, aseton
Almond
Sinida
Bawang putih
Arsenik, selenium, talium
Telur busuk
Hidrogen sulfida, mekraptan
Warna urin
Warna
Penyebab
Hijau/ biru
Metilin biru
Kuning-merah
Rimfapisin, besi/ fe
Coklat tua
Fenol, kresol
Butiran keputihan
Primidon
Coklat
Mio/ haemoglobinuria
Ilmu Penyakit Dalam, ed. VI 2014
Gambaran klinis
Kemungkinan etiologi
Pupil pinpoint, frek napas turun
Opioid, inhibitor
kolinesterase(organofosfat, carbamate
insektisida), klonidin, fenotiazin
Dilatasi pupil, laju napas turun
Benzodiazepin
Dilatasi pupil, takikardia
Antidepresan trisiklik, amfetamin,

ekstasi, kokain, antikolinergik,
antihistamin
Sianosis
Obat depresan SSP, bahan penyebab

metHb
Hipersalivasi
Organofosfat/ karbamat, insektisida
Nistagmus, ataksia, tanda

serebelar
Antikonvulsan(fenitoin, CMZ), alkohol
Gejala ekstrapiramidal
Fenotiazin, haloperidol, metoklopramid
Seizures
Antidepresan trisiklik, antikonvulsan,

teofilin, antihistamin, OAINS, fenotiazin,
isoniazid
Hipertermia
Litium, antidepresan trisiklik,

antihistamin
Hipertermia, hipertensi,
takikardi,agitasi
Amfetamin, ekstasi kokain
Pemeriksaan Penunjang
Sampel yang harus di kirim: 50ml urin, 10 ml
serum, bahan muntahan, feses
Pemeriksaan:
Radiologi : curiga adanya aspirasi melalui
inhalasi atau adanya perforasi lambung
Laboratorium klinik: analisa gas darah, fungsi
hati, ginjal, sedimen urin, GDS
EKG: sering terdapat sinus takikardi, sinus
bradikardi, takikardi supraventikular, takikardi
ventikular, asistol, disosiasi elektromekanik, dll
Penatalaksanaan
Stabilisasi (ABC)
Dekontaminasi menurunkan paparan terhadap racun,
mengurangi absorbsi, dan mencegah kerusakan:
Dekontaminasi pulmonal
Dekontaminasi mata
Dekontaminasi kulit
Dekontaminasi GIT
Eliminasi mempercepat pengeluaran racun yang sedang
beredar dalam darah atau dalam saluran GIT setelah >
4jam
Diuresi paksa
Alkalinisasi urin
Asidifikasi urin
Hemodialisis / peritoneal dialisis
Antidotum
Intoksikasi makanan
Intoksikasi Makanan
Makanan beracun karena :
1. Memang mengandung zat kimia
berbahaya ;ex: singkong,jamur,dsb
2. Timbul zat beracun krn proses
penyimpanan dan pemasakan
3. Tercemar oleh zat racun
1. Dg sengaja (zat warna,penyedap,dll)
2. MO (Stafilokokus,Salmonella,dll)
Makanan mengandung Toksin

EKSOTOKSIN
ENTEROTOKSIN
Toksin yang diproduksi &

dikeluarkan oleh mikroorganisme
yang masih hidup
Toksin yg spesifik bagi lapisan

lendir usus, seperti tahan
terhadap enzim tripsin & stabil
terhadap panas)
Makanan non asam kaleng

proses yang kurang sempurna
clostridium botulinum / sporanya
tumbuh
Masa inkubasi 1 96 jam dan

gejala timbul 1 -7 hari
( tergantung penyebab)
7 tipe eksotoksin: A, B, C, D, E, F,
G
Pencemaran terjadi karena

makanan dibiarkan terbuka atau
spora yang masih ada tumbuh
kembali
Pencegahan: makanan kaleng

dapat di masak dulu selama 15
menit
Pencegahan: Makanan di simpan

dalam lemari pendingin
dan penderita infeksi mata &
kulit sebaiknya jangan
mengelola makanan
Makanan mengandung Toksin

EKSOTOKSIN
ENTEROTOKSIN
Gejala klinis (timbul 8jam 8 hari):

muntah, penglihatan ganda,
kelumpuhan otot, diare dan sakit
perut, ptosis dan pupil membesar,
sukar menelan, lemah, kelumpuhan
otot pernapasan, gangguan saluran
cerna (mungkin tak terlihat)
Gejala klinis: muntah, diare,

mual, sakit perut, kejang perut,
dapat demam, dehidrasi dan
syok
Tindakan gawat darurat:

