Toxic Gases

Oxygen; 21%

Trace gases; 1%

Nitrogen; 78%

Severity = f (dose, toxicity)

Dose = Concentration (%/ppm) x

duration of
exposure

Classification
Local poisons (Irritants)
Injury at the point of contact

Systemic poisons
Injuries following absorption

Some poisons can behave in both

ways

What you need to know

Color, odor, characteristic features
Sources, circumstances and manner
of poisoning
Mechanism of toxicity
Fatal Dose
Clinical Features
Diagnosis
Treatment

What are the irritant gases?

Ammonia
Chlorine
Sulfur dioxide
Methyl isocyanate
War gases

Local/Irritant Poisons
Skin: dermatitis
Erythema, macules, papules, vesicles,
bullae

Eye: conjunctivitis, keratitis

Red eye, lacrimation

Napalm death

Acute Alveolar Injury

Mild: Leaky capillaries
Alveolitis
Pulmonary edema

Severe: Dead capillaries

Diffuse alveolar damage
Necrotizing alveolitis
Alveolar rupture and hemorrhage

Treatment for irritant gas exposure is

supportive
Airway Breathing Circulation
Limit further exposure

Delayed effects of irritant gas

exposure
Eye: Vision loss
Airway: bronchiolar fibrosis
Alveoli: alveolar interstitial fibrosis

Chlorin
e
Color

Greenish
yellow

Smell
Fatal
dose
Source
Treatme
nt

Ammoni Sulfur
a
dioxide

MIC

Colorless
Pungent

500ppm

5000ppm

500ppm

20ppm

Industrial plants and laboratories

Supportive

Methyl isocyanate
Bhopal Gas Tragedy
Store as a liquid in stainless steel or
glass containers
Keep containers cool, avoid
exothermic reactions

Combat gases
Mustard gas: WWI, WWII
Tear gas: Riot control
Phosgene: Carbonyl chloride
Colorless, musty-hay odor
Fatal dose is 300ppm
WWI

Gases with systemic toxicity

Carbon Monoxide
Hydrogen cyanide
Hydrogen sulfide
Anesthetic gases

Carbon Monoxide
Colorless, odorless
Incomplete combustion
Cigarettes
Fires
Vehicle exhausts

What makes CO so toxic?

Affinity for Hb and disruption of
oxygen delivery
Peripheral vasodilation leading to
shock
Inhibition of Complex IV of the ETC

O2 content = (O2 binding capacity X %Saturation) +

dissolved O2

Functionally, CO toxicity is similar to

severe anemia

Cherry red discoloration of skin is classic but

rare
Gorman DF,Clayton D,Gilligan JE,Webb RKA longitudinal study of 100
consecutive admissions for carbon monoxide poisoning to the Royal Adelaide
Hospital.Anaesth Intensive Care1992;20:311-316

CO toxicity causes necrosis of

the globus pallidus and
substantia nigra: Parkinsonism
in survivors

Death at blood CO-Hb concentration

>80%
As a function of inspired air:
0.05% in 4 hours
0.1% in 2 hours
0.4% in 1 hour
10% in minutes

Treatment
Terminate exposure
100% oxygen
Hyperbaric oxygen (HBO) in severe
cases
Monitor for cerebral edema
Monitor cardiac function

Hydrogen Cyanide
Colorless
Bitter almond odor
Sources
Vapors from prussic acid (liquid HCN)
Acidification of metallic cyanide salts
Burning of plastic, silk or wool
Cigarette smoke

Mechanism of toxicity
Cyanide inhibits cytochrome oxidase
in the electron transport chain
No ATP production
Anaerobic metabolism
Lactic acidosis

Diagnosing cyanide toxicity

Hypoxia
Brick-red coloration of the skin
Labs
Serum cyanide level
Elevated lactates
High AG metabolic acidosis
Elevated venous oxygen saturation

To treat HCN poisoning you need to

prevent it from reacting with
cytochrome oxidase in the
mitochondrial electron transport chain

How do you do that?

Give the patient a NITRITE
Amyl nitrite and/or sodium nitrite
Oxidizes Hb to methemoglobin

How does that help?

Cyanide binds to MetHb with a
greater affinity than it does to
cytochrome oxidase
What you get is
cyanomethemoglobin instead of a
cyanide-cytochrome oxidase complex

What do you do with the cyano-MetHb then ?

Give the patient a thiosulfate

Sodium thiosulfate will convert
cyanide to thiocyante
Thiocyanate gets excreted in the
urine

What else can you do?

Hydroxycobalamine: binds to CN- and
forms cyanocobalamin
EDTA chelates CN Gastric Lavage if a salt has been
ingested
100% oxygen

Treatment of HCN poisoning:

Summary
Amyl nitrite to generate to Met-Hb,
which scavenges the CN as
cyanomet-Hb then add sodium
thiosulfate to form thiocyanate

Hydrogen Sulfide
Rotten egg odor
Sources
Natural: Sewage, Manure, Caves,
Volcanoes
Laboratory/Industrial

Biological effects similar to HCN

Treat with nitrites to generate MetHb,
which spontaneously forms sulf-MetHb

Anesthetic gases
Nitrous oxide
Halothane
Halogenated ethers

Volatile Substance Abuse

Toluene (glue-sniffing), other
aromatic hydocarbons
Huffing = inhale vapors from a piece
of cloth
Bagging = inhale vapors from a bag
Young drug-nave males
Hallucinations followed by amnesia
Death from arrythmias, hypoxia,
plastic bag asphyxiation, aspiration