Intoxications JESSICA

8/10/2019 Intoxications JESSICA

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POISONING


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Def. Intoksication= development of dose-

related adverse effect following exposure to

chemical, drugs, or other xenobiotik (zat

asing)


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Classification

Etiology

Onset

Self Poisoning

Attempted suicide

Accidental poisoning

Homicidal poisoning

Acute

Chronic

Target Organ

Liver

Heart

Kidney

CNS

Chemical Material

Alcohol

Phenol

Heavy metal

Organochlorin


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Fundamental of Poisoning Management


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Diare/diaforesis

Urination

Miosis

Bradikardi/bronkospasme

Emesis

Lakrimasi

Salivasi

Kolinergik

Kulit kering

Retensi urine

Penurunan bunyi usus

Delirium

Takikardia

Dilatasi pupil

Kejang, Disritmia

Anti-Kolinergik

Depresi respiratorik

Pupil pinpoint

KomaOpioid

Hipertensi

Takikardia

Dilatasi pupil

Delusi

Psikosis

Kejang

Disritmia

Simpatomimetik

Penurunan tingkat kesadaran

Depresi respirasi

Hipotensi

Perubahan pupil yg berbeda-beda

Hipotermia

Kejang

Sedatif-Hipnotik

Toksidrome


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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 CNSTOXEMIA STRYCHNIN .SPINAL CHORD


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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


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GASTER LAVAGE


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ELIMINASI


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FOOD POISONING


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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)


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Foodborne Diseases

Infections

Poisonous

Animal Tissues

Poisonous

Plant Tissues

Chemical

Poisoning

Intoxications

Microbial

Intoxications

Other Neurotoxins Enterotoxins

Toxicoinfection Invasive Infection

Intestinal

Mucosa

Systemic Other Tissues

or Organs

(Muscle, Liver,

Joints, Fetus,

Other)Mycotoxins(Fungal Toxins)

Algal Toxins BacterialToxins

Diarrhogenic Emetic Enterotoxins Neurotoxins Other


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High risk foods

These include:

meat and meat products;

milk and dairy products;

fruit.

If these foods become contaminated with food-poisoning micro-organisms and conditions allow them

to multiply, the risk of food-poisoning increases.


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People at high risk

Elderly people, babies and anyone who is ill orpregnant needs to be extra careful about the foodthey eat.

For example, pregnant women or anyone with lowresistance to infection should avoid high risk foods suchas unpasteurised soft cheese.


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Factors affecting food poisoning

Some common factorsleading to food poisoninginclude:

preparation of food too farin advance;

storage at ambienttemperature;

inadequate cooling;

inadequate reheating;

under cooking;

inadequate thawing.

More common factorsleading to food poisoninginclude:

consuming raw food;

improper warm holding(i.e. holding hotfoodbelow 63C);

infected food handlers;

contaminatedprocessed food;

poor hygiene.


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Symptoms of food poisoning

Food poisoning can be mild or severe.

The symptoms will be different depending on whattype of bacteria is responsible.

Common symptoms include: severe vomiting; diarrhoea; exhaustion;

headache; fever; abdominal pain; tiredness.


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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.


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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.


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3

Type of food

poisoning

Where the

bacteria come

from

Onset time Symptoms

Salmonella Raw meat,

eggs, poultry,

animals

6 - 72 hours Abdominal pains,

diarrhoea, fever,

vomiting, dehydration

Clostridium

perfringens

Raw meat, soil,

excreta, insects

8 - 72 hours Abdominal pain,

diarrhoea

Staphylococcu

s aureus

Skin, nose,

boils, cuts, rawmilk

1 - 6 hours Vomiting, abdominal

pains, lower thannormal temperature

The Main Food Poisoning Bacteria


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6

Date Place People

Affected

Type of Food

Poisoning

Source

June '98 Marmul 23 Salmonellosis Unknown

April'99

Fahud 12 Shigellosis Unknown

April

'99

RAH Club 32 Shigellosis Unknown

May '01 TocoCamp

Saih Rawl

75 Salmonellosis Unknown

Incidents of Food Poisoning in PDO

Name RF Sign & Symptoms


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Name RF Sign & Symptoms

Campylobacter Meat and poultry. Onset 211 days. Fever,headache and dizzinessfor a few hours, followedby abdominal pain. This

usually lasts 27 daysand can recur over anumber of weeks

Clostridium perfringens Raw meat, cooked meatdishes and poultry.

