TOXICOLOGY

ELLA JOY NOGAS-PEREZ, MD, DPSCOT, FPAFP

 OBJECTIVES

By the end of the lecture, we will be able to:

Explore the principles in the management of acute poisoning

Know how to prepare and administer Activated Charcoal and Cathartic

Know the criteria for non-toxic ingestions

DEFINITION OF TERMS
TOXICITY
Inherent ability of a substance to cause harm, injury or death to a
biologic material

RISK
The potential (likelihood) that injury ( biological damage) will
occur in a given situation
EXPOSURE
Contact with a chemical which may or may not enter the
body
POISON
Any substance that has the ability to harm a living organism from
either the plant or animal kingdom.
Refers to any agent that can kill, injure or impair normal
physiologic function in humans

xenobiotic
A chemical compound (as a drug, pesticide or carcinogen) that is
foreign to a living organism

toxin
Poisonous substance produced by plants, animals, or bacteria
POISONING
overdose of drugs, medicaments, chemicals and biological
substances

ingestion of more than the therapeutic dose of a drug

or a substance not intended for consumption, usually by
an adult in a moment of distress

Based on circumstances:
ACCIDENTAL, INTENTIONAL
SUBSTANCE USE DISORDER (DSM-5)

Combined DSM IV criteria for substance abuse and substance

dependence

maladaptive pattern of substance use with impairment or distress, as

manifested by 3 or more of the following factors during a 12-month
period
Factors in Substance Use Disorder
Tolerance
Withdrawal
Substance taken in greater amounts or longer than intended
Persistent desire or unsuccessful efforts to stop use
Considerable time spent to obtain substance
Impairment of social, occupational, or recreational
activities
Use of substance despite knowledge of harm

Drug craving
Quick Screening: CAGE questions

Have you ever felt you needed to Cut down on your drinking?

Have people Annoyed you by criticizing your drinking?

Have you ever felt Guilty about drinking?

Have you ever felt you needed a drink first thing in the morning ( Eye-
opener) to steady your nerves or to get rid of a hangover?

Bernadt, MW; Mumford, J; Taylor, C; Smith B; Murray RM (1982) Comparison of questionnaire

and laboratory tests in the detection of excessive drinking and alcoholism Lancet 6 (8267;325-8
GENERAL PRINCIPLES IN THE
MANAGEMENT OF ACUTE
POISONING
General approach to the poisoning:
I EMERGENGY STABILIZATION
II CLINICAL EVALUATION
III- MINIMIZING THE ABSORPTION OF THE POISON
IV ENHANCING THE ELIMINATION OF THE ABSORBED POISON
V ADMINISTRATION OF ANTIDOTES
VI SUPPORTIVE THERAPY AND OBSERVATION
VII- DISPOSITION
Emergency ABCs of Life Support for Poisoned
Patients
Stabilization
Clinical Evaluation
Maintain adequate Airway
Minimizing Absorption

Enhancing Elimination Ensure adequate Breathing/ventilation

Antidotes Maintain adequate Circulation
Supportive and
Observation
Disturbances of CNS by toxicant. Treat
Disposition convulsions (usually with Diazepam)
Correct metabolic abnormalities
(Electrolytes, glucose, acid-base)
 Emergency
Stabilization COMMON TOXICANTS THAT CAN CAUSE
HYPOXIA
Clinical Evaluation

Minimizing Absorption
Maintain adequate
Alcohol
airway
Enhancing Elimination
Carbon monoxide
OXYGEN
Antidotes
contraindicated in the
initial management:
Ensure adequate Opiates
breathing/
Supportive and - WATUSI
ventilation
Observation
- PARAQUAT
Organophosphates
Disposition
Quinine

Cyanide
Emergency
Stabilization RECOMMENDED iv FLUIDS
Clinical Evaluation
HYPOTENSIVE patients
Minimizing Absorption
NSS
Enhancing Elimination
Maintain Crystalloid solution

adequate
Antidotes
Adult maintenance
circulation
Supportive and D5NSS
Observation
D5AR
Disposition
D5NM

