POISONING

Def. Intoksication= development of doserelated adverse effect following exposure to

chemical, drugs, or other xenobiotik (zat
asing)

Self Poisoning
Attempted suicide
Accidental poisoning
Etiology

Homicidal poisoning
Acute

Classification

Onset

Chronic
Liver

Target Organ

Heart
Kidney
CNS
Alcohol

Chemical Material

Phenol
Heavy metal
Organochlorin

Fundamental of Poisoning Management

Toksidrome
Kolinergik

Diare/diaforesis
Urination
Miosis
Bradikardi/bronkospasme
Emesis
Lakrimasi
Salivasi

AntiKolinergik

Kulit kering
Retensi urine
Penurunan bunyi usus
Delirium
Takikardia
Dilatasi pupil
Kejang, Disritmia

Opioid

Depresi respiratorik
Pupil pinpoint
Koma

Simpatomi
metik

SedatifHipnotik

Hipertensi
Takikardia
Dilatasi pupil
Delusi
Psikosis
Kejang
Disritmia

Penurunan tingkat kesadaran

Depresi respirasi
Hipotensi
Perubahan pupil yg berbeda-beda
Hipotermia
Kejang

TOXICOLOGY
POISON

SUBSTANCE

* CHARACTERISTIC
* ACTION OF DAMAGE
* CLINICAL SIGN
* THERAPEUTIC MANNER

INDIVIDUAL

PHYSIOLOGY
LIFEABILITY
PATOLOGY

DAMAGE OF ACTIONS
LOCAL

DAMAGEOF LOCAL CEL

(SKIN, MUCOUS)
LOCAL PAIN
S/ SYSTEMIC
TOXEMIA

SYSTHEMIC

ABSORPTION CIRCULATION
ORGAN S/SPESIFIC
CYANIDA RESPIRATION
INSECTISIDE CNS
STRYCHNIN .SPINAL CHORD

acute intoxications, from LD50 atau LC50 & how the

toxin enter the body :
Klasifikasi

Cara Masuk
Oral

Dermal

Inhalasi

LD50 (mg/kg BB) LD50 (mg/kg Bb) LC50 (mg/m3)

-

Supertoxic
Extremely toxic
Very toxic
Moderately toxic
Slightly toxic

<5
5 50
50 500
500 5000
> 5000

< 250
250 1000
1000 3000
3000 10.000
> 10.000

< 200
250 1000
1000 10.000
10.000 30.000
> 30.000

GASTER LAVAGE

ELIMINASI

FOOD POISONING

Hazards in food
Physical: glass, stone, metal, wood, etc
Chemical:
- natural toxins
- residues
- metals
- toxins formed during food processing
Microbiological: pathogenic microorganisms
(bacteria, viruses, parasites, etc)

Foodborne Diseases

Infections

Intoxications

Chemical
Poisoning

Poisonous
Plant Tissues

Poisonous
Animal Tissues

Toxicoinfection

Microbial
Intoxications

Other

Neurotoxins

Invasive Infection

Enterotoxins

Intestinal
Mucosa

Mycotoxins
(Fungal Toxins)

Algal Toxins

Bacterial
Toxins

Diarrhogenic

Emetic

Enterotoxins

Neurotoxins

Other

Systemic

Other Tissues
or Organs
(Muscle, Liver,
Joints, Fetus,
Other)

High risk foods

These include:
meat and meat products;
milk and dairy products;
fruit.
If these foods become contaminated with foodpoisoning micro-organisms and conditions allow them
to multiply, the risk of food-poisoning increases.

People at high risk

Elderly people, babies and anyone who is ill or
pregnant needs to be extra careful about the food
they eat.

For example, pregnant women or anyone with low

resistance to infection should avoid high risk foods such
as unpasteurised soft cheese.

Factors affecting food poisoning

Some common factors
leading to food poisoning
include:
preparation of food too far
in advance;
storage at ambient
temperature;
inadequate cooling;
inadequate reheating;
under cooking;

inadequate thawing.

More common factors

leading to food poisoning
include:
consuming raw food;
improper warm holding
(i.e. holding hot food
below 63C);
infected food handlers;
contaminated
processed food;
poor hygiene.

