Principles of Toxicology

Clinical Case 1
Seorang anak laki2, umur 7 tahun dibawa ke IGD karena
muntah-muntah dan penurunan kesadaran. 30 menit
sebelumnya baik-baik saja, lalu ditemukan tidak berespon di
kamar mandi
Bau tidak spesifik dan menyengat
Px fisik: pinpoint pupil (diameter 2 mm), hipersalivasi,
lakrimasi. Masih berespon dengan nyeri, bicara
ngelantur, GCS 9.
HR 117, RR 38, BP 112/58, t 36.8C, SatO2 96%
Paru: Wheezing bilateral; Abdomen: no tenderness
Extremitas: hangat-dingin, capillaery refill <2 detikc
8 menit masuk IGD, HR 50x dan henti nafas.
Dilakukan intubasi orotrakeal, ventilasi mekanik, dan
atropinisasi (0.02 mg/kg every 5 min)...stabil

Clinical Case 2
Seorang wanita, umur 31 tahun dibawa ke IGD karena
ditemukan tidak sadar oleh suami. 1 jam sebelumnya baikbaik saja, hanya mengeluh migren-nya kambuh lagi dan
tampak minum obat yang dia tidak tahu.
HR 136, RR 21, TDS 82 mmHg, SatO2 100% NRM
Jantung: BJ I-II normal, bising -, Gallop
Lain dbn
ECG: Takikardia dengan kompleks QRS lebar, VT

Clinical Case 2: ECG

ECG: Takikardia dengan kompleks QRS lebar

Clinical Case 2: ECG

Terapi: Sodium bikarbonat, hiperventilasi

Definitions
Toxicology

Complex subdivision which deals with

toxic substances: detection, properties,
effects and regulation of toxic
substances, including poisons.
So what is a poison?

Definitions

Toxic refers to the condition of a substance

and the degree to which it can cause damage
to you or any other organism or system. Toxic
can refer to biological organisms and nonbiological substances
Poisonous describes substances that will
disturb organisms, usually in a harmful way.
Poison implies a high level of toxicity, though
any substance is technically poisonous if
taken in a large enough dose. Poison always
refers to biological organisms.

What is a poison?
Poison

Any substance which cause a harmful effect when

administered either by accident or by design to a
living organism
Poisoning is quantitative concept
Any chemical at some specific dose and time is
harmless, while the same chemical at other doses
and time is toxic

What is Toxicology?
1. Primarily a multidisciplinary science that is
based on other sciences including:
Pharmacology
Pathology (disease/death)
Chemistry
Epidemiology

Hazard potential for harm

Risk probability of producing Harm

2. Applied Science
Enhancement of the quality of life
Protection of Environment
To learn about life processes (i.e uncoupling agents)

Dose Response Curve related to

Toxicity

Dose/Time Principle
While dose is the primary determinant of
toxicity, effects of chemicals on the body
are also a function of the length of time
such substances are present.

Blood Plasma Level Toxicity

More simply

Dose makes the poison

It is the primary determinant of Toxicity

Toxicology in Modern Times

During the last 5 decades, toxicology has
taken on new meaning

Thalidomide tragedy (1950s) - phocomelias

and other birth defects
Silent Spring Rachel Carson, DDT
TV CSI, Quincy
Increasing Drug Abuse
Medical Malpractice suits (last 30 years)

Importance of Toxicology

1. Important because chemicals are

responsible for at least 10,000 accidental
deaths annually.
Children under 5 years old are usually poisoned
by:
Plants, cosmetics, salicylates, hydrocarbons,
detergents and acetaminophen.
Adult poisoning usually involves:
Barbituates, carbon monoxide, salicylates,
alcohol, narcotics and acetaminophen

2. Work place accidents associated with

chemicals.
A. Drugs (alcohol, cocaine, marijuana, etc.)
B. Manufactured Products

Importance of Toxicology (cont)