Usahakan muntah (beri natrium
bikarbonat & karbon aktif)
Dapat dilakukan pengurasan
lambung & pembersihan usus
(kecuali diare)
Penanggulangan:
Muntah klorpromazin 25
100mg (IM/rektal)
Keracunan ringan istirahat
sampai muntah berhenti (jangan
di beri apa apa melalui mulut
selama 4 jam) 12-24 jam diberi
makanan cair
Jika diare & muntah berat RS
antimuntah & cairan IV
Tindakan umum:
Depresi pernapasan pernapasan
buatan
Cegah aspirasi oaru
Tempe Bongkrek
Bongkrek sejenis tempe yang dalam proses
pembuatannya di campur dengan ampas kelapa
Terjadi kontaminasi Pseudomonas cocovenenans yg
memproduksi racun as. Bongkrek (tidak berwarna) &
toksoflavin (berwarna kuning)
Gejala klinis: mual, muntah, diare, pingsan dan
meninggal
Penanggulangan:
Bila perlu beri pernapasan buatan
Usahakan untuk muntah (bila tidak muntah)
Lakukan pengurasan lambung
Pencegahan:
Hindari konsumsi tempe bongkrek
Singkong (Cassava)
Patofisiologi :
Singkong mengandung glikosida sianogenik

linamarin (C10H17O6N) lapisan luar
glukosa,aseton dan asam sianida (HCN)
HCN : sianmethemoglobin, keracunan protoplasmik
melumpuhkan pernafasan sel
Mekanisme : berikatan reversibel dengan sitokrom
oksidase seluler menghambat penggunaan o2
asfiksia. Yang tidak terikat -> metabolisme
tiosianat
Uji Guinard uji singkong tersangka warna

asam pikrat kuning mjd kemerahan dalam
15mnt-3 jam
Buku Ajar Anak - IDAI
Manifestasi klinis
Tergantung jumlah kandungan HCN dalam singkong
Jumlah besar : kematian dalam waktu singkat akibat
gagal nafas
Mula-mula : panas pada
perut,mual,pusing,sesak,lemah nafas cepat dg
inspirasi pendek & bau bitter almond (bau nafas dan
muntahan)
Sesak disusul pingsan,kejang
lemas,berkeringat,mata menonjol,pupil melebar tanpa
reaksi
Busa pada mulut tercampur warna darah dan warna
kulit mjd merah bata
Tidak ada sianosis
Tatalaksana
Awal
Eliminasi racun muntah / bilas lambung

Pemberian antidotum
Amil/Na Nitrit
dan Na-tiosulfat
Proses detoksifikasi
Na-Nitrit : metHb cukup banyak
mengikat NaCN tidak merusak enzim
pernafasan dan sel ferisitokrom oksidase
3 % ml iv pelan-pelan
Na-tiosulfat : iket NaCN terbentuk
tiosianat keluar melalui
paru,ludah,kencing
10% iv dg dosis 0,5 ml/kgbb/kali
Resusitasi dan
suportif
Cairan IV dan Oksigenasi dengan tekanan

tinggi
(hiperbarik/CPAP)
Jengkol
Epidemiologi :
: = 9:1
Kejadian tertinggi terdapat pada umur 4-7 tahun
Patof :
jengkol mengandung asam jengkolat (AA yang

mengandung belerang) bertumpuknya asam
jengkolat dalam tubulis distal ginjal (kristal),
ureter dan uretra
Pada anak keluhan mulai timbul 5-12 jam
setelah makan
Timbulnya gejala keracunan jengkol tergantung
dari kerentanan seseorang terhadap asam
jengkolat
Manifestasi klinis
Sakit pinggang, nyeri perut, muntah, sakit
waktu kencing
Air kemih keluar sedikit-sedikit dg butir-butir
putih urin berbau jengkol dg hematuria
Oliguri anuria
Muntah
Pegal
Infiltrat pada penis,skrotum,daerah
suprapubik
GGA
Tatalaksana
Eliminasi racun : muntah/bilas lambung

