Clinical Toxicology

“Poisons & their control”

 Toxicology
“Toxicology is the study of adverse effects of exogenous agents
on biologic systems. The term poison refers to agents that cause
harmful effects.”

 -
 Focuses on the effects of substances in patients caused by
accidental poisonings or intentional overdoses of medications,
drugs of abuse, household products, or various other chemicals

 Intoxication: Toxicity associated with any chemical substance

 Poisoning. A clinical toxicity secondary to accidental exposure
 Overdose. An intentional exposure with the intent of causing self-
injury or death
 Toxidromes. A group of signs, symptoms, and laboratory findings
that suggest a specific ingestion
Introduction
Clinical Toxicology
 This branch of toxicology deals with the harmful effects of chemical
substances on human and animals and examines poisoning from lethal point of
view.
 Clinical toxicology deals with the assessment and treatment of patients
exposed acutely or chronically to potentially harmful agents
 Because of the diverse nature of the substances involved in poisonings and the
wide range of clinical manifestations and their treatment, optimal
management is achieved by an interdisciplinary approach using the
expertise of physicians, nurses, pharmacists, and prehospital professionals.
What is a Poison ?

“A poison is any substance, including

medications, that is harmful (causing death or injury) to your
body if too much is eaten, inhaled, injected, or absorbed
through the skin. ”
(CDC. USA)
An Unintentional poisoning occurs when a person taking or
giving too much of a substance did not mean to cause harm.
 The word poison comes from the Latin word, “potare”,
which means to drink, but the poisons can also enter the
body through other ways as well.
◦ From exposure to radiation
◦ Venom from snake bite, etc.
Poisoning

“The development of dose related

adverse effects following
exposure to chemicals, drugs or
other xenobiotics.”
A xenobiotic is a foreign chemical substance found within an organism
that is not normally naturally produced by or expected to be present
within. E.g., Antibiotics

Poisoning refers to exposure to any agent which is

capable of producing a deleterious response in a
biological system, seriously injuring functions or
producing death.
Types of poisoning
Acute Poisoning
 Acute poisoning is sudden exposure to a poison on one occasion or
during a short period of time.
 Symptoms develop in close relation to the exposure. Absorption of a
poison is necessary for systemic poisoning. In contrast, substances that
destroy tissue but do not absorb are classified as corrosives rather than
poisons.
 Onset of signs and symptoms are abrupt in case of acute poisoning.