3. Litigation
A. ie. Drug/alcohol related accidents

4. Causation
A. Evidence of cause and effect based on
exposure and dose.

Toxicological Terms
1. LD50 dose at which 50% die
Only animals
TD50 dose at which 50% have toxicity
Measure of harmfulness

2. T.I. Therapeutic Index

TD50 / ED50
The larger the number, the safer the drug
Measure of safety

3. Acute Toxicity
Single dose within 24 hrs
Defines intrinsic toxicity

Toxicological Terms (cont)

4. Chronic Toxicity
Daily exposure for up to a lifetime

5. TLV Threshold Limit Value

Concentration below which there is no expected untoward
effect over a period of 8hrs/day 5 days/week
NOEL no observable effect level
ADI allowable daily intake
ADI = (NOEL) / x
x is some safety factor (i.e., 100)

Toxicological Terms (cont)

6. STEL Short term exposure level
4x a day, with the average being equal to the TLV

7. ALD Average Lethal Dose

Estimated from accidental deaths in humans

8. Toxicon
Toxic principle of a given chemical entity

Tylenol quinone imine

CCl4 free radicals

9. Primary Determinant of Toxicology

Dose, Dose and Dose

Selective vs. Nonselective Toxicity

Nonselective
Nearly all chemical are nonselective in their
actions
Few chemicals are sufficiently selective to harm
certain cells

Selective
One mans poison is another mans pill.
What may be harmful to one specimen may be
relatively harmless to another.
Garden spray

II. Management of a Poisoning

Immediate measures are called for in
every case of poisoning regardless of
cause.
1. Support Vital Functions
2. ID drug poisoning as the problem
3. Reduce the amount of drug in the body

Support vital life functions (ABCs)

Airway endotracheal tube if needed, watch for fluid
accumulation in airway (i.e.. Aspiration of vomit)

Breathing Supplemental Oxygen, bag valve mask

(BVM) and respirator.

Circulation Monitor ECG, watch for arrhythmias, cardiac

arrest and shock

Vasogenic Shock faulty vasomotor tone, increase capillary

permeability.
Cardiogenic Shock inadequate cardiac output can be due to
cardiac dilation (barbituate, Ca channel blocker)

General Treatment of a
Comatose Patient
There are several general antidotes that
are used in the treatment of comatose
patients upon presentation at the hospital.
What are they?

Supportive Drug Therapy

Treat all patients who come into the
hospital in a coma with glucose, insulin
and naloxone.
Use drugs to treat emergent conditions, ie:
Seizures anticonvulsants (valium)
Cardiac Dysrhythmias anti-arrhythmias (lidocaine,
digoxin)
Severe Agitation anxiolytics (benzo)

How to ID the poison?

ID the poison
1. Patient history
2. Laboratory testing
3. Comparison of drugs or chemicals with
known toxicology standards.

Identification of the Poison

(Sample Types)
Urine - 1st choice easier to detect presence of
the drug due to the accumulation of drug in the
urine.
Blood/Serum 2nd choice get exact serum
levels to better identify the health effects of the
drug (coma/stimulant panels)
Gastric Contents 3rd choice less helpful, but
can tell if you should perform a gastric lavage.

Identify Poison (Tests)

Urine tests
Immunoassay (EMIT, ELISA) semiquantitative tests usually
with automated instrumentation. Can detect cannabinoids,
amphetamines, cocaine, barbs etc.
Thin Layer Chromatography (TLC) ToxiLab, 4 stage solvents,
qualitative test

Urine/Blood tests
High Performance Liquid Chromatography (HPLC), gas
chromatography and Gas Chromatography/Mass
Spectroscopy (GCMS) are quantitative tests that can detect
many compounds.
Coma and Stimulant panels

Can be done in 2 hours

Removal of the Drug (Emesis)

Utilize syrup of Ipecac to Induce
emesis to remove unabsorbed
drug.
Emesis inducers

Mechanical
Apomorphine
Syrup of ipecac
Contraindications?

