Sara Qaradeh

Clinical Toxicology

"Everything is poison,
there is poison in
everything. Only the dose
makes a thing not a
poison”
Philippus Paracelsus (1493-1541)

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Environmental pollutants:
- Insecticides (organophosphorus, carbamates,
pyrethroid)
- Rodenticides: Warfarin, strychnine, Phosphine
and Phosphides
- Fungicides
- Herbicides
-Gaseous intoxication
- Heavy metals (lead, mercury, Arsenic)
4
Organophosphorus, carbamates insecticides
Mechanism of toxicity
A. Organophosphorus (OP) compounds inhibit the
enzyme acetylcholinesterase leads to the
accumulation of excessive acetylcholine at
muscarinic receptors (cholinergic effector cells), at
nicotinic receptors (skeletal neuromuscular
junctions and autonomic ganglia), and in the CNS

-Permanent inhibition of acetylcholinesterase may

occur through covalent binding by the OP to the
enzyme. This is known as "aging”

5
B. Carbamates inhibit the acetylcholinesterases
and lead to accumulation of acetylcholine,
similar to the effects of OPs.
• CNS effects are often less pronounced than in
OP poisoning because they have more
difficulty crossing the blood-brain barrier.
• Carbamates also do not "age," leading to
faster reactivation of the AChE.

• Aldicarb –watermelon (California 1985)

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• Most OPs and carbamates can be absorbed by
any route: inhalation, ingestion, and
absorption through the skin.

• Highly lipophilic organophosphates

(disulfoton, fenthion, and others) are stored in
fat tissue, and this may lead to persistent
toxicity lasting several days after exposure

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Clinical presentation. Dumbles
A. Muscarinic manifestations include vomiting,
diarrhea, abdominal cramping,
bronchospasm, miosis, bradycardia, and
excessive salivation and sweating. Fluid losses
can lead to systemic hypovolemia, resulting in
shock.
B. Nicotinic effects include muscle
fasciculations, tremor, and weakness.
Respiratory muscle weakness complicated by
bronchorrhea may lead to respiratory arrest
and death. 9
C. Central nervous system: poisoning may cause
agitation, seizures, and coma.

• Chemical pneumonitis may occur if a product

containing a hydrocarbon solvent is aspirated
into the lungs.

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Diagnosis
• is based on the history of exposure
• the presence of characteristic muscarinic,
nicotinic, and CNS manifestations of
acetylcholine excess.
• There may be a solvent odor, and some agents
have a strong garlicky odor.

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Specific levels
Organophosphorus compounds. Laboratory
evidence of poisoning may be obtained by
measuring decreases in the plasma
pseudocholinesterase (PChE) and red blood
cell acetylcholinesterase (RBC AChE) activities.
Carbamate: poisoning produces reversible
acetylcholinesterase inhibition, making these
tests less useful.
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• Treatment
A. Emergency and supportive measures.
Caution: Health-care providers must take
measures to prevent direct contact with the
skin or clothing of contaminated victims
B. Hydrocarbon

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Specific drugs and antidotes.
1. Give atropine, 0.5–2 mg IV initially, then
double the dose every 5 minutes until signs
of atropinization are present
Note: Atropine will reverse muscarinic but not
nicotinic effects.
2. Pralidoxime (2-PAM) or obidoxime is a
specific antidote that acts to regenerate the
enzyme activity at all affected sites prior to
aging.

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a. Pralidoxime should be given immediately to
reverse muscular weakness and fasciculations:
1–2 g initial bolus dose (20–40 mg/kg in
children) IV over 5–10 minutes, followed by a
continuous infusion.
b. still be effective if given later, particularly after
exposure to highly lipid-soluble compounds.
c. Pralidoxime is not recommended for carbamate
intoxication, (if the exact agent is not identified
and the patient has significant toxicity,
pralidoxime should be given .
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• Decontamination (Skin, GI)
• Enhanced elimination

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Pyrethrins and Pyrethroids
• From chrysanthemum plant (‫اﻷﻗﺣوان‬
• They have been used for many years as oral
anthelmintic agents

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Mechanism of toxicity.
-In insects, pyrethrins and pyrethroids rapidly
cause death by paralyzing the nervous system
through disruption of the membrane ion
transport system in nerve axons
-Mammals are generally able to metabolize
these compounds rapidly and thereby render
them harmless.

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• Clinical presentation. Toxicity to humans is
associated primarily with hypersensitivity
reactions and direct irritant effects
(inhilation,eye, skin, ingestion )rather than
with any pharmacologic property.