Chronic Poisoning
 Chronic poisoning is long-term repeated or continuous exposure to a
poison where symptoms do not occur immediately or after each
exposure.
 The patient gradually becomes ill, or becomes ill after a long latent
period. Chronic poisoning most commonly occurs following exposure to
poisons that bio accumulate such as mercury and lead. It is produced by
small doses taken over a long period.
 Onset is usually NOT abrupt.
EPIDEMIOLOGY
 WHO (2004) - 3,46,000 deaths in a year d/t poisoning.
 In Pakistan unintentional poisoning condition was the 26th cause of
mortality in 1990 but increased to the 22nd by 2010
 The NHS Pakistan 1990-1994, a nationally representative household
survey, reported an incidence of 3.3 non-fatal injuries due to poisoning
per 1,000 per year from which 3.4% recovered with handicap.
 Estimates from previous reports
◦ range from 21.5% to 77.0% for non-fatal injuries;
◦ self-inflicted poisoning ranges from 18% to 70% and
◦ homicidal poisoning from 1.8% to 5%
 Commonest cause in PAKISTAN –
◦ Insecticides > Tranquilizers > Narcotics
◦ Among medical drugs, 60% accounted for BZD.
 Reasons – Agriculture based economy
- Easy availability pesticides
- Poverty
 Relevant definitions
Fulminant poisoning
 It is produced by a massive dose of poison. Death occurs rapidly, sometimes
without preceding symptoms and patient collapse suddenly.
Sub acute Poisoning
 Some poison also show a sub acute type of poisoning which lies somewhere
between the latter two extremes mentioned above.
Toxin and Toxicant
 Chemical that can potentially produce harm is termed as toxicant.
 The term toxin is reserved for those chemicals that are produced by the living
organisms. For example rattle snake venom, poisonous mushroom containing
toxin.
Venom
 Venom is an animal poison that is produced in a poison gland or a group of
cells and is delivered to another animal or living animal or living organism via
a bite or sting. This is referred to as envenomation.
“If you bite it and you die, it's poison.
If it bites you and you die, it's venom.”
 Relevant definitions
Corrosives
 Corrosives are the substances that rapidly destroy or decompose the
body tissues at point of contact. Some examples are hydrochloric acid,
nitric acid, sulfuric acids, phenol, sodium hydroxide and iodine etc.
Irritants:
 Substance which, while not corrosive, causes a temporary or reversible
inflammation of living tissue (such as eyes, skin, or respiratory organs)
by a chemical action at the point of contact. The effects of an irritant
may be acute (due to a single high level exposure) or chronic (due to
repeated low level exposures).
Deliriants:
 Deliriants are a class of hallucinogen. Deliriants are considered to be
true hallucinogens, because the visuals they produce are hard or
impossible to tell apart from reality; they are also known for negative
physical effects.
Biocide
 A chemical substance capable of killing living organisms.
Role of pharmacist
Assisting medical team
◦ Correct diagnosis
◦ Assessment of severity
◦ Appropriate initial management
Acts as advisor/consultant (Emergency pharmacist)
Availability of antidotes
Maintenance of inventory
Pharmacist in emergency care unit
Preventing unintentional drug poisoning (awareness &
education)
Plan of therapy (management)
Classification of toxic agents on the basis of treatment by
pharmacist
Role of pharmacist
Plan of therapy
◦ Decrease the absorption of toxin.
 a) Inducing emesis.
 b) Performing gastric lavage.
 c) Using chemical adsorbent.
◦ Enhances the elimination of toxin.
 It includes the study of;
 a) Urinary alkalization/acidification.
 b) Dialysis.
 c) Whole bowel irrigation
◦ Chemical inactivation.
 Antidotes can change the chemical nature of the poison by
 a) Rendering it less toxic.
 b) Preventing its absorption.
◦ General treatment of local exposure.
Classification of poisons
 According to the chief symptoms produced
 Corrosives .
 Systemic
 Irritants
 Miscellaneous

1. Corrosives
a) Strong acids- H2SO4 , HNO3 , HCl
b) Strong alkalis- Hydrates & Carbonates of Na+ , K+ &
NH3
c) Metallic salts – Zinc chloride, Ferric chloride, KCN ,
Silver nitrate, Copper sulphate.
Classification continued….

2. Irritants
a) Inorganic –i) Nonmetallic – Phosphorus, Iodine
Chlorine.
ii) Metallic – Arsenic, Antimony, Lead.
iii) Mechanical – Powdered glass, hair

b) Organic
Vegetable – Abrus precatorius, Castor, Croton,
Calotropis.
Animal – Snake & insect venom,
Cantharides
Classification continued…….

3. Systemic
a) Cerebral
 CNS depressants – Alcohol, opioids, hypnotics, general
anesthetics.
 CNS stimulants – Amphetamines, Caffeine
 Deliriant – Datura (Angel’s trumpets),
Cannabis, Cocaine
b) Spinal – Nux vomica
c) Peripheral – Conium (hemlock), Curare
d) CVS - Aconite (wolf’s bane), Quinine, HCN
e) Asphyxiantes – CO, CO2 , H2S

4) Miscellaneous – Food poisoning, Botulism.

 Biochemical investigations
 Hematologic
 CBC, Platelet count, Coagulation profile
◦ Hemolytic anemia- lead, NSAIDS, Quinidine
◦ Thrombocytopenia- Aspirin, Phenytoin, Procanamide
◦ Coagulopathy- snake venoms, warfarin