Symptoms of food poisoning

Food poisoning can be mild or severe.

The symptoms will be different depending on what

type of bacteria is responsible.
Common symptoms include:
severe vomiting;
diarrhoea;
exhaustion;
headache;
fever;
abdominal pain;
tiredness.

Preventing food spoilage,

contamination and poisoning
Tips for buying food include:
it is illegal to sell food that has passed its use by
date;
dented, blown or rusted cans of food should not be
purchased;
frozen food which has frozen together in the pack
should not be purchased;
do not buy food where the packaging has been
damaged;
only shop in clean and hygienic stores.

Preventing food spoilage,

contamination and poisoning
Tips for transporting food back home:
buy chilled and frozen foods at the end of the
shopping trip;
keep frozen and chilled foods cold, by using cool
boxes/bags and packing these types of foods together;
cooked and uncooked foods
should be kept separate;
dry and moist foods
should be packed separately;
household chemicals
should be packed separately.

Preventing food spoilage,

contamination and poisoning
Tips for storing food in the home:
food should be unpacked as soon as possible;
old stocks of food should be used before buying
new ones (first in, first out theory);
store food in the correct place, i.e. dry food, in cool,
dry clean places and chilled food in the refrigerator.

The Main Food Poisoning Bacteria

Type of food Where the
Onset time
poisoning
bacteria come
from

Symptoms

Salmonella

Raw meat,
eggs, poultry,
animals

Abdominal pains,
diarrhoea, fever,
vomiting, dehydration

Clostridium
perfringens

Raw meat, soil, 8 - 72 hours

excreta, insects

Staphylococcu Skin, nose,

s aureus
boils, cuts, raw
milk

6 - 72 hours

1 - 6 hours

Abdominal pain,
diarrhoea
Vomiting, abdominal
pains, lower than
normal temperature

Incidents of Food Poisoning in PDO

Date

Place

People Type of Food

Affected
Poisoning

Source

June '98 Marmul

23

Salmonellosis Unknown

April
'99

Fahud

12

Shigellosis

Unknown

April
'99

RAH Club

32

Shigellosis

Unknown

May '01 Toco

Camp
Saih Rawl

75

Salmonellosis Unknown

Name

RF

Sign & Symptoms

Campylobacter

Meat and poultry.

Onset 2 11 days. Fever,

headache and dizziness
for a few hours, followed
by abdominal pain. This
usually lasts 2 7 days
and can recur over a
number of weeks

Clostridium perfringens

Raw meat, cooked meat

dishes and poultry.

Onset 8 22 hours.
Abdominal pain,
diarrhoea and nausea.
This usually lasts 12 48
hours.

E Coli 0157

Raw meat and dairy

products.

Diarrhoea, which may

contain blood, can lead
to kidney failure or death.

Listeria Monocytogenes

Unpasteurised milk and

dairy products, cook-chill
foods, pate, meat,
poultry and salad
vegetables

Ranges from mild, flu-like

illness to meningitis,
septicaemia,
pneumonia. During
pregnancy may lead to
miscarriage or birth of an

Name

RF

Sign & Symptoms

Bacillus cereus

Rice, meat, seafood,

salads, potatoes, and
noodles

Ranges nausea and vomiting and

abdominal cramps and has an
incubation period of 1 to 6 hours .
This usually lasts less than 24 hours
after onset.

Clostridium
botulixnum

Inadequately
processed canned
meat, vegetables
and fish (faulty
canning)

Onset 24 72 hours. Voice change,

double vision, drooping eyelids,
severe constipation.
Death within a week or a slow
recovery over months.

Salmonella

Raw meat, poultry

and eggs, and raw
unwashed
vegetables.

Onset 12 36 hours. Headache,

general aching of limbs, abdominal
pain and diarrhoea, vomiting and
fever. This usually lasts 1 7 days,
and rarely is fatal.

Staphylococcus
aureus

Meat, dairy products

and poultry.

Onset 1 6 hours. Severe vomiting,

abdominal pain, weakness and
lower than normal temperature.
This usually lasts 6 24 hours.