• Ingestion. With large ingestions (200–500 mL

of concentrated solution)

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• Diagnosis is based on a history of exposure.
No characteristic clinical symptoms or
laboratory tests are specific for identifying
these compounds.

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Treatment
A. Emergency and supportive measures
B. Specific drugs and antidotes. There is no
specific antidote.
C. Decontamination (surface, GI)
D. Enhanced elimination. These compounds are
metabolized rapidly by the body.

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Warfarin and Related Rodenticides
• superwarfarins" such as brodifacoum, and
bromadiolone, which have profound and
prolonged anticoagulant effects

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• Mechanism of toxicity. All these compounds
inhibit hepatic synthesis of the vitamin K–
dependent coagulation factors II, VII, IX, and
X.
• Kinetics
A. The duration of anticoagulant effect after a
single dose of warfarin is usually 2–7 days.
B. Superwarfarin products may continue to
produce significant anticoagulation for weeks
to months after a single ingestion
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• Toxic dose. The toxic dose is highly variable.

• Clinical presentation.
- Excessive anticoagulation may cause
ecchymoses, bleeding gums, or evidence of
internal hemorrhage (eg, hematemesis,
melena, or hematuria).
- -The most immediately life-threatening
complications are massive GI bleeding and
intracranial hemorrhage.

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A. Anticoagulant effects of warfarin may be
apparent within 8–12 hours, but with
superwarfarins peak effects commonly are
delayed for up to 2 days after ingestion.
B. Evidence of continuing anticoagulant effects
may persist for days, weeks, or even months
with superwarfarin products.

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• Diagnosis is based on the history and
evidence of anticoagulant effects.
A. Specific levels. Brodifacoum levels are
available : Levels less than 4–10 ng/mL are
not expected to interfere with coagulation.
B. An anticoagulant effect is best quantified by
baseline and daily repeated measurement of
the prothrombin time (PT) and calculation of
the International Normalized Ratio (INR),
which may not be elevated until 1–2 days
after ingestion. A normal PT 48 hours after
exposure rules out significant ingestion.
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Treatment

A. Emergency and supportive measures. If

significant bleeding occurs, be prepared to
treat shock with transfusions of blood and
fresh frozen plasma and obtain immediate
neurosurgical consultation if intracranial
bleeding is suspected.

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B. Specific drugs and antidotes.
- Vitamin K1 (phytonadione, effectively restores
the production of clotting factors.
- It should be given if there is evidence of
significant anticoagulation.
- Note, if it is given prophylactically after an
acute ingestion, the 48-hour prothrombin time
cannot be used to determine the severity of the
overdose, and it is suggested that the patient be
monitored for a minimum of 5 days after the
last vitamin K1 dose.
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• Administer oral vitamin K1 every 6 hours
Doses of up to 800 mg daily have been
required to maintain a satisfactory INR

• Prolonged dosing of vitamin K may be

required for several weeks in patients who
have ingested a long-acting superwarfarin
product.

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• Decontamination
• Enhanced elimination

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 Phosphine and Phosphides
• Phosphine is a colorless gas

• Magnesium phosphide and aluminum phosphide

are available in pellets or tablets and are used as
rodenticides

• Zinc phosphide is a crystalline dark gray powder

mixed into food as rodent bait.
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• Mechanism of toxicity.
- The action of phosphine is not clearly understood
but may be related to inhibition of electron
transport in mitochondria.

- Phosphides liberate phosphine gas upon contact

with moisture, and this reaction is enhanced in
the acidity of the stomach.
- Phosphine is then absorbed through the GI and
respiratory tracts.

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• Toxic dose
• Phosphides. Ingestion of as little as 500 mg of
aluminum phosphide has caused death in an
adult.
• In a reported case series, survivors ingested
about 1.5 g
• The LD50 for zinc phosphide in rats is 40
mg/kg; the lowest reported lethal dose in
humans is 4 g

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• Clinical presentation.
- Inhalation of phosphine gas is associated with
cough, dyspnea, headache, dizziness, and
vomiting.
- Phosphide ingestion may cause nausea,
vomiting, diarrhea, hypotension unresponsive
to pressors, and a rotten fish or garlicky odor.
- Adult respiratory distress syndrome (ARDS),
acute renal failure, hepatitis, seizures, and
coma may occur.
- Myocardial injury
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Diagnosis is based on a history of exposure to
the agent.