 Liver function tests

 S. bilirubin , enzymes – AST,ALT , ALP, coagulation profile
◦ Acetaaminophen, sulfonamides, rifampicin, TCA, INH,

 Renal functions tests

◦ Aspirin, lead, barbiturates, alcohol, amphetamines,
copper sulphate
Principles of Management
 InitialABC assessment if necessary (ABC stands for
airway, breathing, circulatory resuscitation)
 A secondary survey for infection or trauma of the head or
cervical spine, if the patient mental or metabolic activities
are abnormal.
 Supportive care with continuous assessment and
monitoring
 Case specific management such as preventing further
absorption using antidotes or enhanced the elimination of
poison
 Rapid evaluation of poison from blood, vomitus or from
other body fluids or parts
 In case of extensive poisoning, early treatment and supportive care
should be provided to the patient prior to extensive investigations or
apparent diagnosis
 Attention must be given to maintain patient vital signs and providing
immediate treatment of life threatening conditions such as
hypotension, hypertension, bradycardia, tachycardia, cardiac
arrhythmias, hyperthermia, hypothermia, respiratory depression.
 Cardiac monitoring and immediate treatment is needed for
arrhythmias and conduction defects.
Initial Steps to stabilizing
patients
Get Help

Prioritize this patient over not sick patients

Rapidly assess the patient

Simultaneously stabilize the patient

Expedite diagnostic workup and management

Initial assessment of acutely ill patient

Identify and treat immediate life

threats

Perform A-B-C-D
Say “OMI” Oxygen, Monitor,
IV
 ABCs of assessment

AIRWAY BREATHING CIRCULATION

Talking = good Look: work of Look: mental status,

breathing, respiratory color
rate
Look: edema, blood,
vomitus, foreign body Feel: Peripheral pulses
Listen: Breath sounds
Listen: Noisy = Check: Heart rate,
obstructed Check: Pulse oximetry cardiac rhythm, blood
pressure
 Supportive Management
ABCD principle
A for airway
B for breathing
C for circulation
D for diagnosis and drugs
Airway
 Airway obstruction can cause death
 First evaluate mental status and cough reflex to check if the patient is conscious or
unconscious.
 In the unconscious patient, the priority is airway management, to avoid a preventable
cause of hypoxia. Common problems with the airway of patient with a seriously
reduced level of consciousness involve blockage of the pharynx by the tongue,
a foreign body, or vomit.
 At a basic level, opening of the airway is achieved through manual movement of the
head using various techniques, with the most widely taught and used being the "head
tilt — chin lift", although other methods such as the "modified jaw thrust" can be used,
especially where spinal injury is suspected, although in some countries, its use is not
recommended for lay rescuers for safety reasons.
 Interventions which can be used to facilitate airways are:
◦ Sniffing position
◦ Jaw thrust
◦ Head-down, left-sided position
◦ Examine the oropharynx
◦ Clear secretions
◦ Use of Airway devices
 Before considering Intubation…
◦ Consider naloxone first
Breathing
 Determine if respirations are adequate
 Give supplemental oxygen
 Assist with bag-valve-mask
 Check oxygen saturation, and consider Air Blood Gases
(ABG) tests.
 In the unconscious patient, after the airway is opened the next area to
assess is the patient's breathing, primarily to find if the patient is
making normal respiratory efforts. Normal breathing rates are between
12 and 20 breaths per minute, and if a patient is breathing below the
minimum rate, then CPR should be considered, although professional
rescuers may have their own protocols to follow, such as artificial
respiration.
 Auscultate lung fields
◦ For Bronchospasm: Albuterol nebulizer
◦ For Bronchorrhea/rales: Atropine
◦ For Stridor: Determine need for immediate intubation
If Airway/Breathing are impaired
Begin high-flow oxygen Prepare to manage the
• To reduce hypoxemia
airway
• Remove obstacles
• Or intubation in severe cases

Stabilizing
A&B
Auscultate lungs Obtain STAT chest X-
carefully ray
• Checking lung sounds • To get an idea about what’s
going on physiologically
Circulation
 Once oxygen can be delivered to the lungs by a clear airway and
efficient breathing, there needs to be a circulation to deliver it to the rest
of the body.
 For an appropriate circulation, we should have normal blood pressure
(120/70 mmHg) and a normal rhythmic pulse/heart rate (between 60-80
beats per minute).
 Interventions which can be done to secure circulation:
◦ Secure the IV access for fluid replacement in states of shock.
◦ Obtain blood work/laboratory tests
◦ Measure & monitor blood pressure, & pulse
◦ Hypotension treatment:
 Normal saline fluid challenge, 20 mL/kg
 Vasopressors (adrenaline, noradrenaline, isoproterenol) if still hypotensive
 Packed Reb Blood Cells (PRBC) /Blood transfusion if bleeding or anemic
◦ Hypertension treatment:
 Nitroprusside, beta blocker, or nitroglycerin
◦ Continuous ECG monitoring
 To assess for arrhythmias, & treat accordingly
Vital signs related to Circulation

