KLASIFIKASI RACUN

Toxicology Definition

• Study of the adverse effects of

chemicals or physical agents on living
organisms
• Kajian terhadap bahan kimia atau agen fizikal yang
bertindakbalas dengan sistem biologi dan menghasilkan kesan
merbahaya

+ =
 TOXICOLOGY

POISON * CHARACTERISTIC
* ACTION OF DAMAGE
* CLINICAL SIGN
* THERAPEUTIC MANNER
SUBSTANCE INDIVIDUAL

PHYSIOLOGY
LIFEABILITY
PATOLOGY

DAMAGE OF ACTIONS

LOCAL SYSTHEMIC

DAMAGEOF LOCAL CEL ABSORPTION  CIRCULATION 

(SKIN, MUCOUS) ORGAN  S/SPESIFIC

LOCAL PAIN CYANIDA  RESPIRATION

S/ SYSTEMIC INSECTISIDE  CNS
TOXEMIA STRYCHNIN .SPINAL CHORD
POISONING PROCESS
• ACUTE  24 HOURS
• SUBCHRONIC REPEATE UNTIL 90 DAYS
• CRONIC Up than 6 mounth
Klasifikasi Racun

• Racun dapat diklasifikasikan

berdasarkan atas berbagai hal seperti:
• sumber,
• sifat kimiawi dan fisikanya,
• bagaimana dan kapan terbentuknya,
• efek terhadap kesehatan,
• kerusakan organ, dan
• hidup/tidaknya racun tersebut
Klasifikasi berdasar sumber :
• Sumber alamiah/buatan.
• Klasifikasi ini membedakan racun asli
yang berasal dari flora dan fauna dan
kontaminasi organisme dengan berbagai
racun yang berasal dari bahan baku
industri beracun ataupun buangan
beracun dan bahan sintetis beracun.
• Sumber berbentuk titik, area dan
bergerak. Klasifikasi sumber seperti ini
biasanya dipergunakan orang yang
berminat melakukan pengendalian.
Tentunya sumber titik lebih mudah
dikedalikan daripada sumber area dan
bergerak.
Sumber domestik, komersial dan industri :

• Sumber domestik biasanya berasal dari

permukiman, kurang beracun kecuali
bercampur dengan buangan pestisida,
obat-obatan dll.
• Buangan komersial dapat sangat
beragam, demikian pula dengan
buangan industri
KLASIFIKASI ATAS DASAR WUJUD

Sangat bermanfaat dalam memahami efek

yang mungkin terjadi serta
pengendaliannya
Wujud pencemar :

• Padat : padatan yang sangat halus dapat

terbang bersama udara, disebut debu, fume,
mist, sehingga dampaknya dapat sangat
luas.
• Cair : banyak dipergukan dalam pertanian
dan biasanya ditambah pengencer
dampaknya tidak secepat gas.
• Gas : dapat berdifusi sehingga menyebar
lebih cepat dari pada cairan dan zat padat.
Ukuran pencemar, densitas, serta
komposisi :

• Hal ini akan memberikan petunjuk

mudah tidaknya pencemar
memasuki tubuh host dan cepat
tidaknya menimbulkan efek serta
seberapa jauh efeknya.
Klasifikasi atas dasar sifat fisika dan kimia (B3) :

• Korosif
• Radioaktif
• Evaporatif
• Eksplosif
• Reaktif
Semua nya memerlukan penanganan,
transportasi, dan pembuangan yang
berbeda, karena bahaya yang
mungkin timbul akan berbeda.
Klasifikasi atas dasar terbentuknya
pencemar/xenobiotik:

• Pencemar yang terbentuk dan keluar

dari sumber disebut pencemar primer.
• Pencemar yang sudah bereaksi
dilingkungan disebut pencemar
sekunder.
• Pencemar sekunder yang bereaksi
menjadi pencemar tersier dst.

k/e tgl 27/9/05

Klasifiaksi atas efek kesehatan:

• Fibrosis : terbentuknya jaringat ikat secara

berlebihan;
• Granuloma : didapatnya jaringan radang kronis;
• Demam : suhu badan melebihi suhu normal;
• Asfiksia : keadaan kekurangan oksigen;
• Alergi : sensitifitas yang berlebihan;
• Kanker : tumor ganas;
• Mutan : generasi yang berbeda dg gen induknya
• Teratogenik : cacat bawaan
• Keracunan sistemik : keracunan yang menyerang
seluruh tubuh.
Klasifikasi atas dasar kerusakan organ
target :

• Hepatoksik : beracun pada hati;

• Nefrotoksik : beracun pada ginjal;
• Neurotoksik : beracun pada saraf;
• Hematotoksik : beracun pada sel
darah;
• Pneumotoksik : beracun pada paru-
paru.
Klasifikasi atas dasar hidup/matinya racun :

• Klasifikasi ini dibuat berdasarkan

pertimbangan bahaya yang
ditimbulkannya
• Zat yang hidup dapat berkembang biak
bila lingkungannya mengijinkan
• Zat abiotis dapat berubah menjadi
berbagai senyawa
• Sehingga pengendaliannya berbeda
 Racun biotis atau biotoksin

• Adalah racun yang berasal dari biota;

• Dapat berupa racun asli/racun primer
(biota tsb beracun);
• Racun sekunder : Akibat kontaminasi dg
lingkungannya;
Ada dua jenis racun asli :

• Organisme itu sendiri beracun bagi

manusia atau organisme lain yg
memakannya;
• Racun dari biota sengaja dimasukkan
ke dlm tubuh organisme lain sebagai
defens biota tadi.
Ada 3 macam biotoksin :

• Mikroba;
• Tanaman;
• Hewan.
Racun mikroba :

• Racun di dalam mikroba dapat

berupa :
• racun yang dibuat oleh mikroba itu
sendiri atapun
• dapat berupa sisa metabolismenya
 Mikroba pembentuk racun atau toksin :