Tidak ada antidotum yang khas
Cairan IV bila px tidak dapat minum banyak
GGA : dialisis
Ringan (muntah, sakit perut / pinggang saja) tidak perlu
dirawat, cukup dinasehati untuk banyak minum serta
memberikan Natrium bikarbonat saja
Berat (oliguria, hematuria, anuria dan tidak dapat minum)
penderita dirawat dan diberi infus natrium bikarbonat dalam
larutan glukosa 5%. Dosis dewasa dan anak 2-5mEq/kgBB dan
natrium bikarbonat diberikan secara infus selama 4-8 jam.
Antibiotik (jika ada infeksi sekunder)
Pencegahan : masak biji jengkol dg soda/ bikarbonat lain

Botulisme
Kontaminasi o/ Clostridium botulinum
dan/atau Bacteria cocovenans gliserin mjd
racun toksoflavin media minyak,daging,ikan
yang tidak sempurna
diproses/diawetkan,makanan kaleng
GK/:
Kelainan mata (lumpuh otot mata)

Lumpuh N. Kranialis simetris
Disfagia/disartria
Lumpuh otot pernapasan
Muntah pada permulaan penyakit dan seringkali
hebat
Talaks/:
Eliminasi racun : bilas lambung,obat
pencahar
Depresi napas berat: pernafasan
mekanis buatan
Antidotum : antitoksin botulisme IV
10-50 ml setelah dilakukan tes kulit
Kuanidin hidroklorida lwn blokade
neuromuskular dg dosis 15-35
mg/kgBB/hari dibagi dalam 3 dosis
Makanan tercemar bakteri

Endotoksin o/ Salmonella/Stafilokokus
tumbuh dalam suhu hangat
mudah dihancurkan dalam panas
Ex : sosis,ham,ikan,susu
GK/:
Muntah dan diare 3-6 jam , berlanjut 1224 jam dan kemudian mereda
Kadang timbul nyeri perut
hebat,demam,dehidrasi dan kaku otot
Talaks/:
Suportif dan simptomatis Cairan IV
dan obat u/ meredam gerakan usus
Makanan yang belum dimakan
dipanaskan kembali slm 15 menit u/
menghancurkan toksin tsb
Corrosives compounds
sodium hydroxide, potassium
hydroxide, acids, bleaches or
disinfectants
Managements
Do not induce vomiting or use activated
charcoal when corrosives have been
ingested
may cause further damage to the mouth,
throat, airway, lungs, oesophagus and
stomach
Give milk or water as soon as possible to

dilute the corrosive agent
nothing by mouth and arrange for surgical
review to check for oesophageal damage
or rupture, if severe
Pocket book of hospital care for
children; WHO: 2013
Petroleums compound
kerosene, turpentine
substitutes, petrol
Hidrokarbon
Gol minyak tanah,bensin,terpentin,pelarut
cat
GK/:
Pernafasan : batuk,edema
paru,pneumonitis,pneumonia
SSP : letargi,semikoma,koma
Pencernaan : mual,kembung,sakit perut
Demam,dll
Leukositosis dan demam bukan tanda

infeksi yang jelas
Penyebab meninggal :
Pernafasan : hiperemia,edema paru,jar

hemoragik,nekrosis jaringan paru dan
salurannya,sumbatan PD,necrotizing
bronchopneumonia
Keracunan alveolar,kolaps dan menutupnya

saluran udara bag distal
hipoxia,sianosis,koma
Kelainan SSP o/k hipoxia
Talaks
Eliminasi racun
Tanpa melakukan evakuasi isi

lambung rangsang muntah
dan bilas lambungaspirasi
dan berat intoksikasi
Biasanya masuk melalui
inhalasi (lewat paru) bukan
lewat GIT/langsung ke SSP
Antimikroba
Dipertimbangkan anak gizi

buruk + keracunan parah (t1
24-96 jam pertama)
Kortikosteroid
u/ mencegah fibrosis dan

edema paru teori
O2 dan perbaiki Ventilasi
Suportif
Upaya paling mendasar
Terutama hipoxia kasus berat
CPAP(continous positive
airway pressure)/IPBB
(intermittent positive pressure
breathing) perbaikan
proses disosiasi gas dalam
paru
Pencegahan
Simpan barang beracun di