Pulse/ Cardiac Blood

Heart rate rhythm pressure
If Circulation is impaired
Establish two large-bore IVs Identify cardiac rhythm
• Differentiate from sinus to non-
• For backup incritically ill patients
sinus arhythmias

Stabilizing
circulation Consider IV fluids
Consider treating non-sinus
rhythms • Not all patients require fluids but
majority benefits from fluid
optimization.
• Fluid wont help in valvular disease
Clinical presentation & diagnosis
Substance. Pertinent information includes the quantity of each ingredient in the product. The
history may be unreliable or unavailable in suicidal patients or substance abusers; patients
with altered mental status or those exposed to a substance in an unmarked container or who
ingest an unidentified plant may be unable to provide a history.

Amount. If an accurate determination of the amount ingested is not possible and the substance is
toxic, a potentially toxic dose should be assumed. For intentional exposures, the patient's report of
the dose is suspect.

Time since exposure. This information coupled with information on the onset and duration of
action of the substance, allows assessment of whether clinical manifestations are consistent
with the history of dose and time since exposure. Whether to institute some therapeutic
options, including GI decontamination, is determined by time since ingestion.

Clinical manifestations. Evaluate if clinical effects are consistent with the substance(s); if
not, evaluate for other substances and/or medical conditions. Severe effects (respiratory and
cardiovascular depression) necessitate immediate treatment.

Patient's age and weight. Determine the toxicity of the substance, dosing of antidotes, and likely
reason for the exposure based on this information.
ANTIDOTAL THERAPY
NON-SPECIFIC
SPECIFIC
NON SPECIFIC ANTIDOTES
 Activated Charcoal
 Activated charcoal by virtue of its large surface
area adsorbs many drugs and toxins. It is used
orally to limit the drug or toxin absorption.
 Initial dose
 1.0g /kg orally or via gastric tube
 Repeat dose
 15-30 g every 2-4 hours. Administer small dose of
cathartic with every 2nd or 3rd charcoal dose
 Patients showing nausea and vomiting require
antiemetic drugs also.
SPECIFIC ANTIDOTES
1 N-AcetylCysteine Paracetamol Poisoning

2 Flumazenil BDZ Poisoning

3 Atropine/pralidoxime Pesticide Poisoning

4 Oxygen Carbon Monoxide

Poisoning

5 Pencillamine Heavy metal Poisoning

6 Deferoxamine Iron poisoning

Common Emergency Treatments for poisoning
Poisoning Antidote/Treatment Mechanism
Paracetamol N-acetyl cysteine Act as –SH group donor,
(acetaminophen) increasing glutathione
production.
Morphine, Codeine, Heroine, Naloxone Competitive antagonism
Methadone,
Iron Deferoxamine Chelation
Copper (in Wilson’s disease) Penicillamine Chelation
Salicylates Charcoal, Alkalization Decreased Absorption
(NaHCO3) Increased elimination
Petroleum distillates & Activated charcoal, Decreased Absorption
Solvents (insecticides). Supportive treatment
Methanol (wood alcohol) gastric lavage. Decreased Absorption
Hemodialysis
folic acid, thiamine, and breakdown of toxic
pyridoxine metabolites
BZD Flumezanil Competitive antagonism
Most Common Anti Dotes
Activated Charcoal
 It contains the extremely small particles and have pores that’s
why it absorbs the toxins. The particle surface area may exceed
from 3000 m2. A substance that is absorbed to activated charcoal
cannot be absorbed from GIT.
 Activated Charcoal is a highly absorbent gritty black material
that is commonly found in air and water filters.

