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UNIT 2: POISONS AND POISONING

CLASSIFICATION OF POISONS
 Agents are generally classified in accordance with the interest and needs of the classifier.
 Classified in terms of: source, use, target organs, effects
 May also be classified in terms of: physical state, chemical stability, general chemical
structure, poisoning potential
SOURCES OF POISONS
1. Industrial
Cyanide1 – is used in hardening of metals in electroplating
2. Household
Drain cleaners2 – concentrated acids and bases (liquid Sosa)
b. Sodium hypochlorite
3. Pharmacologic
Clinically used drugs become a poison usually in high doses
4. Environmental – mostly air pollutants like:
CO – automobile exhaust system; fire
Pb – also in automobile exhaust system
SO2 – from the combustion of sulfur-containing fuels
Nitrogen oxides – associated with fires
Ozone – occurs normally in the earth’s atmosphere; important absorbent of UV light;
high-voltage electrical equipment; air and water purification
Hg – atmospheric (when burning fossil fuels) and ecological contaminant

KINDS OF POISONS (PROPERTY)


1. Corrosive poisons
They cause local destruction of parts but they are not poisonous if they are highly
diluted

2. True poisons
They are still poisonous no matter how highly diluted (cyanide)

3. Cumulative poisons
They are poisons which increases suddenly in its intensity of action after slow addition
to it (asbestosis, silica)

KINDS OF POISONS (MOA)


1. LOCAL
These poisons destroy or cause serious injury to mucous membranes or tissues with
which they come in contact or may cause inflammatory reactions

2. SYSTEMIC
Following local action, the poison is absorbed into the bloodstream and produces
harmful effects on vital organs of the body
ROUTES OF POISONS

PO IV SQ

SKIN INHALATION

MECHANISM OF TOXIC ACTION


 May interfere with the transport tissue utilization of oxygen resulting in hypoxia
(carbon monoxide and cyanide )
 May depress or stimulate the CNS, producing coma (sedative-hypnotics ) or
convulsions (sympathomimetic agents)
 May affect the ANS, producing cholinergic (organophosphates) or anticholinergic
actions (belladonna alkaloids)
 May affect the lungs by aspiration (hydrocarbons) or systemically (paraquat)
 may affect the heart and vasculature1
 may produce local damage (caustics & corrosives)
 may have delayed effects on the liver (acetaminophen)
 may have delayed effects on the kidneys (heavy metals)

TYPES OF POISONING
ACCORDING TO MEDICAL VIEWPOINT
 Acute – prompt and there is marked disturbances of function or death within a short
period of time
 Chronic – gradual and there is progressive deterioration of the functioning of tissue
 Cumulative - suddenly increases in its intensity of action when a certain limit is
reached

ACCORDING TO LEGAL POINT OF VIEW


 Accidental - poison was taken without intention to cause death
 Suicidal - poison was taken by victim voluntarily for the purpose of taking his own
life
 Homicidal - poison was given willfully and with intent to cause death to the victim
 Undetermined - the history is hazy as to how the poison was obtained and why it
was administered

TYPES OF POISONING EFFECTS


LOCAL EFFECTS
 The impression is made directly upon that part of the body with which the poison comes
in contact (ex. Corrosives)
 Two kinds of local effects:
o Corrosion or chemical destruction – is illustrated by the effect of strong
mineral acids or bases
o Irritation or inflammation – which ranges from simple redness in its simple form to
ulceration or gangrene in its more severe form

