Toxic Gases

TOXIC GASES
Classification
1-simple asphyxiant:
Nonpoisonous inert gases that displace oxygrn from the ispired air
causeing hypoxia.
eg:
• co2
• methan
• helium
• nitrogen
• propane.

2-Chemical asphyxiant:
Act by alteration of oxygen carring capacity and biochemical
changes of respiratory enzymes eg:
• Co
• hydrogen sulfiedeand hydrogen cyanid.

3-Irritant gases:
-gases with immediat toxicity
Ammonia, chlorine,and sulphur dioxid.
-gases with delayed toxicity:
Phosphagenand nitrogen dioxid.

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Carbon monoxide

Carbon monoxide, or CO, is an odorless,

colorless gas. It is a product of combustion of
organic matter under conditions of restricted
oxygen supply, which prevents complete
oxidation to carbon dioxide (CO2)

Where is CO found?
CO is found in combustion fumes, such as those produced by cars
and trucks, small gasoline engines, stoves, lanterns, burning charcoal
and wood, and gas ranges and heating systems. CO from these
sources can build up in enclosed or semi-enclosed spaces. People and
animals in these spaces can be poisoned by breathing it.

What is carbon monoxide

poisoning?
It occurs when enough
carbon monoxide is inhaled for
it to replace oxygen in the
blood. The more carbon
monoxide is present in the
blood, the less organs and
tissue are able to function
normally. Poisoning mainly
affects the cardiovascular and
nervous systems.

Toxic dose: a level higher than 50 ppm (parts per million) with
continuous exposure over an eight hour period

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Incidence
extrapolations for USA for Carbon monoxide poisoning:113,333
per year, 9,444 per month, 2,179 per week, 310 per day, 12 per hour,
0 per minute, 0 per second. [Source statistic for calculation: "25,000
annual cases of home exposure in the UK

Egypt: Extrapolated Incidence is 31,715 , from 76,117,4212

Population Estimated Used

Circumstances of poisoning.
Accidental: automobile exhaust,
faulty domestic appliances and
policeman on traffic duty.

Suicidal: by breathing the exhaust

fumes in closed grage.

Homecidal: it is rare may be

infanticide method.

N.B/ The severity of carbon monoxide poisoning depends on a

number of factors: The concentration of carbon monoxide in the
air (measured in parts per million [ppm]), length of exposure
(measured in hours or minutes), and individual state of health and
susceptibility to the effects of the gas

Who is most vulnerable to carbon monoxide poisoning?

Carbon monoxide poisoning can occur more quickly in certain people,
such as:

 Pregnant women and their fetuses

 Newborns and children (because their breathing is quicker and
shallower)
 Seniors (because their breathing is quicker and shallower)
 People with pulmonary, respiratory or cardiovascular problems

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 People suffering from anemia

 Smokers
 People engaged in intense physical activity in a poorly ventilated
area contaminated with carbon monoxide
 People living at altitude

Toxicokinetics

-inhaled by nose.

-absorbed readily from lung.

-rapidly bounded to
hemoglobin

-elemination mainly through

respiratory systm

-plasma half life 4-5 hours.

Pathophysiology

(chemical asphyxiant) leading

to :

i. Hypoxia and cellular

asphyxia.
ii. Ischemia.
iii. Reperfusion
injury.

This is due to its effects on the following:

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Hemoglobin:

CO combines preferentially with hemoglobin to produce COHbCO

binds reversibly to hemoglobin with an affinity 200- 230 times that of
oxygen. Consequently, relatively minute concentrations of the gas in
the environment can result in toxic concentrations in human blood.

COHbCO decreases the oxygen-

carrying capacity of the blood and
inhibits the transport, delivery, and
utilization of oxygen by the body

Hemoglobin is a tetramer with four

oxygen binding sites. The binding of
carbon monoxide at one of these sites
increases the oxygen affinity of the
remaining three sites, which causes
the hemoglobin molecule to retain
oxygen that would otherwise be
delivered to the tissue. This situation is described as carbon monoxide
shifting the oxygen dissociation curve to the left. Because of the
increased affinity between hemoglobin and oxygen during carbon
monoxide poisoning, the blood oxygen content is increased. But
because all the oxygen stays in the hemoglobin, none is delivered to
the tissues cause cherry red appearance of victim.