Caution: Pulmonary edema may have a delayed

onset, and initial respiratory symptoms may
be mild or absent.
Specific levels. Body fluid phosphine levels are
not clinically useful.

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Treatment
Emergency and supportive measures
• In severe poisoning, adrenal function may be
compromised and intravenous hydrocortisone
should be considered
Specific drugs and antidotes. There is no
specific antidote.
Decontamination
Enhanced elimination.

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Phosphorus
• Red and yellow. Red phosphorus is not
absorbed and is essentially nontoxic. In
contrast, yellow phosphorus (also called
white phosphorus) is a highly toxic cellular
poison
• Mechanism of toxicity
Phosphorus is highly corrosive and is also a
general cellular poison.

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Fungicides

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 Herbicides
• Glyphosate
Mechanism of toxicity.
A. It has been hypothesized that toxicity is related to the
presence of the surfactant rather than to the
glyphosate itself. Surfactants may impair cardiac
contractility.

B. Glyphosate is a phosphorus-containing compound, ( it

does not inhibit acetylcholinesterase).

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Toxic dose.
• Glyphosate itself has very low toxicity by the oral
and dermal routes, with an LD50 in animals of >
5000 mg/kg and > 2000 mg/kg, respectively.

• The surfactant (polyoxyethyleneamine ) is more

toxic, with an oral LD50 of 1200 mg/kg.
• Ingestion of > 85 mL of a concentrated
formulation is likely to cause significant toxicity in
adults.

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Clinical presentation
A. Dermal. Prolonged exposure to the skin can cause dermal
irritation.
B. Ocular exposure can cause a mild superficial corneal injury. No
serious eye injury occurred among 1513 consecutive ocular
exposures reported to a poison control center.
C. Inhalation is a minor route of exposure. oral or nasal
discomfort and throat irritation.
D. Ingestion. After acute ingestion of a large amount of a
glyphosate/surfactant-containing product, serious GI,
cardiopulmonary, and other organ system
toxicity may occur.

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• Diagnosis is based on the history of contact with
or ingestion of glyphosate-containing products
Treatment
A. Emergency and supportive measures
B. Specific drugs and antidotes. No specific antidote
is available
C. Decontamination
1. Skin and eyes
2. Ingestion. For small ingestions =no need.
For larger ingestions, Gastric lavage.
The efficacy of activated charcoal is unknown.
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 Paraquat and Diquat
• Recently a formulation containing diquat 0.73%
and glyphosate 18% was marketed (Roundup
Grass and Weed Killer).

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• Mechanism of toxicity
- They are strong cations in aqueous solution,
and concentrated solutions (eg, > 20%) may
cause severe corrosive injury when ingested,
injected, or applied to the skin, eyes, or
mucous membranes.

- They are extremely potent systemic toxins

when absorbed and can cause multiple system
organ damage.
-
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Mechanism of toxicity (continue)
1. Paraquat is selectively taken up and
concentrated by pulmonary alveolar cells,
leading to cell necrosis followed pulmonary
fibrosis.
2. Diquat accumulates in the kidney, causing
renal failure. It is also associated with GI fluid
sequestration and cerebral hemorrhagic
infarctions.

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Pharmacokinetics
Absorption. Paraquat and diquat are rapidly
absorbed from the GI tract, and peak serum
levels are reached within 2 hours of ingestion.

Toxic dose. Diquat is slightly less toxic than

paraquat. Both compounds are extremely
poisonous.
• Patients with ingestions of less than 20 mg/kg
usually recover fully.

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• Clinical presentation (like mech.)
A. Paraquat.
- leads to corrosive GI injury, rapid onset of renal failure,
necrosis, shock, and death within hours to a few days.
- Most patients dying from pulmonary fibrosis after days
to weeks
B. Diquat
- Severe gastroenteritis and GI fluid sequestration may
cause massive fluid and electrolyte loss that
contributes to renal failure. Agitation, seizures, and
coma have been described.
- Cerebral and brainstem hemorrhagic infarctions may
occur.
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Diagnosis
• It is based on a history of ingestion
• and the presence of gastroenteritis and oral
burns.
• Rapidly progressive pulmonary fibrosis
suggests paraquat poisoning.
• Plasma paraquat levels associated with a high
likelihood of death are 2 mg/L at 4 hours, 0.9
mg/L at 6 hours, and 0.1 mg/L at 24 hours
after ingestion.