REMOTE EFFECTS
o The effect is produced or developed in an area other than that site of application (e.g
atropine causing blurred vision)
o The remote action of poisons following absorption on certain organs more than others is
the “localization of poisons”
o Example:
BRAIN: opium, morphine, barbiturates, alcohol
HEART: Digitalis
SPINAL CORD: Strychnine
LUNGS: chlorine (gaseous form)
COMBINED EFFECTS
o Local + Remote effects
o Arsenic – local effects upon the stomach; remote effects upon the brain.
o Cantharides – locally produce blisters and remotely influences the kidney and
bladder, sometimes bloody urine
FACTORS AFFECTING POISONING EFFECTS
PATIENT-RELATED FACTORS
1. Size POISON-RELATED FACTORS
2. Age 1. Physical state and chemical
3. Species and strain properties
4. Feed and feeding 2. Routes and rate of administration
5. Changes in the internal environment 3. Previous or coincident exposure to
6. Habitually used drugs other chemical

PATIENT-RELATED FACTORS

SIZE
 If the same amount of a chemical is given to individuals of different sizes, then the
concentration of the chemical attained in the tissues will be different and, hence, the
effect induced will vary
 The metabolism and activity are proportional to the surface area of the body
AGE
 The difference in response during early life is a consequence of the relative inefficiency
of various metabolic1 and excretory pathways, the greater susceptibility of certain
tissues, immaturity of the blood-brain barrier, and other factors
SPECIES AND STRAINS
 Often, differences in toxicity are due to different types of biotransformation, which can
take place in various tissues
 Differences in the strain of animals also induce a variation in response of chemical agents
 Because humans are a remarkably heterogeneous species, the rate of metabolism of any
compound may differ greatly from person to person
SEX
 The sex of an animal often has an influence on the toxicity of a chemical agent. Major
differences are shown to be under direct endocrine influence1
 Pregnancy & lactation
FEED AND FEEDING
 The composition of the feed or food can affect the results of toxicity tests.
 It may be of significance to mention that the activity of hepatic drug-metabolizing
enzyme systems decreases in mice fed a low-protein diet
 some food ingredients might induce a toxic reaction during a drug treatment1
CHANGES IN THE INTERNAL ENVIRONMENT
 physical activity, stress conditions, hormonal state of animals, and degenerative
changes in internal organs, are known to influence the toxicity of any compound
 Also includes induction/inhibition of liver microsomal enzymes, displacement of
protein binding of a chemical, or inhibition of its renal clearance
 Pathological conditions
HABITUALLY USED DRUGS
 The habitual use of certain psychoactive drugs by humans is known to augment or
decrease toxic reactions to drugs in humans
 The habitual, and particularly excessive, use of these chemicals could affect the
sensitivity of humans to toxic doses of drugs and other chemicals

POISON-RELATED FACTOR

PHYSICAL STATE AND CHEMICAL PROPERTIES OF THE TOXICANT


• Solubility in water • Rate of
• Solubility in disintegration of
vegetable oil formulation
• Suspending • Particle size
medium • Crystal form
• Stability of the • Grittiness of inert
agent substances given
in bulk amounts
ROUTES AND RATES OF ADMINISTRATION
Generally, toxicity is the highest by the route that carries the compound to the blood stream most
rapidly

PREVIOUS OR COINCIDENT EXPOSURE TO OTHER CHEMICALS (DRUGDRUG


INTERACTIONS)
EVIDENCES OF POISONING
1. CIRCUMSTANCIAL/MORAL EVIDENCE
a. That which are contributed by the circumstances or deduced from various
occurrences and facts (ex. Statements from witnesses)
2. SYMPTOMATIC EVIDENCES
a. Those that are contributed by symptoms
3. CHEMICAL EVIDENCES
a. Obtained by means of chemical analysis of the substances supposed to have
caused the poisoning, or of what has been vomited, or of materials found in some
parts of the body, or in its excretion
EXAMPLES OF CHEMICAL EVIDENCE
Protamines – (animal alkaloids, cadaveric alkaloids, or putrefactive
alkaloids) – they are alkaloidal substances resulting from the decomposition
of albuminous materials under the influence of bacteria
Tyrotoxin – it is any toxin developed in cheese or milk by bacillus
Tyrotoxicon – a poisonous crystalline ptomaine or diazobenzene hydroxide,
sometimes occurring in state milk, cheese, or ice cream
Toxin