• Vibrio cholera;
• Clostridium botulinum;
• Pseudomonas cocovenans;
• Staphilochoccus aureus;
• Michotoksin;
• Algatoksin;
• dll
Racun Biotis (Biotoksin)

• Vibrio Cholerae
• Sebagai penyebab penyakit cholera
• Meski sudah di cegah, namun masih saja
terjadi kasus dan manusia termasuk salah
satu mata rantainya.
• Masuk melalui makanan dan minuman
secara selanjutnya menkontaminasi usus
halu, di dalam usus halus merangsang
enzim adenylcyclase sehingga ion Na tidak
dapat terserap dan terjadi keluarnya ion Cl
kedalam lumen usus, akibat terganggunya
balans osmosis maka banya cairan yang
masuk ke usus, sehingga terjadi diare.
• Pengobatan dengan rehidrasi
Racun Biotis (Biotoksin)

• Clostridium Botulinum
• Penyebab keracunan Botulism
• Gejala keracunan :
- mata tidak fokus
- kelemahan otot.
• Masa tunas : 24 jam – 7 hari dan bila
tidak cepat ditolong maka dalam 3-7 jam
akan terjadi sulit menelan dan sulit
bernapas.
Racun Biotis (Biotoksin)

• Clostridium Botulinum
• Karanteristik :
• Anaerobik
• Gram positif
• Membentuk spora
• Tamperatur optimum 42,5 °C
• pH 5,5 – 8
• Habitat aslinya adalah tanah.
• Resisten terhadap panas diatas 120 °C selama
30 menit.
• Tahan terhadap pendinginan, keadaan aerobik
dan anaerobik, radiasi pengion, dan berbagai
zat kimia.
Racun Biotis (Biotoksin)

• Clostridium Botulinum
• Toksin bakteri ini disebut botulin dengan
LD 50 adalah 0,5 µg.
• Resisten terhadap panas, tetapi botulin
dapat dihancurkan pada suhu 80-100 °C
selama 10 menit.
• Toksin bakteri labil terhadap panas,
berupa protein dan hanya keluar saat sel
pecah atau lisis.
• Sewaktu bakteri ada didalam makanan,
membuat protoksin yang akan dikeluarkan
sebelum dan sewaktu lisis.
Racun Biotis (Biotoksin)

• Pencegahan botulism
• Ph < 4,5
• Garam = 10 % dari berat
• Disimpan pada suhu 3 °C
• Proses masak sampai dengan 90 °C
sebelum dikonsumsi
• Cegah kontaminasidengan tanah, saat
pemrosesan dan penyajian
Racun Biotis (Biotoksin)

• Clostridium Tetani
• Habitat sama dengan botulinum yaitu di
tanah, namun hidup komensal di usus
kuda.
• Penyebab penyakit tetanus
• Toksin yang masuk akan menghambat
glisin sehingga terjadi kejang.
Racun Biotis (Biotoksin)

• Pseudomonas Cocovenans
• Terkenal di daerah banyumas Jateng.
• Terkandung pada tempe bongkrek
(kedelai, bungkil kacang tanah, ampas
kelapa, dan diberi bibit jamur.)
• Racun berasalkan dai ampas kelapa yang
terkontaminasi Pseudomonas Cocovenans
yang memproduksi asam bongkrek.
(cairan tidak berwarna)
• Gejala keracunan terjadi hiperglikemia.
Racun Biotis (Biotoksin)

• Pseudomonas Cocovenans
• Keracunan dimulai dengan hiperglikemi, karena
menghambat ATP, sehingga terjadi glikolisis dari
glikogen mjd glukosa
• Setelah glikogen habis maka terjadi hipoglikemi.
• Merupaka trikarboksilat C28H38O7 dengan berat
molekul 486
• Asam bongkrek merupakan antibiotik terhadap
aspergillus niger dan cladosporium cucumerin.
• LD 50 1,4 mg/kg.
• Saat ini sudah dilarang
Racun Biotis (Biotoksin)

• Staphylococcus Aureus
• Terdapat dimana-mana, kulit, permukaan tubuh,
selaput lendir, hidung, dll
• Menyebabkan, bisul bernanah, pada neonatus
menyebabkan epidemi pneumonia (infeksi paru)
• Karakteristik :
• Gram + pada usia 18-24 jam selanjutnya sesuai
variabel
• Habitat : kult, faring, air susu, tinja, dll
• Temperatur optimum pertumbuhan : 35-37 °C
• Bersifat fakultatif anaerob
• Membentuk enim koagulase
• Hancur pada pH 2 dan oleh pepsin
• Keracunan akut dengan Masa tunas 6-8 jam
Racun Biotis (Biotoksin)

• Corynebacterium diphteriae
• Penyebab diphteri (menyerang
saluran pernapasan dan kulit)
• Mengeluarkan exotoksin oleh
bakteri aerob.
• Efek toksiknya meghentikan sintesa
protein.
• Sifatnya irreversibel
Racun yang berupa metabolit organisme :

• Ammonia;
• Nitrat, nitrit;
• CO, CO2, derifat sulfur dll.
Racun biotis ada disebut exo dan endo-
toksin :

• Exotoksin : dibuat dan dikeluarkan dari

tubuhnya oleh bakteri semasa masih
hidup serta sehat; dan efeknya dapat
dirasakan dari efek yang sangat jauh.
• Endotoksi : hanya dapat dirasakan bila
terjadi kehancuran sel bakteri.
 Perbedaan endotokisn dan exotoksin :

