FCM West Visayas State University – College of Medicine – Batch 2020

Lecture 1
Block XVIII Toxicology
Module 1
10/ 18/ 19
Dr.Cruz

TOPIC OUTLINE 10. Highly hazardous pesticides

I. Chemicals What is important is the clinical (appearance) of the
II. 10 CHEMICALS OR GROUPS OF CHEMICALS OF patient
MAJOR PUBLIC HEALTH CONCERN (WHO 2013)
A. Air pollution
Difficult due to the high number of differential
B. Arsenic diagnosis
C. Asbestos First 24 hours is the most crucial.
D. Benzene
E. Cadmium
A. AIR POLLUTION
F. Dioxin
G. Fluoride • Indoor pollution and outdoor pollution
H. Lead Est. to be responsible for 3.1 million premature
I. Mercury deaths worldwide yearly
J. Pesticides Est. to be responsible for 3.2% global burden of
III. Poisoning disease
A. 3 leading causes of poisoning ─ Respiratory infections
B. Other commonly used agents
─ Cardiovascular diseases
C. Definitions
D. Criteria establishing substance dependence
─ Lung cancer
E. Patient management INDOOR POLLUTION
F. Metabolic abnormalities • Solid fuel combustion
G. Coma of unknown etiology Wood
IV. Clinical evaluation
A. History Dung
B. Physical exam Crop residues
C. Toxidromes • Tobacco smoke
D. Laboratory evaluation
• Outdoor air pollutants
E. Elimination of poison
F. Excretion of absorbed sibstances • Emissions from construction materials & furnishings
G. Antidotes • Improper maintenance of ventilation & air condition
H. Supportive therapy systems
I. Disposition
Review Questions ‘Sick building’ syndrome
References
OUTDOOR POLLUTION
LECTURER BOOK REFERENCE OLD TRANS • Fossil fuel combustion
Vehicle (CO)
Stationary sources
I. CHEMICALS
─ Power generating stations
• Are part of our daily lives
─ Industry
• All living and inanimate matter is made up of chemicals
• Forest fires
• Many chemicals, properly used, contribute significantly
• Deliberate biomass burning
to improvement of life, health and well-being
• Nature
• Others are hazardous and can negatively affect health
Wind-blown soil
and environment when improperly managed
Natural events (e.g. volcanic eruptions)
II. 10 CHEMICALS OR GROUPS OF CHEMICALS OF
MAJOR PUBLIC HEALTH CONCERN (WHO 2013) B. ARSENIC
1. Air Pollution • Soluble inorganic arsenic is acutely toxic
2. Arsenic • Intake of inorganic arsenic over a long period can lead
3. Asbestos to chronic arsenic poisoning (arsenicosis)
4. Benzene Est. arsenic-contaminated drinking water in
5. Cadmium Bangladesh alone was attributed 9,100 deaths and
6. Dioxin & dioxin-like substances 125,000 Disability Adjusted Life Years (DALYs) in
7. Inadequate or excess fluoride
2001
8. Lead
9. Mercury