Contraindications of Emesis
Emesis is contraindicated in cases of:
Petroleum hydrocarbon solvent chemical
pneumonitis
Caustic acid or alkali agent (rupture)
Seizing Patient
Comatose Patient

Removal of the Drug

(Gastric Lavage)
Gastric Lavage washing of
the stomach. (early tx.)
A tube is inserted through the
nose or mouth, down the
esophagus, and into the
stomach. Sometimes a topical
anesthetic may be applied to
minimize irritation and gagging
as the tube is being placed.
Stomach contents can be
removed using suction
immediately or after irrigating w/
fluids through the tube.

Activated Charcoal/Cathartics
Activated Charcoal (AC)
Used to bind compounds and to prevent absorption in the
GI tracts. (many drugs)
Contraindicated with caustic agents and petroleum
distillates due to the lack of absorption of these agents by
the charcoal and risk of vomiting associated with the
charcoal

Order of use of charcoal and ipecac

Cathartics
Promotes rapid passage of poison through the GI tract
Counteracts the constipative effects of AC
I.E. sorbitol, Mg Citrate, Mg Sulfate

Removal of the Drug (Other)

Alteration of pH of urine to enhance excretion of the drug,
useful for salicylates, chlorpropamide, etc ( tx)
Diuresis often used in conjunction with urine pH alteration
Dilution with water useful in the treatment of skin or eye
exposure to harmful agents. ( no neutralizers)
Demulcents soothes mucous membranes and coats the
stomach, i.e. milk of magnesia
Hemodialysis blood transverses a semipermeable
membrane that is bathed in dialysis solution or dialysate. Drugs
or toxins diffuse across this membrane. (protein binding)

B. Antidotal Treatments (1. Complexation)

A. Heavy Metals
Chelators (BAL, EDTA) complexes with the metals
making them inert

B. Heparin
Protamine (base) binds to acidic heparin to terminate its
action and is excreted by glomerular filtration.

C. ToxinsBotulinum Toxin ALD- < 0.5mcg LD50=10ng/kg

Most potent poison known, rapidly absorbed and
prevents ACH release from nerve terminals
Tx: ABCs, lavage, emesis, charcoal,Trivalent anti-toxin
Mortality of 70% to 10% with treatment

Complexation (cont)
D. Organophosphates
Pralidoxime is a nucleophillic reagent that ties up
the organophosphates and permits its excretion.

E. Cyanide
Binds to cytochrome oxidase, LD50= 2mg/kg
Causes death in 1 to 15 minutes at high doses.
Chelator is made in the body, methemoglobin
(Fe3+)
Give Amyl Nitrites and Na Nitrite with O2 and whole
blood to convert hemoglobin to methemoglobin
(LD50 increases 5 fold) .

Patofisiologi
OP menghambat asetilkolinesterase (AChE) yang menghidrolisa
asetilkolin. Inhibisi AChE oleh OP mengakibatkan akumulasi asetilkolin
stimulasi yang berlebihan pada reseptor asetilkolin di sinaps sistem
saraf otonom, sistem saraf pusat, dan neuromuscular junction.
Gambar.2. Mekanisme keracunan organofosfat

Sumber : Department of environmental and occupational health sciences. 2007

Gambaran Klinis
Gambaran klinis dari keracunan OP
dari 3 fase :

terdiri

Worthley LIG. Clinical Toxicology: Part II. Diagnosis and management of uncommon poisonings.
Critical Care and Resuscitation.2002;4:216-230
Goel A, Aggarwal P. Pesticide poisoning. Natl Med J India. 2007;20:182-91