Pediatric maintenance
D50.3NaCl
Emergency
Stabilization Causes of convulsion in poisoned patients
Clinical Evaluation Direct convulsant effect
Minimizing Absorption Cerebral hypoxia
Treat Elimination
Enhancing CNS Hypoglycemia
disturbances
Antidotes Severe muscle spasm
convulsions
coma
Supportive and
Withdrawal reactions
Observation

Disposition
Decreased seizure threshold in an
epileptic patient
 Emergency
Stabilization Causes of convulsion in poisoned patients
Clinical Evaluation Direct convulsant effect
Minimizing Absorption Aminophylline Mefenamic acid
Treat Elimination
Enhancing CNS Amphetamines Opioids
disturbances Carbon monoxide Organophosphates
Antidotes
convulsions Cocaine Phenothiazines
Cyanide
coma
Supportive and Salicylates
Observation Ethylene glycol Strychnine
Hypoglycemic agents Theophylline
Disposition
Isoniazid Tricyclic antidepressants
Lead Withdrawal of narcotics,
MAO inhibitors diazepam, or ethanol
Emergency
Stabilization MANAGEMENT OF SEIZURE
Clinical Evaluation General management of seizure
Minimizing Absorption Diazepam
Lorazepam
Treat Elimination
Enhancing CNS
disturbances Management of uncontrolled seizure
Antidotes
convulsions Phenytoin
coma
Supportive and
Observation Management of seizures of unknown etiology
Disposition Pyridoxine (Vitamin B6) therapeutic trial
Adult: 5g IV
Pedia 80 to 120 mg/kg/dose IV
Emergency
Stabilization MANAGEMENT OF COMA
Clinical Evaluation Coma of unknown etiology
Minimizing Absorption
100% oxygen
Treat Elimination
Enhancing CNS Thiamine or Vitamin B complex 100mg
disturbances
Antidotes Glucose
convulsions Adult: 50-100ml Dextrose 50%
coma
Supportive and
Pedia: 1-2ml/kg dose Dextrose 10%
Observation
Naloxone
Disposition 400mcg IV every 3 minutes (max: 2mg)
0.1 mg/kg

Emergency
Stabilization Causes of Hypokalemia
Clinical Evaluation
Alkalinizing agents
Minimizing Absorption
(NaHCO )
Enhancing Elimination
Correct 3
Metabolic
Antidotes Bronchodilators
Abnormalities
Supportive and
Observation (theophylline, salbutamol)
Disposition
Corticosteroids

Diuretics (Furosemide)
 Emergency
Stabilization Causes of Hyperkalemia
Clinical Evaluation
ACE inhibitors
Minimizing Absorption

Enhancing Elimination
Beta blockers
Correct
Metabolic
Antidotes Cardiac glycosides
Abnormalities
Supportive and
Observation
Cyanide
Disposition Oral potassium
Potassium-sparing
diuretics
Emergency
Stabilization Clinical
Evaluation
Complete Clinical Evaluation
Minimizing Absorption Enhancing
Good History Taking
Elimination Antidotes

Supportive and Complete Physical Examination

Observation Evaluate the general status

Disposition Examine the patients skin

Characterize the odor of the patients breath

Auscultate the lungs

Listen to the heart

Check the abdomen

Do a complete neurologic examination

Check for toxidromes

Laboratory examinations
Emergency
Stabilization

Clinical
Poisons with delayed manifestations

Evaluation Ethylene glycol 6 hours

Minimizing Absorption Salicylates 12 hours
Enhancing Elimination
Paracetamol 36 hours
Antidotes
Paraquat 48 hours
Supportive and
Observation
Methanol 48 hours
Disposition Coumatetraryl 72 hours
Thyroxine 4 weeks
Emergency
Stabilization Evaluation
Minimizing Absorption Enhancing Elimination Antidotes
Clinical
Supportive and
 Observation

Disposition
HISTORY
Type and amount of poison

Time of exposure

Mode of Exposure

Intake of other substances

Circumstances prior to the poisoning

Past medical history and current
medications

Home remedies given

Emergency
Stabilization
Preliminary survey of the patient
Clinical
Evaluation Sharpen your basic senses
Minimizing Absorption
Minimizing Absorption
Look for telltale signs residues, needle
Enhancing Elimination
Enhancing Elimination
tracks, evidence of physical injuries
Antidotes
Antidotes Smell poisons may have particular odors
Supportive and