Therapeutic Uses for Activated Charcoal

 1. Universal antidote for drugs, chemicals and poisons.
 2. Systemic clearance of drugs and intoxicants.
 3. General detoxification.
 4. Anti-aging and life extension.
 5. Reducing cholesterol, coronary disease and arteriosclerosis.
 6. Counteracting pathogens.
 7. Intestinal complaints.
Factors affecting charcoal activity:
1. The type of toxicant (its chemical structure and
physical properties).
2. The amount and type of charcoal ingested.
3. The length of time from toxin ingestion to
Activated Charcoal ingestion.
4. The contents of your intestinal fluids and
intestinal transport efficiency

Dose
Child Dose under 12 years (1g/kg body weight)
Adult Dose 50grams
N-Acetyl Cysteine
 It is an antidote for paracetamol poisoning

Mechanism of action
 It acts as a sulfhydral group donor, substituting glutathione.
It rapidly binds with the reactive metabolites. The toxic
metabolites N-acetyl Para benzo quinine imines in the liver.
The glutathione conjugates these toxic metabolites and
prevent hepatotoxicity.
Naloxone
 It is indicated in the patients with opiate drugs such as Morphine,
Codeine, Heroine, Methadone
 These drugs tend to produce extreme drowsiness associated with
respiratory compromise and hypoxia

Mechanism Of Action
 It acts as competitive antagonist
Chelating Agents
The agents that posses the ability to form complex with the
heavy metals and there by prevent or reverse the binding of
metallic cat ions to body ligands are known as chelating
agents.
Mechanism of action
 Chelating agents are large anionic molecules that
reversibly bind with high affinity to di and trivalent metals
cat ions to form a metal complex and then this complex is
eliminated from the body by using body’s natural
mechanism of waste product removal.
Route of administration of chelating agents
 The chelating agent may be administered intravenously,
intramuscularly, or orally, depending on the agent and the
type of poisoning.
Deferoxamine
 Deferoxamine (also known as desferrioxamine B,
desferoxamine B, DFO, DFOA, DFB or desferal) is a
bacterial side rophore produced by the actinobacter
Streptomyces pilosus. It has medical applications as a
chelating agent used to remove excess iron from the body.
Mechanism
 Deferoxamine acts by binding free iron in the bloodstream
and enhancing its elimination in the urine. By removing
excess iron, the agent reduces the damage done to various
organs and tissues, such as the liver. A recent study also
shows that it speeds healing of nerve damage (and
minimizes the extent of recent nerve trauma).
Deferoxamine may modulate expression and release of
inflammatory mediators by specific cell types.
Uses
 Deferoxamine is used to treat acute iron poisoning,
especially in small children.
 Treatment with this agent is also frequently necessary to
treat hemochromatosis, a disease of iron accumulation that
can be either genetic or acquired.
 Acquired hemochromatosis is common in patients with
certain types of chronic anemia (e.g. thalassemia and
myelodysplastic syndrome. Administration for chronic
conditions is generally accomplished by subcutaneous
injection (SQ) over a period of 8-12 hours/Day
 Can be used to treat aluminium toxicity
 Deferoxamine can be used to speed fracture healing.