Onset 822 hours.Abdominal pain,

diarrhoea and nausea.This usually lasts 1248hours.

E Coli 0157 Raw meat and dairyproducts.

Diarrhoea, which maycontain blood, can lead

to kidney failure or death.Listeria Monocytogenes Unpasteurised milk and

dairy products, cook-chillfoods, pate, meat,poultry and saladvegetables

Ranges from mild, flu-likeillness to meningitis,septicaemia,pneumonia. Duringpregnancy may lead tomiscarriage or birth of an


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Salmonella Outbrakes associated with grade A eggs. Preparation of Poultry.


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Salmonella g gg p ySources : Chocolate mousse ; Ceasar salad ; ChickenGram - rodKilled 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 Four different types


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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 12-48 hrs (14 days)

N/V/D

abdominal distention

constipation (as disease progresses)

Neurologic disturbances : dysarthria, dysphagia, dry mouth

With disease

progression

descending paralysis ; respiratory weakness; respiratory failure ;

oculobulbar symptomsTreatment stabilization of airway

history upper and lower GI decontamination trivalent antitoxin

(ABE)

watch for hypersensitivity call CDC

DD Neuromuscular disorders


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DD 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 laboratoryconfirmation

Treatment /

profilaksis

Ventilatory assistance and supportive careBotulinum antitoxin

Trivalent equine product against types A,B, and E available from CDCMost effective if given early

Antibiotics for wound botulismPenicillin

Recovery may be prolonged with supportive care necessaryVaccine investigational

not available


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1

1

1

1

1

1

2

1

1

1

11

1

1

Laboratory Capacity for

Botulinum Toxin Testing


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

Staphylococcus Enterotoxins


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p y

aureus 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 usedj k l f d i di k l i lf i ki d f b ( i h l bi


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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 36hours.abdominal pain/discomfort after eating few jengkolVomit , colic pain at micturition.Urine volume also decreased, even can be anuria. hematuria can be found. Alsourine and breath smells jengkol.

LAB In urine examination with microscope, can be found jengkolic acid crystal thatbeing 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 Root and leaf of cassava have hydrocyanate acid(HCN).


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(Singkong) 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 bloodSign &

symptoms

More quantitydeath due to respiratory failure

initiallyheat to the abdomen, nausea, dizziness, spasms, weakbreathing fast and

short

Smelly breath and vomitbitter almondsmell

Fainting, seizures, weakness, sweating, eyes bulging wide pupils without reaction

Mouth foam mixed with the color of blood Skin colorbrick red (light skin), cyanosis usually (-) appears

Test Giunard u / cassavapicric acid color changeyellow to red (15minutes ~ 3 hours)

Treatment Commonly sametoxin eliminated (vomited, rinse the hull(gaster), antidot

amil/na nitrit, Na-tiosulfat

Na-nitritNaCN bindprevent damage to cells ferisitokrom oxidase enzyme

Na-tiosulfatNaCN bindstable tiocynatatexcretion 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

O2th suportif & antidotum (t.u O2 high tension/CPAP)

Ok O2 competitive against bond ferisitokrom oxidase enzyme with cyanide


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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 acid from tempe bongkrek (manufacture with coconut


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bongkrek, asam

bongkrek)

pulp fermentation and peanuts)

Etiology coconut pulpbongkrek acid (Pseudomonas cocovenenan)

iron pedestalClostridium botulinum contamination

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

ptosis, Strabismus

severe : Respiratory and circulatory failure, seizure, death

Treatment Spesific Antidotnot yet. Prevent further absorption of toxins and accelerate the

excretion Rinse the hull

Catharsis

General improvement

IV plasma liquid & NaCl

IV glukosa

activated charcoalu / impaired circulation and respiration.

Ne


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PLANT & ANIMAL TOXINS

T i A d U


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Toxins Around Us

Have you every eaten

too much puffer fish

or the wrong

mushroom or been

bitten by a snake?