Myoglobin

Carbon monoxide also

binds to the hemeprotein
myoglobin. It has a high affinity
for myoglobin, about 60 times
greater than that of oxygen.
Carbon monoxide bound to
myoglobin may impair its ability
to utilize oxygen. This causes
reduced cardiac output and
hypotension, which may result in
brain ischemia. A delayed return
of symptoms have been

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reported. This results following a recurrence of increased

carboxyhemoglobin levels; this effect may be due to a late release of
carbon monoxide from myoglobin, which subsequently binds to
hemoglobin.

Cytochrome oxidase

Another mechanism involves effects on the mitochondrial

respiratory enzyme chain that is responsible for effective tissue
utilization of oxygen. Carbon monoxide binds to cytochrome oxidase
with less affinity than oxygen, so it is possible that it requires
significant intracellular hypoxia before binding. This binding interferes
with aerobic metabolism and efficient adenosine triphosphate
synthesis. Cells respond by switching to anaerobic metabolism, causing
anoxia, lactic acidosis, and eventual cell death. The rate of dissociation
between carbon monoxide and cytochrome oxidase is slow, causing a
relatively prolonged impairment of oxidative metabolism.

Central nervous system effects

Damage Mechanism: Oxidative Destruction. (delayed action)

The injury potential of carbon monoxide also arises from oxidative

damage, and associated complex biochemical processes that can
directly injure perivascular, neuronal, cardiovascular, and other
structures and organs. Understanding this mechanism of injury begins
with a discussion of the concept of oxidative destruction.

1. Initial Platelet-Neutrophil Reaction.

Carbon monoxide---an unnatural

stranger in the bloodstream---
triggers the platelets to
discharge nitric oxide (an
oxidant) into the bloodstream.
Superoxide is released from
neutrophils---in part as a
reaction to nitric oxide oxidants
and in part as a direct reaction
to the presence of carbon
monoxide in the blood stream.
The two compounds (nitric oxide
and superoxide) interact, producing reactive nitric oxide-associated
species molecules (ROS molecules), including peroxynitrite, in their

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biochemical clash. Peroxynitrite is the most oxidizing substance to be

found in mammalian systems.

An unfortunate characteristic of this species of molecule (reactive nitric

oxides, including peroxynitrites which in turn can produce nitrotyrosine)
is that it causes platelets and neutrophils to adhere or aggregate (a
process called heterotypic aggregation) rather than keeping their safe
Hatfield-McCoy distance. Nitrotyrosine is a culprit in this "stickiness" or
adherence. It gets produced from the series of interactions kicked off
by carbon monoxide---initiating the discharge of nitric oxide from
platelets, the triggering of superoxide release into the bloodstream
from the neutrophils, then a reaction between nitric oxide and
superoxide to generate peroxynitrite, and finally the emergence of
nitrotyrosine.

2. Platelet-Neutrophil Linkage. Once the platelets and neutrophils are

physically linked, two things happen:

• Cascade of ROS Molecules. The neutrophils experience an

oxidative burst. While a neutrophil will safely package or contain
oxygen radicals (oxidants) until they are needed to attack an
organism (such as a bacteria when we are sick), the oxidative
burst releases them prematurely and they attack healthy cells
pathologically. Thus, additional reactive nitric oxide-associated
species molecules are formed. So the production of even larger
numbers of ROS molecules (which includes the reactive nitric
oxide species) within the bloodstream is enhanced---a cascading
effect.
• Vascular Damage and Destruction of Lipids and Myelin
Sheath. The physical association of platelets and neutrophils
precipitates neutrophil degranulation---releasing myeloperoxidase
(MPO), an enzyme that resides in the granules. Granules are
typically located within the cell's cytoplasm and those tiny
structures will safely confine products, including myeloperoxidase,
that would be toxic if allowed to escape. With "degranulation," the
granules move to the neutrophil's cell surface, a portal opens to
release the products within the granules, and the cell membrane
then closes---but only after the MPO has escaped the confines of
the granules and cell structure. Once poured into the bloodstream,
three destructive biochemical processes are initiated by the
myeloperoxidase (MPO):
o Accelerated MPO Release. Some of the released MPO
adheres to the outer surface of the neutrophils, triggering
additional neutrophil activation, additional degranualtion, and
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additional release of more MPO from the neutrophil's cell