4. ANTE-MORTEM EVIDENCES
a. Those evidences obtained before death

5. POST-MORTEM EVIDENCES
a. Those obtained by an examination of the organs and tissues of the body after
death

6. EXPERIMENTAL EVIDENCES
Evidence obtained by administering suspected substances to some living animals and
observing the effects

SYMPTOMATIC EVIDENCES
 Blood changes
 Breath odor
 Skin discoloration
 Vomitus
 Stool color
 Urinary changes
 Gum discoloration
 Visual disturbances
 Others
BLOOD CHANGES
BLOOD CHANGE SUBSTANCE
Decreased blood coagubility Heparin, benzene, fluorine, phosphorus
Cherry red blood Carbon monoxide, cyanide
Dark red blood Nicotine
Chocolate blood Aniline, nitrites, nitro derivatives

ODOR OF BREATH
ODOR SUBSTANCE
Shoe polish Nitrobenzene
Fruity odor Ethanol
Garlic Arsenic, Phosphorus, Malathion,
Thallium
Mouse urine Coniine
Stale tobacco Nicotine
Bitter almonds Cyanide
Sweet, penetrating odor Acetone, chloroform
Pearl-like Chloral hydrate
Rotten egg Hydrogen sulfide
Mothballs Naphthalene
Wintergreen Methyl Salicylate

SKIN DISCOLORATION
COLOR SUBSTANCES
Yellow Picric acid, nitric acid
Bleaching white Phenol
Ash grey Mercuric chloride, physostigmine
Deep brown Bromine
Brown black Sulfuric acid, iodine, silver nitrate
Bluish grey Silver salts
Blue Cyanotics (opium, aniline, sulfides)
Pale bonds on fingernails (Mee’s lines) Arsenic
Boiled lobster appearance Boric acid

VOMITUS
COLOR SUBSTANCE
Blue-green Copper
Ground coffee Sulfuric acid
Luminous vomit Phosphorus, arsenic
Yellow green Chromium

BOWEL CHANGES
COLOR SUBSTANCE
Black Charcoal, bismuth, iron, lead, magnesium
dioxide, silver nitrate
Clay-like Alcohol, barium
White Aluminum hydroxide
Blue Boric acid, methylene blue, iodine
Green Indomethacin, iron, Cupric acid
Red Hemolytic substances

URINARY CHANGES
COLOR SUBSTANCE
Dark yellow Picric acid
Yellow brown Aloe, Senna
Violet Turpentine
Green blue Phenols & derivatives; Methylene blue
Wine or red brown Caffeine, benzene, rifampicin, lead,
mercury, carbon tetrachloride

DISCOLORATION OF GUMS
COLOR SUBSTANCE
Blue line gum Bismuth, lead
Black line gum Mercury, Arsenic

VISUAL DISTURBANCES
DISTURBANCE SUBSTANCE
Purple vision Digitalis, marijuana
Blurred vision Anticholinergics
Partial/total blindness Methanol, formic acid, solanine
Optic neuritis Ethambutol
Blood shot eyes Marijuana

RESPIRATORY CHANGES
CHANGES SUBSTNACE
Violent sneezing Veratrine
Irritation Sulfur dioxide
Dyspnea Carbon monoxide
General respiratory depression Opium, barbiturates; benzodiazepine,
cyanide

OTHERS
CHANGE SUBSTANCE
Alopecia Arsenic
Tinnitus Salicylates, quinine
Ototoxicity Aminoglycosides, loop diuretics
Xerostomia Anticholinergics
Bloody sputum Cadmium
Muscular twitching, loss of voice Barium
Loose teeth Mercury, lead, phosphorus
Bleeding gums Arsenic, mercury
CHANGE SUBSTANCE
Lock jaw Strychnine
Blister formation Cantharides
Whitened mucous membrane Oxalic acid
Scalded appearance of the mouth Acetic acid
White stains on lips becoming brown on Phenol
exposure to air
Reddening of the mucuous membranes of Formalin
mouth and eyes; hardening of mucosa
with hemorrhage
Mild GI irritation with green stains Copper
Fatty degeneration of liver and/or Phosphorus
kidneys
Inflammation of the kidneys, with cantharides
bleeding