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Plant Toxins


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Skin

Gastrointestinal System

Cardiovascular Systems

Nervous System

Liver

Reproductive Effects

Plant Toxins

Example Jimson Weed


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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 asign of allure and beauty

Atropine is drug responsible for effects

Counteracts the effects of pesticides and

chemical warfare agents that act by inhibiting

acetylcholinesterase

ExampleJimson Weed

Example Mushroom Poisoning


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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

ExampleMushroom Poisoning

Skin Allergic DermatitisPlant Rashes, itchy skin

Phil d d i i h b lb f d ff dil h i th


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Philodendron, poison ivy, cashew, bulbs of daffodils, hyacinths,

tulips (antibody mediated)

Allergic DermatitisPollen Sniffles & sneezing, runny eyes

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

mediated)

Contact Dermatitis OralSwelling and inflammation of mouth Skin

pain & stinging sensation

Dumb cane (Dieffenbachia)Nettles (Urtica)

Contact Dermatitis Skinpain & stinging sensation

Calcium oxalate crystals coated with inflammatory proteinscontain

histamine, acetylcholineGI 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 toxicitynausea, diarrhea, headache, confusion, dehydration,

death

Wisteria, castor bean (Ricinus communis)

Ricinblock protein synthesis very toxic 5 to 6 beans can kill a child

Liver Hepatitisand cirrhosis of liver - From contaminated grain

R d l


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Ragwort or groundsel

Pyrrolizidine alkaloidsattack liver vesselseffects 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

Alfaltoxinsproduced by fungus in poorly stored grain

CV Digitalis like glycosidescardiac arrhythmias

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

Heart nervesdecreased 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


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Reproductions Teratogenmalformations in offspring (sheep)

Veratrum californicumnative to North America

Veratrumblocks cholesterol synthesisseenoffspring of mountain sheep

Abortifacients

Legumes (Astrogalus)

Bitter melon seeds (Momordica)Swainsonine toxinstops cell division

Lectins - halt protein synthesisused by humans

Animal Toxins


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Arachnids - Scorpions, Spiders,

Ticks

Insects Snakes

Lizards

Fish, and frogs

Animal Toxins

Example Puffer Fish


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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

ExamplePuffer Fish

Arachnids

Scorpions Spiders

ScorpionsStingerlow toxicity

Spider bites


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Scorpions, Spiders,

Ticks

Spider bites

Widow spiders -Neurotoxin

Brown or Violin -Tissue Damage

TicksNeurotoxinTransmits other diseases

Insects Moths and caterpillarsIrritating to eatAntsProteins, formic acid Irritation to allergic response

Honey beesProteinsSwelling, allergic response

WaspsFormic acid

Reptiles LizardsIrritating to eat

Snakes

VipersRattlesnakes, Water moccasins, Copperheads

Complex enzymesTissue necrosis, allergic response,

shock

Elapidae Cobras, Kraits, Coral SnakesProteins

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)


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WHY TALK ABOUT VENOMOUS

ANIMALS?

SO THAT YOURE NEITHER OVERLY

WORRIED


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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.


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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, makingsure not to put fingers under the rock/wood, always

lift it so that the rock/wood is between you and thepotential animal, and always check underneath. It isbest to use a tool to lift a rock/wood.


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POISONOUS VS VENOMOUS?

Poisonousanimals 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 thetoad!

e.g., Parotoid Gland


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POISONOUS VS VENOMOUS?

Venomousanimals inject their

toxins.

For example, this rattlesnake

produces toxins in modifiedsalivary glands then injects

toxins through hollow fangs.

THE CHARACTERS


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THE CHARACTERS:

MILDLY VENOMOUS ANIMALS

Non-life-threatening except by anaphylactic shockin those that are allergic.

Wasps, bees, ants, most spiders, most scorpions,

etc.

THE CHARACTERS


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THE CHARACTERS:DANGEROUSLY VENOMOUS ANIMALS

Life-threatening. Need to seek medical attention.

Bark scorpion, black widow, brown spider, gilamonster, coral snake, rattlesnakes.
http://www.enature.com/guides/show_species_fgl.asp?fromWhere=&curPos=59&recsFound=76&curGroup=Reptiles_and_Amphibians&recNum=AR0198&guideID=ng&beautyID=8870&searchType=&color=&size=&shape=546&leafShape=&fruit=&habitat=&range=&useFreeText=&freeText=


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TYPES OF VENOM

Hemolytic: affects circulatory system(hemo= blood) by destroying bloodcells and vessels. Symptoms include severepain, swelling, discoloration, and localtissue death. Shock can occur. Example:

most rattlesnakes.