Drawback
 Administration of deferoxamine after acute intoxication may
color the urine a pinkish red, a phenomenon termed "vin
rose urine".
Penicillamine
Penicillamine is a pharmaceutical of the chelator class. The
pharmaceutical form is D- penicillamine, as L-penicillamine is toxic
(it inhibits the action of pyridoxine). It is a metabolite of penicillin,
although it has no antibiotic properties.
Uses
 Penicillamine is used as a form of immunosuppression to treat
rheumatoid arthritis. It works by reducing numbers of T-
lymphocytes, inhibiting macrophage function, decreasing IL-1,
decreasing rheumatoid factor, and preventing collagen from
cross-linking
 It is used as a chelating agent:
◦ In Wilson's disease, a rare genetic disorder of copper metabolism
penicillamine treatment relies on its binding to accumulated copper
and elimination through urine.
◦ In cystinuria, a hereditary disorder featuring formation of cystine
stones, penicillamine binds with cysteine to yield a mixed disulfide
which is more soluble than cystine.
◦ Penicillamine has been used to treat mercury poisoning.
Adverse effects
 Glomerulonephritis
 Antibody-mediated myasthenic syndrome which may
persist event after its withdrawal.
 Drug-induced systemic lupus erythematosus.
Some common poisoning and Management
Acetaminophen
 Acetaminophen (paracetamol) is a common analgesic found in
many nonprescription and prescription products. After absorption, it
is metabolized mainly by glucuronidation and sulfation, with a small
fraction metabolized via the P450 mixed-function oxidase system to a
highly toxic reactive intermediate. This toxic intermediate is
normally detoxified by cellular glutathione.
 With acute acetaminophen overdose (> 150–200 mg/kg, or 8–10
g in an average adult), hepatocellular glutathione is depleted and
the reactive intermediate attacks other cell proteins, causing
necrosis.
Clinical Findings
 Shortly after ingestion, patients may have nausea or vomiting.
 With severe poisoning, fulminant hepatic necrosis may occur,
resulting in jaundice, hepatic encephalopathy, renal failure, and
death.
 The diagnosis after acute overdose is based on measurement of the
serum acetaminophen level.
Treatment
 Emergency and Supportive Measures
 Administer activated charcoal within 1–2 hours of the
ingestion.
 Although charcoal may interfere with absorption of the
oral antidote acetylcysteine, this is not considered
clinically significant.

 Specific Treatment
 Begin treatment with a loading dose of N-acetylcysteine,
140 mg/kg orally, followed by 70 mg/kg every 4 hours.
Dilute the solution to 5% with water, juice, or soda.
 If the precise time of ingestion is unknown or if the patient
is at higher risk of hepatotoxicity (eg, alcoholic, liver
disease, chronic use of P450-inducing drugs), then use a
lower threshold for initiation of N-acetylcysteine.
Opioids
 Opioids (morphine, heroin, codeine, oxycodone, fentanyl,
hydromorphone, etc) are popular drugs of abuse and the
cause of frequent hospitalizations for overdose. All of
these agents decrease central nervous system activity and
sympathetic outflow by acting on opiate receptors in
the brain.
Clinical Findings
 Mild intoxication is characterized by euphoria, drowsiness,
and constricted pupils. More severe intoxication may
cause hypotension, bradycardia, hypothermia, coma, and
respiratory arrest. Pulmonary edema may occur.
 Death is usually due to apnea or pulmonary aspiration of
gastric contents.
 Methadone has been associated with QT interval
prolongation and torsades de pointes.
Treatment
 Emergency and Supportive Measures
 Protect the airway and assist ventilation.
 Administer activated charcoal.
 Specific Treatment
 Naloxone is a specific opioid antagonist that can rapidly
reverse signs of narcotic intoxication.
 Administer 0.4–2 mg intravenously, and repeat as needed
to awaken the patient and maintain airway protective
reflexes and spontaneous breathing.
 Caution: The duration of effect of naloxone is only
about 2–3 hours; repeated doses may be necessary for
patients intoxicated by long-acting drugs such as
methadone. Continuous observation for at least 3 hours
after the last naloxone dose is mandatory.
Salicylates
 A single ingestion of more than 200 mg/kg of salicylate is
likely to produce significant acute intoxication. Poisoning
may also occur as a result of chronic excessive dosing over
several days.
Clinical Findings
 Acute ingestion often causes nausea and vomiting,
occasionally with gastritis.
 Moderate intoxication is characterized by hyperpnea
(deep and rapid breathing), tachycardia, tinnitus, and
elevated anion gap metabolic acidosis.
 Serious intoxication may result in agitation, confusion,
coma, seizures, cardiovascular collapse, pulmonary
edema, hyperthermia, and death.
 The prothrombin time is often elevated owing to salicylate-
induced hypoprothrombinemia.
Treatment
 Emergency and Supportive Measures
 Administer activated charcoal.
 Gastric lavage followed by administration of extra doses of
activated charcoal may be needed in patients who ingest more
than 10 g of aspirin.
 Treat metabolic acidosis with intravenous sodium bicarbonate.
This is critical because acidosis (especially acidemia, pH < 7.40)
promotes greater entry of salicylate into cells, worsening toxicity.
 Specific Treatment
 Alkalinization of the urine enhances excretion. Add 100 mEq
(two ampules) of sodium bicarbonate to 1 L of 5% dextrose in
0.2% saline, and infuse this solution intravenously at a rate of
about 150–200 mL/h.
 ·Hemodialysis may be lifesaving and is indicated for patients
with severe metabolic acidosis, markedly altered mental status,
or significantly elevated salicylate levels.
Snake Bites
 The venom of poisonous snakes and lizards may be
predominantly neurotoxic or cytolytic