membrane. It is an "outside-in" neutrophil activation.

Lipid Destruction and Vascular Damage. The MPO molecules

deposit along the vascular lining of the blood vessels (the
endothelium)---the interior lumen surface---and interact with
nitrotyrosine, the culprit in causing the platelets and
neutrophils to stick together. In a series of biochemical
reactions, the interaction results in the destruction of the
constituents in cells used for fuel, the lipids, and thus the
destruction of the cells themselves within the endothelium of
the blood vessels, most particularly the blood vessels of the
brain but also in the lungs and the cardiovascular system. It
is a process known as lipid peroxidation---where the
perivascular cells are damaged by oxidative destruction. The
damage to lipids is not limited to their fuel function, however.
A lipid is a fatty structure and---in addition to be used as a
source for cellular energy---is an important constituent for
membranes and cell structure and can be used as a fuel, a
barrier, and an insulator. The myelin sheath surrounding
axons, for instance, is composed of lipids. Thus, the oxidative
destruction of lipids has consequences beyond the
destruction of a cell's fuel source. The MPO-nitrotyrosine
interaction also activates the endothelial cells---and their
adherent or attraction characteristics---which causes the
neutrophils themselves to adhere to the perivascular lining.
When the neutrophils adhere, they are more likely to release
damaging substances such as myeloperoxidase, cytokines,
thromboxanes, and oxygen radicals.

The damage to the endothelium---whether from lipid

peroxidation or from the adherence of neutrophils---kicks off
yet another destructive cycle. Platelets are designed to
respond to damage because of their clotting properties.
Platelets, then, will adhere to the damaged endothelium and
activate, releasing nitric oxide, and triggering (through the
processes described earlier with the initial platelet-neutrophil
interaction) the production of peroxynitrite, the most
oxidizing substance found in mammalian systems. The
platelet adherence---in activating the clotting process---can
also cause fibrin to be deposited, which can disrupt local
blood and nutrient flow.

Destruction of Myelin Sheath.

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The release of MPO has resulted,

then, in the destruction of lipids and
the cells they are to fuel through lipid
peroxidation---as well as lipids that
are the constituents of membranes.
But that process also has a second---
and entirely separate---level of
damage because byproducts are
generated in the degradation of the
lipids that have their own dangerous
properties: lipid peroxides. They attack the myelin sheath, the
protective and insulating sheath that surrounds the axon of
nerve cells. That sheath's primary structure is composed of
myelin basic protein (MBP). Through peroxidation, the
byproducts attack the MBP (and, thus, the integrity of the
protective sheathing for the nerves), damaging it in two ways---
damaging its three dimensional structure and altering its charge
pattern. An inflammatory process---also called an
immunological response---is initiated: the alteration gets
"perceived" by inflammatory cells as a foreign body and there is
an influx of the inflammatory cells to attack the MBP. This
damage is critical because the axons are the "wires" or
pathways over which the nucleus of a nerve "fires" its signal.
Destruction of the myelin sheath around the axon---and there
are billions of them in the brain alone---disrupts the
transmission capacity of nerve cells and can cause profound
neurological damage. The inflammatory process also causes the
release of yet more by-products that damage adjacent tissue.