Sindrom kolinergik akut

Efek Muskarinik
Miosis

Efek Nikotinik
Fasikulasi otot

Efek SSP
Penurunan
kesadaran

Diaphoresis/berkeringa Paralisis
t

Kejang

Bronchorrhea/
Bronchospasme

Kelemahan
otot

Depresi pernafasan

Bradikardi

Hipertensi

Ataksia, disartria

Salivasi

Takikardi

Gejala
Ekstrapiramidal

Hipotensi

Letargi

Lakrimasi
Diare/Diuresis berlebih

Sumber : Lau CL, Chung KL, Kam CW. Hong Kong Journal of Emergency

Muntah

Penegakkan Diagnosa
Keracunan organofosfat dapat didiagnosa dengan
adanya 2 dari gejala berikut :
1. Riwayat terpapar organofosfat
2. Manifestasi dari gejala muskarinik atau nikotinik.
3. Timbulnya efek antikolinergik setelah pemberian
atropine. Keraguan terhadap keracunan organofosfat
pemberian atropine chalange :1 mg atropine dosis
0,01-0,02 mg/kg. Tidak terdapat gejala antikolinergik
keracunan asetilkolinesterase inhibitor
4. Konfirmasi hasil laboratorium : pengukuran AChE di
sel darah merah, atau pseudo AChE di plasma darah.
Koirala DP, Rao KS, Malla KK, Malla T. A study of clinical features, management and outcome of
organophosphate and carbamate poisoning in children. J. Nepal Paediatr.Soc. 2013;33(2):85-90

Antidotal Treatments (cont)

2. Enhancement of metabolic conversion to a
safer form
Example: Cyanide Poisoning and thiosulfate
treatment (LD50 increases 3 fold)

CN-

SCN
Rhodanese

Sulfur

Treatment: Give
Thiosulfate
(Sulfur source)

Antidotal Treatments (cont)

3. Inhibition of metabolic conversion to
toxic forms.
A. Ethylene glycol / Methanol ethanol
administration prevents Alcohol dehydrogenase
(ADH) from converting these substances into toxic
forms. (Km Mechanism of Toxicity)

4. Accelerating rate of excretion

Compete with reabsorption (Renal Tubules).
I.e. For Sr2+ or Ra2+ radiation give Ca2+; For Br1poisoning give Cl1- to aid in excretion.

5. Competition for Essential receptors

A. Carbon Monoxide
CO is found in cigarette smoke (5%) and auto
exhaust (9%). Not in natural gas itself.
Commonly used as a means of suicide; over 5000
fatalities a year from CO poisoning.
Carboxyhemoglobin is found in very small amounts
in non-smokers ~2.5% of the bodys hemoglobin and
7-10% for smoker
TLV 35ppm STEL 200ppm (15min)
ALD - 0.1%
CO has a 210x greater affinity for Hb than O2 does

Carbon Monoxide Poisoning

Carboxyhemoblobin
Concentration

Symptoms

0-10%

None

20-30%

Slight headache, exertional dyspnea

30-40%

Throbbing headache, fatigue, dizziness,

SOB

40-60%

Severe headache, weakness, dizziness,

confusion, dimness of vision (some have a
cherry red appearance)

>60%

Convulsions, coma, Respiratory collapse

leading to death

Treatment: Artificial Respiration with pure O 2 to promote

displacement of CO

Competition for Essential receptors

(cont)
B. Turbocurare/pancuronium
Cause a competition between the poison and Ach at the
skeletal muscle endplate.
Treatment: Cholinesterase Inhibitors (i.e. Neostigmine and
physostigmine)
Administration of ACH alone ineffective

C. Coumarin
Anticoagulant that interferes with synthesis of coagulation
factors II, VII, IX and X.
Treatment: Vitamin K

D. Opiates
Competition at opiate receptors with antagonists like
naloxone and naltrexone.

6. Repair or Bypass effect of poison

A. Nitrites/sulfa drugs
Converts hemoglobin into methemoglobin, which reduces
the ability of the blood to carry O2.
Methylene blue causes a direct reduction of
methhemoglobin back to hemoglobin.

B. Digitalis
Toxic effects include GI disturbances, neurologic, disorders
and cardiac arrhythmias.
Give antidote of Digibind

C. 5-Fluorouracil and 5-fluodeoxyuridine

Antitumor agents used to decrease DNA synthesis.
Thymidine is a specific and effective antidote.