• Endotoksin
• Karakteristik • Exotoksin
• Lisis sel
• Pelepasan toksin Sel yang baik
• Komposisi • Protein = antigen Protein
• Polisakarida =
zat immun
• Lipida = toksin
• Neutralisasi • Homolog,
Positif
• Termostabilita negative
Kurang stabil
s • Lebih stabil
Positif
• Pewarnaan Gram • Negative
Lebih toksik
• Toksisitas • Kurang toksik
RACUN JAMUR/FUNGI
ATAU MIKOTOKSIN
Mikotoksin

• Adalah racun yang dibuat oleh fungi

atau jamur;
• Habitatnya dialam sangat luas;
• Ada yg di gudang, lapangan, pada
semua pelapukan dan pembusukan.
Beberapa fungi yg beracun :

• Claviceps purpurea;
• Aspergilus flavus;
• Fusarium roseum;
• Fusarium tricintum;
• Penilicium sp;
• Aspergilus sp.
Racun Biotis (Biotoksin)

• Racun Jamur/Fungi atau mikotoksin

• Mikotoksin adalah racun yang dibuat oleh
fungi atau jamur.
• Jamur bisa ditemukan di berbagai macam
tempat dan bahan.
• Beberapa Fungi yang beracun adalah sbb :
• Caviceps Pupurea
• Adalah jamur yang hidup sebagai parasit dalam
butiran gandum
• membuat toksin ergot, yakni suatu alkaloid sehingga
terjadi orgotisme.
• Jamur berbentuk spora dan terbawa angin
Racun Biotis (Biotoksin)

• Keracunan ergot dikenal sejak

600 tahun SM
• Sifat keracunan akut dan kronis
• Gejalanya akut: kontraksi otot,
otot kebas, gangren, bingung,
depessi, dll
• Gejala kronis : mual, muntah,
diare, keguguran, pingsan, mati
Racun Biotis (Biotoksin)

• Aspergilus flavus
• Merupakan aflatoksin yang karsinogenik
• Terdapat pada makanan, maupun
makanan yang menbusuk
• Di absorsi tubuh melalui oral, mudah larut
dalam air, dan mudah diabsorbsi lewat
usus, dan masuklah ke sel hati.
• Didalam hati terjadi mutagenik terjadilah
kanker hati.
Racun Biotis (Biotoksin)

• Aflatoksin di Indonesia juga dikenal

sebagai tempe dan oncom.

Fusarium roseum
• Jamur ini mensintesa Zearalenone
• Zearalenone merupakan kontaminan
jagung dan gandum.
• Juga makanan yang di fermentasi spt bir,
inuman asam, dll
Racun Biotis (Biotoksin)
• Jamur yang juga membuat racun :
• Fusarium Sporotrichoides, racunnya adalah
sporogenin
• Fusarium Poae racunnya Poae fusarigenin
• Clapidosporium epiphyllum racunnya
epicladosporic acid
• Cladosprium fagi racun fagi cladosporic acid
• Aspergilus ochraceous membuat okratoksin
• Phytomyces chartarum racunnya sporidesmin
• Penicillium islandium racunnya ilanditoksin
Racun Biotis (Biotoksin)

• Fusarium trinicinctum
• Jamur lain yang terdapat pada gandum dan
jagung
• Memproduksi toksin Mycotoxin T-2 atau
mykotoksin trikotesena
• LD 4,0 mg/kg per oral
• Masa tunas 1-12 jam
• Gejala : pusing, mual, muntah, kulit melepuh dan
membusuk, diare, dan mati.
• Disinyalir digunakan dalam perang kamboja
dikenal sbg yellow rain, menyebabkan kematian
karena asfiksia
Racun Biotis (Biotoksin)

• Penicillium Sp dan Aspergilus Sp

• Enam spesies pennicillium dan tujuh
spesies aspergilus menghasilkan
okratoksin
• Okratoksin sering ditemukan pada
tumbuhan gandum, kopi, jagung, pakan
hewan, dll
• Penyebab kelainan ginjal/Nefropati
RACUN ALGAE
BANYAK TERDAPAT DI ALAM :

• Pyrrophyceae merupakan protozoa,

hewan laut, mastigofora.
• Cyanophyceae disebut juga blue
green algae,
• Cyanobacterium, suatu organisme air
tawar;
• Chrysophyceae, algae yang hidup di
air payau.
Pyrrophyceae

• Adalah algae beracun dan berwarna

merah;
• Bila nutrien cukup, berkembang biak
dg pesat, shg laut berwarna merah yg
disebut “red tides”
• Bila terdapat ini kerang-kerang banyak
mengandung racun shg tdk dapat
dikonsumsi
• Keracunan kerang (shelfish)
menyebabkan paralisis;
Kasus yang terjadi :

• Dilaporkan sekitar 1600 kasus;

• Daerah kasus : Indonesia, Malaysia,
Filipina, di tahun1970-1980.
• Tahun 2001 terjadi red tides shg
pengusaha udang tambak merugi,
• Tahun 1987 di Amerika Latin tjd
epidemi dikota champerico,
Guatemala, sebanyak 186 kasus, dg
kematian 26 orang.
Cyanophyceae

• Algae yg berwarna biru;

• Jenis yg beracun : Mycrocytis;
Anabaena; Aphanizomenon,
kesemuanya hidup di air tawar dan
membuat endotoksin.
• Bila terdpat banyak pupuk terjadilah
eutrofikasi menyebabkan : populasi
banyak, oksigen terlarut kurang,
terjadi kematian hewan aquatik
Dapat terjadi fluktuasi diurnal karena:
• Siang terjadi fotosintesis maksimum, shg
DO menjadi maksimum, dan pH menuju
9,5. karena toksin labil dalam alkali,
maka terjadi pengurangan toksisitas.
• Pada malam hari, terjadi yg sebaliknya,
shg terjadi kematian ikan, burung
pemakan ikan dan ternak.
Chrysophyceae