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MD 3 Surname 1, Surname 2, Surname 3
• Sources of arsenic: E. CADMIUM
Natural activities – volcanic activities, dissolution of • Exerts toxic effects on the kidney, the skeletal and the
minerals (esp. in groundwater), windblown respiratory systems
Human activities – mining, metal smelting, fossil • Classified as a human carcinogen
fuel combustion, timber treatment with • Generally present in the environment at low levels, but
preservatives human activity has greatly increased those level
Mobilization into drinking water from natural • Can travel long distances from the source of emission
deposits (tube-well drilling) or from mine drainage by atmospheric transfer
water • Readily accumulated in many organisms, notably
mollusk and crustaceans
• Lower concentrations are found in vegetables, cereals
and starchy roots
• Human exposure occurs mainly from
Consumption of contaminated food
Active & passive inhalation of tobacco smoke
Inhalation by workers in the non-ferrous metal
industry
Figure 1. Effects of Arsenic. Source: Upclass Notes
F. DIOXIN & DIOXIN-LIKE SUBSTANCES
C. ASBESTOS
• Are persistent organic pollutants (POPs) covered
• All types are known to cause
by the Stockholm Convention
Asbestosis (fibrosis of the lungs)
• Are byproducts of combustion & various industrial
Lung Cancer
processes, such as chlorine bleaching of paper
Mesothelioma
pulp and smelting
Cancer of larynx
• Can travel long distances from the source of
Cancer of ovary
emission
• Exposure through inhalation of fibers in
• Bio-accumulate in food chains
Air in the working environment
• Human exposure has been associated with a range of
Ambient air in the vicinity of point sources such as:
toxic effects, including:
─ Factories handling asbestos
Immunotoxicity
─ Indoor air in housing and buildings containing
Developmental & neuro-developmental effects
friable (crumbly) asbestos materials
Changes in thyroid & steroid hormones
• Currently about 125 million people in the world are
• Developmental effects are the most sensitive toxic
exposed to asbestos at the workplace
endpoint making children, particularly breastfed infants,
• In 2004, asbestos-related lung cancer, mesothelium &
the population most at risk
asbestos from occupational exposures resulted in
• Human exposure occurs mainly through consumption
107,000 deaths & 1,523,000 Disability Adjusted Life
of contaminated food
Years (DALYs)
• Also, several thousands of deaths can be attributed to
G. INADEQUATE OR EXCESS FLUORIDE
other asbestos-related diseases, as well, as to non-
• Inadequate or excess fluoride
occupational exposures to asbestos
• Fluoride intake has beneficial effects
Reducing the incidence of dental caries and
D. BENZENE
negative effects
• Human exposure to benzene has been associated with
Causing enamel & skeletal fluorosis following
a range of acute and long term adverse health effects
prolonged high exposure
and diseases, including cancer & aplastic anemia
• The ranges of intakes producing these opposing effects
• Occupational & domestic exposure happens as a result
are not far apart
of the everywhere use of benzene containing
• Dental health benefits are obtained when the
petroleum products including motor fuels & solvents
concentration of fluoride in drinking water is 0.8-1.0
• Active & passive exposure to tobacco smoke is also a
mg/L
significant source of exposure
• Excessive fluoride intake usually occurs through the
• Benzene is highly volatile and exposure occurs mostly
consumption of
through inhalation
Ground water naturally rich in fluoride
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 Crops that take up fluoride and are irrigated with
this water H. LEAD
• Toxic effects of high fluoride intake are due to the fact • A toxic metal
that it is a direct cellular poison • A cumulative toxicant that affects multiple body
Binds calcium and interferes with the activity of systems, including:
proteolytic and glycolytic enzymes Neurologic
• This can lead to Hematologic
Enamel fluorosis Gastrointestinal
Crippling skeletal fluorosis, which is associated Cardiovascular
with Renal Systems
─ Osteosclerosis • Children are particularly vulnerable to the neurotoxic
─ Calcification of tendons & ligaments effects of lead
─ Bone deformities Even relatively low levels of exposure can cause
serious and in some cases irreversible cases,
irreversible neurological damage.
E.g. paint with lead in cribs, plastic toys
• Lead exposure is estimated to account for 0.6% of the
global burden of diseases, with the highest burden in
developing regions
• Widespread occurrence of lead in the environment is
largely the result of human activity
• As lead is an element, once it is released into the
environment, it persists!
HUMAN ACTIVITIES RELEASING LEAD IN THE
ATMOSPHERE
Figure 2. Effects of fluoride on teeth. Source: Upclass Notes • Mining, smelting, refining and informal recycling of lead
• Use of leaded petrol (gasoline)
• Production of lead-acid batteries and paints
• Jewelry making, soldering, ceramics and leaded glass
manufacture in informal and cottage (home-based)
industries
• Electronic waste
• Use in water pipes and solder
• It is estimated that in 2004, lead exposure was
responsible for 143,000 deaths and 0.6% of the global
burden of disease (DALYs), taking into account mild
mental retardation and cardiovascular outcomes
resulting from exposure to lead
• Lead in the body is distributed to the brain, liver, kidney
Figure 3. Effects of fluoride. Source: Upclass Notes and bones; stored in the teeth and bones, where it
• Dental Fluorosis accumulates over time
Mild • Young children absorb 4-5 times as much lead as
Moderate adults (apart from pregnant women)
Severe • Infants, young children (especially those <5 years of
• Skeletal Fluorosis age) and pregnant women are most susceptible to the
• No age limit for fluorosis. adverse effects of lead
• The most critical effect of lead in young children is that
on the developing nervous system
• Subtle effects on intelligence quotient (IQ) are
expected from blood lead levels at least as low as 5
μg/dl (50 μg/l) and the effects gradually increase with
increasing levels of lead in blood

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Figure 4. Lead poisoning. Opaque metaphyseal bands in the lower
femur, upper tibia, and the upper fibula secondary to lead poisoning in
a child. Source: Medscape
Figure 6. Heavy metals and the environment. Upclass Notes
• Once in the environment, elemental mercury is
naturally transformed into methyl mercury that bio-
accumulates in fish and shellfish
• Human exposure occurs mainly through
Inhalation of elemental mercury vapors during
industrial processes
Consumption of contaminated fish and shellfish

Figure 5. Lead poisoning. Upclass Notes

I. MERCURY
• Mercury is toxic to human health particularly to the
development of the child in utero and early in life
• Mercury exists in various forms, which all have different
toxic effects:
Elemental (or metallic)
Inorganic (e.g. mercuric chloride)
Organic (e.g., methyl- and ethylmercury) Figure 7. Congenital Minamata Disease from severe mercury
poisoning. Upclass Notes
• Mercury toxicity affects
The nervous, digestive and immune systems
J. HIGLY HAZARDOUS PESTICIDES
Lungs, kidneys, skin and eyes • May have acute and/or chronic toxic effects
• It is estimated that among selected subsistence fishing • Pose particular risk to children
populations, between 1.5/1,000 and 17/1,000 children • Global impact of self-poisoning (suicides) from
showed cognitive impacts caused by the consumption preventable pesticide ingestion has however been
of fish containing mercury estimated to amount to 186,000 deaths and 4,420,000
• Mercury release in the environment is a result mainly Disability Adjusted Life Years (DALYs) in 2002
from human activity • Environmental contamination can also result in human
Coal-fired power stations exposure through consumption of residues of
Residential heating systems pesticides in food and, possibly, drinking water
Waste incinerators • Sources of exposure to highly hazardous pesticides:
As a result of mining for mercury, gold and other Agriculture and public health workers
metals. Domestic use
Food and drinking water
Exposure of children
• Health Effects:

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 Unintentional and self-inflicted (suicides) acute 3 LEADING CAUSES OF POISONING
poisoning National Poison Control & Information Service - NCPIS)
• Acute hazard is highly variable depending on the 1. Alcohol Intoxication
2. Methamphetamine (Shabu)
pesticide; includes:
3. Isoniazid (INH) Toxicity
Peripheral and central neurotoxicity
Reduced blood clotting capacity OTHER COMMONLY USED AGENTS
• Chronic exposure to highly hazardous pesticides can 1. Pesticides (Organophosphates & N-
result in effects: methylcarbamates)
Skin 2. Hydrocarbons (Kerosene)
Eyes 3. Acids (Hydrochloric Acid)
Nervous system 4. Alkalis (Sodium Hypochlorite)
5. New toxicants being seen:
Cardiovascular system
dancing firecrackers (watusi) commonly composed
Gastrointestinal tract
of yellow (or white) phosphorus
• Children are more vulnerable to the effects of
trinitrotoluene (TNT)
pesticides because of their smaller size
potassium nitrate
Greater exposure (on a milligram per kilogram
potassium chlorate
body weight basis)
Jatropha curcas (tuba-tuba)
Different metabolism and still developing internal
organs
• Some highly hazardous pesticides may also affect the
immune system
• Some obsolete pesticides may cause cancer, including
childhood cancer

POISONING
• Poisoning is a significant global health problem.
Figure 8. Jatropha curcas (tuba-tuba): a poisonous shrub, currently
Est. 346,000 people died worldwide from promoted agriculturally for the production of biodiesel, an alternative
unintentional poisoning in 2004. fuel source. Upclass Notes
91% occurred in low- and middle-income countries
Unintentional poisoning caused the loss of over 7.4
million years of healthy life (disability adjusted life
years, DALYs)
• Poisoning is an increasing health problem in both
industrialized and developing nations.
The Centers for Disease Control & Prevention
(CDC) US, reports 31,758 poisoning deaths
nationwide in 2009, ranking second only to motor
vehicle deaths.
• The Philippines is not an exception. Figure 9. Jatropha podragrica (Buddha belly): A poisonous shrub,
The National Poison Control & Information Service promoted by garden enthusiasts for butterfly attraction; falsely sold by
some plant vendors as “ginseng” Upclass Notes
(NPCIS) of the UP-PGH reports an increase from Table 1. international poisoning cases.Source: Doc’s PPT
271 patients seen in the emergency room in 1990 INTERNATIONAL POISONING CASES
to 1,049 in 1996. § 65.3% (1983-87)
Some cases in WVSUMC, if you don’t know what § 67.0% (1995)
the patient took, you can call the National Police § 63.1% (1996)
Institution and ask for samples in patients with the § Suicides: 29.4% of all cases seen (1996)
Table 2. Accidental Ingestion/exposure. Source: Doc’s PPt
same condition. ACCIDENTAL INGESTION/ EXPOSURE
PE & History are very specific for the time, cause, § 17.1% (1983)
path of intake, circumstance (accidental, suicidal, § 23.5% (1996)
Table 3. mortality rates. Source: Doc’s PPT
etc); very important is how much and what the
MORTALITY RATES
patient took.
§ 3.86 (1983)
§ 3.0% (1995)
§ 2.4% (1996)
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Case Fatality Ratio: 4.9/100 patients, with
organophosphates as the agent most commonly
associated with mortalities
DEFINITIONS
• Poisoning
An overdose of drugs, medicaments, chemicals
and biological substances
• Self-Poisoning & Para-Suicide
Deliberate 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)
Mortalities are classified as suicides rather than
para-suicides (regardless of whether or not this
was the intended outcome)
• Accidental Poisoning
Non-intentional ingestion, overdose or exposure to
drugs, medicaments, or biological substances
• Substance Abuse/Dependence
Maladaptive pattern of substance use with
impairment or distress
CRITERIA ESTABLISHING SUBSTANCE
DEPENDENCE
AMERICAN PSYCHIATRIC ASSOCIATION CRITERIA
FOR DRUG DEPENDENCE
• 3 or more of the following factors during a 12-month
period:
• Physiologic dependence is specified with the
presence or absence of criteria 1 or 2
1. Tolerance: need for greater amounts or
experiencing less effect with same amount
2. Withdrawal: experiencing symptoms of
withdrawal or substance has to be taken to
relieve or avoid symptoms
3. Substance taken in greater amounts or for a
longer period than intended
4. Persistent desire or unsuccessful efforts to
decrease or control use
5. Considerable time spent in obtaining substance
(e.g., driving long distances or visiting multiple
physicians)
6. Important social, occupational, or recreational
activities given up or decreased because of use
of substance
7. Use of substance despite knowledge of
persistent or recurrent physical or psychological
harm that is likely to be caused or exacerbated
by it
• Administration of Antidotes
• Supportive Therapy & Observation
• Disposition
We have to be careful of the katas when cleaning
the patient. Toxic particles might still be present
in the external body of the patient
EMERGENCY STABILIZATION
• Life-saving measures should take priority.
• Management is directed towards:
Airway obstruction (maintain adequate
airway)
Breathing difficulties (provide adequate
oxygenation/ventilation)
Circulatory inadequacy (maintain adequate
circulation)
Drug-induced CNS depression (treat
convulsions/coma)
Electrolyte or metabolic abnormalities (correct
metabolic abnormalities)
MAINTAIN ADEQUATE AIRWAY
• Conscious patients are more likely to have intact
airways.
Objective is to give oxygen.
• Decreasing sensorium may compromise airway.
• Gag or cough reflex is an indirect estimate of the
patient's ability to keep the airway clear.
Be careful of the fumes that might come from the
patient which might be toxic.
In the Event of an Obstructed Airway:
• Place patient in supine position.
• Rule-out possible cervical fracture before
attempting chin-lift/jaw-thrust maneuver and/or
intubation.
• Chin-lift/jaw-thrust maneuver (refer to succeeding
figure) is done to position the tongue away from the
airway.