Salmonella

Outbrakes associated with grade A eggs. Preparation of Poultry.

Sources : Chocolate mousse ; Ceasar salad ; Chicken
Gram - rod
Killed by high temperatures

Sign & Symptoms

12-36 hours ; low grade fever ; abdominal pain ; diarrhea; chills

Diagnose

patient history
stool culture
Microscopic examination
leukocytes
occult blood

Treatment

Supportive
fluid and electrolyte
NO antibiotics
does not alter the severity
prolongs the carrier state
Do NOT give anti-motility drugs
lead to intestinal perforation

Clostridium
botulinum

Four different types

food borne
infant
wound
undetermined

Resistant

heating, freezing, ionizing radiation

Destroyed by

boiling >120 degrees for >20 min

Toxin

Very powerful : 0.5 nanograms (lethal)

Heat sensitive : 80 degrees for 30 min

Sign & symptoms

With disease
progression

descending paralysis ; respiratory weakness; respiratory failure ;

oculobulbar symptoms
stabilization of airway
history
upper and lower GI decontamination
trivalent antitoxin
(ABE)
watch for hypersensitivity
call CDC

Treatment

12-48 hrs (14 days)

N/V/D
abdominal distention
constipation (as disease progresses)
Neurologic disturbances : dysarthria, dysphagia, dry mouth

DD

Treatment /
profilaksis

Neuromuscular disorders
Stroke syndrome
Myasthenia gravis
Guillain-Barre syndrome (Miller-Fisher variant)
Tick paralysis
Atropine poisoning
Paralytic shellfish/puffer fish poisoning
Diagnosis based on clinical presentation with subsequent laboratory
confirmation
Ventilatory assistance and supportive care
Botulinum antitoxin
Trivalent equine product against types A,B, and E available from CDC
Most effective if given early
Antibiotics for wound botulism
Penicillin
Recovery may be prolonged with supportive care necessary
Vaccine investigational
not available

Laboratory Capacity for

Botulinum Toxin Testing
1

1
2
1

1
2
11
1
1
1
1
1
1
1
1

Arnon SS et al, JAMA 2001:285:1059-70

Staphylococcus
aureus

Enterotoxins
Found :
protein rich foods : ham, poultry, fish, milk and other dairy
improper food handling

Mechanism

entrotoxin acts as a superantigen

stimulates intense cytokine production
toxic shock like syndrome

Sign & Symptoms

2-6 hrs
abdominal pain
N/V/D

Treatment

mild
self limiting
death is rare
elderly
debilitated

JengKOL

not well for people outside indonesia, because not many cultures that used
jengkol as food ingredients. Jengkol itself is a kind of beans (Pithecolobium
lobatum). : = 9:1 (Highest 4-7 years old)
intoxication occurs depends on individual susceptibility to jengkolic acid

Symptoms

caused by obstruction of urinary tract by jengkolic acid crystal.

Complains in 5-12 hours after eating jengkol. Fastest 2 hours, the latest after 36
hours.
abdominal pain/discomfort after eating few jengkol
Vomit , colic pain at micturition.
Urine volume also decreased, even can be anuria. hematuria can be found. Also
urine and breath smells jengkol.

LAB

In urine examination with microscope, can be found jengkolic acid crystal that
being seen as sharp needle or sometimes agglutinated as bound or rosette

Diagnose

Parents told us, after hours eat jengkol, sign and symptoms appear
mild (vomit, abdominal/flank pain only) advice to drink a lot and giving

sodium bicarbonate.
severe (oliguria, anuria, hematuria and can't drink), hospital or opname

and receive Sodium bicarbonate in 5 % glucose I.V (adult and child

doses 2-5 mEq/kgBB with Natrium bicarbonat IV for 4-8 hours.
Antibiotik (if suspect secundary infections)

Prognose

Bonam, still have some patient die cause acute kidney failure

Advise

Dont EAT JENGKOL

Cassava
(Singkong)

Sign &
symptoms

Treatment

Root and leaf of cassava have hydrocyanate acid (HCN).