• Adalah flagellata bersel tunggal,

berwarna kuning coklat, hidup di air
payau,dg kadar NaCl 0.12%.
• Spesies Prymnesium parvum bersifat
racun bagi ikan.
• Algae ini membuat toksin hemolisin,
sitotoksin, banteriolitik, dan
ichtyotoksin.
Tanaman beracun
 Tanda-tanda tanaman beracun :
• Rasa pahit, bergetah seperti susu;
• Racun dapat terdapat pada buah, daun, biji,
dan akar;
• Jamur liar;
• Tanaman dengan kuncup berlaminasi;
• Racun labil terhadap panas, dan larut dalam
air, shg air bekas masak sebaiknya tdk
diminum;
• Tanaman liar tdk dikenal jangan dimakan;
• Bagian tanaman yg tdk lazim dimakan, jangan
dimakan.
Racun yg didapat dlm tanaman berupa :

• HCN didapat pada Cassava, Acacia,

Sorghum muda, dll.
• Asam oksalat didapat pada
Chenopodiaceae, Rumex, Oxilidaceae;
• Fosfor organik tdp pada Oxylobrium
paviflorum, Gatrolobium bilobium;
Beberapa tanaman yg beracun :

• Curare :
• banyak ditemukan di Indiana.
• Sbg racun panah utk melumpuhkan
hewan;
• Kemudian utk anestesi;
 Plant Toxins

 Skin
 Gastrointestinal System
 Cardiovascular Systems
 Nervous System
 Liver
 Reproductive Effects
Example – Jimson Weed

 Deadly nightshade plant (Atropa

belladonna)
 Used in the Roman Empire and
during the Middle Ages both as cure
and a poison
 Women used preparations to dilate
their pupils a sign of allure and
beauty
 Atropine is drug responsible for
effects
 Counteracts the effects of pesticides
Example – Mushroom Poisoning
 Most dangerous mushrooms are the
“death cap” (Amanita phalloides) or
the “death angel” (Amanita
ocreata).
 Most susceptible are children less
than 10 years of age
 Initial symptoms are nausea,
vomiting, diarrhea and irregular
heart rate
 Amatoxin, damages the liver cells
causing liver and kidney failure and
possibly death
 Plant Toxins - Skin
 Allergic Dermatitis – Plant Rashes, itchy skin
 Philodendron, poison ivy, cashew, bulbs of daffodils,
hyacinths, tulips (antibody mediated)

 Allergic Dermatitis – Pollen Sniffles & sneezing, runny eyes

 Ragweed (North America), Mugwort (Europe), grasses
(antibody mediated)

 Contact Dermatitis Oral – Swelling and inflammation of

mouth Skin – pain & stinging sensation
 Dumb cane (Dieffenbachia)Nettles (Urtica)

 Contact Dermatitis Skin – pain & stinging sensation

 Calcium oxalate crystals coated with inflammatory
proteins – contain histamine, acetylcholine
Plant Toxins – Gastrointestinal
 Direct stomach irritation - Nausea, vomiting and diarrhea
 California buckthorn (sacred bark), tung nut, horse
chestnut, pokeweed

 Antimitotic (stops cell division) – Nausea, vomiting,

confusion, delirium
 Lily family, glory lily, crocus, may apple
 Colchicine (gout treatment)

 Lectin toxicity – nausea, diarrhea, headache, confusion,

dehydration, death
 Wisteria, castor bean (Ricinus communis)
 Ricin – block protein synthesis very toxic 5 to 6 beans
can kill a child
Plant Toxins – Cardiovascular

 Digitalis like glycosides – cardiac arrhythmias

 Foxglove (Digitalis purpurea), squill, lily of the valley
 Contain glycosides that are similar to digitalis

 Heart nerves – decreased heart rate and blood pressure,

general weakness
 Lily, hellebore, death camas, heath family, monkshood,
rhododendron
 Alkaloids, aconitum, grayanotoxin (concentrated in
honey)

 Blood vessel constriction (vasoconstriction)

 Mistletoe (berries contain toxin)
 Toxin is called phoratoxin
Plant Toxins - Nervous System I
 Seizures
 Water hemlock, (parsley family), mint family

 Stimulation – Excitatory Amino Acids – headache,

confusion, hallucinations
 Red alga (red tide), Green alga
 Mushrooms– Amanita family (fly agaric), Flat Pea
(Lathyrus)

 Aberrant behavior – very excitable, muscle weakness, death

 Locoweed - Australian & Western U.S. plant

 Stimulation
 Coffee bean, tea, cola nut
 Caffeine, most widely consumed stimulant in the world
Plant Toxins - Nervous System II
 Neurotoxic – death
 Poison hemlock (Conium maculatum)
 Coniine – neurotoxic alkaloid – Poison used by Socrates

 Paralysis – demyelination of peripheral nerves

 Buckthorn, coyotillo, tullidora (U.S., Mexico)

 Atropine like effects – dry mouth, dilated pupils, confusion,

hallucinations, memory lose
 Solanaceae family – jimsonweed, henbane, deadly
nightshade (Atropa belladonna), angles trumpet
(atropine and scopolamine)

 Neuromuscular – mild stimulation to muscle paralysis,

respiratory failure (curare), deathCoffee bean, tea, cola nut
 Tobacco – South American – Strychnos family (curare)
Blue green alga (anatonin A)
Plant Toxins – Liver

 “Hepatitis” and cirrhosis of liver - From contaminated grain

 Ragwort or groundsel
 Pyrrolizidine alkaloids – attack liver vessels – effects
humans, cattle but some species resistant

 Liver failure and death

 Mushrooms – “Death cap” (Amanita phalloides)
 Amatoxin and phalloidin effects RNA and protein
synthesis

 Liver cancer
 Fungus that grows on peanuts, walnuts, , etc…plant
 Alfaltoxins– produced by fungus in poorly stored grain
Plant Toxins – Reproductive