PATIENT MANAGEMENT
• Emergency Stabilization
Figure 10. Chin lift/ Jaw-thrust maneuver. Source: Upclass notes
• Clinical Evaluation
• Elimination of the Poison
• Excretion of Absorbed Substances
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• Remove any foreign body (dentures, secretions, or SBP <80 mmHg in patients <40 yrs
vomitus). • Insert central venous line for severe hypotension.
• Endotracheal intubation should be done by trained or
experienced personnel. CONVULSIONS
• Humidified air should be given. POSSIBLE CAUSES IN POISONED PATIENTS
• Bronchial toilet on a regular basis should be done. Direct convulsant effect of poison (e.g., INH toxicity)
• Spasms are common in pesticide poisoning Take note of the patient’s medication history.
Cerebral hypoxia from respiratory or cardiovascular
ADEQUATE OXYGENATION/ MECHANICAL depressive effect of drugs (e.g., opiates)
VENTILATION • Hypoglycemia
• Accurately assess ventilation by determining arterial • Severe muscle spasm due to spinal or peripheral
blood gases (ABG). effects on mechanism controlling muscle tone
Initiate oxygenation with pO2 <80 mmHg. Withdrawal reaction in patients with physical
• Oxygen can be given via the following means: dependence on abused drugs (e.g., alcohol, opiates)
nasal cannula • Decreased threshold in epileptic patient
plastic mask • Treatment should be directed towards the etiology.
rebreathing mask “Amuyin mo nalang”
ventilator
• Evaluate the need for bronchodilators in patients POISONS COMMONLY ASSOCIATED WITH
manifesting bronchospasm. CONVULSIONS
• Aminophylline
COMMON CAUSES OF HYPOXIA • Amphetamines
• Alcohol • Carbon monoxide (CO)
• CO • Cocaine
Common in people who stay inside their running • Cyanide
cars, then sleep. • Ethylene glycol
• Opiates • Hypoglycemic agents
Cause secretions causing DOB. • Isoniazid (INH)
• Organophosphates Common in children.
Bronchoconstriction • Lead
• Cyanide • Lithium
• Quinine • MAO inhibitors
• Mefenamic acid
WARNING! • Opiods
CONTRAINDICATIONS TO THE USE OF OXYGEN AS • Organophosphates
INITIAL MANAGEMENT: Very common
• Watusi - flammable • Phenothiazine
• Zinc phosphide (Zn3P2), a rodenticide – flammable • Salicylates
• Paraquat poisoning (N,N′-dimethyl-4,4′-bipyridinium Body rubs are sometimes orally fed to children
dichloride), a common herbicide - oxygen increases • Strychnine
pulmonary fibrosis • Theophylline
• Tricyclic antidepressants (TCAD)
ADEQUATE CIRCULATION • Withdrawal of narcotics, diazepam or ethanol in
• Secure venous access/initiate IVF of appropriate fluids. abusers
Hypotensive patients: NSS, Crystalloid solution
Don’t give D5, increases urination -> dehydration
Adult maintenance: NSS, D5AR
Pediatric maintenance: D5 0.3NaCl
Nifedipine (Ca Ch-Blocker) given before, can cause
sudden drop in BP.
• Hypotension: Elevate legs about 15 cm above the
horizontal plane.
SBP <90 mmHg in patients >40 yrs
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 METABOLIC ABNORMALITIES • Especially in treating pregnant women for preeclampsia
HYPOKALEMIA (seizure prevention)
• Common in overdoses of bronchodilators (e.g.,
theophylline, salbutamol, terbutaline) HYPOTHERMIA
• Forced alkaline diuresis (furosemide) because of K+-H+ • Rectal temp of <30°C
exchange • Only supportive measures are needed in general.
• Treatments is based on restoring acceptable lower
limits of serum K+ Drugs Associated with Hypothermia
KCl solution up to 40 mEq/hr, not to exceed 60 • Alcohol
mEq/L • Barbiturates
• Weakness of the legs occur before other symptoms • CO
• Deaths can happen very early in the morning • General Anesthetics
• Opioids
HYPERKALEMIA • Phenothiazine
• Seen in: • Sedative-hypnotics
Overdoses of drugs that inhibit Na+-K+ pump, • TCADs
allowing K+ leakage into the extra cellular fluid
(e.g., β-blockers, cardiac glycosides) HYPERTHERMIA
Cyanide or CO poisoning (interference with ATP to • Rectal temp of >40°C
the N+-K+ pump) • Immediate body cooling to a body temp of 39°C to
Intake of oral K+ prevent death or severe brain damage
Patatas, Saging, Vitamins and other supplements External cooling: sponge bath, fanning, ice-water
Use of K+-sparing diuretics immersion (control shivering with diazepam)
Toxin-induced acute renal failure Iced gastric or colonic lavage
Rhabdomyolysis (disruption of membrane integrity) • Subsequent treatment is directed towards the
• Treatment: underlying cause.
Glucose-Insulin infusion: 50 ml D50-50 and 10 U
regular insulin Drugs Associated with Hyperthermia
Sodium bicarbonate after glucose-insulin, at 1 • Amphetamines
mEq/kg/dose • Anticholinergics
10% calcium gluconate as alternative to sodium • Antihistamines
bicarbonate, given 5-10 ml slow IV push under • Cocaine
cardiac monitoring • Isoniazid (INH)
Dialysis for intractable hyperkalemia • Phenytoin
• Quinidine
HYPOMAGNESEMIA • Salicylates
• Commonly observed: • Sulfonamides
With administration of diuretics, xanthines, • Xanthines
aminoglycosides, cardiac glycosides (digoxin • Aminophylline
induced, due to inhibition of Na+-K+ ATPase • Theophylline
pumps in renal tubules)
Chronic alcoholism (due to poor nutrition, ketosis, HYPOGLYCEMIA
GI losses, hyperaldosteronism) • Common in alcohol and salicylate intoxication
• Treatment of Severe Cases: (prolonged glucose utilization and depletion of hepatic
Loading dose of 600 mg elemental Mg++ in D5W glycogen stores)
over 3 hrs (not exceeding 15 mg/min) • Treatment:
Maintenance dose of 600-900 mg elemental Mg++ Glucose infusion: 50-100 ml D50-50 (adult); D10
per 24 hrs (pediatric)
MgSO4 IM 200 mg q 4 hrs for 24 hrs, then 100 mg Thiamine: in cases of alcoholism, 100 mg given
q 4 hrs prior to glucose infusion to prevent development of
To avoid toxicity, MONITOR heart rate, respiratory rate, Wernicke's encephalopathy
deep tendon reflexes, and urine output. ECG
monitoring is also recommended.
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HYPOCALCEMIA
Common with dancing firecrackers (watusi) & Jatropha
seed ingestion
Sea urchins
Also seen in bites or stings of spiders & sea urchins
Treatment: parenteral administration of calcium salt
Calcium chloride preferred because of better and
predictable body retention as vs. calcium gluconate
Adults: 2.25 to 4.5 mmol calcium by slow IV push
Pedia: 100-300 mg/kg/day IV
• Companions/relatives to search where poisoning took
place
• Containers of substances: exposure or ingestion of
another intoxicant
d. Circumstances prior to poisoning
• Activities/events, e.g., field spraying (pesticides), fire
(CO/cyanide)
• Patient's emotional stability (have a bearing on long-
term management)