HCN + cytochrome oxydase cytochrome oxydase HCN compleks, (oxydation in the
tissu would be inhibited)
HCN cyanmethemoglobin, toxic respiratory cel, disruption to the process of oxidation
enzymes
Enzim distruption tissue, neuron cell cant take the O2 Venous blood is bright
red as arterial blood
More quantity death due to respiratory failure
initially heat to the abdomen, nausea, dizziness, spasms, weak breathing fast and
short
Smelly breath and vomit bitter almond smell
Fainting, seizures, weakness, sweating, eyes bulging wide pupils without reaction
Mouth foam mixed with the color of blood
Skin color brick red (light skin), cyanosis usually (-) appears
Test Giunard u / cassava picric acid color change yellow to red (15minutes ~ 3 hours)
Commonly same toxin eliminated (vomited, rinse the hull(gaster), antidot
amil/na nitrit, Na-tiosulfat
Na-nitrit NaCN bind prevent damage to cells ferisitokrom oxidase enzyme
Na-tiosulfat NaCN bind stable tiocynatat excretion through the lungs, saliva,
urine
Na-nitrit 3% ml iv slowly, Na tiosulfat 10% IV slowly (0.5mL/kgBB/x or 10-50ml)
if Na nitrit (-), Na tiosulfat is fine
O2 th suportif & antidotum (t.u O2 high tension/CPAP)
Ok O2 competitive against bond ferisitokrom oxidase enzyme with cyanide

Advise

Processing HCN : peeled tubers with - washed - dried, soaked, heated

PATPI (Perhimpunan Ahli Teknologi Pangan Indonesia):
Bulbs soaked with 8% salt solution in 3 days , or
Tuber slices heated in boiling water 30 min > effective
How linase enzyme (-) Active
If the consumption of cassava alone FR low protein calori, & iodium

Bongkrek (tempe
bongkrek, asam
bongkrek)

Bongkrek acid from tempe bongkrek (manufacture with coconut

pulp fermentation and peanuts)

Etiology

coconut pulp bongkrek acid (Pseudomonas cocovenenan)

iron pedestal Clostridium botulinum contamination

Symptoms

Mild : headache, nausea, Abdominal pain, anoreksia, diplopia,

ptosis, Strabismus
severe : Respiratory and circulatory failure, seizure, death

Treatment

Spesific Antidot not yet.

Prevent further absorption of toxins and accelerate the
excretion
Rinse the hull
Catharsis
General improvement
IV plasma liquid & NaCl
IV glukosa
activated charcoal u / impaired circulation and respiration.
Ne

PLANT & ANIMAL TOXINS

Toxins Around Us

Have you every eaten

too much puffer fish
or the wrong
mushroom or been
bitten by a snake?

Ancient
Awareness
399 BC Death of
Socrates by Hemlock
Charged with religious
heresy and corrupting the
morals of local youth.
Active chemical is the
alkaloid coniine which
when ingested causes
paralysis, convulsions and
potentially death.

Historical
Awareness
From Romeo and
Juliet - act 5
Come bitter pilot, now
at once run on
The dashing rocks thy
seasick weary bark!
Heres to my love! O
true apothecary!
Thy drugs are quick.
Thus with a kiss I die.

Historical Events Plant Toxin?

Opium War of 1839-42
Great Britain has a monopoly on the sale of opium
which it forces on China. Eventually getting control
of Hong Kong.
Consider our societies current wars on drugs.

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 and
chemical warfare agents that act by inhibiting
acetylcholinesterase

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
Amatoxin is very potent: only 0.1 to 0.3 mg/kg of
body weight results in death

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

GI

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

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, , etcplant
Alfaltoxins produced by fungus in poorly stored grain

CV

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

Neuro 1

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
Neuro 2

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)

Reproductions

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

Animal Toxins
Arachnids - Scorpions, Spiders,
Ticks
Insects
Snakes
Lizards
Fish, and frogs

Example Puffer Fish

Tetrodotoxin
100 different species of puffer fish
Tetrodotoxin used by fish to discourage
consumption by predators
Low dose of tetrodotoxin produces tingling
sensations and numbness around the
mouth, fingers, and toes
As little as 1 to 4 mg of the toxin can kill an
adult

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 Animal

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)

WHY TALK ABOUT VENOMOUS

ANIMALS?
SO THAT YOURE NEITHER OVERLY
WORRIED

NOR OVERLY
WELL, YOU KNOW
Most rattlesnake bite victims are young
men (18-28 yrs old) who are bitten while
handling or provoking the snake.