 Teratogen – malformations in offspring (sheep)

 Veratrum californicum – native to North America
 Veratrum – blocks cholesterol synthesis – seen offspring
of mountain sheep

 Abortifacients
 Legumes (Astrogalus)
 Bitter melon seeds (Momordica)
 Swainsonine toxin – stops cell division
 Lectins - halt protein synthesis– used by humans
Hewan beracun
 Arachnids
Scorpions, Spiders, Ticks

 Scorpions – Stinger – low toxicity

 Spider bites
 Widow spiders -– Neurotoxin
 Brown or Violin -– Tissue Damage
 Ticks – Neurotoxin – Transmits other
diseases
 Insects

 Moths and caterpillars – Irritating

to eat
 Ants – Proteins, formic acid –
Irritation to allergic response
 Honey bees – Proteins –
Swelling, allergic response
 Wasps – Formic acid
 Reptiles

 Lizards – Irritating to eat

 Snakes
 Vipers – Rattlesnakes, Water
moccasins, Copperheads –
Complex enzymes – Tissue
necrosis, allergic response, shock
 Elapidae Cobras, Kraits, Coral
Snakes – Proteins – Neurotoxin,
paralysis
Marine Animals

 Shellfish (filter-feeding mollusks)

 Mussels, clams, oysters, scallops
 Jelly fish, anemona, coral
 Sea Snail (cigua) and some fish,
oysters and clams
 Puffer Fish (fugu, blowfish, toadfish
… some frogs, starfish, octopus
 Tuna, shark, sword fish (mercury)
Summary

Be aware of
what plants or
animals you
eat!
Common Environmental Toxins

1. Hydrocarbons
2. Inhaled toxins
3. Pesticides
4. Heavy Metals
Hydrocarbons

Introduction:

• One of most frequently reported poisonings

• Presentation to ED classified into 4 types:
1.) Accidental ingestion,
- most common
- in children less 5yrs
2.) Intentional inhalation,
- abuse of volatile hydrocarbons
- recreational
3.) Accidental inhalation / exposure,
- household or workplace
4.) Massive oral ingestion,
- suicide attempts
Hydrocarbons

Pharmacology:

• Diverse group of organic compounds

• Contain hydrogen and carbon
• Most are petroleum distillates (e.g. gasoline)
- derived from crude oil and coal
- turpentine derived from pine oil
• 2 Main categories (classified by structure)
(i) Aliphatics – straight chain hydrocarbons
~ paraffin (lamp oil)
~ mineral turpentine
~ thinners
~ petrol
~ diesel
~ benzine
 Hydrocarbons

Pharmacology:

(ii) Aromatics – ring structure hydrocarbons

~ lubricating oil
~ liquid paraffin
~ baby oil
~ suntan oils
~ petroleum jelly
~ grease

• Hydrocarbons commonly used as solvent base for toxic

chemicals like
• insecticides and metals
Hydrocarbons
Pathophysiology:

• 3 main target organs effected:

# CNS
# Lungs
# Heart
• Most acute damage in the lungs
• Potential for acute toxicity depends on 4 characteristics
1.) Viscosity (resistance to flow)
low viscosity = high toxicity
eg. Lubricants + mineral oil
* high viscosity + low toxicity
Furniture oil
* low viscosity + high toxicity + aspiration
 Hydrocarbons

Pathophysiology:

2.) Volatility (capacity of liquid to turn into gas)

- displaces alveolar O2
- petrol

3.) Surface tension

4.) Chemical side chains

- often high toxicity
- e.g.. Heavy metals
Hydrocarbons

Pathophysiology:
LUNG DISEASE:

• Fatalities after ingestion, accompanied by aspiration

• 1ml in trachea can cause chemical pneumonitis

Mechanisms
1) Penetrates lower airways ~ produces bronchospasm +
inflammation
2) Displaces alveolar O2 (volatile hydrocarbon)
3) Inhibits surfactant

4) Damaging alveoli and capillaries

Hydrocarbons

Pathophysiology:

These effects cause:

• Alveolar disfx
• Vent / Perfusion mismatch
• Hypoxia
• Resp. failure
Hydrocarbons

CNS:

• Narcotic – like effects:

~ euphoria
~ disinhibition
~ confusion
• Usually substance abusers - recreational use
• Single exposure with rapid onset of intoxication + recovery
• Chronic use causes:
~ peripheral neuropathy
~ cerebellar degeneration
~ neuropsychiatric disorders
~ dementia
~ chronic encephalopathy
Hydrocarbons

CARDIAC:

• Sudden death

• Sudden physical activity during / after intentional inhalation

• Myocardial sensitization to endogenous + exogenous catecholamines

• Precipitates vent. dysrythmias + myocardial dysfx

Hydrocarbons

Clinical presentation:

4 typical presentations:
1.) Accidental ingestion:
• Usually toddlers
• Reused beverage containers storing hydrocarbon
• Mild Sx include ~ tachypnoea
~ dyspnoea
~ bronchospasm
~ fever within 6 hours
Hydrocarbons

Clinical presentation:(cont.)

1.) Accidental ingestion:(cont.)

• Severe poisonings ~ early resp. Sx

~ cyanosis
~ grunting
~ coughing
~ repeated vomiting
~ these findings suggests aspiration
• Change in mental status ~ direct CNS effect OR
~ caused by hypoxia
Hydrocarbons

Clinical presentation:

2.) Intentional inhalation:

• Substance abuse
• Mechanisms include: - “bagging”- hydrocarbon poured into
bag/container
+ deeply inhaled
- “huffing” - inhaling through a saturated
cloth
- “sniffing”
• Mostly volatile hydrocarbons - petrol
- paint
- glue
Hydrocarbons

Clinical presentation:

2.) Intentional inhalation: (cont.)