Supportive and
Observation Listen carefully to the chest and abdomen
Disposition Observation
DO NOT TASTE
Disposition
Feel the surface of the scalp and skin but do
not forget personal protection
Emergency
Stabilization Clinical
Evaluation
TOXIDROMES
Conglomeration of signs and symptoms that
will suggest a specific toxicant

Valuable in arriving at a tentative diagnosis when the toxicant is

unknown or when the effects of the alleged toxicant are not
compatible with the patients presentation

Valuable in guiding initial steps in the

management of the patient
Organophosphate
Emergency TOXIDROMES
Stabilization
Carbamates
Clinical
Pyrethroids
Evaluation
Minimizing Absorption

Enhancing Elimination

Antidotes

Supportive and
Observation

Disposition
Stabilization
Emergency
TOXIDROMES

Clinical
Evaluation
Minimizing Absorption
 A
E
Anti-depressants
nhancing Elimination
Anti-
histamines ATROPINE S

TOXICITY
ntidotes
BLOOD PRESSURE :
upportive and
Disposition
Observation 190/ 100 mmHg
Emergency
Stabilization TOXIDROMES
Heart Rate: 150 bpm
Clinical
Evaluation SYMPATHOMIMETIC TOXIDROME
TEMPERATURE: 40 C
MYDRIASIS
Minimizing Absorption

E
Cocaine seizures
A
Methamphetamine Estacy S
TACHYCARDIA
(MDMA)
Disposition
 HYPERTENSION
HYPERTHERMIA
SEIZURES Blood pressure:
Emergency
80/50 mmHg
Stabilization TOXIDROMES
Clinical Heart rate: 50 bpm
OPIATE/NARCOTIC toxicity
Evaluation
Minimiz
Respiratory rate: 12 cpm
ingMorphine
Absorption MIOSIS
Enhanci
ngNalbuphine
Elimination GCS: E1V1M3
Antidot HYPOTENSION
Suppor es
Heroin
Oxycodone BRADYCARDIA
Codeine
Dispositi tive and
Observation
Fentanyl
H POVENTIL COMA

Y ATION
BLOOD PRESSURE :
Emergency
Stabilization 190/ 100 mmHg
TOXIDROMES
Clinical
nhancing Elimination Heart Rate: 150 bpm
Evaluation SYMPATHOMIMETIC TOXIDROME
ntidotes
TEMPERATURE: MYDRIASIS
Minimizing Absorption

E upportive
and 40 C
Cocaine
nhancing Elimination
Observation
A
Methamphetamine
ntidotes Estacy
seizures S
TACHYCARDIA
(MDMA)
upportive and
Disposition
Observation
 HYPERTENSION
HYPERTHERMIA
SEIZURES
Emergency
Minimizing
Stabilization Absorption SKIN SIGNS
Diaphoresis
Enhancing Elimination
Clinical
Evaluation
Antidotes

Supportive and
Observation sympathomimetics, organophosphates, aspirin, phencyclidine

Dry skin anti-histamines, anticholinergics

Disposition
Bullae barbiturates and other sedative hypnotic agents
Acneiform rash bromides, chlorinated aromatic hydrocarbons
Flushing anticholinergics, disulfiram
Cyanosis ergotamine, nitrates, nitrites, aniline dyes
 Skin Irritation/Burns
nickel, hydrochloric acid, sodium hydroxide, hydrofluoric acid

Skin Cancers/hyperpigmentation/hyperkeratosis arsenic

Emergency
Stabilization
Complete Clinical Evaluation
Clinical Good History Taking

Evaluation Complete Physical Examination

Minimizing Absorption Evaluate the general status

Enhancing Elimination Antidotes Examine the patients skin

Characterize the odor of the patients breath

Supportive and
Observation Auscultate the lungs

Disposition Listen to the heart

Check the abdomen

Do a complete neurologic examination

Check for toxidromes

 Laboratory

examinations
Emergency
Stabilization
EXTERNAL DECONTAMINATION
Clinical Evaluation