How to avoid being bitten or stung

Never handle venomous animals
Never place your hands or feet anywhere you cant
see (and havent checked). For example:
Never step into or over bushes
Never reach up onto a rock or ledge
Always pick up rocks, wood, etc. carefully, making
sure not to put fingers under the rock/wood, always
lift it so that the rock/wood is between you and the
potential animal, and always check underneath. It is
best to use a tool to lift a rock/wood.

POISONOUS VS VENOMOUS?
Poisonous animals possess toxins.
For example, this Sonoran Desert Toad produces
and secretes toxins from glands on its skin. The
toads toxins are able to kill dogs that bite the
toad!

e.g., Parotoid Gland

POISONOUS VS VENOMOUS?
Venomous animals inject their
toxins.
For example, this rattlesnake
produces toxins in modified
salivary glands then injects
toxins through hollow fangs.

THE CHARACTERS:
MILDLY VENOMOUS ANIMALS
Non-life-threatening except by anaphylactic shock
in those that are allergic.
Wasps, bees, ants, most spiders, most scorpions,
etc.

THE CHARACTERS:
DANGEROUSLY VENOMOUS ANIMALS

Life-threatening. Need to seek medical attention.

Bark scorpion, black widow, brown spider, gila
monster, coral snake, rattlesnakes.

TYPES OF VENOM
Hemolytic: affects circulatory system
(hemo = blood) by destroying blood
cells and vessels. Symptoms include severe
pain, swelling, discoloration, and local
tissue death. Shock can occur. Example:
most rattlesnakes.

Rattlesnake bite picture source

http://www.venomous.com/snake/armpic.jpg

TYPES OF VENOM
Neurotoxic: affects nervous system (neuro).
Symptoms may include local pain, headache,
lethargy, paralysis and occasionally death by
circulatory arrest or respiratory paralysis.
Usually no swelling, discoloration, or tissue
death. Examples include Black Widow,
Scorpions, and Coral Snake.

TYPES OF VENOM
Other:
Gila Monster toxin causes
pain.
Brown (Recluse) Spider
toxin destroys proteins,
thus tissues.

Likely brown spider bite

WHY BE VENOMOUS?
1. Subdue Prey: allows predator to reduce chance of
injury and to eat larger prey.
2. Defense: protects animal from predators and other
potential threats.
3. Digest Food: venom is modified saliva, produced by
modified salivary glands. Most contain compounds
that aid in digestion (thought to be the original
use of venom).

WHY NOT BE VENOMOUS?

1. Takes Special Equipment: requires glands to
produce toxins and often specialized
apparatus for injecting venom (teeth,
modified ovipositor, etc.).
2. Takes Energy and Materials: toxins are
expensive to produce.

WAYS TO AVOID WASTING TOXIN

Match amount of venom to prey: use less
for smaller prey, use more for prey that can
get away easier (e.g., birds).

AVOID USING TOXIN

Hide (use cryptic coloration): camouflage.
Warn (use aposematic coloration): bright, memorable colors and/or patterns.

AVOID USING TOXIN

Retreat

ONE MORE WAY TO AVOID USING TOXIN

Dont produce toxins at all be a Fake!
Batesian Mimics just pretend to be dangerous or
inedible. Thus potential predators avoid them, but it
doesnt cost them.

Some useful terms

Nocturnal: active at night (e.g., scorpions)
Diurnal: active during daylight hours (e.g., gila
monsters)
Crepuscular: active during dawn and dusk
(e.g., deer tend to be most active around
sunrise and sunset)

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged)
bark scorpion: of 30 AZ species of scorpion, only
the bark scorpion sting is considered lifethreatening. Identified by long, thin pincers.
Climbs, is nocturnal, and is neurotoxic.
Bark scorpion

Stripe-tailed scorpion
Compare
pincer
shapes

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged)
black widow: Nocturnal, makes strong,
messy web. Neurotoxic.