• Presentation:
- sudden cardiac arrest
- CNS intoxication with euphoria, agitation, hallucinations +
confusion
• Chronic abusers similar to long-term alcoholics
- peripheral neuropathy
- cerebellar degeneration
- encephalopathy
Hydrocarbons

Clinical presentation:

3.) Accidental dermal exposure or inhaled resp.

exposure:
• In workplace / home
• Not life threatening
• Asymptomatic or transient non-specific symptoms
• Sx resolve with fresh air / removal from offending environment

4.) Intentional ingestion / intravenous injection:

• Rare
• Suicide attempts
• Used in combination with other substances
• Massive oral ingestion not associated with significant morbidity
Hydrocarbons

Diagnosis:

• Clinically
• History from parents / family / bystanders
• Contact local poison control centre to identify product
• CXR: - radiographic changes can occur within 30 min
- findings of chemical pneumonitis include:
1.) bilat. perihilar infiltrates
2.) gradually: forms patchy infiltrates
3.) finally: large areas of consolidation
• Pulse oximetry
• ABG
Hydrocarbons

Management:

• Observe for 4 – 6 hours (even if asymptomatic)

• If any Sx present: do CXR, pulse oximetry, ABG
• Supportive care
• Gastric lavage should be avoided
- increased risk of aspiration
• No antidote
• If any Sx present suggestive of aspiration – admit for 24 hour
observation
• Manage resp. complications appropriately – give O2, intubate +
ventilate if necessary
• No prophylactic A/B!!
INHALED TOXINS

1. Smoke inhalation
2. Cyanide
3. Carbon monoxide
Smoke inhalation

Introduction:

• Inhalation injury common

• Fires in enclosed spaces like homes / factories

• Injury typically irritant in nature

• Heated particulate matter + absorbed toxins injure normal mucosa

• Carbon monoxide + Cyanide poisoning often associated with

smoke inhalation
- these are systemic ( not resp.) toxins
Smoke inhalation

Principles:

• Fires involves variable fuels + burning conditions

- character of smoke not always identified

• Irritant toxins are produced which damages the airway mucosa

Clinical presentation:

• Morbidity + mortality related to resp. tract damage

- thermal / irritant in nature
• Time between smoke exposure + onset of Sx – highly variable
• May always be delayed
• Depend on degree + nature of exposure
Smoke inhalation

Clinical presentation: (cont.)

• Cough + stridor
- thermal + irritant induced laryngeal injury
• Cough, stridor + bronchospasm
- caused by soot + irritant toxins in the airways
• Subsequently – a cascade of:
- airway inflammation
- acute lung injury with pulm. edema
- resp. failure
• Burned nasal hair + soot in the sputum suggest substantial
exposure
• Always consider CO + cyanide inhalation
- in pt`s exposed to filtered / distant smoke ( different room) OR
- relatively smokeless combustion
Smoke inhalation

Management:

• Rapid assessment of the airway + early intubation mandatory

(prior to deterioration!!)

• Supportive care

• Intraveneous fluid resuscitation

• Maintenance of adequate oxygenation

- suctioning + pulm. toilet

• Admit to ICU / transfer to Burn Centre

Cyanide

• One of the most rapidly acting poisons

Causes:
1.) Smoke inhalation:
- most common
- compounds containing carbon + nitrogen produce hydrogen CN
gas when burned
- natural compounds (silk + wood) produces HCN as a combustion
product
- burning of household furniture + plastics also causes HCN gas
Cyanide

Causes: (cont.)

2.) Intentional poisoning:

- uncommon
- cyanide salts in hospitals + labs

3.) Industrial exposure:

- Occupations with easy access to cyanide
* chemists
* jewelers
* pest control
* mineral refining
* photography
* electroplating
* dying + printing
Cyanide

Pathophysiology:

• Cyanide inhibits mitochondrial cytochrome oxidase + blocks

electron transport ( binding with ferric iron Fe3+ )
• aerobic metabolism + O2 utilization decreases
• Lactic acidosis occurs as a consequence of anaerobic metabolism
• O2 metabolism @ cellular level is grossly hampered
• Cyanide rapidly absorbed from:
- stomach
- lungs
- mucosal surfaces
- skin
Cyanide

Clinical presentation:

• Sx appear seconds to minutes after exposure

• HCN gas can lead to cardioresp. arrest + death within minutes
• Onset of effects after ingestion / skin contamination:
- much slower (several hours)
- early signs:
i) dizziness
ii) bronchospasm
iii) dyspnoea
iv) confusion
v) paresis
- Later:
i) cardiovasc. collapse
ii) seizers
Cyanide

Prognostic features:

1.) Ingestion of few hundred mg of cyanide salt = FATAL

2.) Pt`s surviving to reach the hospital after HCN inhalation

- unlikely to have suffered significant poisoning

3.) Lactic acidosis + pulm. edema = severe poisoning

Cyanide

Management:

• Avoid mouth – to – mouth resuscitation!

• Give 100% O2
- tight fitting facemask
- ventilate via ET tube if necessary
• O2 contributes to reversal of cyanide-citochrome complex
• Skin contamination – wash thorough with soap + H2O
• Antidote therapy:
- given ASAP, if available
- Regimens:
1.) dicobalt edetate
~ toxic
~ only given in confirmed cyanide poisoning
Cyanide

Management: (cont.)

2.) Nitrate / Sodium Thiosulphate Regimen

~ safer
~ antidote kit with:
* amyl nitrate
* sodium nitrate
* sodium thiosulphate
~ Nitrates oxidizes Hb to MetHb - which has greater affinity for
cyanide
- leading to dissociation of
cyanide
citochrome complex
~ Thiosulphate mediates conversion of cyanide to less toxic
substance
Cyanide

Management: (cont.)

Doses:
1.) Inhalation of 0.3ml amyl nitrate (emptied on a gauze)

2.) Then 10ml Sodium Nitrate given ivi over 3min.