COMA OF UNKNOWN ETIOLOGY e. Current medications

• Challenge with (adults) Naloxone (Narcan) 2.0 mg IV, • Medications for existing disease/s
repeated every 3-5 minutes if necessary • Intake of other substances (e.g., barbiturates with
• If no response observed (improvement of respiration, alcohol, salicylate with warfarin, marijuana with CNS
sensorium, dilatation of miotic pupils) after a total of 10 stimulants/depressants)
mg dose, cause of coma other than opioid overdose
should be considered f. Past Medical History
Neonates: 10 mcg/kg IV followed by a larger dose • Existing disease/s (heart, liver, lung)
of 100 mcg/kg • Psychiatric history & history of recent traumatic life
• Opiate overdose events
Naloxone (Narcan)
Warning: Chronic opiate abusers may have g. Any home remedies taken
withdrawal reaction. • May improve or complicate condition
• Thiamine (possible alcohol intoxication): 100 mg IV, • There are several important and potentially fatal acute
followed by 50-100ml D50-50 poisons with delayed symptoms. Observe
• Glucose: for suspected diabetic coma (hypoglycemia) asymptomatic patients with history of these poisonings.
• Take note of what patients do at home; special mixes
CLINICAL EVALUATION of common ingredients.
A. HISTORY •
• Identify type and amount of poison to which patient was Table 3. Poisons with Delayed Manifestations. Source: Doc’s PPT
exposed to establish toxicity POISONS WITH DELAYED
Poison can still be extracted if patient comes in 30 MANIFESTATIONS
minutes or less after ingestion
ETHELYNE
• 80% adults who take poison are conscious on arrival 6 HOURS
GLYCOL
• Some patients reluctant to admit taking poison (pay
attention to patient's signs and symptoms; SALICYLATES 12 HOURS
toxidromes) PARACETAMOL 36 HOURS
PARAQUAT 48 HOURS
a. Time of exposure
METHANOL 48 HOURS
• Crucial in cases of caustic ingestion (decision
regarding NGT insertion) THYROXINE 4 WEEKS
• Gives idea of poison's phase of biotransformation at
time of admission

b. Mode of exposure
• Oral, inhalational, dermal(pesticide)
• Establish route of entry in initial examination for
guidance in subsequent management

