INTOKSIKASI

Dr. dr. Shahrul Rahman, Sp.PD, FINASIM

Departemen Ilmu Penyakit Dalam

Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara
 Acute exposure is a single contact that lasts for
seconds, minutes or hours, or several
exposures over about a day or less. Chronic
exposure is contact that lasts for many days,
months or years.
 A poison may get into the body through
ingestion, inhalation (gas, vapors, dust,
fumes, smoke, spray), skin contact
(pesticides), or injection (bites and stings,
drug injection
History taking
 What poison was ingested.
 Time since ingestion.
 Total amount of poison ingested.
 Route of exposure.
 Progression of signs and symptoms since ingestion.
 Family history of epilepsy, mental sub normality,
bleeding disorder.
 Whether the patient is receiving other medications
which may interact with the poison.
General Management
1. PREVENT FURTHER POISONING

2. KEEP PATIENT ALIVE

3. ANTIDOTE S AND ANTAGONIST

PREVENT FURTHER POISONING
 The patient should be separated from the source of
poison immediately
 Removal of contaminated clothings
 Cleaning of skin and mucous membrane
 Gastric lavage are important
 Vomiting may be induced
 The mouth must be at a lower level than the larynx
KEEP PATIENT ALIVE
 Management of coma
 Management of shock
 Management of respiratory failure
 Good appropriate nursing management
ANTIDOTES AND ANTAGONISTS
 The term “ Universal antidote “ implies an emetic
agent
 Less than 2% instances of poisoning is there a spesific
pharmacological antidotes
 Very few poisons will be antagonised in vivo
Initial resuscitation
stabilization
 Includes airway- proper positioning head tilt and chin
lift, suction of secretions from oropharynx, falling
back of tongue is prevented by suitable airway tube.
 Breathing- oxygen via a mask, when gag/cough
reflects is absent- ET tube inserted. if necessary
positive pressure ventilation with ABG monitoring,
respiratory stimulants for severe respiratory
depression.
 Circulation- proper IV access, maintenance of fluid &
electrolyte balance, IV drugs for treatment.
 Gastric Lavage. If the vomiting does not occur
quickly, gastric lavage should be done
promptly to remove the poison. In a
symptomatic but alert patient with minor
ingestion, activated charcoal alone by mouth is
sufficient for gastrointestinal
decontamination
Insecticides
1. Phenolic substance, e.g. Dinitrophenol
This causes anxiety, tachycardia, arrhythmias,
pyrexia, perspiration and mucosal burns
Treatment : Intensive supportive therapy
Ice packs
Sedation
2. Organophosphorus, e.g. Parathion,
Malathion
This cause restlessness, fibrillary twitches, fits, colic,
salivation, hypotension, unconscious.

Mild Poisoning
INSECTICIDE POISONING
 Cause :
 Suicide
 Homicide
 Accident due to :
 No follow direction use
 Not known (children)

 Route of poisons :
 Airway (inhalation)
 Skin (contact)
 GI Tract

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The most common insecticides that cause poisoning are:
- Organophosphate and Carbamat
- Chlorinated Hydrocarbon
 Organophosphat dan Carbamat.
 organophosphat groups :
 Highly toxicity :
-Octamethyl pyro phospharamide (OMPA)
- Tetraethyl pyrophosphate (TEPP)
- Diisoprophylfluorophosphate (DFP)
- Sulfo tetraethyl pyrophosphate (Sulfo TEEP)
- Parathion
- Phosphamidon
Moderate Toxicity : Low Toxicity :
- Dichlovos
- Quinalphos - Malathion
- Fenthion - Temephos
- Diazinon
- Fenitrothion

Carbamat groups :
Highly toxicity :Aldicarb, Apocarb, Carbofuran.
Moderate toxicity : Carbaryl, Primicarb, Propoxur
Low toxicity : Metam sodium
Mechanism of action of organophosphat & carbamat

 Inhibition of asetylcholinesterase

asetylcholine

Parasymphatic activity
Neuromuscular Activity
Alteration of CNS
Symptoms & Signs
 1. Parasymphatic activity
( Muscarinic effect) :

 Hypersalivation, hypersecretion of bronchial.