Minimizing EMPTY THE STOMACH

Absorption ADMINISTER SINGLE DOSE ACTIVATED

Enhancing Elimination CHARCOAL
Antidotes
ADMINISTER CATHARTIC
Supportive and
Observation
USE DEMULCENTS/
Disposition

NEUTRALIZING AGENTS
Emergency
Stabilization
EXTERNAL DECONTAMINATION
Clinical Evaluation

Skin and hair decontamination

Minimizing
Whole body bath
Absorption
Remove all clothing, jewelries, dentures
Enhancing Elimination
Mildly alkaline soap (e.g. Perla, ivory US)
Antidotes

Supportive and Running water

Observation
Drying patient
Disposition
New clothing

Ocular decontamination: sterile NSS

Emergency Clinical Evaluation
Stabilization
Minimizing
Empty the stomach: GASTRIC LAVAGE
Absorption
Enhancing Elimination

Antidotes Should Not Be Routinely Used

Supportive and
Ingested potentially life threatening
Observation amounts of poison
Disposition
1 hour
Up to 4 hours

Plain NSS

Activated Charcoal
Emergency Clinical Evaluation
Stabilization
Minimizing
Absorption
Activated Charcoal
Adsorption

actC ivat edC - a adu ds int gi ac cs id/ ac ndy sa ten ai md te o

carbonaceous
A materials
Alcohol
ca paci ty
very fine particle size that increases the overall surface area and adsorptive
Enhancing Elimination
L Lithium
Antidotes
A standard 50-gram dose of activated charcoal has the
Supportive and
surface area of 10 football fields
I
Observation
P Petroleum distillates
Disposition
not "digested," it stays inside the GI tract and eliminates the toxin when
the person has a bowel movement
Emergency Clinical Evaluation
Stabilization
Minimizing
Single Dose Activated Charcoal
Absorption
Enhancing Elimination
ADULT: 50 to 100 mg of activated
Antidotes
charcoal in 100 to 200 ml water
Supportive and
Enhancing Elimination
Observation
Antidotes PEDIA: 1 g/kg in water as 1:3 dilution eg: 10 kgs child
Disposition
Supportive and 10g in 30 ml water to make a slurry
Emergency Observation
Stabilization
Disposition Cathartics
Clinical Evaluation

Hasten intestinal elimination of the unabsorbed toxic

Minimizing agent or the adsorb toxic
agents
Absorption
 AACT/EAPPCT: No role when used alone

NPMCC: use of cathartics alone have been helpful in

accelerating expulsion of large amounts of poison such as
kerosene, thereby reducing contact time of the poison in the
gut
Emergency
Enhancing
Stabilization Elimination
Cathartics
Clinical
AntidotesEvaluation

Minimizing
Supportive and SODIUM SULFATE
Observation
ADULT: 15g in 100 ml lukewarm water
Absorption
Disposition
PEDIA: 250mg/ kg given as a 10 solution
eg: 20 kgs
5g in 50ml lukewarm water
 Should be
administered
after the
charcoal
lavage
Emergency Observation
Stabilization
Disposition
Clinical Evaluation

Minimizing
Absorption
Enhancing Elimination

Antidotes

Supportive and
USE OF commonly used demulcent for mild caustic
DEMULCENTS ingestion and watusi poisoning
AND ADULT: 8 to 12 eggs
NEUTRALIZING
AGENTS PEDIA: 4 to 6 eggs

RAW EGG SODIUM BICARBONATE or baking soda (1-5%)

WHITE can serve as neutralizing agents in iron toxicity
(Albumin and red tide poisoning
only) is a NaHCO3 (8.4%): 1 vial of 8.4% sodium bicarbonate in
250 ml water to makes a 2% solution
Emergency
Stabilization

Enhancing Elimination of Absorbed Poisons

Clinical Evaluation

Minimizing
Absorption

Multiple-dose activated charcaol

Enhancing
Elimination Alkalinization Therapy*
Antidotes
Acidification Therapy*
Supportive and
Observation
Dialysis and Hemoperfusion
Disposition