The biochemical interactions resulting from carbon monoxide

poisoning, then, can be profound. Separate and apart from the hypoxic
damage, carbon monoxide is a neurotoxin, triggering biochemical
processes that will kill cells, that accelerates apotosis (programmed cell
death), and that damages significant neuronal structures, including the
protective sheathing around axons. It is believed that the presence of
carbon monoxide can also cause iron release in molecules. Iron is
highly reactive and can trigger its own inflammatory processes. The
different biochemical processes, moreover, do not reach a quick
conclusion. They occur over a period of time, thereby accounting for
damage that can be developing over a period of weeks or more after
the exposure.

Co poisoning causes delayed reversible demyelinization of white matter

in the central nervous system, which can lead to edema and necrosis
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within the brain. This brain damage occurs mainly during the recovery
period. This may result in cognitive defects, especially affecting
memory and learning, and movement disorders. These disorders are
typically related to damage to the cerebral white matter and basal
ganglia. Hallmark pathological changes following poisoning is bilateral
necrosis of the white matter, globus pallidus, cerebellum, hippocampus
and the cerebral cortex.

Pregnancy

Carbon monoxide poisoning in pregnant women may cause severe

adverse fetal effects. Poisoning causes fetal tissue hypoxia by
decreasing the release of maternal oxygen to the fetus. Carbon
monoxide also crosses the placenta and combines with fetal
hemoglobin, causing more direct fetal tissue hypoxia. Additionally, fetal
hemoglobin has a 10 to 15% higher affinity for carbon monoxide than
adult hemoglobin, causing more severe poisoning in the fetus than in
the adult. Elimination of carbon monoxide is slower in the fetus, leading
to an accumulation of the toxic chemical. The level of fetal morbidity
and mortality in acute carbon monoxide poisoning is significant, so
despite mild maternal poisoning or following maternal recovery, severe
fetal poisoning or death may still occur

Clinical picture:
The severity of the poisoning depends on:
• How much carbon monoxide is actually present in the
environment.
• The duration you are exposed to carbon monoxide.
• The age of the individual concerned - elderly, children and
the fetus are all at greater risk.
• The general state of health.
• The extent of physical activity - effects are increased with
higher activity levels.

 Acute poisoning:

o Symptoms:
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 Mild to moderate cases( 25% -

30%COHB )
o Malaise, flu-like symptoms,
fatigue
o Dyspnea
o Chest pain, palpitations
o Lethargy
o Confusion
o Depression
o Hallucination, confabulation
o Agitation
o Nausea, vomiting
o Abdominal pain
o Headache, drowsiness
o Dizziness, weakness
o Low levels of carbon monoxide poisoning can be
confused with flu symptoms, food poisoning .However, unlike
flu, CO poisoning does not cause a high temperature.

 Severe >50%COHb

o Visual disturbance
o Syncope
o seizures
o Memory and gait
disturbances
o Bizarre neurologic
symptoms
o coma
o Mild fever

 COHb Levels and Symptomatology

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Asymptomatic or may have

10%
headaches
Dizzyness, nausea, and
20%
syncope
30% Visual disturbances
40% Confusion and syncope
50% Seizures and coma
Cardiopulmonary
60%
dysfunction and death
More than
death
70-80%%

Signs
Physical examination is of limited value. Inhalation injury or burns
should always alert the clinician to the possibility of CO exposure

.In mild cases:

• Tachycardia
• Tachypnia

In severe cases

• Vital signs
o Tachycardia
o Hypertension or hypotension
o Hyperthermia
o Marked tachypnea (rare; severe intoxication often
associated with mild or no tachypnea)
• Skin
o Classic cherry red skin
 (ie, "When you're cherry red, you're dead")
 Pallor is present early more often .
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• Ophthalmologic
o Flame-shaped retinal hemorrhages
o Bright red retinal veins (a sensitive early sign)
o Papilledema
• Metabolic acidosis leading to rhabdomyolysis and then renal
failure
• pulmonary edem
• Neurologic and/or neuropsychiatric
o Patients display memory disturbance (most
common amnesia with amnestic confabulatory states).
o Patients may experience emotional lability,
impaired judgment, and decreased cognitive ability.
o Other signs include stupor, coma, gait disturbance,
movement disorders, and rigidity.
o Patients display hearing and vestibular dysfunction,
blindness, and psychosis.
o Long-term exposures or severe acute exposures
frequently result in long-term neuropsychiatric
sequelae.
o Additionally, some individuals develop delayed
neuropsychiatric symptoms, often after severe
intoxications associated with coma.