 Sweating
 Hyperperistaltic  nausea, vomiting, diarrhea
 Pinpoint pupil (myosis)
 Bradycardia
 Bronchospasm
 Incontinence urine and faecal
Neuromuskular stimulation :
- Twitching - Convulsion

Muscles weakness Paralysis

Resp.muscles
Death
 Alteration of CNS :

 Confusion
 Psychosis
 Coma
 Convulsion
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Management :
 General :
 Gastric lavage (if less than 4 hours)
 Oxygen with Mechanical Ventilation
 IVFD Ringer Lactate / NaCl
 Body cleansing
 Charcoal active : 1 gr / kg BW
 Specific :
 Antidote : Atropine ( Sulphas Atropine / SA)

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 Tidak sadar : 16 ampul (4 mg) iv  8 ampul (2 mg)
per 30 menit sampai sadar

Sadar : 8 ampul (2 mg) iv  2 ampul (0.5 mg)/30 menit

sampai atropinisasi

Atropinisasi : 1 ampul (0.25 mg)/4 jam selama 24 jam

Atropinisation :
Mydriasis, dry skin, dry mouth, flushing and warm,
tachycardia
 Maintenance Dose.
 0,5 mg / 30 minutes or 1 hour or 2 hour or 4 hour (depend
on you need)

 NB :
 Contra indication SA : cyanosis --> VF
 Maximal Dose : 50 mg / 24 hours.
 1 amp SA = 0,25 mg
Obat lain yang diberikan setelah atropinisasi:
 Diazepam : 5 - 10 mg IV

 Pralidoksim :
 Dosis - Inisial : 2 gr IV
- Maintenance : 8 mg/kgBB/jam selama 24 j

 Obidoksim :

Dosis : - Inisial : 250 mg / IV

- Maintenance : 0,5 mg/kgBB/jam selama 24 j

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Organo Klorin
 Jenisnya :
 Toksisitas tinggi : - Toksisitas rendah :
 Aldrin - Ethylan
 Endrin - Hexachlorbenzene
 Dieldrin - Methoxychlor
 Endosulfan
 Toksisitas sedang :
- Chlordane - DDT
- Heptaklor - Kepone
- Lindane - Minex - Toxaphene
Tanda &Gejala Klinis
 Gelisah, gemetar, lemah
 Sakit kepala, vertigo
 Kesadaran menurun (delirium, koma)
 Kejang, paralisis --> apnu
 Takikardia, vibrilasi ventrikel
 Takipnu, sianosis, edema paru.
 Kalau tertelan : muntah, diare, sakit perut
 Kalau terinhalasi : hidung / tenggorokan terasa
spt terbakar
 Kalau kena mata : iritasi, spt terbakar
 Kalau kena kulit : iritasi, bintik-bintik merah
Keracunan kronis :
Sakit kepala, insomnia, gangguan jiwa, sulit konsentrasi,
depressi, twitching, kejang, gangg. spermatogenesis, Ca
 Penatalaksanaan:
 Bersihkan kulit dan mata.
 Bila tertelan : rangsang muntah, kumbah lambung dan
beri arang aktif.
 Bila kejang : Diazepam 10 mg IV
 Antidotum : tidak ada.
 Phenobarbital 100-200 mg/ hari selama beberapa hari - 2
minggu untuk :
 Mempercepat metabolisme organoklorin
 Mengurangi keluhan