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Treatment
A. Emergency and supportive measures.
Avoid excessive oxygen administration in patients with
paraquat poisoning ------related to oxygen-radical
production which lead to cytotoxicity
.Treat significant hypoxemia with supplemental oxygen,
but use only the lowest oxygen concentration
necessary
B. Specific drugs and antidotes. There is no
specific antidote

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C. Decontamination
- Ingestion.

- Immediately administer 100 g of activated

charcoal and repeat the dose in 1-2 hours.

- Gastric lavage may be helpful if performed within

an hour of the ingestion but should be preceded
by a dose of activated charcoal

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 Gaseous intoxication

• Carbon monoxide (CO) is a colorless, odorless,

tasteless, and nonirritating gas produced by the
incomplete combustion of any carbon-containing
material.

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• Mechanism of toxicity. Toxicity is a
consequence of cellular hypoxia and ischemia.
A. CO binds to hemoglobin with an affinity 250
times that of oxygen, resulting in reduced
oxyhemoglobin saturation and decreased
blood oxygen-carrying capacity.

B. CO may also directly inhibit cytochrome

oxidase, possibly contributing to impaired
myocardial contractility.

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Toxic dose: ????
Clinical presentation. Symptoms of intoxication are
predominantly in organs with high oxygen
consumption such as the brain and heart.
• The majority of patients complain of headache,
dizziness, and nausea.
• Patients with coronary disease may experience
angina or myocardial infarction.
• With more severe exposures, impaired thinking,
coma, convulsions, cardiac arrhythmias,
hypotension, and death may occur.
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• Diagnosis
- a history of exposure (eg, the patient was found
in a car in a locked garage).
- There are no specific reliable clinical findings;
cherry-red skin coloration or bright red venous
blood is highly suggestive but not frequently
noted.

- Specific levels. Obtain a specific carboxyhemoglobin

concentration

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Treatment
A. Emergency and supportive measures
B. Specific drugs and antidotes. Administer
oxygen in the highest possible concentration
(100%).
C. Decontamination. Remove the patient
immediately
D. Enhanced elimination. Hyperbaric oxygen
provides 100% oxygen under 2–3
atmospheres of pressure and can enhance
elimination of CO (half-life reduced to 20–30
minutes)
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Heavy metals: lead
• Mechanism of toxicity
The multisystem toxicity of lead is mediated by
several mechanisms, including inactivation or
alteration of enzymes and other
macromolecules by binding to sulfhydryl,
phosphate, or carboxyl ligands and interaction
with essential cations, most notably calcium,
zinc, and iron

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• Pharmacokinetics.
- Inhalation of lead fume or other fine, soluble
particulate results in rapid and extensive
pulmonary absorption by ingestion,

- After absorption, lead is distributed via the

blood to multiple tissues, including
transplacental transport to the fetus, and CNS
transport across the blood-brain barrier.

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Toxic dose
• Dermal absorption is minimal with inorganic
lead but may be substantial with organic lead
compounds, which may also cause skin
irritation.
• Ingestion. Depend on solubility.
Gastrointestinal lead absorption is increased by
iron deficiency and low dietary calcium.
- Acute symptomatic intoxication is rare after a
single exposure

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• Inhalation. Unprotected exposure to the
massive airborne lead levels (> 2500 mcg/m3)
(welding, or torch cutting metal surfaces
coated with lead-based paint) has resulted in
symptomatic lead intoxication from within a
day to a few weeks.

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Clinical presentation. The multisystem toxicity
A. Acute ingestion????? of very large amounts
of lead (gram quantities) may cause
abdominal pain, anemia, toxic hepatitis, and
encephalopathy.
B. Subacute or chronic exposure (plumbism,
saturnism) is more common than acute
poisoning.

1. Gastrointestinal effects include crampy

abdominal pain (lead colic, painter's colic),
nausea, constipation 62
2. Central nervous system manifestations
- Impaired concentration, headache, diminished
visual-motor coordination, and tremor
- In infants and children may lead to decreased
intelligence and impaired neurobehavioral
development
3. Peripheral motor neuropathy, can cause
severe extensor muscle weakness ("wrist
drop").

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4. Hematologic effects include normochromic or
microcytic anemia, Hemolysis may occur after
acute or subacute high-dose exposure.
5. Nephrotoxic
6. Adverse reproductive outcomes may include
diminished sperm production, increased rate of
miscarriage, preterm delivery, decreased
gestational age, low birth weight, and impaired
neurologic development.