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Carbon monoxide poisoning: Acute CO poisoning causes a cherry red

discoloration of the brain and can also cause necrosis of the globus
pallidus, as seen in this slide.

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 Chronic co poisoning:
 Exposure to low levels of CO that occurs more than once and lasts
longer peroid
 Usually involves lower CO levels / lower COHb saturations
(otherwise victims would not survive)
 Exposure usually continues for many days, months, years
 Boundary limit between acute and chronic exposure indistinct

Characteristics:
 Often goes long undetected
 Often many people "sick"
simultaneously
 May go away upon leaving poisoning
site (to work, on vacation, etc.)
 Nearly always misdiagnosed by
physicians
 May involve pets "sick", dead at
same time

Differences from Acute CO

Poisoning:
 May not elicit the typical symptoms of (acute) CO poisoning:
- vomiting
- altered conscious state
- Lactic acidosis
- ataxia
- mucous membranes almost never cherry pink
 COHb is usually not excessively elevated
 More difficult to recognize than acute CO poisoning
 CT and MRI rarely useful, except to rule out stroke, tumor, etc.

Problems in Dealing with Chronic CO Poisoning:

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 Fact of exposure usually recognized only later, the time we call

"discovery"
 Good COHb level measurements usually not obtained
 Residual effects commonly occur, but often subtle; thus usually
unrecognized by untrained physicians.
 Considerable variability of effects from one individual to the next

Delayed neuropsychatric sequelea of co

poisoning:
Neuropsychiatric sequelae of CO poisoning occur in up to 50% of all
patients. Symptoms may arise immediately or follow an asymptomatic
period. Lucid intervals of up to 2-40 days have been observed after CO
poisoning
All patients with suspected CO poisoning may be at risk and should
be treated aggressively—with at least 100% normobaric oxygen or
HBO2 if there is evidence of severe poisoning (metabolic acidosis [pH <
7.1], myocardial ischemia, chest pain, loss of consciousness, or, in
pregnant women.
Neuropsychological deficits
and neuroimaging-confirmed
lesions after CO poisoning are
numerous and diverse; there are
no pathognomonic findings.
However, observed deficits can
be divided into 3 categories:
affective, behavioral (motor), and
cognitive, with most patients
demonstrating abnormalities in
more than 1 area of function.
Up to 30% of patients with CO
poisoning exhibit some degree of
cognitive decline, ranging from
subtle impairments that are only
detectable on neuropsychological
testing to a decline in gross
intellectual function with dementia.
Findings commonly observed include
disorientation and deficits in attention,
concentration, executive function,
verbal fluency, speed of information
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processing, and memory. impairment in attention and concentration

often have profound effects on the ability to learn new tasks.
In a case presented, neuropsychological testing immediately after
CO poisoning was unremarkable, although 3 weeks later, the patient
exhibited marked cognitive changes, decreased verbal expression, and
an inability to care for herself.
Movement disorders are also well documented, particularly delayed-
onset parkinsonian symptoms (including bradykinesia, masked facies,
reduced facial expression, rigidity, and shuffling gait). Urinary and fecal
incontinence is also a common problem in those who have been
severely affected.
Fortunately, the prognosis for recovery from motor symptoms
appears good, with 75% of patients resolving their parkinsonism 1 year
after its onset Although several of the patient's motor patterns may be
also catatonia (e.g., purposeless, repetitive movements with posturing,
waxy flexibility, and a resistance to passive movement).
Affective disturbances after CO poisoning have been described
less often and are difficult to distinguish from premorbid disorders,
particularly in cases of suicide. Personality changes may occur, and
case studies have described prominent depression, anxiety, and
irritability several years after accidental CO poisoning Residual
cognitive deficits, executive dysfunction, and impairments in memory
and concentration may
all contribute to
deterioration in mood.
Conversely, impairment
in attention,
concentration, and
memory may be
symptoms of depression
and may be falsely
attributed to cognitive
decline.