7. Blockade of receptors
responsible for Toxic Effects
The toxic action and the therapeutic action
are mediate by different receptors.
A. Anticholinesterases
Found in pesticides and chemical warfare agents.
increases level of acetylcholine resulting in
Cholinomimetic effects
Atropine blocks muscarinic receptors to block the
effect of the ACHe inhibitors. (anticholinesterases)

Toxicology

Toxidromes
Toxidromes are clinical syndromes that are
essential for the successful recognition of
poisoning patterns sindroma toksik.
The most important toxidromes, clinically,
are:
Sympathomimetics
Sedative Hypnotics
Opiates
Anticholinergics

Cholinergics
Tricyclics (TCAs)
Salicylates

Sympathomimetic Toxidrome
CNS

Agitation, hallucinations, paranoia

Respiration

--

Pupils

Mydriasis

Other

Seizure, hypertension, tremor,

hyperreflexia, hyperthermia

Drugs

Cocaine, amphetamines, PCP

Sedative/Hypnotic Toxidrome
CNS

Coma

Respiration

Decreased

Pupils

Mydriasis

Other

Hypothermia, decrease reflexes,

hypotension

Drugs

Alcohol, barbiturates,
benzodiazepines

Opioid/Opiate
CNS

Coma

Respiration

Depression

Pupils

Pinpoint

Other

Hypothermia, hypotension, triad,

histamine release

Drugs

Opiates, morphine, codeine,

propoxyphene, oxycodone,
hydrocodone

Anticholinergic Toxidrome
CNS

Agitation

Respiration

---

Pupils

Mydriasis

Other

Fever, dry skin, flushing, urinary

retention (ACS) [Hot, dry, mad, red,
blind]

Drugs

Anticholinergics, antidepressants

Cholinergic Toxidrome
CNS

Coma (not quaternary)

Respiration

---

Pupils

PPP

Other

Fasciculation, incontinence,
salivation, wheezing, lacrimation,
bradycardia (SLUDE)

Drugs

Organophosphates, carbamates,
nicotine

Tricyclic Antidepressant Toxidrome

CNS

Coma

agitation

Respiration

----

Pupils

Mydriasis

Other

Arrythmias, convulsions,
hypotension, mycoclonus,
hyperthermias

Drugs

TCAs, amipramine, imipramine,

desipramine

Salicylate Toxidrome
CNS

Variable up or down

Respiration

Can increase or normal

Pupils

-----

Other

Diaphoresis, tinnitis, agitation,

alkalosis (early), acidosis (late),
fever

Drugs

ASA, aspirin, (salicylates)

Specific Poisons Frequently

Encountered
2. Base
Source

Lye, liquid plumber, oven cleaner

Signs

Swallowing is painful and difficult,

vomitus thick and slimy and may
contain blood, shock, esophageal
strictures, causes progressive
damage25% mortality

Treatment

ABCs, demulcents, lots of water,

analgesics, steroids, antibiotics, no
lavage or emetics

Differences between acids and Bases

Acids
1. Immediate pain in
buccal cavity and
esophagus

Bases
1. Primary cause of
chemical burns
2. Rapidly penetrating
liquefactive necrosis.

2. Less often
swallowed than bases

3. Primary effects on
esophagus and only 20% on
stomach.

No esophageal
perforation

4. Esophageal damage
severe including perforation.

Specific Poisons Frequently

Encountered
3. Opiates
Source

Heroin, morphine, oxycodone,

hydrocodone

Signs

Bilateral miosis (PPP), CNS

depression, apnea, decrease in body
temperature, heart rate and
respiratory depression/arrest.

Treatment

ABCs, Naloxone, gastric lavage and

supportive care.

Specific Poisons Frequently

Encountered

4. Meperidine
Source
Signs

Demerol
Dilated pupils due to antimuscarinic
effects, increase in HR, convulsions
due to metabolite (nor-meperidine),
respiratory depression/arrest, coma.
Few fatalities with meperidine
(tolerance).