tempat rapi dan jauh dari
jangkauan anak
Manifestations &
management
Manifestations
Inhalation
pulmonary oedema and lipoid pneumonia
respiratory distress with hypoxaemia
Ingestion encephalopathy
Management
Do not induce vomiting or give activated
charcoal
Specifi c treatment includes oxygen therapy
if there is respiratory distress
children; WHO: 2013
Irons intoxication
Clinical features
nausea, vomiting
abdominal pain
Diarrhoea
Gray/black vomit and stools
Severe
gastrointestinal haemorrhage, hypotension,
drowsiness
convulsions and metabolic acidosis
children; WHO: 2013
Management
Consider gastric lavage if potentially
toxic amounts of iron were taken
Administration of antidote
deferoxamine
slow IV infusion: initially 15 mg/kg per h
reduced after 46 h so that the total dose does not
exceed 80 mg/kg in 24 h
Maximum dose, 6 g/day
IM: 50 mg/kg every 6 h. Maximum dose, 6 g/day
End-points clinically stable patient

and serum iron < 60 mol/litre
children; WHO: 2013
Pesticides intoxication
Organochlorine Pesticides
aryl, carbocyclic, or heterocyclic
compounds containing chlorine substituents
The individual compounds differ widely in their
biotransformation and capacity for storage in
tissues
toxicity and storage are not always correlated
can be absorbed through the skin as well as

by inhalation or oral ingestion
DDT in solution is poorly absorbed through the
skin
dieldrin absorption from the skin is very efficient
Katzung BG, Masters SB, Trevor AJ,
Basic Clinical Pharmacology. 11th
edition. US: McGraw-Hill, 2007
Agents

Human toxicology
Acute toxic properties
inactivation of the sodium channel in excitable membranes

+ calcium ion transport is inhibited
rapid repetitive firing in most neurons
affect repolarization and enhance the excitability of neurons
Manifestations
Tremor convulsions (especially DDT)
Carcinogenic properties
enhanced tumorigenicity (in animals)

association between prepubertal exposure to DDT and brain
cancer
testicular cancer is increased in persons with elevated DDE
levels
risk of non-Hodgkin's lymphoma (NHL) also seems to be
increased
Management
No specific treatment in acute
intoxications
Symptomatic treatment

Organophosphorus
Pesticides
based on compounds such as
soman, sarin, and tabun, which were
developed for use as war gases
used to combat a large variety of pests
absorbed by the skin as well as by

the respiratory and gastrointestinal
tracts
Biotransformation is rapid
Agents

Human toxicology
inhibition of acetylcholinesterase through phosphorylation

of the esteratic site
accumulation of acetylcholine direct cholinergic activity
Manifestations
Altered neurologic and cognitive functions
capable of phosphorylating another enzyme (neuropathy

target esterase) present in neural tissue
progressive demyelination of the longest nerves paralysis

and axonal degeneration (organophosphorus ester-induced
delayed polyneuropathy/OPIDP)
Manifestations
burning and tingling sensations

motor weakness a few days later
ataxia may be present
Central nervous system and autonomic changes

Carbamate Pesticides
= organophosporus pesticides
clinical effects due to carbamates are of
shorter
Spontaneous reactivation of cholinesterase
is more rapid

Management (organophosporus &

carbamate intoxications)
Acute intoxication
Dominant initial sign must be recognized
miosis, salivation, sweating, bronchial constriction,
vomiting, and diarrhea
CNS involvement (cognitive disturbances, convulsions,
and coma)
depolarizing neuromuscular blockade
Therapy
maintenance of vital signs

decontamination to prevent further absorption
atropine parenterally in large doses;
Pralidoxime NOT recommended for carbamate
intoxication
benzodiazepines for seizures
Chronic exposure
Sign & symptoms
neuropathy target esterase (NTE) inhibition

weakness of upper and lower extremities, unsteady
gait in 1-2 weeks
intermediate syndrome (muscle weakness) occurs 14
days
Therapy
Triorthocresyl phosphate (additive in lubricating oils)
Preventive therapy
Pyridostigmine
prior binding to the enzyme impedes binding of

organophosphate agents
Botanical Pesticides
Nicotine
leaves of Nicotiana tabacum and N rustica
rapidly absorbed from mucosal surfaces; free

alkaloid, but not the salt, is readily absorbed
from the skin
Nicotine reacts with the acetylcholine receptor of
the postsynaptic membrane depolarization of
the membrane
Toxic doses cause stimulation rapidly followed by
blockade of transmission
Treatment
maintenance of vital signs and suppression of

convulsions
Rotenone
Derris elliptica, D mallaccensis,
Lonchocarpus utilis, and L urucu
oral ingestion gastrointestinal

irritation; or conjunctivitis, dermatitis,
pharyngitis, and rhinitis
Treatment
Symptomatic
Pyrethrum
pyrethrin I, pyrethrin II, cinerin I, cinerin II, jasmolin I, and jasmolin II
may be absorbed after inhalation or ingestion