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Diagnosis
Specific levels. The whole-blood lead level is
the most useful indicator of lead exposure
- Blood lead levels are less than 5 mcg/dL in
populations without occupational or specific
environmental exposure.
1. Levels between 5 -25 mcg/dL have been
associated with subclinical decreases in
intelligence and impaired neurobehavioral
development

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2. Blood lead levels of 25-60 mcg/dL may be
associated with headache, irritability, difficulty
concentrating, slowed reaction time, and other
neuropsychiatric effects. Anemia may occur
3. Blood levels of 60-80 mcg/dL may be associated
with GI symptoms and subclinical renal effects.
4. With blood levels in excess of 80 mcg/dL,
serious overt intoxication may occur, including
abdominal pain (lead colic) and nephropathy.
A blue line (Burton line) along the gum, is another
indication of chronic lead poisoning
5. Encephalopathy and neuropathy usually are
associated with levels over 100 mcg/dL. 66
• Treatment
A. Emergency and supportive measures
B. Specific drugs and antidotes. Treatment with
chelating agents decreases blood lead
concentrations and increases urinary lead
excretion.
1. Encephalopathy. Administer intravenous
calcium EDTA [Calcium Disodium EDTA,
Calcium Disodium Edetate]. Some clinicians
initiate treatment with a single dose of BAL
(British anti-Lewisite), followed 4 hours later
by concomitant administration of calcium
EDTA and BAL. 67
2. Symptomatic without encephalopathy.
- Administer oral succimer (Dimercaptosuccinic
acid, DMSA).
- Parenteral calcium EDTA is preferred as initial
treatment if the patient has severe GI toxicity (eg,
lead colic) or if the blood lead concentration is
extremely elevated (eg, > 150 mcg/dL).

- Unithiol (2,3-Dimercapto-1-propanesulfonic
acid[DMPS]) may be considered as an alternative
to DMSA.
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3. Asymptomatic children with elevated blood
lead levels. The Centers for Disease Control
and Prevention (CDC) recommend treatment
of children with levels of 45 mcg/dL or higher.
Use oral succimer (DMSA).
4. Asymptomatic adults. The usual treatment is
removal from exposure and observation.
Consider oral succimer (DMSA] for patients with
markedly elevated levels (eg, > 80-100
mcg/dL).

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 Mercury
Mechanism of toxicity. Mercury reacts with sulfhydryl
(SH) groups, resulting in enzyme inhibition and
pathologic alteration of cellular membranes.

A. Elemental mercury and methylmercury are

particularly toxic to the CNS. Metallic mercury
vapor is also a pulmonary irritant. Methylmercury
is associated with neurodevelopmental disorders.

B. Inorganic mercuric salts are corrosive to the skin,

eyes, and GI tract and are nephrotoxic-mercuric
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chloride
Toxic dose.
• Elemental (metallic) mercury is a volatile
liquid at room temperature. Hgo vapor is
absorbed rapidly by the lungs and distributed
to the CNS.

• Liquid metallic mercury is poorly absorbed

from the GI tract

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• Organic mercury
• Mercury-containing antiseptics such as
mercurochrome have limited skin penetration;
Oral absorption is significant
• Methylmercury is well absorbed after inhalation,
ingestion, and probably dermal exposure. (fish and
shellfish ): Minamata disease
• Dimethylmercury, a highly toxic synthetic liquid
used in analytic chemistry, is well absorbed
through the skin, and cutaneous exposure to only a
few drops has resulted in a delayed but fatal
encephalopathy.
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• Thimerosal (ethylmercury thiosalicylate), a
preservative that undergoes metabolism to
ethylmercury, was removed from most childhood
vaccines in the United States on a precautionary
basis.

• No causal link between thimerosal-containing

vaccines and neurodevelopmental disorders has
been established.

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Diagnosis depends on integration of
characteristic findings with a history of known
or potential exposure and the presence of
elevated mercury blood levels or urinary
excretion.
A normal mercury level is less than 10 µg/L

74
• Treatment
• Emergency and supportive measures
• Specific drugs and antidotes
1. In acute or chronic poisoning, oral succimer
(DMSA)or oral unithiol (DMPS) may enhance
urinary Hg excretion
2. Organic mercury. In methylmercury intoxication,
limited data suggest that oral succimer (DMSA)
and oral N-acetylcysteine) may be effective in
decreasing Hg levels in tissues, including the
brain
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Decontamination
Inhalation
a. Immediately remove the victim from exposure
b. Even minute indoor spills (eg, 1 mL) of metallic mercury
can result in hazardous chronic airborne levels.