Treatment

ABCs, Gastric lavage (if oral),

diazepam for seizures and naloxone
for depressive effects (not for tremors)

Specific Poisons Frequently

5. Atropine Encountered
Source

Atropine, Deadly Nightshade plant

Signs

Dry mucous membranes, burning in

throat, intense thirst, dilation of pupils,
hot dry skin, hyperpyrexia, tachycardia,
mania and delirium; death from
respiratory failure
Hot, dry, mad, red and blind.

Treatment

ABCs, Lavage with 4% tannic acid,

pilocarpine or physostigmine, aspirin
(antipyretic) and alcohol sponges.

Specific Poisons Frequently

Encountered
6. Barbiturates
Source
Signs

Treatment

Suicide, automatism (forget you

already took your dose)
CNS depression (progressive),
drowsiness, shallow rapid respiration,
CV collapse, low body temp and death
due to respiratory depression
ABCs, Lavage with KmNO4, charcoal,
alkaline diuresis (NaHCO3),
hemodialysis (long acting barbs)

Specific Poisons Frequently

Encountered
7. Benzodiazepines
Source
Signs

Treatment

Diazepam (long acting), alprazolam

(short acting), triazolam (ultra short)
Same as barbiturates, rarely fatal
unless taken with ETOH or other CNS
depressant due to synergistic CNS
depression
ABCs, emesis, gastric lavage,
antidote: flumazenil short T1/2 may
require multiple doses.

Specific Poisons Frequently

Encountered
8. Ethanol
Source

Whisky, wine, beer etc.

Signs

Odor on breath, impaired motor

coordination, slurred speech,
dehydration, gastritis, hypothermia,
coma and death due to respiratory
depression

Treatment

ABCs, gastric lavage with bicarb,

caffeine, hemodialysis (if >500mg%)

Specific Poisons Frequently

Encountered
9. Neuroleptics
Source
Signs

Major tranquilizers, antipsychotic agents

(phenothiazines, thioxanthenes)
Extrapyramidal signs (EPS),
hyperactive, tardive dyskinesia, CNS
depression, seizures, hypotension,
poikilothermia

Treatment ABCs, lavage (even hours hours later

due to lower gastric motility), Treat
arrhythmias as needed and
diphenhydramine for EPS.

Specific Poisons Frequently

Encountered
10. Kerosene
Source

Illuminating fuels, paint thinners

Signs

Euphoria, burning in the chest,

headache, weakness, drowsiness,
convulsions, death due to respiratory
arrest or ventricular fibrillation

Treatment

ABCs, large amounts of water, olive

oil and saline cathartic, antibiotics,
corticosteroids to reduce kerosene
pneumonitis, no emetics or lavage.

Specific Poisons Frequently

Encountered
11. Parathion
Source

Organophosphate insecticide

Signs

SLUDE, fixed pin point pupils, loss of

muscle coordination, muscle twitching,
mental confusion, death due to
respiratory arrest.

Treatment

ABCs, atropine, pralidoxine, lavage

with 5% NaHCO3, wash affected
areas, avoid morphine, barbituates
and phenothiazines.

Specific Poisons Frequently

Encountered
12. Salicylates
Source

Aspirin, percodan

Signs

Deep and rapid breathing, tinnitis,

hallucinations, convulsions, resp.
alkalosis (adult), metabolic acidosis
(child), respiratory and CV collapse
Serum level > 400mcg/ml

Treatment

ABCs, emetics, gastric lavage 5%

NaHCO3, monitor pH, barbituates or
benzos for seizures, hemodialysis if
needed.

Specific Poisons Frequently

Encountered
13. Acetaminophen
Source

Tylenol, Vicodin, Percocet

Signs

After depletion of glutathione, nausea,

vomiting, elevated liver enzymes
(SGOT, SGPT, bilirubin), hepatic
necrosis and death due to hepatic
failure.