DANGEROUSLY VENOMOUS ANIMALS:

ARACHNIDS (8-legged)
brown spider: thin, spindly spider with three
pairs of eyes in semicircle (difficult to see). May
have violin-shaped marking on cephalothorax
(head). Bite causes tissue damage.
Compare to Wolf Spider which is not deadly
marking

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES
Gila monster: only other known venomous lizard in the
world is Mexican beaded lizard (in Mexico).
Diurnal, but spends 98% of time in burrow; peak activity in
spring when hunting nestlings/eggs. Has leaky skin.
Venom for defense (pain) only.

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES

coral snake: member of cobra family. Has

highly toxic venom but small fangs and
mouth so difficult to bite humans.
Nocturnal. Neurotoxic.
Identified by the phrase: red and
yellow kill a fellow (notice how red
band touches yellow bands); versus
red and black friend of Jack (nondangerous snakes have red
touching black).

DANGEROUSLY VENOMOUS ANIMALS:

REPTILES
Rattlesnakes: 11 species (17 subspecies) of
rattlesnakes in Arizona

TRUE OR FALSE?
You can tell the age of a rattlesnake by counting the
segments of its rattle.
Baby rattlesnakes are more dangerous.
Rattlesnakes must be coiled to strike.
Rattlesnakes always rattle before striking
Rattlesnake eggs are good eating
Rattlesnake bites are always fatal
All False
Source: AGFD

RATTLESNAKE SENSE ORGANS

Nostrils to smell
Eyes: to see

Pit Organ to sense heat

Body to feel ground vibrations

Cont >>

RATTLESNAKE SENSE
ORGANS
Jacobsons Organ to augment
smell by analyzing chemicals
brought to it by the tongue which
picks up the chemicals from the air
and ground.

MEDICATION POISONING

Acetaminophen
Rosens Emergency Medicine 7th ed, vol 2

A typical time course of rise, peak, and fall of

laboratory values in patients with acetaminopheninduced hepatic dysfunction who survive. Peaks are not
proportional. Not all laboratory abnormalities occur in
all patients, and significant individual variation may
occur.
ALT: alanine transaminase
AST: aspartate transaminase
CR: creatinine
INR: international normalized ratio.

Acetaminophen
Rosens Emergency Medicine 7th ed, vol 2

Acetaminophen
Rosens Emergency Medicine 7th ed, vol 2

Risk Assessment in Pregnant Women

Fetal acetaminophen toxicity : jarang terjadi tapi fatal
Acetaminophen bisa tembus sawar janin; konsentrasi @ fetus
> ibu
Risk assesment & pendekatan dx = wanita tak hamil
Gunakan normogram
Toksisitas kronik: (aspartat aminotransferase) AST > 50IU atau
[acetaminophen] serum segera NACth/ (N-acetylcysteine)

Acetaminophen
Rosens Emergency Medicine 7th ed, vol 2

Management:
Stop absorpsi o/ GIT: pengosongan lambung, karbon aktif
Th/ NAC secepatnya (efektif 6-8 jam post ingest)
Supportive care: mual, muntah, hepatic injury, renal dysfx

Aspirin
Rosens Emergency Medicine 7th ed, vol 2

Gejala keracunan salisilat:

Asymptomatic
Mild:
hyperpnea tinnitis + lethargy

Moderate:
Hyperpnea berat
g3 neurologic nyata: letargi, agitasi
Tidak koma / konvulsi

Severe:
Hyperpnea berat
Koma, semikoma + konvulsi

Aspirin
Rosens Emergency Medicine 7th ed, vol 2

Treatment of acute salicylate poisoning:

Treat dehydration; maintain urine output at 23 mL/kg/hr with 5% dextrose (D5) in

lactated Ringers solution or normal saline.
Correct potassium depletion.
Alkalinize urine.

Obtain baseline arterial blood gas values. If pH is <7.4, administer sodium bicarbonate to obtain pH
of 7.4 (50 mL bicarbonate increases serum pH by 0.1 in an adult).
Infuse intravenous fluids: D5 with 100150 mEq bicarbonate/L.
Monitor serum pH; do not cause systemic alkalosis.
Do not attempt forced diuresis.