DETECTION OF POISON
TEST, POISON DETECTED, IMPORTANT NOTES
TEST POISONS (S) IMPORTANT NOTES
DETECTED
Beilstein Chlorine Green flame
Benzoldt Gunning Acetone Indigotine
Fresh colored ppt
Bromine water Aniline
(tribromoaniline)
FeSO4 + H2SO4 brown ring
Brown Ring Nitrite & nitrate
at interface
KI Mercury Orange precipitate
Lieben’s iodoform
Methanol Yellow ppt (iodoform)
(distinguish from ethanol)
Mirror-like ppt soluble in
Marsh Arsenic
NAOCl
Modified Duquenois marijuana Red color (THC) on TLC
Mitscherlich Phosphorus Phosphorescence
Chloroform
Nessler (Nessler’s reagent -
(distinguish from chloral Yellow ppt (iodoform)
mercuric KI)
hydrate)
White ppt (bismuth
Nylander Bismuth
subnitrate)
+ chloroform -> aniline &
Nitrobenzene
Phenylisocyanide phenylisocyanide (irritable
(found in shoe polish)
odor)
Picrate Prussic acid Yellow to brick red ppt
Schonbien-Pagenstecher Prussic acid Deep blue on guaiac paper
Scherer Phosphorus Black ppt
Yellowish red color with
Schwartz’s Resorcinol Chloroform yellowish green
fluorescence
Light to dark red color
Rodillon/millon’s Phenol
(mercurous phenate)
Mirror-like ppt (elemental
Tollent’s Reducing substances
Ag)
Xanthogenate CS2 Release of H2S

TEST POISONS (S) IMPORTANT NOTES


DETECTED
Dark purple/black (Ecstacy,
propoxyphene);
Marquis Common drugs of abuse orange to brown (amphetamine,, meth);
pink to purple (heroin & opioates);
red (aspirin)
Purple-black (Sb);
dull black (As);
shiny black (Bi);
Reinsch Heavy metals
silvery (Hg)

Needs confirmation via AAS

DIAGNOSIS OF POISONING
FOUR ELEMENTS OF DIAGNOSIS
Cause: Poison
Subject: Poisoned organism
Effect: injury to cells
Consequence: signs and symptoms, death

PRINCIPLES OF DIAGNOSIS
 Most poisoning incidents are dose-related
 Poisoning should be distinguished from hypersensitivity and idiosyncratic reactions,
which are undesirable and not dose-related, and distinguished from intolerance, which
is a toxic reaction to an unusually nontoxic dose of a substance
 DIAGNOSIS is the evaluation of signs and symptoms of a disease or dysfunction to
arrive at a cause
 Diagnosis of poisoning is a difficult task and cannot be based on a single observation;
often rests on appropriate findings and should take into account several points1
 clinical examination gives some valuable clues that can help to narrow the differential
diagnosis
Recognition of the cause and severity of poisoning depends largely on the following:
1. Clinical History
o Performing a thorough general history of the patient aids in the effective treatment
of intoxication
o “everybody lies..”
o Essential and helpful information include:
1. 5W-2H
2. Pre-existing conditions or allergies
3. Medications or substances currently used
4. Pregnant?
o If symptomatic, immediately transport to healthcare facility with original
container or poison

o If asymptomatic, obtain AMPLE information:


AGE and ALLERGIES
MEDICATIONS
PAST HISTORY
Time of LAST meal
EVENTS leading to present condition
2. Physical examination
o A thorough examination of the patient is required to assess the patient’s
condition
o Clinical signs examined (refer to SYMPTOMATIC EVIDENCES), including
skin marks
o Most symptoms of poisoning like vomiting, convulsions, coma, dilatation or
contraction of the pupils, slow or rapid respiration, delirium, dyspnea, and
cyanosis are also symptoms of diseases