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BOTULISMUS
 Definisi : adalah suatu bentuk keracunan akibat
memakan makanan yang mengandung toksin
botulin yang dihasilkan oleh Clostridium
botulinum.
 Etiologi : Clostiridium botulinum
menghasilkan endotoksin / neurotoksin
tdd 7 strain : A-G
yg paling sering : A,B,E
 Spora : -mati pd temp.1200C selama 30 mnt
-tahan temp 1000C beberapa jam pada
Toksin : rusak pd - temp.1000C selama 1 mnt
- temp 800C selama 20 mnt
 Pertumbuhan di hambat oleh Nitrat.
 Pathogenesis :
 Keracunan terjadi melalui berbagai cara :
1. Termakan makanan yang mengandung toksin
botulin (makanan basi, diasapi, peragian)
diabsorbsi, terutama di lambung &
usus halus bagian atas
Absorbsi di bagian bawah usus halus &
kolon : lambat.
2. Wound botulism:
C. botulinum masuk melalui luka / suntikan
subkutan (ok tdk tepat) berkembang biak
menghasilkan toksin.
Masa inkubasi : 4 - 14 hari

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 Effek dari toksin botulinum :
 Antikolinergik (parasimpatolitik) : menghambat
pelepasan asetil kolin
 Tidak menembus sawar darah otak.
 Dosos toksik : 0,05 mikrogram.

 Gejala klinik:
 Dimulai stlh 12-36 jam (bisa 8 hari) termakan toksin.
 Makin cepat makin berat.
 Mual, muntah, lemah, vertigo.
 Mulut/tenggorokan terasa kering ; sakit menelan.
 Mata : kabur, diplopia.
 Otot (termasuk otot pernafasan) lemah
 apnu kematian
 Pemeriksaan Fisik:

 Kesadaran : normal sampai somnolen

 Mata : ptosis, midriasis, refleks pupil melemah
 Mulut : mukosa & lidah kering
 Paru : obstruksi jln nafas, infeksi sekunder.
 Abdomen : distensi, peristaltik lemah/hilang
 V. urinaria : retensi urin

 EKG : gangguan irama jantung

 Diagnosa :
 Ada riwayat memakan makanan tercemar
 Ada gejala/tanda klinis :
 Laboratorium :
 Mendeteksi toksin pada makanan, muntahan, tinja ----
lama pemeriksaan :24 jam
 Diagnosa Banding:
 Miastenia gravis
 Guillain Barre Syndrome
 Poliomielitis akut
 Stroke
 Keracunan atropin (Belladona)

 Infant Botulismus:
 tjd pd bayi 1 mgg- 6 bulan
 terutama yang diberi madu
 Gejala : Hipotonia
Sulit menelan
Takikardia
 Penatalaksanaan :

 Perbaiki jalan nafas:

 Kalau tjd obstruksi : - trakeostomi
- resp. mekanik
 Cleansing enema.
 Bersihkan luka ( Wound Botulisme)
 Antitoksin : Trivalent (ABE) antitoksin botulin
 diberikan secara IV.
 Hati-hati anafilaktik --- Test dulu

 Antibiotik : Penisilin, Amoksilin, Ampisilin

 Prognosa:

Angka kematian tinggi :

 Strain A : 60 - 70 %
 Strain B : 10 - 30 %

 Strain E : 30 - 50 %

 Makin dini diagnosa ditegakkan :

Makin baik prognosa.
Kerosene
Poisoning
Clinical Presentation
1. Pharynx, esophagus, gastric and small intestine
irritation  burning sensation in mouth, throat
esophagus and mucosa ulcers
2. Ventricle fibrillation  rare
3. CNS : somnolent or coma, rapidly after ingestion
4. Bronchopneumonia
5. Inhalation sign: euphoria like alcohol intoxication
6. Severe Intoxication : albuminuria

Asphyxia  Death
Management
# Induction of emesis  absolute contraindicated
# Adrenalin  contraindicated
# Don’t give Alcohol & Mineral oil
# True therapy :
1. Supportive
2. Oxygen
3. Intravenous fluid line
4. Antibiotic for prophylaxis
5. CNS symptoms  caffeine
Intoksikasi