Monitor for dialysis indications:

Coma, seizure
Renal, hepatic, or pulmonary failure
Pulmonary edema
Severe acid-base imbalance
Deterioration in condition
Serum salicylate concentration 100 mg/dL after acute ingestion
Serum salicylate concentration 40 mg/dL after chronic ingestion

HEAVY METAL

Timbal
symptom(akut) :

Colicky abdominal pain

Constipation
Headache
Irritability

Severe intoxication
comma & seizure
Chronic intoxication:
Learning disorders (in
children)
Motor neuropathy (eg.
Wrist drop)

Diagnosis :
Blood lead level :
< 10 mcg/dL nontoxic
10 25 mcg/dL impaired
neurobehavioral
development in children
25 50 mcg/dL
headache, irritability,
subclinical neuropathy
50 70 mcg/dL moderate
toxicity
70 100 mcg/dL severe
poisoning

Microcytic anemia with

basophilic stippling
Elevated free erythrocyte
protoporphyrin

Timbal
Emergency and supportive measures :
Encephalopathy patent airway, treat coma and convulsion
Recent acute ingestion whole bowel irrigation, endoscopy, or
surgical removal

Specific treatment :
Severe toxicity edetate calcium disodium (EDTA) 1500
mg/m2/kg/d (approximately 50 mg/kg/d) in four to six divided
doses or as a continuous intravenous infusion. Some clinicians
also add dimercaprol (BAL) 4-5 mg/kg intramuscularly every 4
hours for 5 days
Less severe toxicity edetate calcium disodium (EDTA)
(dosage as above); mild to modereate intoxication succimer
(DMSA) 10 mg/kg orally every 8 hours for 5 days, then every 12
hours for 2 weeks

Mercuri
Gejala klinis (akut) :
Burning sensation in the
throat
Discoloration and edema
of oral mucous
membrane
Abdominal pain
Vomiting
Bloody diarrhea
Shock

Direct nephrotoxicity
acute kidney injury

Inhalation of high
concentrations of
metallic mercury vapor
acute fulminant
chemical pneumonia
Intoksikasi kronik :

Weakness
Ataxia
Intention tremors
Irritability
Depression

Mercuri
Treatment :
Acute poisoning :
Mercury vapor pneumonitis no specific treatment
Ingested mercuric salts lavage + activated charcoal
Acute ingestion of mercuric salts dimercaprol (BAL)

Chronic poisoning :
Remove from exposure
Neurologic toxicity is not considered reversible with
chelation (DMSA or unithiol ?)

Arsen
Gejala klinis (akut) :

Abdominal pain
Vomiting
Watery diarrhea
Skeletal muscle cramps
Dehydration and shock

Intoksikasi kronik :
Pancytopenia
Painful peripheral
sensory neuropathy
Skin changes including
melanosis, keratosis, and
desquamating rash

Emergency measures :
Recent ingestion (1 2 hours)
gastric lavage + 60 100 g
of activated charcoal
Vomiting and diarrhea
intravenous fluids

Antidote :
Severe acute intoxication
dimercaprol injection (BLA)
10% solution in oil, 3 5
mg/kg intramuscularly every
4 6 hours for 2 days; follow
with oral succimer (DMSA) 10
mg/kg every 8 hours for 1
week.

Organophosphates and carbamates are

potent cholinesterase inhibitors capable of
causing severe cholinergic toxicity following
cutaneous exposure, inhalation, or ingestion.
World Wide:
3,000,000 per yr people are exposed.
up to 300,000 fatalities.
15 to 18 % of all poisoning in Aleppo.
Chemical weapons (nerve gases) are
organophosphate agents.

Organophosphorous compounds bind to

acetylcholinesterase
overabundance of acetylcholine in the synapse
By time the compound undergoes a
conformational change (aging) renders the
enzyme irreversibly resistant to reactivation.

Carbamate compounds unlike

organophosphates, are transient cholinesterase
inhibitors.

Generally oral or respiratory exposures result in

signs or symptoms within three hours.

while symptoms of toxicity from dermal

absorption may be delayed up to 12 hours.