3. Analytical evidences
o The common proof of poisoning lies in the detection of a significant amount of
toxic material in the body tissues

Often times, it is difficult to make the diagnosis. The following rules are frequently of great
value in distinguishing poisoning from disease
TO DISTINGUISH POISONING FROM DISEASE
1. In cases of poisoning, the symptoms usually appear suddenly even when the patient is in good
health
2. In cases of poisoning, the symptoms commonly make their appearance after taking food,
drink or medicine
3. If several persons are taking the same food or drink, they show similar symptoms
TREATMENT OF POISONING

GENERAL MANAGEMENT
 Ensure airway is clear so that breathing and circulation are adequate
 Remove unabsorbed material
 Limit the further absorption of toxicant
 Hasten toxicant elimination
GENERAL PRINCIPLES IN THE TREATMENT OF POISONING
 Initial management (A.B.C.D.E.F)
o AIRWAY
o BREATHING
o CIRCULATION
 In cases of circulatory collapse, cardiac massage at a ratio of 5:1 is
indicated
 60 heart massages and 12 resuscitation attempts per minute
o DRUGS, DISABILITY
o EXPOSURE, ECG
o FIBRILLATION (defibrillation)1

 Overtreatment of the poisoned patient with large doses of antidote often does far more
damage than the poison itself
 The most important treatment measure for poisoning is prevention1
 Of course, once poisoning occurs, it is important to be able to provide highly skilled
supportive medical care
 It is sufficient to focus only on simple first-aid measures and antidotal therapy or
home remedies1,2,3
 Actually, there are very few poisons for which there are effective antidotes (<5%). For
most cases of poisoning, good supportive care is all than can be offered and all that is
needed
 Even in those instances where antidotes are available, supportive care is at least as
important.
 indeed, the best antidote in the world is of little value without good supportive care

PRIMARY CARE GIVEN BY A PHYSICIAN


“Five-finger rule”
Elementary aid
Decontamination
Antidote therapy
Transport
Securing of evidence
PRINCIPLES OF TOXIN MANAGEMENT
1. SEPARATE THE PATIENT FROM THE POISON
Remove the individual from the contaminated air if the toxic substance is airborne
Remove the person’s clothing immediately if the clothing is soaked in the poison
Dermal: Rinse & wash w/ large amounts of water (slightly cool)
Ocular: Irrigation for 15 mins with isotonic NaCl
When the poison has been ingested, induce vomiting (contraindicated for hydrocarbon
poisoning) or use gastric lavage

2. GIVE SUPPORTIVE THERAPY1


Provide basic respiratory support
Provide basic cardiovascular support
If necessary:
Artificial air, 100% CO2
Assisted intubation
Bronchodilators
3. GIVE ANTIDOTE
Few poisons have specific antidotes
The most common substance that is effective and generally available in the household
is _____2

PRINCIPLES OF TOXIN ELIMINATION


1. INDUCE VOMITING
 Emetics are substances that cause regurgitation of gastric contents by either locally
irritating the stomach or stimulating the medullary chemoreceptor trigger zone (CTZ)
 IPECAC is the emetic best recommended. It is best administered with a glass of warm
water because this produces a diluting effect and solubilizes stomach contents.
SYRUP OF IPECAC

AGE DOSE (mL)