- Cover the spill with powdered sulfur and carefully clean

up and discard all residue and contaminated carpeting
- Do not use a home vacuum cleaner, as this may disperse
the liquid mercury, increasing its airborne concentration.
- For large spills, professional cleanup with self-contained
vacuum systems is recommended.
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Household Intoxication:
• Corrosives
• Hydrocarbons (kerosene)

77
 Caustic and Corrosive Agents
• They include mineral (Hydrochloric acid) and
organic acids (e. g. Acetic acid, Lactic acid, Citric
acid, carbolic acid), alkalis (Sodium hydroxide -
often called "caustic soda“), oxidizing agents
• some hydrocarbons, and agents that cause
exothermic reactions
• Button batteries are small disk-shaped
batteries used in watches, calculators, and
cameras. They contain caustic metal salts such
as mercuric chloride that may cause corrosive
injury. 78
Toxic dose.
• There is no specific toxic dose or level because
the concentration of corrosive solutions and
the potency of caustic effects vary widely.
• The concentration or the pH of the solution
may indicate the potential for serious injury.

79
Clinical presentation
A. Inhalation of corrosive gases (eg, chlorine)
may cause upper respiratory tract injury, with
hoarseness, wheezing, and noncardiogenic
pulmonary edema.
B. Eye or skin exposure to corrosive agents
usually results in immediate pain and
redness, followed by blistering. Lacrimation is
common. Serious full-thickness burns and
blindness can occur.

80
Ingestion
• Cause oral pain, dysphagia, and pain in the
throat, chest, or abdomen.
• Esophageal or gastric perforation may occur,
manifested by severe chest or abdominal pain,
signs of peritoneal irritation, or pancreatitis.

• Hematemesis and shock may occur.

• Scarring of the esophagus or stomach may
result in permanent stricture formation and
chronic dysphagia.
81
Diagnosis is based on a history of exposure to a
corrosive agent and characteristic findings.
Endoscopy.
- Esophageal or gastric injury is unlikely after
ingestion if the patient is completely
asymptomatic. For this reason, many
authorities recommend endoscopy for all
patients regardless of symptoms.
- X-rays of the chest and abdomen usually reveal
impacted button batteries. X-rays may also
demonstrate air in abdomen from esophageal
perforation.
82
Treatment
A. Emergency and supportive measures
1. Inhalation
2. Ingestion
a. Immediately give water or milk to drink.
b. If esophageal or gastric perforation is
suspected, obtain immediate surgical or
endoscopic consultation
B. Specific drugs and antidotes. For most
agents, there is no specific antidote.

83
3. Decontamination
a. Prehospital. Immediately give water or milk to
drink. Do not induce vomiting or give pH-
neutralizing solutions (eg, dilute vinegar or
bicarbonate).
b. Hospital. Gastric lavage to remove the corrosive
material is controversial
4. Enhanced elimination. There is no known role
for any of these procedures.

84
 Hydrocarbons
• Mechanism of toxicity. direct injury to the lung
after pulmonary aspiration or systemic
intoxication after ingestion, inhalation, or skin
absorption
A. Pulmonary aspiration.
- Chemical pneumonitis is caused by direct tissue
damage and disruption of surfactant.

- Aspiration risk is greatest for hydrocarbons with

low viscosity and low surface tension (eg,
gasoline, turpentine). 85
B. Ingestion
1. Aliphatic hydrocarbons and simple petroleum
distillates (e.g. kerosene, furniture polish, and
gasoline) are poorly absorbed from the GI tract
and do not pose a significant risk of systemic
toxicity after ingestion as long as they are not
aspirated.
2. Camphor (Eugenol, safrol, camphor), phenol,
halogenated or aromatic compounds are
capable of causing serious systemic toxicity, such
as coma, seizures, and cardiac arrhythmias
86
3. Inhalation of hydrocarbon vapors in an
enclosed space may cause intoxication as a
result of systemic absorption or by displacing
oxygen from the atmosphere.

87
Toxic dose.
The toxic dose is variable, depending on the
agent involved and whether it is aspirated,
ingested, injected, or inhaled.
A. Pulmonary aspiration of as little as a few
milliliters may produce chemical pneumonitis.
B. Ingestion of as little as 10–20 mL of some
systemic toxins, such as camphor and carbon
tetrachloride, may cause serious or fatal
poisoning

88
Clinical presentation?????

Diagnosis
A. Aspiration pneumonitis.
- Diagnosis is based on a history of exposure and
the presence of respiratory symptoms such as
coughing, tachypnea, and wheezing.
- If these symptoms are not present within 6
hours of exposure, it is very unlikely that
chemical pneumonitis will occur.