Treatment

ABCs, emetics, lavage, charcoal, Nacetylcysteine to restore glutathione

earlier the better (grapefruit juice),
monitor liver enzymes.

Acetaminophen Blood level

Effects
Plasma levels of > 250mcg/ml at 3-5
hours post ingestion.
Rumack Matthew nomogram Probable
toxicity
Children (9-10yrs) are less susceptible to
the toxic effect of acetaminophen.

Specific Poisons Frequently

Encountered
14. Cocaine
Source

Coca plant, cocaine, crack

Signs

CNS stimulation, euphoria, cocaine

bugs,halo lights, seizures, hallucinations,
cardiac arrhythmias lead to cardiac
arrest

Treatment ABCs, charcoal, diazepam (seizures),

lidocaine (arrhythmias), no dialysis or
lavage.

Forms of cocaine
Crack (type of free base)
Baking soda, hard rock, volatile

Cocaine HCL (salt)

Non-volatile, white crystalline powder

Specific Poisons Frequently

Encountered
15. Phencyclidine (PCP)
Source
Signs

Treatment

Angel dust, Sernyl (old veterinary

general anesthetic)
Psychosis, sensory analgesia, rotary
nystagmus, hypertension, hyperactive
reflexes, seizures.
Lock in padded room, diazepam,
antipsychotic agent (Haloperidol),
cranberry juice (100x increase in
excretion)

Specific Poisons Frequently

Encountered
16. Tricyclic Antidepressants
Source

Amitryptyline, imipramine, doxepin

Signs

Anticholinergic Syndrome (ACS) [dry

mouth, mydriasis, hyperpyrexia, increase
HR, decreased GI motility] hallucinations,
seizures, respiratory depression, cardiac
arrhythmias (quinidine-like effect)

Treatment

ABCs, emesis, lavage, physostigmine

(till ACS stops), treat arrhythmias
(phenytoin, bicarb)

Specific Poisons Frequently

Encountered
17. Methaqualone
Source

Quaalude, ludes (sedative/hypnotic)

Signs

Depersonalization, tongue
discoloration, dizziness, nausea,
hemorrhage, abstinence syndrome

Treatment

ABCs, emesis, lavage, hemodialysis

Specific Poisons Frequently

18. Digoxin Encountered
Source

Digitalis, digoxin

Signs

Headache, nausea, vomiting, blurred

vision, delirium, slowed pulse, cardiac
irregularities, hypokalemia,
arrhythmias, ventricular fibrillation
low TI

Treatment

ABCs Dose adjustment, drug

withdrawal, lavage, charcoal, emesis,
Digibind, K+ supplement, treat
arrhythmias (lidocaine, phenytoin,
propranolol)

Specific Poisons Frequently

Encountered
19. Phenytoin
Source

Dilantin

Signs

Nystagmus, ataxia, drowsiness,

seizuresdeath is rare but is usually
due to ventricular fibrillation and
cardiac arrest. Toxicity >25mcg/ml

Treatment

ABCs, emesis (if conscious), lavage,

charcoal, cathartics, discontinue
phenytoin

Specific Poisons Frequently

Encountered
20. Theophylline
Source

Aminophylline

Signs

CNS stimulation, hyperreflexia,

cardiac arrhythmia, convulsions, death
is due to respiratory failure. Toxic
plasma level >20mcg/ml.

Treatment

ABCs, discontinue drug, charcoal,

emesis, fluids and anticonvulsants
(diazepam) as needed.

21. Dioxin (2,3,7,8 TCDD)

Source

Herbicides, cigarette smoke, smoke

from burning trash and debris

Signs

Chloracne (small yellow comedones)

mainly on the face can last 30 years,
hepatomegaly, fatigue, irritability,
blurred vision, porphyria cutanea tarda
(slate gray skin pigmentation), limited
systemic effects, Death??

Treatment

ABCs, alkaline diuresis, If recent

ingestion: [emesis, lavage, charcoal,
cathartic], mainly supportive care

Dioxin Poisoning

Viktor Yushchenko: Ukraine President