c. Intake of other substances

• Any substance that may contribute to intoxication

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 PHYSICAL EXAMINATION Heart
General status of patient Irregular rhythm or presence of arrhythmia
Several medical conditions can be associated with
certain drugs or substances Table 5. Irregular heart rhythms and associated toxicities. Source:
Doc’s PPT
Table 4. substances and drugs causing hypertension and hypotension. IRREGULAR HEART RHYTHMS & ASSOCIATED
Source: doc’s PPT TOXICITIES
HYPERTENSION HYPOTENSION Tachycardia Bradycardia
COCAINE CLONIDINE Iron Propanolol & other β-
THEOPHYLLINE RESERPINE & OTHER Carbon Monoxide blockers
ANTIHYPERTENSIVES Cyanide Anticholinesterases
SYMPATHOMIMETICS Organophosphates Clonidine
ANTIDEPRESSANTS
(AMPHETAMINES, PPA) Phenothiazine Ca++ channel blockers
CAFFEINE SEDATIVE-HYPNOTICS Ethylene glycol Codeine & other opioids
HEROIN & OTHER Ethanol Ethanol
ANTICHOLINERGICS Free-base cocaine Digitalis
OPIATES
Anticholinergics
NICOTINE
Antihistamines
Amphetamines
Patient's skin
Warm or cold Sympathomimetics
Needle tracks, bruises, lacerations Salicylates
Cutaneous bullae (barbiturates & CO poisoning) Solvents
Diaphoresis (carbamate, organophosphate, Theophylline
salicylate, amphetamine toxicity)
Always wear gloves Abdomen
Jaundice (delayed manifestation of paracetamol or Organomegaly,
other hepatotoxic agents) Normality of bowel sounds
Dry skin & hyperpyrexia (atropine, TCADs & other Possible GI disturbances
anti-cholinergic agents toxicity) Drugs that can affect peristalsis
Flushing (anticholinergics, alcohol & cyanide)
Complete neurologic exam
Characteristic odor of patient's breath Glasgow Coma Scale (GCS)
Odors associated with drugs or chemical Certain neurologic signs aid in identification of
substances etiologic agents
─ Bitter almonds (cyanide) Some chemicals may produce masking effects
─ Fruity odor (diabetic ketoacidosis, isopropyl (consider possible multiple drug intoxication with
alcohol) mixed presentations)
History of fainting, comatose. Structural neurologic problems (trauma to head in
─ Oil of Wintergreen (methylsalicylate) process of losing consciousness)
─ Rotten eggs (sulfur dioxide, hydrogen sulfide) In organophosphate poisoning, pinpoint pupils are
─ Pears (choral hydrate) observed. Atropine is usually given; pupil size is
─ Garlic (arsenic, organophosphates, dimethyl then monitored together with reduction in
sulfoxide [DMSO]) temperature
─ Mothballs (camphor)

Lung sounds
Rales:
─ Pulmonary edema ~ pesticide, INH, opiate, β-
blockers or TCAD toxicity
Plus anti-depressants
─ Aspiration pneumonia ~ a primary concern in
hydrocarbon (kerosene) ingestion
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Table 6 . Neurologic Signs and Related Etiologies.Source: Doc’s • Cholinergics (Organophosphates, Carbamates)
ppt
Diarrhea, diaphoresis
NEUROLOGIC SIGNS AND RELATED CERTAIN ETIOLOGIES Urination
Mydriasis Miosis Miosis, muscle fasciculation's
Antihistamines Cholinergics / Clonidine Bradycardia, bronchoconstriction
Emesis
Antidepressants Opiates /
Lacrimation
Sympathomimetics Oragnophosphates
Salivation
(methamphetamine, Phenothiazines /
• Narcotics/Opiates
cocaine) Pilocarpine / Pontine
Miosis
Isoniazid Bleed
Bradycardia
Anticholinergics Sedative-Hypnotics
Hypotension
Hypoventilation
GLASGOW COMA SCALE
• Verbal Response
Coma
5= Oriented conversation
4 = Confused conversation LABORATORY EXAMINATIONS
3 = Inappropriate words • Adjuncts to diagnosis, but sometimes important to
2 = Incomprehensible sounds clinch diagnosis
1 = No response • Be aware of possible false positives or negatives
• Motor Response • Bedside toxicology: simple screening tests performed
6 =Obeys commands on urine samples, interpretations based on color
5= Localizes pain changes (e.g., Forrest Test for phenothiazine
4= Withdraws from pain overdose)
3= Decorticate rigidity
2= Decerebrate rigidity
SPECIMEN COLLECTION
1 = No response
• Timing of collection (important for accurate
• Eye opening
4 = Spontaneous interpretation of results)
3 = To speech • Pharmacokinetic characteristics of substance dictate
2 = To pain when the sample is collected
1= No response • Should include blood and urine tests for suspected
poison
• Total Score within 3 - 15 Blood: 5-10 ml heparinized & clotted samples (test
• In general, a score of 8 or less is correlated with a tubes kept in ice)
poor prognosis. Urine: 200 ml, preferably first void
• A score of 3 - 4 has an 85% chance of mortality Specimens placed in sealed container and stored
in freezer (-20°C) if cannot be examined right away
TOXIDROMES
• Signs & symptoms that can characterize suspected GENERAL LABORATORY EXAMINATIONS
toxicants when taken collectively • CBC: anemia or leucocytosis
• Observed to occur consistently with particular poisons • Urinalysis: urine pH and SpGr for baseline
• Anticholinergics/ antidepressants • FBS, BUN Creatinine & Electrolytes: any abnormalities
Hot as a hare (hyperthermia) • ABG: acid-base disturbances & hypoxemia
Dry as a bone (dry mucosa) • ECG: arrhythmias
Red as a beet (flushed skin) • Liver function tests & Pro-time: hepatotoxicity
Blind as a bat (dilated pupils) • Upright Chest X-ray: aspiration pneumonia, pulmonary
Mad as a hatter (confusion/delirium) edema, perforated ulcer
• Sympathomimetics (Cocaine, Amphetamines) • Abdominal X-ray: radio-opaque drugs & ruptured
Mydriasis viscus
Tachycardia • Conditions or Agents Predisposing to Metabolic
Hypertension Acidosis or Elevated Anion Gap
Hyperthermia Methanol
Seizures Ethylene glycol
Toluene, Theophylline