major site of toxic action is the central nervous system
Voltage-gated sodium, calcium, and chloride channels &
benzodiazepine receptors
Manifestations
excitation, convulsions, and tetanic paralysis

irritant asthma, reactive airways dysfunction syndrome (RADS),
anaphylaxis
Cutaneousparesthesias
Treatment
management of symptoms
Anticonvulsants are not consistently effective
chloride channel agonist, ivermectin
pentobarbital and mephenesin
Drugs intoxication
Acetaminophen
Acute ingestion of more than 150200
mg/kg (children) or 7 g total (adults)
highly toxic metabolite is produced in the liver
Manifestations
Asymptomatic, mild gastrointestinal upset

(nausea, vomiting)
elevated aminotransferase levels and
hypoprothrombinemia (2436 hours)
fulminant liver failure occurs hepatic
encephalopathy and death
Renal failure may also occur
Treatment
antidoteacetylcysteine
glutathione substitute binding the toxic
metabolite as it is produced
most effective when given early and should
be started within 810 hours if possible
Liver transplantation for patients with

fulminant hepatic failure

Anticholinergic Agents
inhibit the effects of acetylcholine at muscarinic
receptors
Manifestations
"red as a beet" (skin flushed)

"hot as a hare" (hyperthermia)
"dry as a bone" (dry mucous membranes, no sweating)
"blind as a bat" (blurred vision, cycloplegia)
"mad as a hatter" (confusion, delirium)
Muscle twitching
seizures are unusual
unless the patient has ingested an antihistamine or a
tricyclic antidepressant
Urinary retention

Treatment
Agitated patients benzodiazepine or an
antipsychotic agent (eg, haloperidol)
specific antidote for peripheral and central
anticholinergic syndrome
Physostigmine 0.51 mg IV + monitoring
(bradycardia and seizures)
should not be given to a patient with suspected
tricyclic antidepressant overdose aggravate
cardiotoxicity, resulting in heart block or asystole
Catheterization prevent excessive

distention of the bladder
Antidepressants
Tricyclic antidepressants
amitriptyline, desipramine, doxepin
more than 1 g of a tricyclic (or about 1520

mg/kg) lethal
Manifestations
tachycardia, dilated pupils, dry mouth; vasodilation
Centrally mediated agitation and seizures followed
by depression and hypotension
Quinidine-like cardiac toxicity wide QRS interval
and depressed cardiac contractility arrythmia
(ventricular conduction block and ventricular
tachycardia)
Treatment
Endotracheal intubation and assisted
ventilation
Intravenous fluids are given for hypotension
+ dopamine/NE (if necessary)
antidote for quinidine-like cardiac toxicity
(manifested by a wide QRS complex)
sodium bicarbonate; bolus of 50100 mEq
(or 12 mEq/kg)
Do not use physostigmine!
aggravate depression of cardiac conduction
and cause seizures
Monoamine oxidase inhibitors

tranylcypromine, phenelzine
Manifestations
severe hypertensive reactions when interacting foods or

drugs are taken
interact with the selective serotonin reuptake inhibitors
(SSRIs)
Newer antidepressants
fluoxetine, paroxetine, citalopram, venlafaxine (SSRIs)

can cause seizure
interact with each other or especially with monoamine
oxidase inhibitors to cause the serotonin syndrome
agitation, muscle hyperactivity, and hyperthermia
Bupropion seizure

Antipsychotics
phenothiazines and butyrophenones +
newer atypical drugs
Manifestations
CNS depression, seizures, and hypotension
QT prolongation
potent dopamine D2 blockers
parkinsonian movement disorders (dystonic
reactions)
neuroleptic malignant syndrome
"lead-pipe" rigidity, hyperthermia, and autonomic
instability
Aspirin (Salicylate)
Acute ingestion of more than 200 mg/kg
chronic overmedication
uncoupling of oxidative phosphorylation and
disruption of normal cellular metabolism
Manifestations
hyperventilation and respiratory alkalosis

