Sheany - Pemicu6 KGD

PROBLEM 6
SHEANY LESTATILA
405110062
Group 3, Emergency Medicine Block
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), 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,
demam, pusing
Pertolongan Segera pada Keracunan

yang Mengancam Nyawa (1st survey)
Pastikan jalan napas terbuka
Dapat diberikan tambahan oksigen, 12 L/mnt
Intubasi apabila refleks 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 1020mg
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
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
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 >>
dengan tanda kesadaran menurun
Klasifikasi
Menurut cara terjadinya
Self poisoning
Pasien makan obat dengan dosis berlebihan

tetapi dengan pengetahuan dosis ini tidak
akan membahayakan, tidak bermaksud
bunuh diri
Attempted
suicide
Pasien memang bermaksud bunuh diri
Accidental
poisoning
Faktor kecelakaan
Homicidal
poisoning
Keracunan
akut
Keracunan
kronik
Seseorang
sengaja
Menurut
mulameracuni
waktu orang lain
Terjadi mendadak setelah memakan sesuatu, banyak
orang (makanan)
Gejala perlahan & lama setelah terpajan
Zat penyebabnya diekresi > 24 jam, T panjang
akumulasi
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
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, feses
Pemeriksaan:
Radiologi : curiga adanya aspirasi melalui
inhalasi atau adanya perforasi lambung
Laboratorium klinik: analisa gas darah,
fungsi hati, ginjal, sedimen urin, GDS
EKG
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
Tertelan
Bila tertelan bahan korosif(asam/basa) atau produk
petroleum jangan lakukan yang no2
1. Usahakan px minum 1/> cairan berikut u/
mengencerkan racun dan menghambat
penyerapannya : susu, suspense terigu,starch /
kentang tumbuk yang dilumatkan dalam air, air.
2. Rangsang px muntah : usapp dinding faring dan
belakang lidah (jari/gagang sendok) tidak
muntah 15 mL (1 sendok makan) sirup Ipecac
3. 1 sendok makan penuh natrium sulfat dilarutkan
dalam 1,5 gelas
4. Pertahankan suhu tubuh dg meggunakan selimut.
Hindari sumber panas external
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.
2.
Dg sengaja (zat warna,penyedap,dll)

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 kaleng proses yang

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

gejala timbul 1 -7 hari
( tergantung penyebab)
Pencegahan: makanan kaleng

dapat di masak dulu selama 15
menit
Pencemaran terjadi karena

makanan dibiarkan terbuka
atau spora yang masih ada
tumbuh kembali
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
Singkong (Cassava)
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 15mnt3 jam
Buku Ajar Anak - IDAI
Patofisiologi :
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
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
Patof :
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
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
Tatalaksana
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 12-24 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
Drugs
intoxication
Acetaminophen
Acute ingestion of more than 150200 mg/kg
(children) or 7 g total (adults)
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
Katzung BG, Masters SB,

Trevor AJ, Basic Clinical
Pharmacology. 11th edition.
US: McGraw-Hill, 2007
highly toxic metabolite is produced in the liver
Treatment
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

antidoteacetylcysteine
Anticholinergic Agents
inhibit the effects of acetylcholine at muscarinic
receptors
"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

Manifestations
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

Treatment
Antidepressants
Tricyclic antidepressants
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)

amitriptyline, desipramine, doxepin
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

Treatment
Monoamine oxidase inhibitors

tranylcypromine, phenelzine
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

Manifestations
Antipsychotics
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

phenothiazines and butyrophenones + newer

atypical drugs
Aspirin (Salicylate)
Acute ingestion of more than 200 mg/kg
chronic overmedication
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

uncoupling of oxidative phosphorylation and

disruption of normal cellular metabolism
Treatment
aggressive gut decontamination
Intravenous fluids
intravenous sodium bicarbonate (for moderate
toxicity)
emergency hemodialysis
poisoning (eg, patients with severe acidosis, coma, and
serum salicylate level > 100 mg/dL)

gastric lavage, repeated doses of activated charcoal,

whole bowel irrigation
Aspirin and other salicylat
Beta Blockers
The most toxic blocker is propranolol
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

At high doses it may cause sodium channel blocking effects

similar to those seen with quinidine-like drugs + lipophilic
(enter the CNS)
Calcium Channel Blockers

Small dose toxicity
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

depress sinus node automaticity and slow AV node

conduction

Carbon Monoxide & Other

Toxic Gases
Cholinesterase Inhibitors
organophosphate or carbamate poisoning
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

Manifestations
Treatment
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

Blood testing
Cyanide
Manifestations
shortness of breath, agitation, and tachycardia
followed by seizures, coma, hypotension, and death
Severe metabolic acidosis
venous oxygen content may be elevated

binds readily to cytochrome oxidase inhibiting

oxygen utilization within the cell cellular
hypoxia and lactic acidosis
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