6-9 months 5
9-12 months 10
1-12 years 15
More than 12 years 30

CONTRAINDICATIONS ON EMESIS
RELATIVE ABSOLUTE
-Very young (<1y) or very old patient -Convulsions, or ingestion of a
-Pregnancy convulsant
-Heart disease impaired gag reflex
-Bleeding diathesis -Coma
-Ingestion of cardiotoxic poison -Foreign body ingestion
-Time lapse of more than 6-8 hours -Corrosive ingestion1
-Ingestion of petroleum distillates1, or
those drugs which cause altered mental
status
-All poisons that are emetic in nature
OTHER EMETICS:
Apomorphine1 - only other acceptable method of inducing emesis that is
advocated (CI for CNS depression)
Stimulation of the posterior pharynx – unsuccessful and incomplete
Obsolete emetics: warm saline, mustard water, copper sulfate, Zinc sulfate2
2. USE GASTRIC LAVAGE
 By passing a large-bore tube through the mouth into the esophagus and stomach
 Stomach lavage can be achieved with 250-ml aliquots of water and saline
 Less effective than emesis but have the advantage of allowing other medicines to be
given immediately
 Especially useful in treating poisoning by aromatic substances e.g. perfumes
 AACT & EAPCCT: should not be employed routinely1
 Lavage should be considered only if a patient has ingested a life-threatening amount of a
poison and presents to the hospital within 1 to 2 hours of ingestion.

3. USE OF CATHARTICS
 Substances that enhance the transit of materials through the GIT, so decreasing the
contact time with stomach and intestines
 2 main groups of cathartics:
o Ionic or Saline: Mg citrate, Mg sulfate, Na sulfate1
o Saccharides: Sorbitol (Cathartic of choice for adults)
 Generally used after a chemical antidote, to remove the compounds formed
 Useful for the ingestion of hydrocarbons and enteric-coated tables

CONTRAINDICATIONS FOR CATHARSIS


 Corrosives
 Existing electrolyte imbalance
 Paralytic ileus
 Severe diarrhea
 Recent bowel surgery
 Abdominal trauma
 Renal failure
 Oil based cathartics should never be used:
1. Increase the risk of lipid pneumonia
2. Increase the absorption of fat soluble poisons
Inactivates activated charcoal’s effects when administered along the

4. USE OF ACTIVATED (MEDICINAL) CHARCOAL


 A number of studies have documented clearly the efficacy of activated charcoal as the
sole decontamination measure in ingested poisoning

CONTRAINDICATIONS TO THE USE OF ACTIVATED CHARCOAL


 Absent bowel sounds or proven ileus
 Small bowel obstruction
 Caustic ingestion
 Ingestion of petroleum distillates
5. WHOLE BOWEL IRRIGATION (WHOLE GUT LAVAGE)
 This is a method that is being increasingly recommended for late presenting overdoses
when several hours have elapsed since ingestion.
 Previously used was saline. Today, special solutions are used such as PEG-GELS and
PEG-3350
 Indications:
o Ingestion of large amounts of toxic drugs in patients presenting late ( > 4 hours
post-exposure)
o Overdose with sustained-release preparations.
o Ingestion of substances not adsorbed by activated charcoal, particularly heavy
metals.
o Ingestion of foreign bodies such as miniature disc batteries (button cells), cocaine
filled packets (body packer syndrome),** etc.
o Ingestion of slowly dissolving substances: iron tablets, paint chips, bezoars,
concretions, etc
6. EXTRACORPOREAL METHODS
6.1 HEMODIALYSIS
 a dialysis machine and a special filter called an artificial kidney, or a dialyzer, are used to
clean your blood
 Many factors affect drug removal in hemodialysis
1. Drug characteristics (solute size, lipid solubility, protein binding)
2. Vd
3. Concentration gradient between plasma & dialysate
4. Physical factors (dialysis set-up)
 Ideal dialyzable drug:

 Drug removal is limited by membrane surface area & permeability


1. Low MW 3. Low protein
binding
2. Water soluble 4. Low Vd

6.2 HEMOPERFUSION
 the method by which anticoagulated blood is passed through a column containing sorbent
particles
 Hemoperfusion uses the physical process of drug adsorption1
 and in many instances, drug removal is superior to hemodialysis, peritoneal dialysis, or
diuresis
 Disadvantage: does not correct electrolyte imbalance