Symptoms:
 Neurotoxins cause respiratory paralysis; cytolytic venoms
cause tissue destruction by digestion and hemorrhage due to
hemolysis and destruction of the endothelial lining of the
blood vessels.
 The manifestations of rattlesnake envenomation are mostly
local pain, redness, swelling, and extravasation of blood.
Perioral tingling, metallic taste, nausea and vomiting,
hypotension, and coagulopathy may also occur.
 Neurotoxic envenomation may cause ptosis, dysphagia,
diplopia, and respiratory arrest.
Treatment
 Emergency Measures
 Immobilize the patient and the bitten part in a neutral position. Avoid
manipulation of the bitten area.
 Transport the patient to a medical facility for definitive treatment.
 Do not give alcoholic beverages or stimulants; do not apply ice; do not
apply a tourniquet.
 Specific Antidote and General Measures
 Pit viper (eg, rattlesnake) envenomation
 For local signs such as swelling, pain, and ecchymosis but no systemic
symptoms, give 4–6 vials of crotalid antivenin (CroFab) by slow
intravenous drip in 250–500 mL saline.
 Monitor vital signs and the blood coagulation profile. The adequacy of
venom neutralization is indicated by improvement in symptoms and
signs, and the rate that swelling slows.
 Elapid (coral snake) envenomation
 Give 1–2 vials of specific antivenom as soon as possible. To locate
antisera for exotic snakes, call a regional poison control center.
Petroleum Distillates & Solvents
 Petroleum distillate toxicity may occur from inhalation of
the vapor or as a result of pulmonary aspiration of the
liquid during or after ingestion.

 Symptoms:
 Acute manifestations of aspiration pneumonitis are
vomiting, coughing, and bronchopneumonia.
 Hydrocarbons can also cause systemic intoxication by
inhalation. Vertigo, muscular incoordination, irregular
pulse and seizures occur with serious poisoning and may
be due to hypoxemia or the systemic effects of the agents.
 Chlorinated and fluorinated hydrocarbons and many other
hydrocarbons can cause ventricular arrhythmias due to
increased sensitivity of the myocardium to the effects of
endogenous catecholamines.
Treatment
Move the patient to fresh air.
Gastric emptying and activated charcoal are
recommended, for the preparation contains toxic
solutes (eg, an insecticide) or is an aromatic or
halogenated product.
Observe the victim for 6–8 hours for signs of
aspiration pneumonitis (cough, localized rales or
rhonchi, tachypnea, and infiltrates on chest
radiograph).
If fever occurs, give a specific antibiotic only
after identification of bacterial pathogens by
laboratory studies.
Methanol & Ethylene Glycol
 Methanol (wood alcohol) is commonly found in a variety of
products, including solvents, duplicating fluids, record
cleaning solutions, and paint removers. Ethylene glycol is
the major constituent in most antifreeze compounds.
 The toxicity of both agents is caused by metabolism to
highly toxic organic acids—methanol to formic acid;
ethylene glycol to glycolic and oxalic acids.
Clinical Findings
 Shortly after ingestion of either of these agents, patients
usually appear "drunk."
 After several hours, metabolism to toxic organic acids
leads to a severe anion gap metabolic acidosis,
tachypnea, confusion, convulsions, and coma.
 Methanol intoxication frequently causes visual
disturbances, while ethylene glycol often produces oxalate
crystalluria and renal failure.
Treatment
 Emergency and Supportive Measures
 For patients presenting within 30–60 minutes after
ingestion, empty the stomach by gastric lavage.