Rattlesnake bite picture source

https://reader010.{domain}/reader010/html5/0608/5b19caef0c197/5b19cb14b106a.jpg


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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.


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TYPES OF VENOM

Other:

Gila Monster toxin causes

pain. Brown (Recluse) Spider

toxin destroys proteins,

thus tissues.

Likely brown spider bite
http://www.pharmacy.arizona.edu/centers/poisoncenter/apdicindex.html


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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

useof venom).


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WHY NOTBE 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

expensiveto produce.

WAYS TO AVOID WASTING TOXIN


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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


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AVOID USING TOXIN

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

AVOID USING TOXIN


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AVOID USING TOXIN

Retreat


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ONE MORE WAY TO AVOID USING TOXIN

Dont produce toxins at allbe a Fake!

Batesian Mimics just pretend to be dangerous orinedible. Thus potential predators avoid them, but it

doesn

t cost them.


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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)


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DANGEROUSLY VENOMOUS ANIMALS:


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ARACHNIDS (8-legged)

black widow

: Nocturnal, makes strong,

messy web. Neurotoxic.



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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



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REPTILES

Gila monster: only other known venomous lizard in theworld is Mexican beaded lizard (in Mexico).

Diurnal, but spends 98% of time in burrow; peak activity in

spring when hunting nestlings/eggs. Has leakyskin.Venom for defense (pain) only.



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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 (non-

dangerous snakes have red

touching black).



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REPTILES

Rattlesnakes: 11 species (17 subspecies) of

rattlesnakes in Arizona


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RATTLESNAKE SENSE

ORGANS

Jacobsons Organto augment

smell by analyzing chemicals

brought to it by the tongue which

picks up the chemicals from the airand ground.


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MEDICATION POISONING

Acetaminophen


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Rosens Emergency Medicine 7thed, vol 2

Acetaminophen

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

laboratory values in patients with acetaminophen-induced hepatic dysfunction who survive. Peaks are not

proportional. Not all laboratory abnormalities occur inall patients, and significant individual variation mayoccur.

ALT: alanine transaminase

AST: aspartate transaminase

CR: creatinine

INR: international normalized ratio.

Acetaminophen


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A p

Acetaminophen


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A p

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


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A pManagement:

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


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A pGejala 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


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A pTreatment 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


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HEAVY METAL

Timbal


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symptom(akut) :

Colicky abdominal pain

Constipation

Headache

Irritability

Severe intoxication

comma & seizure

Chronic intoxication:

Learning disorders (inchildren)

Motor neuropathy (eg.

Wrist drop)

Diagnosis :

Blood lead level :

< 10 mcg/dLnontoxic

1025 mcg/dLimpairedneurobehavioraldevelopment in children

2550 mcg/dLheadache, irritability,

subclinical neuropathy

5070 mcg/dLmoderatetoxicity

70100 mcg/dLseverepoisoning

Microcytic anemia withbasophilic stippling

Elevated free erythrocyteprotoporphyrin

Timbal


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Timbal

Emergency and supportive measures : Encephalopathypatent airway, treat coma and convulsion

Recent acute ingestionwhole bowel irrigation, endoscopy, orsurgical removal

Specific treatment :

Severe toxicityedetate calcium disodium (EDTA)1500mg/m2/kg/d (approximately 50 mg/kg/d) in four to six divideddoses or as a continuous intravenous infusion. Some cliniciansalso add dimercaprol (BAL)4-5 mg/kg intramuscularly every 4hours for 5 days

Less severe toxicityedetate calcium disodium (EDTA)(dosage as above); mild to modereate intoxicationsuccimer(DMSA)10 mg/kg orally every 8 hours for 5 days, then every 12hours for 2 weeks

Mercuri


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Mercuri

Gejala klinis (akut) : Burning sensation in the

throat

Discoloration and edema

of oral mucousmembrane

Abdominal pain

Vomiting

Bloody diarrhea

Shock

Direct nephrotoxicityacute kidney injury

Inhalation of highconcentrations of

metallic mercury vapor

acute fulminant

chemical pneumonia

Intoksikasi kronik :

Weakness

Ataxia Intention tremors

Irritability

Depression

Mercuri


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Mercuri

Treatment :

Acute poisoning :

Mercury vapor pneumonitisno specific treatment

Ingested mercuric saltslavage + activated charcoal

Acute ingestion of mercuric saltsdimercaprol (BAL)

Chronic poisoning :

Remove from exposure

Neurologic toxicity is not considered reversible with

chelation (DMSA or unithiol?)