 Generally manifests in minutes to hours

Evidence of cholinergic excess
SLUDGE = Salivation,
Lacrimation,
Urination,
Defecation,
Gastric Emptying.
BBB

= Bradycardia,
Bronchorrhea,
Bronchospasm.

 Respiratory insufficiency can result from

muscle weakness, decreased central drive,
increased secretions, and bronchospasm
and it is the lead cause of death.
Cardiac arrhythmias, including heart block
and QTc prolongation may be due to
hypoxemia.

ACH: acetylcholine; Epi: epinephrine; NE: norepinephrine; NMJ: neuromuscular junction.

 In children
Seizures are more common (22%-25%).
Lethargy and coma (54%-96%).
Flaccid muscle weakness,
miosis,
excessive salivation
are common presenting signs.

10 to 40 % of organophosphorous agent
poisoned patients.

Occurs 24-96 hours after exposure

Bulbar, respiratory, and proximal muscle

weakness are prominent features.

Generally resolves completely in 1-3 weeks.

Organophosphate Induced Delayed

Neuropathy (OPIDN).
specific organophosphorous agents.
Usually occurs several weeks after exposure.
Primarily motor involvement (symmetrical motor

polyneuropathy) flaccid weakness of lower

extremities, ascends to involve upper extremities.

Sensory disturbances are usually mild.

May resolve spontaneously, but can result in
permanent neurologic dysfunction.

88% of parents initially deny any exposure

history.

petroleum or garlic-like odor.

If doubt exists a trial of Atropine (0.01 to 0.02

mg/kg) may be employed.
The absence of signs or symptoms of
anticholinergic effects following atropine
challenge strongly supports the diagnosis

 RBC acetylcholinesterase activity:

provides a measure of the degree of toxicity.
determine the effectiveness of antidote therapy.

plasma (or pseudo-) cholinesterase activity:

more easily performed.
not correlate well with the severity of poisoning.
a depression of 25% or more is strong evidence of
excessive organophosphate absorption.

Do not delay the treatment until laboratory

confirmation is obtained.

 Deliver 100 % oxygen via facemask

Strongly consider intubation:
patients who appear mildly poisoned may rapidly
develop respiratory failure.
Consider volume resuscitation with normal saline or
ringer to treat Bradycardia and hypotension.
Use activated charcoal within one hour of an ingestion.
In cases of dermal exposure aggressive
decontamination with complete removal of the patient's
clothes and vigorous irrigation of the affected areas
should be performed.

 Competes with acetylcholine at muscarinic

receptors.
Initial dose 0.05 mg/kg IV bolous.
Doubled every 3 to 5 min until bronchial
secretions and wheezing stop (SaO2).
Repeat every 10 to 30 min until all absorbed
organophosphate metabolized (few hours to
several days; usually 2 to 12 hours).

Keep a maintenance dose of atropine for 2-3

days after disappearing of manifestation.

Tachycardia and mydriasis are not appropriate

markers for therapeutic improvement, as they
may indicate continued hypoxia, hypovolemia, or
sympathetic stimulation.

Fever, muscle fibrillation, and delirium are the

main signs of atropine toxicity that indicate that
atropine administration should be discontinued,
at least temporarily.

 Cholinesterase reactivating agent that are

effective in treating both muscarinic and
nicotinic symptoms.
Use within 48 hours after poisoning.
Use with concurrent of atropine.
Use only for moderate to severe
Organophosphate poisoning and not
carbamate.
Use if neuromuscular dysfunction is present.

25-50 mg/kg IV in 100 ml NS over 30 min.

Repeated after 1 to 2 hours, then every 10 to 12

hour interval if needed
Or
Continuous infusion at 10-20 mg/kg/hour.

Monitor Blood pressure during administration

Prophylactic diazepam has been shown to

decrease neurocognitive dysfunction after
poisoning.
Diazepam 0.1-0.2 mg/kg IV, repeat as necessary
if seizures occur.

phenytoin has no effect on organophosphate

agent-induced seizures.

Organophosphates are usually dissolved in

hydrocarbon bases; thus, the clinician should
consider hydrocarbon pneumonitis and not to do
gastric lavage.