89
B. Systemic intoxication. Diagnosis is based on a
history of ingestion or inhalation,
accompanied by the appropriate systemic
clinical manifestations.
C. Specific levels. Specific levels are generally
not available or useful.

90
Treatment
A. Emergency and supportive measures
• Pulmonary aspiration. Patients who remain
completely asymptomatic after 4–6 hours of
observation may be discharged. In contrast, if
the patient is coughing on arrival, aspiration
probably has occurred.
a. Administer supplemental oxygen and treat
bronchospasm and hypoxia if they occur.
b. Do not use steroids or prophylactic antibiotics.

91
B. Specific drugs and antidotes
A. There is no specific antidote for aspiration
pneumonitis; corticosteroids are of no
proven value.
B. Specific drugs or antidotes may be available
for systemic toxicity of some hydrocarbons
(eg, acetylcysteine for carbon tetrachloride
and methylene blue for methemoglobin
formers) or their solutes (eg, chelation
therapy for leaded gasoline and antidotes for
pesticides, etc).
92
• Treatment
A. Administer intravenous calcium EDTA [Calcium
Disodium EDTA, Calcium Disodium Edetate].
B. Some clinicians initiate treatment with a single
dose of BAL (British anti-Lewisite),
- Administer oral succimer (Dimercaptosuccinic
acid, DMSA).
- Unithiol (2,3-Dimercapto-1-propanesulfonic
acid[DMPS]) may be considered as an
alternative to DMSA.

93
C. Decontamination
Ingestion
- For agents with no known systemic toxicity, gut
decontamination == risk of aspiration.
- For systemic toxins, consider aspiration of the
liquid via nasogastric tube and administration of
activated charcoal.
- Take precautions to prevent pulmonary
aspiration if the patient is obtunded.
D. Enhanced elimination. There is no known role
for any of these procedures.
94
Animal bites

95
Scorpions

Leiurus spp. Androctonus spp.

96
Mechanism of toxicity.
• The venom of scorpion contains numerous digestive
enzymes (eg, hyaluronidase and phospholipase) and
several neurotoxins.
• These neurotoxins can cause alterations in sodium
channel flow, resulting in excessive stimulation at
neuromuscular junctions and the autonomic
nervous system.

Toxic dose.
Variable amounts of venom
97
Clinical presentation
A. Common scorpion stings. Most stings result only in local,
immediate burning pain. Some local tissue inflammation
.Symptoms usually resolve within several hours.
B. Dangerous scorpion stings. In some victims, especially
children under age 10 years, systemic symptoms can
occur after stings, including weakness, restlessness,
diaphoresis, diplopia, nystagmus, muscle fasciculations,
salivation, slurred speech, hypertension, tachycardia,
and, rarely, convulsions, paralysis, and respiratory arrest.
Envenomations by Androctonus, and Leiurus species have
caused pulmonary edema, cardiovascular collapse, and
death.
98
Diagnosis. Either the patient saw the scorpion
or the clinician must recognize the symptoms.

A. Specific levels. Body fluid toxin levels are not

available.
B. No other useful laboratory studies are
needed for minor envenomations. For severe
envenomations, obtain CBC, electrolytes,
glucose, BUN, creatinine, coagulation profile,
and arterial blood gases.
99
Treatment. The majority of scorpion stings can
be managed with symptomatic home care
consisting of oral analgesics and cool
compresses or intermittent ice packs.
A. Emergency and supportive measures
. Do not apply a tourniquet.
. Do not over treat with excessive sedation.
. Clean the wound and provide tetanus
prophylaxis.
. Do not immerse the injured extremity in ice or
perform local incision or suction.
100
B. Specific drugs and antidotes.
• An antivenom was available at one time in
Arizona.
• Specific antivenoms against may be available
in other parts of the world but are not
approved in the United States.

101
Snakebite

102
• Mechanism of toxicity. Snake venoms are
complex mixtures of 50 or more components
produce local "digestive" or cytotoxic effects
on tissues as well as hemotoxic, neurotoxic,
and other systemic effects (e.g. cardiotoxin).

103
Clinical presentation

1. Local effects. Within minutes of

envenomation, burning pain begins.
Progressive swelling, erythema, ecchymosis,
and hemorrhagic blebs may develop over the
next several hours.