Arsen


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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, anddesquamating rash

Emergency measures :

Recent ingestion (12 hours)gastric lavage + 60100 g

of activated charcoal

Vomiting and diarrhea

intravenous fluids

Antidote : Severe acute intoxication

dimercaprol injection (BLA)

10% solution in oil, 35

mg/kg intramuscularly every

46 hours for 2 days; followwith oral succimer (DMSA) 10

mg/kg every 8 hours for 1

week.


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Organophosphates and carbamates arepotent cholinesterase inhibitors capable of

causing severe cholinergic toxicity following

cutaneous exposure, inhalation, or ingestion.

World Wide:

3,000,000 per yrpeople are exposed.

up to 300,000fatalities.

15 to 18 % of all poisoning in Aleppo.

Chemical weapons (nerve gases) are

organophosphate agents.


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Organophosphorouscompounds bind toacetylcholinesterase

overabundance of acetylcholinein the synapse

By time the compound undergoes aconformational change (aging) renders the

enzyme irreversiblyresistant to reactivation.

Carbamatecompounds unlikeorganophosphates, are transient cholinesterase

inhibitors.


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Generally oral or respiratory exposures result in

signs or symptoms within threehours.

while symptoms of toxicity from dermal

absorption may be delayed up to 12 hours.


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Generally manifests in minutes to hours

Evidence of cholinergic excess

SLUDGE= Salivation,

Lacrimation,Urination,

Defecation,

Gastric Emptying.

BBB = Bradycardia,

Bronchorrhea,

Bronchospasm.


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


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Organophosphate Induced DelayedNeuropathy (OPIDN).

specific organophosphorous agents.

Usually occurs several weeks after exposure.

Primarilymotor involvement (symmetrical motorpolyneuropathy) 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.


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88% of parents initially deny any exposurehistory.

petroleumor 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


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RBC acetylcholinesterase activity:

provides a measure of the degree of toxicity.

determine the effectiveness of antidotetherapy.

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.


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Do not delay the treatment until laboratory

confirmation is obtained.


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Deliver 100 % oxygenvia facemask Strongly consider intubation:

patients who appear mildly poisoned may rapidly

develop respiratory failure.

Consider volume resuscitation with normal saline orringer to treat Bradycardia and hypotension.

Use activated charcoalwithin one hour of an ingestion.

In cases of dermal exposure aggressive

decontaminationwith complete removal of the patient'sclothes and vigorous irrigation of the affected areas

should be performed.


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Competes with acetylcholine at muscarinicreceptors.

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 toseveral days; usually 2 to 12 hours).


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Keep a maintenance dose of atropine for 2-3days after disappearing of manifestation.

Tachycardia and mydriasisare not appropriate

markers for therapeutic improvement, as theymay indicate continued hypoxia, hypovolemia, or

sympatheticstimulation.

Fever, musclefibrillation, and deliriumare the

main signs of atropine toxicitythat indicate that

atropine administration should be discontinued,

at least temporarily.


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Cholinesterase reactivating agent that areeffective in treating both muscarinic and

nicotinic symptoms.

Use within 48 hours after poisoning. Use withconcurrent of atropine.

Use only for moderateto severe

Organophosphatepoisoning and notcarbamate.

Use if neuromuscular dysfunctionis present.


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

Repeatedafter 1 to 2 hours, then every10 to 12

hour interval if needed Or

Continuous infusionat 10-20 mg/kg/hour.

Monitor Blood pressure during administration


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Prophylactic diazepamhas been shown todecrease neurocognitive dysfunction after

poisoning.

Diazepam 0.1-0.2 mg/kg IV, repeat as necessary

if seizures occur.

phenytoinhas no effect on organophosphate

agent-induced seizures.


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Organophosphates are usually dissolved inhydrocarbon bases; thus, the clinician should

consider hydrocarbon pneumonitisand not to dogastric lavage.

Intoxications JESSICA

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