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MD 2
 Alcoholic acidosis Need to drink sodium sulfate to avoid constipation
Lactic Acidosis Pedia: 1g/kg or 30-50 g in 100 ml H2O
Aminoglycosides (uremic agents) • Demulcents/Neutralizing Agents/Cathartics
Cyanide, CO Demulcent: raw egg albumin only commonly used
Isoniazid, Iron Adult: 8-12 eggs
Diabetic ketoacidosis Pedia: 4-6 eggs
Grand mal seizures • Neutralizing Agents
Aspirin (salicylates) Sodium bicarbonate (iron poisoning)
Paraldehyde, Phenoformin Starch (iodine ingestion)
Potassium permanganate solution – diluted
ELIMINATION OF THE POISON (1:10,000) (nicotine, quinine & strychnine
• External decontamination poisoning)
Discard clothing • Cathartics
Thoroughly bath or shower Used to hasten intestinal elimination of unabsorbed
Copious irrigation (eyes) with free-flowing water for toxic agent (little known of efficacy in poisoning)
30 minutes Contraindicated in Caustic ingestion
Avoid neutralizing agents (may cause further injury Poisoning from readily absorbable drugs/chemicals
from resultant exothermic reactions) Pts with paralytic ileus, severe fluid electrolyte
Health personnel involved with decontamination disturbances
should also be properly protected Extremes of age
Sodium-containing cathartics are contraindicated in
EMPTY THE STOMACH pts with CHF
• Emesis Magnesium- or phosphate-containing cathartics
Done when toxicity is expected and medical contraindicated in pts with bowel disorders, renal
facilities are inaccessible impairment CNS depression (grades 3 & 4)
Consider only when:
─ There are no absolute contraindications and WHOLE BOWEL IRRIGATION
when definitive treatment will be delayed • “Flushes” poison down GI tract, removing & preventing
1-2 glasses warm water, then apply pressure on further absorption
posterior pharynx with blunt instrument • Polyethylene glycol (PEG) electrolyte is used
Kinchay (Apium graveolens):1 tbsp of juice of Small children: 0.5 L/hr
pounded kinchay followed by a glass of water Adolescents: 1-2 L/hr
Adults: 3-4 L/hr
GASTRIC LAVAGE Irrigation process continued until rectal effluent is
• May be of benefit up to 6-12 hrs post-ingestion clear (usually 2-6 hrs)
• Poisoning with drugs that delay gastric emptying time Table7 .Organic Compounds Effectively Absorbed by Activated
(TCAD, salicylates, opiates) Charcoal. Source: Doc’s ppt.
• Drugs with slow release preparations can form a large SUBSTANCES EFFECTIVELY ADSORBED BY
bezoar in stomach (theophylline) ACTIVATED CHARCOAL (ORGANIC COMPOUNDS)
• Contraindications: • Amphetamines • Glibenclamide
• Antidepressants • Glipizide
Ingestion of caustics or kerosene
• Antiepileptics • Indomethacin
Presence of frank convulsions
• Antihistamines • Kerosene
• Risk of aspiration should be anticipated when
• Aspirin • Malathion
performed • Atropine • NSAIDs
• Barbiturates • Paracetamol
LIMIT GI ABSORPTION • Benzodiazepines • Phenol
• Activated charcoal: effective in decreasing absorption • β-blockers • Phenothiazines
of some drugs, adsorbing these in the charcoal • Chloroquine • PPA
surfaces • Cimetidine • Quinine
Multiple doses are helpful in Tx of poisoning with • Dapsone • Salicylates
• Digitalis • Strychnine
substances that undergo entero-hepatic
• Furosemide • Tetracyclines
recirculation
• Theophylline
Adult: 50-100 g activated charcoal in 200 ml H2O

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MD 2
 Scrombroid poisoning - eating of fish with EXCRETION OF ABSORBED SUBSTANCE
prolonged time between catch and cooking; caused FORCED DIURESIS
by metabolites (histamine from histidine) produced • Less frequently used since many drugs metabolized in
by bacteria. liver
Treated with charcoal lavage, not antihistamine • Useful in toxicity with barbiturates, amphetamines, PCP
& salicylates
Table 8. Inorganic Compounds Effectively Absorbed by • 20% Mannitol
Activated Charcoal. Source: Doc’s ppt Test dose
SUBSTANCES EFFECTIVELY ABSORBED BY ACTIVATED ─ Adult: 200mg/kg or 1 ml/kg within 10 min
CHARCOAL (INORGANIC COMPOUNDS) ─ Pedia: 750 mg/kg or 3.75 ml/kg within 10 min
• Antimony
─ With good urine output (1 ml/kg/hr) continue at
• Arsenic
0.5-1.0 g/kg or 2.5-5.0 ml/kg q 6 hrs x 8 doses
• Iodine
• Mercury chloride
─ If diuresis does not occur in 2 hrs, discontinue
• Permanganate Mannitol
• Phosphorus Maintenance dose (with good kidney function)
• Potassium ─ Adult: 75-100 ml q 6 hrs
• Silver ─ Pedia: 0.5-1.0 g/kg/dose or 2.5-5.0 ml/kg/dose
• Tin q 6 hrs
Duration of Mannitol treatment will depend on half-
Table 9 . Substances Not Effectively Absorbed by Activated life of ingested poison, but should not exceed 48
Charcoal. Source: Doc’s ppt
hours
SUBSTANCES NOT EFFECTIVELY ADSORBED BY
• Furosemide (1 mg/kg/dose) reserved for cases of
ACTIVATED CHARCOAL
pulmonary edema
• Alcohol
• Cyanide
• Iron ALKALINIZATION THERAPY
• Lithium • Ionizes weak acids (salicylates, barbiturates, INH)
• Petroleum distillates
ACIDIFICATION THERAPY
Table10 .Substances with Entero-Hepatic Recirculation. • Ionizes weak bases (amphetamines, PCP, phenytoin,
Source: Doc’s ppt theophylline)
SUBSTANCES WITH ENTERO-HEPATIC
RECIRCULATION DIALYSIS & HEMOPERFUSION
• Anti-coagulants • Paracetamol • Employed in life-threatening poisoning, electrolyte &
• Aspirin • Phenyclidine acid-base disturbances
• Carbamazepine • Phenobarbital
• Cyclosporine • Phenothiazine
Indications for Hemoperfusion
• Dapsone • Phenytoin
• Barbiturates
• Digoxin • Piroxicam
• Glutethimide • Salicylate
Short & medium acting
• Meprobamate • Theophylline • Disopyramide
• Methamphetamine • TCAD • Gluthetimide
• Organocholine pesticides • Meprobamate
• Phenobarbital*
• Salicylates*
• Theophylline
*2-3 times more efficient than dialysis