3.) 50ml 50% Sodium Thiosulphate given over 10min.

Carbon Monoxide

• Most common cause of poison - + fire – related deaths

• Generated through incomplete combustion of all carbon –

containing products

Sources:
1.) Smoke inhalation
2.) Poorly maintained domestic gas
appliances
3.) Deliberate inhalation of car exhaust
fumes
Carbon Monoxide

Pathophysiology:

Intense tissue hypoxia + cell injury caused by

2 mechanisms:
1.) Interrupts electron transport in the mitochondria (like cyanide),
leading to anaerobic metabolism

2.) Reduces O2 delivery by:

- competing with O2 for binding to Hb (CO has much higher affinity
for
Hb, than O2!)
- Shifting the HbO2 dissociation curve to the left
Carbon Monoxide

Pathophysiology: (cont.)

REMEMBER!!

Affinity of fetal Hb for CO even higher than that of adult

Hb!

Therefore fetal exposure higher than that of predicted

maternal
exposure!
Carbon Monoxide

Clinical presentation:

• Hypoxia without cyanosis

• Myocardium + Brain mostly affected ( high O2 consumption)

• Sx include:
- dizziness - convulsions
- headaches - coma
- confusion - cardio/resp. dysfx + death
- chest pain
- dyspnoea
- palpitations
- syncope
Carbon Monoxide

Clinical presentation: (cont.)

• COHb levels correlate poorly with clinical features – only used to

confirm
exposure

• “cherry – red” skin + mucus membranes found post mortem

 Carbon Monoxide
Complications:

• Outcome depends on degree + duration of peripheral tissue

hypoxia
1.) CNS:
- cerebral, cerebellar + midbrain fx affected

2.) Myocardium:
- ischemia + infarction

3.) Skeletal muscle:

- rhabdomyolysis
- myoglobinuria
Carbon Monoxide

Complications:(cont.)

4.) Skin:
- erythema
- severe blistering
Carbon Monoxide

Management:

• AIM: minimize + Rx Complications

• Admit to ICU
• Give 100% O2 - tight fitting facemask
- ventilate via ET-tube if necessary
( O2 decreases half life of COHb)
• Continuous cardiac monitoring
• Pulse oximeter useless!!
- cannot distinguish COHb from HbO2
Carbon Monoxide

Management:(cont.)

• Hyperbaric O2 preferred only if readily available in:

- unconscious pt
- severe metabolic acidosis
- pregnancy
- COHb level 25 – 40%
- neurological signs
• Supportive care:
- Rx arrhythmias
- correction of acid base + electrolyte abnormalities
- Rx convulsions
Carbon Monoxide

Management:(cont.)

• Ensure F/U as neuropsychiatric squeal may take many

weeks
to evolve!
Pesticides

1.) Organophosphates + Carbamates

2.) Paraquat + Diquat Poisoning

Organophosphates + Carbamates

• Poisoning commonly seen in:

- accidental ingestion (kids)
- suicide attempts
- agricultural workers
- pest control

Introduction:

• Potent cholinesterase inhibitors

• Accumulation of acetylcholine (Ach)
• Indirect stimulation of nicotinic + muscarinic receptors
Organophosphates + Carbamates

Introduction: (cont.)

• Absorbed through: - skin

- inhalation
- ingestion
• Carbamate + OP poisoning clinically indistinguishable
• Differences: - OP forms irreversible complex with cholinesterase
- Carbamate complex reversible, with shorter
duration of
action ( less than 24 h)
- Carbamates penetrates blood-brain barrier
poorly,
therefore less CNS effects
Organophosphates + Carbamates

Clinical presentation:

• Minutes to 12 hours after exposure

1.) Muscarinic effects: (post ganglionic)
- hyper secretion (sweating, salivation + bronchial secretions)
- constricted pupils
- bradycardia + hypotension
- vomiting + diarrhoea
- urinary incontinence
- bronchoconstriction
- Also commonly referred to SLUDGE syndrome:
Organophosphates + Carbamates

Clinical presentation: (cont.)

S – salivation
L – lacrimation
U – urinary incontinence
D – diarrhoea
G – G.I cramps
E – emesis
Organophosphates + Carbamates

Clinical presentation: (cont.)

2.) Nicotinic effects: (preganglionic)

- muscle weakness
- fasciculations
- resp. muscle weakness

NB: Sometimes nicotinic effects overrides muscarinic effects!

Causes:
- tachycardia
- hypertension
- dilated pupils
Organophosphates + Carbamates

Clinical presentation: (cont.)

3.) CNS effects:

- restlessness
- anxiety
- headaches
- convulsions
- coma
 Organophosphates + Carbamates

Complications:

Mortality + Morbidity caused by:

1.) Seizers / Coma

2.) Pulm. hypersectretion

3.) Resp. muscle weakness

 Organophosphates + Carbamates

Diagnosis:

1.) Clinically (cholinergic syndrome)

2.) Cholinesterase level

 Organophosphates + Carbamates

Management:

1.) Decontamination: - remove contaminated clothing

- activated charcoal within 1-2 hours

2.) Supportive care: NB airway management!

- suctioning of secretions
- O2
- ventilate via ET-tube if necessary
( avoid Scoline / succinylcholine!!!)
( may have extremely prolonged duration)
 Organophosphates + Carbamates

Management:(cont.)

3.) Definitive Rx: - Atropine administration!

- ASAP
- test dose 1mg adults, 0.01mg/kg children
- then: 0.05mg/kg (2-4mg) given every 15 min
- until full atropinisation achieved
- maintenance: iv infusion of 0.05mg/kg/hour
- high doses required sometimes
- control of bronchial / oral secretions indicates
adequate therapy
 Organophosphates + Carbamates

Management:(cont.)