* Ion Trapping
Emergency Clinical Evaluation
Stabilization
Minimizing
Absorption MULTIPLE-DOSE ACTIVATED CHARCOAL
Enhancing Enhance pre-absorptive elimination of drugs which decrease gastric
motility, and sustained-release agents that have erratic absorption of
Elimination
GI tract
Antidotes

Supportive and
Observation Gut dialysis of drugs that are lipophilic, have low protein-binding
Disposition
capacity, have small volume of distribution and long half-lives

Interrupt enterohepatic recirculation

ACCT/EAPCCT 1999
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
DOSE OF MDAC
Elimination
Antidotes ADULT: 50g in 100 ml of water to make a slurry
Supportive and
Observation
PEDIA: 0.5 g/kg in water as 1:3 dilution
Disposition

Given every 2, 4, 6, 8 hours

CATHARTIC:
every 4 th dose of MDAC
goal: 1 bowel movement/day
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Dangers of MDAC
Elimination
Antidotes Intestinal impaction
Supportive and
Observation

Disposition Gut obstruction

Antidotes
Pulmonary aspiration
Supportive and
Observation Ensure that bowel movement is observed daily.
Emergency
Disposition Absorption
Stabilization

Clinical Evaluation Enhancing

Minimizing
Elimination
Alkalinization/Acidification Therapy

Alkalinization of the urine ionizes weak acids.

It inhibits passive renal tubular reabsorption of non-

ionized molecules thus enhancing excretion

Salicylates, isoniazid, barbiturates, 2,4D

Acidification ionizes the weak bases. It is no longer recommended

metabolic acidosis, rhabdomyolysis and renal failure
Methamphetamine toxicity, phenytoin, theophylline
Emergency
Absorption
Stabilization

Clinical Evaluation Enhancing

Minimizing Elimination
Antidotes

Supportive and Alkalinization/Acidification Therapy

Observation

Disposition Alkalinization Therapy

Sodium bicarbonate (8.4%)
1 mEq/kg/dose or 1 mL/kg/dose IV every 6 hours
until urine pH is 7.5 8.5

Acidification Therapy
Ascorbic acid q6h until urine pH<5.5
Adult: 1g IV
Pedia: 20mg/kg IV
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Dialysis and Hemoperfusion
Elimination
Antidotes
Life-threatening poisoning
Supportive and
Observation Electrolyte and acid-base disturbances
Disposition
Cases involving dialysable toxins with poor
body clearance and high plasma toxin
Antidotes concentrations
Supportive and Cases where the patient has underlying
Observation
kidney or liver problems
Disposition
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Elimination
DIALYSIS

Properties of drugs that are dialyzable

Insoluble
Small volume of distribution

Low protein binding

Low molecular weight (<500 daltons)

Complications:
hypotension, bleeding, nosocomial infection and air embolism
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Elimination
DIALYSIS is indicated
Antidotes

Supportive and
Observation
Amanita phalloides
Disposition
Antifreeze (glycol type)
Heavy metals in soluble compounds
Heavy metals after therapy with chelating
agents

Methanol
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Elimination
Antidotes
HEMOPERFUSION
Supportive and Barbiturates
Observation

Disposition
Short and medium acting
COMPLICATIONS
Phenobarbital Hypotension, bleeding,
nosocomial infection, air
embolism, leucopenia,
Salicylates thrombocytopenia and
hypocalcemia
Theophylline
ACTIVATED CHARCOAL is the most popular
adsorbent used in hemoperfusion
Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing
Elimination
Use of Antidotes
Antidotes
Seldom necessary in poisoning
Supportive and
Observation

Disposition
Benefit outweighs potential harm

Depends on clinical status, or laboratory

results
Emergency
Stabilization Antidotes
Clinical Evaluation Supportive and
Observation
Minimizing
Disposition
Absorption

Enhancing
Elimination
 mech
anism Accelerated detoxification
of Reduction on conversion to more toxic
antid
otes compounds
Competitive inhibition at receptor sites
Inert
By passing the effects of the poison
complex
Antibodies interacting with poisons
formation
Inert Complex Formation

Chelating agents
Facilitate the formation of a stable
complex with the poison, which can
be readily excreted