Indications for Dialysis

• Amanita phalloides (a deadly poisonous basidiomycete
fungus)
• Antifreeze (glycol type)
• Heavy metals in soluble compounds
• Heavy metals after therapy with chelating agents
• Methanol

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MD 2
Dialysis is Dependent on Patient’s Condition • N-N-N-N acid
• Alcohols
• Ammonia Table . Chelators of Choice For Selected Metals. Source:
• Amphetamines Doc’s ppt
• Aniline CHELATORS OF CHOICE FOR SELECTED METALS
Element 1st choice 2nd choice contra-
• Barbiturates
indicated
• Boric acid
• Arsenic • DMSA • BAL •-
• Bromides
• DMPS
• Calcium • Lead • DMSA • EDTA • BAL
• Chloral hydrate • PEN
• Diphenylhydrantoin • Methyl- • DMPS • NAPA • BAL
• Ethclorvynol mercury • DMSA
• Fluorides • Cadmium • EDTA • DMSA • BAL
• Iodides • Copper • PEN • DTPA • BAL
• Isopropanol • DMSA
• INH
• Lithium ACCELERATE DETOXIFICATION
• Meprobamate • e.g., thiosulphate in cyanide toxicity
• Paraldehyde
REDUCTION OF CONVERSION OF MORE TOXIC
• Potassium
COMPOUNDS
• Quinidine
• e.g., ethanol used to inhibit conversion of methanol and
• Quinine
ethyl glycol to their toxic metabolites
• Salicylates
• Strychnine COMPETITIVE INHIBITION AT RECEPTOR SITES
• Thiocynate • e.g., Naloxone blockades receptor sites in CNS, except
in spinal column
Dialysis NOT indicated • Atropine blocks action of acetylcholine at muscarinic
• Antidepressants receptor sites
• Belladonna compounds
• Benzodiazepines BY-PASSING EFFECTS OF THE POISON
• Chlordiazepoxide • e.g., oxygen can by-pass effects of cyanide
• Dextropropoxyphene •
• Digitalis ANTIBODIES INTERACTING WITH POISON
• Diphenoxylate • Digoxin-specific antibodies (Fab fragments) reverse
• Gluthetimide binding of digitalis compounds to cardiac receptors
• Heroin & other opiates
• Synthetic anticholinergics SUPPORTIVE THERAPY AND OBSERVATION
• Essential in the management of poisoning especially
ADMINISTRATION OF ANTIDOTES where intensive care is required
• Specific antidotes are seldom necessary except when IV fluids for maintenance & replacement of losses
their administration is beneficial & lifesaving. Frequent blood & urine pH determination when
alkaline/acid Tx employed
INERT COMPLEX FORMATION Intensive nursing care to avoid aspiration &
• Chelating agents used in heavy metal poisoning decubitus ulcer development
Tx metabolic disturbances: electrolyte imbalance,
Chelating Agents (Chelators of Choice for Selected hypoglycemia, hypothermia, hyperthermia
Metals) Monitor vital signs
• DMPS = 2,3 dimercapto-1-propane sulphonate Monitor input/output
• BAL = British anti-Lewisite
• EDTA = disodiumedetate
• PEN = penicillamine
• NAPA = N-acetyl penicillamine
• DTPA = diethylene triamineopiate pentaacetic-N-
CCetC Block XII: Pulmonary Vaccinations
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MD 2
 DISPOSITION
• Observe for 24 hrs. (if admission not required)
• Psychiatric evaluation
• Child abuse not discounted
• Family counseling & education while patient is in
hospital, continued during out-patient ff. up

REVIEW QUESTIONS
1. Which of the following substances is/ are not
effectively absorbed by activated charcoal
a. Iron
b. Iodine
c. Potassium
d. Digitalis
2. Dr. X plans on doing gastric lavage on his patient
who had drug overdose. He knows one of the
contraindications of gastric lavage is:
a. Ingestion of Aspirin
b. Presence of frank convulsions
c. Both A and B
d. There are no contraindications in doing gastric
lavage
3. Maladaptive pattern of substance use with
impairment or distress
a. Substance Abuse/Dependence
b. Suicide
c. Poisoning
d. Self-poisoning

4. Gives idea of poison's phase of biotransformation

at time of admission
a. Current medications
b. Mode of exposure
c. Time of exposure
d. Past medical history

5. Is done to position the tongue away from the

airway.
a. CPR
b. Chin-lift/jaw-thrust maneuver
c. Mouth-to-mouth resuscitation
d. Finger swipe

Answers: ABACB

REFERENCES
• Upclass notes
• Doctor’s lecture

CCetC Block XII: Pulmonary Vaccinations

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MD 2