3.) Definitive Rx: - Atropine administration!

- reduce dose slowly
- do not stop abruptly

- Cholinesterase reativator:
- e.g. obidoxime
- early Mx of moderate – severe OP poisoning
- atropine always given first
- Contraind. in carbamate poisoning
Paraquat + Diquat

• Most toxic herbicide known ( weed-killers )

• Multiorgan toxicity

• Death due to delayed pulm. fibrosis + resp. failure

Paraquat + Diquat

Pathophysiology:

- Cytotoxic O2 radicals generated

- selectively accumulates in the lungs
- Lungs major target organs (except diquat)
- also liver, kidneys, heart + CNS
- Absorption: * skin
* GIT
* resp. tract
 Paraquat + Diquat
Clinical presentation:

1.) Chemical burns of oropharynx

2.) Esophageal perforation + mediastinitis (extreme cases)
3.) N+V
4.) Skin irritation
5.) Resp. injury:
- high doses cause dyspnoea, ARDS + rapid multiorgan failure
- progressive pulm. Injury over 1 – 3 weeks with irreversible
pulm. fibrosis
Paraquat + Diquat

Management:

• Aggressive early decontamination

• Gastric lavage
• Activated charcoal
• Rx resp. complications appropriately BUT high insp. O2 concentration
worsens resp.
toxicity!!!
• Use low FiO2 mixtures with CPAP + PEEP
Heavy Metal Toxicity

- Uncommon dx

- Exceptions: 1.) acute iron toxicity (intentional /

unintentional)
2.) lead exposure

- Unrecognized / inappropriately Rx result in significant

morbidity + mortality

- Other examples: arsenic, mercury, cadmium.

Heavy Metal Toxicity

- Toxicity depends on:

1.) ? Metal
2.) Total dose absorbed
3.) Acute/Chronic exposure
4.) Age – children more susceptible to toxic effects +
prone to
accidental exposures
5.) Route of exposure - e.g. Elemental mercury, not
dangerous
if ingested / absorbed through
skin
- disastrous if inhaled / injected
Heavy Metal Toxicity

- Sources:
Exposure through:
* Diet supplements
* Medications ( herbal remedies )
* Environment
* Occupational / Industrial
( most acute presentation)
* Ingestion of non food items e.g.Toys, paint chips,
ballistic
devices,
fishing sinkers,
curtain
weights
* Retained bullets ( rarely causes lead toxicity)
Heavy Metal Toxicity

Pathophysiology:

- Remains relatively constant for all heavy metal

toxidromes
- Binds to O2, Nitrogen + sulphydryl groups in proteins
- Result in: ALTERATIONS OF ENZYMATIC ACTIVITY
- Nearly all organ systems involved:
* CNS
* PNS
* Haemapoietic
* GIT
* Cardiovasc.
* Renal
Heavy Metal Toxicity

Clinical presentation:

- History NB!
* diet
* occupation
* hobbies
- Nausea, persistent vomiting, diarrhoea, abd. pain
- Dehydration
- Metal salts = corrosive
Heavy Metal Toxicity

Clinical presentation: (cont.)

- Acute high dose exposures:

• Encephalopathy ( leading cause of mortality!)
• Cardiomyopathy
• Dysrhythmias
• ATN
• Metabolic acidosis
- Chronic exposures:
• Anaemia
• “Mees lines” on nails (horisontal hypopigmented lines across all
nails)
• Subtle neurological signs
Heavy Metal Toxicity

Diagnosis:

- History
- FBC
- U+E
- LFT
- Urine analysis
- LFT
- AXR in ingested heavy metals
- some radio opaque
Heavy Metal Toxicity

Management:
(in Emergency Room)

1.) Decontamination ( MOST NB!)

* removal from source of exposure
* gastric lavage if ingested

2.) Resuscitation:
- supportive care
- airway protection
- Rx arrhythmias
- replace fluids + electrolytes
Heavy Metal Toxicity

Management:(cont.)
(in Emergency Room)

3.) Chelation:
* rarely indicated in emergency setting
* possible exceptions: Lead encephalopathy!
* routine chelation not recommended!
* Always in conjunction with Medical toxicologist + Local
Poison
Centre.
* Chelation Rx supplies sulphydryl groups for heavy metals to
attach to + be eliminated from the body.
Heavy Metal Toxicity

Management:(cont.)
(in Emergency Room)

Excamples:
- Dimercaprol (mercury + arsenic)

- Calcium disodium edetate (acute / chronic lead poisoning)

- Penicillamine (mercury, arsenic, lead, copper poisoning)

All available in SA!

Cara terjadinya keracunan pada
manusia :
1. Sengaja bunuh diri.
Penderita sengaja menelan,
menghirup, menyuntikan obat
dengan dosis tinggi,serta benda lain
yang tidak ditujukan untuk
dikonsumsi.
contoh :
- minum racun serangga
- obat tidur berlebihan.
seriang mengakibatkan kematian,
kecuali penderita ditemukan dan
2. Keracunan tidak disengaja.
terjadi akibat terpapar bahan
beracun secara tidak sengaja.
misal :
a. mengkonsumsi bahan makanan /
minuman yang tercemar oleh
kuman / zat kimia tertentu.
b. Salah minum obat biasanya pada
anak / orang tua yang sudah pikun.
c. makan singkong yang
mengandung sianida tinggi
d. udara yang tercemar zat beracun.
3. Penyalahgunaan obat.
terjadi karena obat dikonsumsi karena
tujuan selain pengobatan.
bila berhadapan dengan kasus
keracuan upayakan untuk mencari :
a. apa kira – kira bahan penyebabnya
?
banyak produk yang sama, cari
ejaan yang tepat, bawa produk /
pembungkusnya ke sarana
kesehatan.
b. Berapa jumlah zatnya
dapat diperkirakan berapa jumlah