Metabolic acidosis follows, an increased anion gap
Body temperature may be elevated
Severe hyperthermia + Vomiting and hyperpnea
fluid loss and dehydration
seizures, coma, pulmonary edema, and
cardiovascular collapse
Treatment
aggressive gut decontamination
gastric lavage, repeated doses of activated
charcoal, whole bowel irrigation
Intravenous fluids
intravenous sodium bicarbonate (for
moderate toxicity)
emergency hemodialysis
poisoning (eg, patients with severe acidosis,
coma, and serum salicylate level > 100
mg/dL)
Aspirin and other salicylat
Beta Blockers
The most toxic blocker is propranolol
At high doses it may cause sodium channel blocking effects

similar to those seen with quinidine-like drugs + lipophilic
(enter the CNS)
Manifestations
Bradycardia and hypotension

Agents with partial agonist activity (eg, pindolol)
tachycardia and hypertension
Propanolol Seizures and cardiac conduction block (wide
QRS complex)
Treatment
Glucagon is a useful antidote
high doses (520 mg intravenously) improve heart rate and blood

pressure
Calcium Channel Blockers

Small dose toxicity
depress sinus node automaticity and slow AV node

conduction
Manifestations
Serious hypotension (nifedipine and related dihydropyridines)
Treatment
general supportive care

initiate whole bowel irrigation + oral activated charcoal ASAP
Calcium
intravenously in doses of 210 g antidote for depressed cardiac
contractility
glucagon, vasopressin, epinephrine & high-dose

insulin+glucose
Carbon Monoxide & Other Toxic

Gases

Cholinesterase Inhibitors
organophosphate or carbamate poisoning
Manifestations
Stimulation of muscarinic receptors
abdominal cramps, diarrhea, excessive salivation,

sweating, urinary frequency, and increased bronchial
secretions
Stimulation of nicotinic receptors
hypertension and either tachycardia or bradycardia
Muscle twitching and fasciculations eakness

and respiratory muscle paralysis
CNS effects
agitation, confusion, and seizures
Treatment
Blood testing
document depressed activity of red blood cell
(acetylcholinesterase) and plasma
(butyrylcholinesterase) enzymes
General supportive care

ensure that rescuers and health care
providers are not poisoned by exposure to
contaminated clothing or skin
Antidotal treatment
atropine and pralidoxime
Cyanide
binds readily to cytochrome oxidase
inhibiting oxygen utilization within the cell
cellular hypoxia and lactic acidosis
Manifestations
shortness of breath, agitation, and tachycardia
followed by seizures, coma, hypotension, and
death
Severe metabolic acidosis
venous oxygen content may be elevated
Treatment
rapid administration of activated
charcoal + general supportive care
nitrites induce methemoglobinemia,
which binds to free CN
thiosulfate is a cofactor in the enzymatic
conversion of CN
Hydroxocobalamin (one form of vitamin
B12) combines rapidly with CN to form
cyanocobalamin
Ethanol & SedativeHypnotic Drugs

Manifestations
euphoric and rowdy ("drunk") or in a state
of stupor or coma ("dead drunk")
Comatose depressed respiratory drive
aspiration of gastric contents
Hypothermia
Ethanol blood levels greater than 300
mg/dL deep coma
gamma-hydroxybutyrate [GHB] overdose
deeply comatose for 34 hours and then
awaken fully in a matter of minutes
Treatment
protecting the airway (including
endotracheal intubation) + ventilation
Hypotension IV fluid
body warming if cold
benzodiazepine overdose intravenous
flumazenil
Ethylene Glycol & Methanol

CNS depression and a drunken
state similar to ethanol overdose
products of metabolism formic acid
(from methanol) or hippuric, oxalic, and
glycolic acids (from ethylene glycol)
severe metabolic acidosis and can lead to
coma
blindness (in the case of formic acid)
renal failure (from oxalic acid and glycolic
acid)
Manifestations
appears drunk
severe anion gap metabolic acidosis +
hyperventilation
methanol poisoning visual disturbances
Treatment
fomepizole (4-methylpyrazole)
inhibiting the enzyme alcohol dehydrogenase
Digoxin
accumulation of digoxin in a patient with
renal insufficiency
some patient also taking diuretics
electrolyte depletion
Manifestations
Vomitting
Hyper- (overdose) /hypokalemia (diuretic effects)
cardiac rhythm disturbances may occur
sinus bradycardia, AV block, atrial tachycardia with
block, accelerated junctional rhythm, premature
ventricular beats, bidirectional ventricular tachycardia,
and other ventricular arrhythmias
Treatment
Atropine is often effective for
bradycardia or AV block
digoxin antibodies
intravenously in the dosage indicated in the
package insert
improve within 3060 minutes after antibody
administration
Theophylline
dose of 2030 tablets can cause serious or fatal
poisoning
Manifestations
sinus tachycardia and tremor