OPIAT
 Effects of Opiate Administration and Opiate Withdrawal

Opiate Administration Opiate Withdrawal

Hypothermia Hyperthermia
Decrease in blood pressure Increase in blood pressure
Peripheral vasodilation, skin flushed and warm Piloerection (gooseflesh), chillines
Miosis (pupillary constriction) Mydriasis (pupillary dilation)
Drying of secretions Lacrimation, rhinorrhea
Constipation Diarrhea
Respiratory depression Yawning, panting
Antitusive Sneezing
Decreased sex drive Spontaneous ejaculations and orgasms
Relaxation Restlessness, insomnia
Analgesia Pain and irritability
Euphoria Depression

Source.From Jaffe (1985) and Jaffe and Martin (1985)

 Bila pemberian morfin dihentikan secara tiba-tiba maka
akan menimbulkan gejala :

- Craving (mendambakan obat)

- Gelisah, mudah tersinggung dan lekas marah
- Peningkatan kepekaan terhadap rangsang nyeri
- Mual, muntah
- Piloereksi (bulu roma berdiri)
- Disforia (suasana hati tidak nyaman)
- Dilatasi pupil
- Berkeringat
- Takikardia
- Nyeri otot
- Kejang otot (kram)
- Diare
- Hipertensi
- Demam
- Menguap
Heroin yang disuntikkan sendiri
Heroin yang disuntikkan saling bergantian
Over dosis Heroin, menemui ajal dgn mengeluarkan buih dari mulut
 DIAGNOSIS
INTOKSIKASI
• Trias:
 Pinpoint
 Depresi napas
 Penurunan kesadaran (sampai koma)
• Bekas suntikan (needle track sign)
• Pemeriksaan kualitatif urin
Penatalaksanaan
Kegawatan
A (Airways) bebaskan jalan napas dari sumbatan
bahan muntahan, lendir, gigi palsu, dll. Bila perlu
dengan perubahan posisi dan oropharyngeal airway
dan alat penghisap lendir.
B (Breathing) jaga agar pernapasan sebaik mungkin
dan bila memang diperlukan dapat dengan alat
respirator.
C (Circulation) tekanan darah dan volume cairan harus
dipertahankan secukupnya dengan pemberian cairan.
Bila terjadi henti jantung lakukan RJP (Resusitasi
Jantung Paru).
 Protokol Penanganan Overdosis Opiat

B. Pemberian antidotum nalokson :

 Tanpa hipoventilasi: Dosis awal diberikan 0,4 mg iv

(pelan-pelan atau diencerkan)
 Dengan hipoventilasi: Dosis awal diberikan 1-2 mg iv
(pelan-pelan atau diencerkan)
 Bila tidak ada respon diberikan nalokson 1-2 mg iv
tiap 5-10 menit hingga timbul respon atau mencapai
dosis maksimal 10 mg
 Protokol Penanganan Overdosis Opiat

 Efek nalokson berkurang 20–40 menit dan pasien dapat jatuh

kedalam keadaan overdosis kembali, sehingga perlu pemantauan
ketat tanda-tanda penurunan kesadaran, pernapasan dan
perubahan pada pupil serta tanda vital lainnya selama 24 jam.
Untuk pencegahan dapat diberikan drip nalokson satu ampul
dalam 500 cc D5% atau NaCl 0,9% diberikan dalam 4 – 6 jam.
 Simpan sampel urin untuk pemeriksaan opiat urin dan
lakukan foto toraks.
 Protokol Penanganan Overdosis Opiat

 Pertimbangkan pemasangan ETT (endotracheal tube) bila :

A. Pernapasan tidak adekuat setelah pemberian nalokson
yang optimal.
B. Oksigenasi kurang meski ventilasi cukup
C. Hipoventilasi menetap setelah 3 jam pemberian nalokson
yang optimal.
 Pasien dipuasakan  6 jam untuk menghindari aspirasi
akibat spasme pilorik
Hipotensi diberikan cairan IV yang adekuat, dapat
dipertimbangkan pemberian dopamin dengan dosis
2 - 5 mcg/Kg BB/menit dan dapat ditritasi bila diperlukan.
Terima Kasih