Heavy metal poisoning

Lead
Arsenic
Methylmercury
Cadmium
Copper
 DMSA (succimer) dimercapto succinic acid
Inert Complex
Formation Arsenic, lead, methylmercury

Cadmium, copper

DMPS dimercapto propane sulphonate

Arsenic, methylmercury

Penicillamine
Lead, copper

EDTA disodium edetate

Cadmium

Lead

BAL British anti-Lewisite

Arsenic

NAPA n-acetyl penicillamine

methylmercury
 Accelerated Detoxification
Enhances formation of a non-toxic or less toxic
compound

Na thiosulfate for cyanide poisoning

Produce thiocyanate (less toxic) which is readily
excreted through the kidneys
Reduction in Conversion to More Toxic
Compounds

Inhibits formation of metabolites which

are more toxic than the parent compound
Ethanol for methanol or
ethylene glycol poisoning
Ethanol competes for the same enzyme
that metabolizes methanol and
ethylene glycol to more toxic
compounds

Phenytion in malathion
Competitive Inhibition at Receptor Sites
Competes for the receptor sites where the poison
attaches thereby dislodging from the receptors

Naloxone for opioid poisoning

Blocks opioid receptors in the CNS

Atropine for organophosphate or

carbamate poisoning
Binds to muscarinic receptors thereby blocking the action
of acetylcholine
 Bypassing the Effect of the Poison

Indirectly counters the effect of the poison

Oxygen for cyanide poisoning

Synergistic antidotal action when given with sodium nitrite and sodium
thiosulfate

Pyridoxine for INH poisoning

Pyridoxine is a needed cofactor for the synthesis of GABA which is
depleted in INH poisoning
Antibody Interacting with Poison

Antibody binds to poison rendering in

inactive

Digoxin-specific antibody fragments

(Digibind) for digitalis poisoning
Binds digoxin, limiting the cardiotoxic effects

Cobra antivenom for cobra envenomation

Neutralizes the venom
Emergency
Absorption
Stabilization
Enhancing Elimination
Clinical Evaluation
Antidotes
Minimizing
Supportive
and supportive therapy and observation
Observatio
n
Disposition IV fluids

Frequent test for blood and urine pH

Avoid aspiration and decubitus ulcers

Treat metabolic disturbances

Monitor vital signs

Monitor input and output

Emergency
Minimizing
Stabilization
Absorption
Clinical Evaluation
Enhancing Elimination
Antidotes Observation at the emergency room:
at least 24 hours may be warranted
Supportive
and
Observation Frequent re-evaluation

Disposition Psychiatric evaluation: suicidal patients

and
substance abusing patients
Childhood poisoning: evaluate for possible
child abuse or neglect
Family counseling and education
Physical/sexual abuse women
Domestic violence
Examples of Non-Toxic Ingestions:

Criteria :
Absolute identification

Time and amount of ingestion is known

Amount ingested relative to patients weight is less than the smallest

amount known or predicted to induce toxicity

Time elapsed since ingestion is greater than the longest

predicted interval between ingestion and peak toxicity

Detailed history includes no symptoms or signs of toxicity

Usually non-toxic ingestions
Air fresheners Dehumidifying products
Antacids Deodorants
Disposable diapers
Antibiotic ointments Dog food
Antiperspirants Erasers
Ashes (wood, fireplace) Felt-tip markers
Glade
Baby products Fish bowl additives
Ballpoint pen inks Glitter glue
Calamine lotion Glowstick
Grease
Catfood Gums
Chalk Gympsum
Charcoal Iodophor
Lipstick
Cigarette ashes
Make-up
Clay Douches
Contraceptive pills w/o iron Mascara
Corticosteroids (single dose) Acrylic and latex paints
Pastes
Cold packs
Crayons
Crayola markers
Crazy glue
Usually non-toxic ingestions

Pencil lead (graphite)

Styrofoam
Petroleum jelly
Plastics Sunscreen and tan preparations
Plaster Super glue
Rouge Toothpaste
Rust
Vaseline
Rubber cement
Vitamins (w/o Iron)
Shampoo (non-medicated)
Shaving cream Watercolor paint
Shoe polish Zinc oxide
Silica gel Zirconium oxide
Soaps and soap products
Starch
END OF PRESENTATION