 Specific Treatment
 Patientswith significant toxicity (manifested by severe
metabolic acidosis, altered mental status, and markedly
elevated osmolar gap) should undergo hemodialysis as
soon as possible to remove the parent compound and the
toxic metabolites.
 Treatment with folic acid, thiamine, and pyridoxine
may enhance the breakdown of toxic metabolites.
Fomepizole (4-methylpyrazole; Antizol) blocks alcohol
dehydrogenase and is easier to use than ethanol.
Benzodiazepines, & Sedative-Hypnotic Agents
 Sedative-hypnotic drugs includes a variety of products
used for the treatment of anxiety, depression, insomnia,
and epilepsy. All of these drugs depress the central nervous
system.
Clinical Findings
 Mild intoxication produces euphoria, slurred speech, and
ataxia. It may produce hypoglycemia, even at relatively
low concentrations.
 With more severe intoxication, stupor, coma, and
respiratory arrest may occur.
 Death or serious morbidity is usually the result of
pulmonary aspiration of gastric contents.
 Bradycardia, hypotension, and hypothermia are common.
 Patients with massive intoxication may appear to be dead,
with no reflex responses and even absent ECG.
Diagnosis
Diagnosis and assessment of severity of intoxication are
usually based on clinical findings. Ethanol serum levels
greater than 300 mg/dL (0.3 g/dL; 65 mmol/L) can
produce coma in persons who are not chronically abusing
the drug. Phenobarbital levels greater than 100 mg/L usually
cause coma.
Treatment
Emergency and Supportive Measures
 Administer activated charcoal. Repeat-dose charcoal may
enhance elimination of Phenobarbital.
 Hemodialysis may be necessary for patients with severe
phenobarbital intoxication.
Specific Treatment
 Flumazenil is a benzodiazepine receptor-specific
antagonist; it has no effect on ethanol,
barbiturates, or other sedative-hypnotic agents. If used,
flumazenil is given slowly intravenously, 0.2 mg over
30–60 seconds, repeated in 0.5 mg increments as needed
up to a total dose of 3–5 mg.
Caution:
 Flumazenil may induce seizures in patients with
preexisting seizure disorder, benzodiazepine addiction,
or concomitant tricyclic antidepressant overdose. If
seizures occur, diazepam and other benzodiazepine
anticonvulsants will not be effective.
Iron
 Iron is widely used therapeutically for the treatment of
anemia and as a daily supplement in multiple vitamin
preparations. Iron is corrosive to the gastrointestinal
tract and, once absorbed, has depressant effects on the
myocardium and on peripheral vascular resistance.
Intracellular toxic effects of iron include disruption of
Krebs cycle enzymes.
Clinical Findings
 Ingestion of less than 30 mg/kg of elemental iron
usually produces only mild gastrointestinal upset.
 Ingestion of more than 40–60 mg/kg may cause
vomiting diarrhea, hypotension, and acidosis.
 Death may occur as a result of profound hypotension
due to massive fluid losses and bleeding, metabolic
acidosis, peritonitis from intestinal perforation, or
sepsis. Fulminant hepatic failure may occur.
Serum iron levels greater than 350–500 mcg/dL are
considered potentially toxic, and levels over 1000 mcg/dL are
usually associated with severe poisoning

Treatment
 Emergency and Supportive Measures
 Treat hypotension aggressively with intravenous
crystalloid solutions (0.9% saline or lactated Ringer
solution).
 Perform whole bowel irrigation to remove unabsorbed pills
from the intestinal tract.
 Specific Treatment
 Deferoxamine is a selective iron chelator. It is not useful as
an oral binding agent. The presence of an iron-
deferoxamine complex in the urine may give it a "vin rosé"
appearance.
 Summary
Poisoning a common problem in our
country
A high index of suspicion required to
diagnose
For any poisoning the mainstay of
treatment is supportive care
Follow the A, B, C
Don’t panic and follow a plan of action
 Decreasing absorption
 Enhancing elimination
 Neutralising toxins
Prevention of re- exposure
Adult education – instructions regarding
safe use of medications & chemicals

Notification of regulatory agencies - in

case of environmental or workplace
exposure

Psychiatric referral- depressed or

psychotic patients should receive psychiatric
assessment, disposition & follow-up
Prevention of re- exposure

Child proofing- In house hold

where children live or visit,
alcohols, medications,
household products ,non edible
plants should be kept out of
reach or in locked, child proof
containers.