Treatment
Ethanol & SedativeHypnotic Drugs

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

Manifestations

protecting the airway (including endotracheal
intubation) + ventilation
Hypotension IV fluid
body warming if cold
benzodiazepine overdose intravenous flumazenil

Treatment
Ethylene Glycol &

Methanol
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)

CNS depression and a drunken state similar to

ethanol overdose
appears drunk
severe anion gap metabolic acidosis +
hyperventilation
methanol poisoning visual disturbances
Treatment
fomepizole (4-methylpyrazole)
inhibiting the enzyme alcohol dehydrogenase

Manifestations
Digoxin
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

accumulation of digoxin in a patient with renal

insufficiency
some patient also taking diuretics electrolyte
depletion

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

Treatment
Theophylline
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

dose of 2030 tablets can cause serious or fatal

poisoning
Treatment
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


Aggressive gut decontamination
Intoxications
managements
ABCDs
Airway
Breathing
assessed by observation and oximetry + arterial
blood gases (if in doubt)
Patients with respiratory insufficiency intubated +
mechanically ventilated

cleared of vomitus or any other obstruction

oral airway or endotracheal tube inserted if needed
lateral decubitus position
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

Circulation
History
family members, police, and fire department or

paramedical personnel should be asked
describe the environment
syringes, empty bottles, household products
over-the-counter medications

Oral statements about the amount and even the

type of drug ingested in toxic emergencies may
be unreliable
Physical examinations
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

Vital signs
Eyes
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

Skin
Laboratory & Imaging Procedures

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

Arterial Blood Gases
Renal function tests

Elevated serum creatine kinase (CK) and myoglobin in the
urine muscle necrosis due to seizures or muscular rigidity
Oxalate crystals in the urine ethylene glycol poisoning
Electrocardiogram
Widening of the QRS complex duration to more than 100
milliseconds
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

tricyclic antidepressant and quinidine overdoses
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 treatment

Toxicology Screening
Tests
Decontamination
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

Skin
GI tract
induced with ipecac syrup
should not be used if the suspected intoxicant is a
corrosive agent, a petroleum distillate, or a rapid-acting
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

Emesis
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, enteric-coated 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

Activated Charcoal

Specific antidote

Methods of Enhancing Elimination

of Toxins
Dialysis Procedures
Peritoneal Dialysis
Hemodialysis
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)

enhance removal of toxic metabolites
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

Forced Diuresis and Urinary pH Manipulation
References
Buku Ajar Ilmu Kesehatan Anak; Ikatan Dokter
Anak Indonesia
Katzung BG, Masters SB, Trevor AJ, Basic Clinical
Pharmacology. 11th edition. US: McGraw-Hill,
2007
Pocket book of hospital care for children; WHO:
2013

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PROBLEM 6

Cara racun masuk ke dalam tubuh : sentuhan kulit,

Pertolongan Segera pada Keracunan

Pertolongan Segera pada Keracunan

Jika diduga keracunan alkohol dan

Bilas lambung apabila diduga

Pasien makan obat dengan dosis berlebihan

Pasien memang bermaksud bunuh diri

Isopropil alkohol, aseton

Arsenik, selenium, talium

Hidrogen sulfida, mekraptan

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

Dg sengaja (zat warna,penyedap,dll)

Makanan mengandung Toksin

Toksin yang diproduksi &

Toksin yg spesifik bagi lapisan

Makanan kaleng proses yang

Masa inkubasi 1 96 jam dan

Pencegahan: makanan kaleng

Pencemaran terjadi karena

Makanan mengandung Toksin

Gejala klinis (timbul 8jam 8 hari):

Gejala klinis: muntah, diare,

Tindakan gawat darurat:

Uji Guinard uji singkong tersangka warna

Buku Ajar Anak - IDAI

Eliminasi racun muntah / bilas lambung

Cairan IV dan Oksigenasi dengan tekanan

Buku Ajar Anak - IDAI

Buku Ajar Anak - IDAI

Eliminasi racun : muntah/bilas lambung

Pencegahan : masak biji jengkol dg soda/ bikarbonat lain

Buku Ajar Anak - IDAI

Kelainan mata (lumpuh otot mata)

Katzung BG, Masters SB,

highly toxic metabolite is produced in the liver

Liver transplantation for patients with fulminant

Katzung BG, Masters SB,

"red as a beet" (skin flushed)

Katzung BG, Masters SB,

Agitated patients benzodiazepine or an

Catheterization prevent excessive distention of

Katzung BG, Masters SB,

Katzung BG, Masters SB,

amitriptyline, desipramine, doxepin

Endotracheal intubation and assisted ventilation

Katzung BG, Masters SB,

Monoamine oxidase inhibitors

Katzung BG, Masters SB,

Katzung BG, Masters SB,

phenothiazines and butyrophenones + newer

hyperventilation and respiratory alkalosis