Vomitting
Hypotension, tachycardia, hypokalemia, and
hyperglycemia
Cardiac arrhythmias
atrial tachycardias, premature ventricular contractions,

and ventricular tachycardia
anticonvulsant-resistant seizure
acute overdose with serum level > 100 mg/L

Treatment
Aggressive gut decontamination
repeated doses of activated charcoal and whole
bowel irrigation
Propanolol or other B-blocker for hypotension

and tachycardia
Phenobarbital
Hemodialysis
serum concentrations greater than 100 mg/L and
for intractable seizures in patients with lower
levels
Intoxications
managements
ABCDs
Airway
cleared of vomitus or any other obstruction
oral airway or endotracheal tube inserted if
needed
lateral decubitus position
Breathing
assessed by observation and oximetry +
arterial blood gases (if in doubt)
Patients with respiratory insufficiency
intubated + mechanically ventilated
Circulation
assessed by continuous monitoring of pulse rate, blood

pressure, urinary output, and evaluation of peripheral
perfusion
intravenous line should be placed
blood drawn for serum glucose and other routine
determinations
Concentrated Dextrose
every patient with altered mental status
unless a rapid bedside blood glucose test demonstrates that the

patient is not hypoglycemic
Adult 25 g (50 mL of 50% dextrose solution) intravenously

Children 0.5 g/kg (2 mL/kg of 25% dextrose)
Alcoholic or malnourished
100 mg of thiamine intramuscularly or in the intravenous infusion
solution
History
Oral statements about the amount and
even the type of drug ingested in toxic
emergencies may be unreliable
family members, police, and fire
department or paramedical personnel
should be asked
describe the environment
syringes, empty bottles, household products
over-the-counter medications
Physical examinations
Vital signs
Eyes
Miosis opioids, clonidine, phenothiazines, and

cholinesterase inhibitors
Mydriasis amphetamines, cocaine, LSD, and atropine
Horizontal nystagmus phenytoin, alcohol,
barbiturates, and other sedative drugs
vertical and horizontal nystagmus phencyclidine
poisoning
Ptosis & ophthalmoplegia botulism
Mouth
Burns corrosive substances & smoke inhalation

Typical odors of alcohol, hydrocarbon solvents, or
ammonia may be noted
odor like bitter almonds cyanide
Skin
flushed, hot, and dry atropine and other

antimuscarinics
Excessive sweating organophosphates, nicotine,
and sympathomimetic drugs
Cyanosis hypoxemia or by methemoglobinemia
Icterus hepatic necrosis due to acetaminophen
or Amanita phalloides mushroom poisoning
Abdomen
Ileus antimuscarinic, opioid, and sedative drugs

Hyperactive bowel sounds, abdominal cramping,
and diarrhea organophosphates, iron, arsenic,
theophylline, A phalloides, and A muscaria
Nervous system

Laboratory & Imaging

Procedures
Arterial Blood Gases
Hypoventilation elevated PCO2
(hypercapnia) and a low PO2 (hypoxia)
PO2 may also be low aspiration
pneumonia or drug-induced pulmonary
edema
total blood oxygen content or
oxyhemoglobin saturation and may
appear normal in patients with severe
carbon monoxide
poisoning
Electrolytes
Sodium, potassium, chloride, and
bicarbonate

Renal function tests

Elevated serum creatine kinase (CK) and
myoglobin in the urine muscle
necrosis due to seizures or muscular
rigidity
normally 280290 mOsm/L
Oxalate crystals in the urine ethylene
glycol poisoning
Serum osmolality
Electrocardiogram
Widening of the QRS complex duration to
more than 100 milliseconds
tricyclic antidepressant and quinidine overdoses
QTc interval may be prolonged to more than

440 milliseconds
quinidine, tricyclic antidepressants, several newer
antidepressants and antipsychotics, lithium, and
arsenic
Variable atrioventricular (AV) block and a

variety of atrial and ventricular arrhythmias
digoxin and other cardiac glycosides
Toxicology Screening Tests

time-consuming, expensive, and
often unreliable
blockers, B-blockers, and isoniazid
are not included in the screening
process
screening tests may be helpful in
confirming a suspected intoxication
or for ruling out intoxication
BUT they should not delay needed
BG, Masters SB, Trevor AJ,
treatment Katzung
Decontamination
Skin
Contaminated clothing should be
completely removed
double-bagged to prevent illness in
health care providers and for possible
laboratory analysis
Wash contaminated skin with soap and
water