104
• Systemic effects may include nausea and
vomiting, weakness, muscle fasciculations,
diaphoresis, thrombocytopenia, and
coagulopathy. Circulating vasodilatory
compounds may contribute to hypotension.
Pulmonary edema and cardiovascular collapse
have been reported.

105
Treatment
A. Emergency and supportive measures.
Regardless of the species, prepare for both local
and systemic manifestations. Monitor patients
closely for at 12–24 hours after snake bite.
1. Local effects
a. Monitor local swelling, the presence and extent of local
ecchymosis, and assessment of circulation.
b. When indicated, obtain consultation with an experienced surgeon
for management of serious wound complications. with tissue
compartment pressure monitoring.
c. Provide tetanus prophylaxis if needed.
d. Administer broad-spectrum antibiotics only if there are signs of
infection. 106
2. Systemic effects
a. Monitor the victim for respiratory
muscle weakness.
b. Treat bleeding complications with fresh-
frozen plasma
c. Treat hypotension with intravenous
crystalloid fluids
d. Treat rhabdomyolysis with fluids and
sodium bicarbonate.

107
B. Specific drugs and antidotes.
• The fixed-dose regimen of 50 ml* V. Palaestinae
antivenom is efficacious for the treatment of
systemic and progressive local manifestations caused
by V. Palaestinae. For most patients, a 1-2 h IV
infusion of 50 mL antivenin preceded by a very slow
test dose over 10 min is sufficient. However, a 24 h
observation period is advised, during which systemic
signs, progression of local signs, complete blood
counts and coagulation profiles are monitored.
Additional antivenin (30 – 50 ml) can be given if
necessary, but this is not common .

• *Suggested 5 ampoules if the volume of each one is108

• Decontamination

109
110
Poisonous plants
• Serious toxicity or death from plant ingestion
is usually a result of intentional abuse (eg,
jimson weed (Datura stramonium)), misuse
(eg, various teas steeped from plants), or
suicide attempts (eg, oleander).

111
Mechanism of toxicity. Plants can be categorized by their
potential toxicity
A. Group 1 plants contain systemically active poisons that may cause
serious poisoning.
B. Group 2a plants contain insoluble calcium oxalate crystals that may
cause burning pain and swelling of mucous membranes. Many
houseplants are found in this category.
C. Group 2b plants contain soluble oxalate salts (sodium or potassium)
that can produce acute hypocalcemia, renal injury, and other organ
damage secondary to precipitation of calcium oxalate crystals in
various organs. Mucous membrane irritation is rare, allowing
patients to ingest sufficient quantities to cause systemic toxicity.
Gastroenteritis also may occur.
D. Group 3 plants contain various toxins that generally produce mild to
moderate GI irritation after ingestion or dermatitis after skin
contact. 112
Toxic dose. The amount of toxin ingested is
usually unknown.
Clinical presentation depends on the active
toxic agent

A. Group 1. In most cases, vomiting, abdominal

pain, and diarrhea occur within 60–90
minutes of a significant ingestion, but systemic
symptoms may be delayed a few hours (eg,
Bitter almonds; cyanogenic glycosides;
Oleander; cardiac glycosides, Atropa
belladonna ). 113
B. Group 2a. Insoluble calcium oxalate crystals
cause immediate oral burning, pain, and stinging
upon contact with mucous membranes. Swelling
of the lips, tongue, and pharynx may occur.
Symptoms usually resolve within a few hours.
• Arum palaestinum or Dracunculus vulgaris

114
C. Group 2b. Soluble oxalates may be absorbed
into the circulation, where they precipitate
with calcium. Acute hypocalcemia and
multiple-organ injury, including renal tubular
necrosis, may result
Garden sorrel

115
D. Group 3. Skin or mucous membrane irritation
may occur, although it is less severe than with
group 2 plants. Vomiting and diarrhea are
common but are usually mild to moderate and
are self-limited.
Cascara Chili pepper

116
Treatment
Specific drugs and antidotes. There are few effective antidotes.
Decontamination
1. Group 1 and group 2b plants. Administer activated charcoal
orally if conditions are appropriate.
2. Gastric lavage is not necessary after small to moderate
ingestions if activated charcoal can be given promptly.
3. Group 2a and group 3 plants
a. Wash the affected areas with soap and water and give
sips of water to drink.
b. Administer ice cream, juice bars, pudding, or cold milk to
soothe irritated oral mucous membranes after exposure to
insoluble oxalate plants.
c. Do not induce vomiting because of potential aggravation
117
or irritant effects. Activated charcoal is not necessary.