GI tract
Emesis
induced with ipecac syrup
should not be used if the suspected intoxicant is a
corrosive agent, a petroleum distillate, or a rapidacting convulsant
Gastric lavage
patient is awake/ airway is protected by an
endotracheal tube using an orogastric or
nasogastric tube
Lavage solutions (usually 0.9% saline) should be at
body temperature
Activated Charcoal
adsorb many drugs and poisons

Ratio 10:1 of charcoal to estimated dose of toxin
by weight
does not bind iron, lithium, or potassium
useful in poisoning due to corrosive mineral acids
and alkali
Cathartics
Whole bowel irrigation with a balanced

polyethylene glycol-electrolyte solution (GoLYTELY,
CoLyte) after ingestion of iron tablets, entericcoated medicines, illicit drug-filled packets, and
foreign bodies
orally at 12 L/h (500 mL/h in children) for several
hours until the rectal effluent is clear
Specific antidote


Methods of Enhancing Elimination of

Toxins
Dialysis Procedures
Peritoneal Dialysis
Hemodialysis
enhance removal of toxic metabolites
formic acid in methanol poisoning
oxalic and glycolic acids in ethylene glycol
poisoning
especially useful in overdose cases +

precipitating drug can be removed
fluid and electrolyte imbalances are present and
can be corrected (salicylateintoxication)
Forced Diuresis and Urinary pH

Manipulation
urinary alkalinization is useful in cases
of salicylate overdose
Acidification may increase the urine
concentration of drugs (phencyclidine
and amphetamines)
not advised worsen renal complications
from rhabdomyolysis
References
Buku Ajar Ilmu Kesehatan Anak;
Ikatan Dokter Anak Indonesia
children; WHO: 2013

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Keracunan pada anak

Curigai keracunan pada anak sehat

WHO pocket book

Anak yang kemasukan bahan korosif atau

Prinsip tatalaksana racun yg

WHO pocket book

WHO pocket book

Prinsip tatalaksana racun yg

WHO pocket book

Prinsip tatalaksana racun yg

WHO pocket book

Prinsip tatalaksana keracunan

WHO pocket book

Prinsip tatalaksana keracunan

WHO pocket book

Prinsip tatalaksana racun yg

WHO pocket book

Korosif : merusak rongga mulut dan saluran

Cara racun masuk ke dalam tubuh : sentuhan kulit,

Membakar : mulut hangus/berdarah, susah

Pertolongan Segera pada Keracunan

Pertolongan Segera pada Keracunan

Jika diduga keracunan alkohol dan malnutrisi

Pasien makan obat dengan dosis berlebihan

Pasien memang bermaksud bunuh diri

Menurut mula waktu

Isopropil alkohol, aseton

Arsenik, selenium, talium

Hidrogen sulfida, mekraptan

Ilmu Penyakit Dalam, ed. VI 2014

Pupil pinpoint, frek napas turun

Dilatasi pupil, laju napas turun

Dilatasi pupil, takikardia

Antidepresan trisiklik, amfetamin,

Obat depresan SSP, bahan penyebab

Organofosfat/ karbamat, insektisida

Nistagmus, ataksia, tanda

Antikonvulsan(fenitoin, CMZ), alkohol

Fenotiazin, haloperidol, metoklopramid

Antidepresan trisiklik, antikonvulsan,

Litium, antidepresan trisiklik,

Amfetamin, ekstasi kokain

Ilmu Penyakit Dalam, ed. VI 2014

Ilmu Penyakit Dalam, ed. VI 2014

Ilmu Penyakit Dalam, ed. VI 2014

Ilmu Penyakit Dalam, ed. VI 2014

Makanan mengandung Toksin

Toksin yang diproduksi &

Toksin yg spesifik bagi lapisan

Makanan non asam kaleng

Masa inkubasi 1 96 jam dan

Pencemaran terjadi karena

Pencegahan: makanan kaleng

Pencegahan: Makanan di simpan

Makanan mengandung Toksin

Gejala klinis (timbul 8jam 8 hari):

Gejala klinis: muntah, diare,

Tindakan gawat darurat:

Hindari konsumsi tempe bongkrek

Singkong mengandung glikosida sianogenik

Uji Guinard uji singkong tersangka warna

Eliminasi racun muntah / bilas lambung

Cairan IV dan Oksigenasi dengan tekanan

jengkol mengandung asam jengkolat (AA yang