 MRI changes
may remain long after
clinical recovery.
Predicting and
preventing long-term complications and delayed encephalopathy
have been the object of recent studies, many of which focus on the
role of hyperbaric oxygen therapy.

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Differential diagnosis:
Alternative diagnoses list for Carbon monoxide poisoning:

For a diagnosis of Carbon monoxide poisoning, the following list of

conditions have been mentioned in sources as possible alternative
diagnoses to consider during the diagnostic process for Carbon
monoxide poisoning:

• Flu like symptoms ( The most common misdiagnosis)

• Food poisoning

A recent report describes a 12 member family that presented

to the emergency department in groups of 4 persons with symptoms
consistent with food poisoning after drinking unrefrigerated milk.6
However, several other affected members of the same household
had not consumed the same milk. Further investigation revealed
severe CO poisoning which was found to be related to indoor
barbecue grill usage that day.

• Viral infections
• Gastroenteritis
• Chronic fatigue syndrome
• Arrhythmia
• Psychic illness
• Cyanide poisoning
• Opoids
• Alcohol
• Sedative overdose
• Methaemoglobinaemia

o Methemoglobin level - Included in the differential

diagnosis of cyanosis with low oxygen saturation but normal
PaO2

• Migraine

N.B Carbon monoxide has been called a “great mimicker” due to

the presentation of poisoning being diverse and nonspecific.

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Mangenent
Diagnosis
:History and clinical picture .1
Misdiagnosis commonly occurs because of the vagueness and
broad spectrum of complaints and symptoms.

Any of the following should alert suspicion in the winter months

when more than one patient in a group or household presents with
similar complaints or if there is history of potential carbon monoxide
exposure, such as being exposed to a residential fire, may suggest
poisoning with carbon monoxide.

2. Laboratory Studies
Because signs and symptoms of carbon monoxide
poisoning are not specific, a blood test to look for CO is the best way to
.ake the diagnosis m

A) HbCO analysis is done by CO- oximetry:

Pulse CO-oximeters estimate

carboxyhemoglobin with a non-invasive finger
clip similar to a pulse oximeter.

The use of a pulse oximeter is not effective

in the diagnosis of carbon monoxide poisoning as patients suffering
from carbon monoxide poisoning may have a normal oxygen saturation
level on a pulse oximeter .This is due to the
carboxyhemoglobin being misrepresented as
oxyhemoglobin on a pulse oximeter.

o Elevated levels are significant;

however, low levels do not rule out exposure.
o The ratio of carboxyhemoglobin to
hemoglobin molecules in an average person
who may be up to 5%

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o Individuals who chronically smoke may have mildly elevated

CO levels as high as 10%.
o Serious toxicity occurs with the carboxyhemoglobin to
hemoglobin ratio above 25%
B) Arterial blood gas
C) Troponin, creatinine kinase-MB fraction, myoglobin
o Myocardial ischemia frequently is associated with CO
exposure.
o Patients with preexisting disease can experience
increased exertional angina with HbCO levels of just 5-10%.
o At high HbCO levels, even young healthy patients
develop myocardial depression.
D) Creatinine kinase, urine myoglobin:
o Non traumatic rhabdomyolysis can result from severe
CO toxicity and can lead to acute renal failure.
E) Complete blood count
o Look for mild leukocytosis.
F) Electrolytes and glucose level
o Lactic acidosis, hypokalemia, and hyperglycemia with
severe intoxication
G) Liver function tests
H) Urine analysis
o Positive for albumin and glucose in chronic intoxication
I) Methemoglobin level

3. Imaging Studies:
• Chest radiography:
o Obtain a chest radiograph with significant intoxications,
pulmonary symptoms.
o Changes such as perihilar haze and intra-alveolar
edema imply a worse prognosis than normal findings.
• MRI & CT scan:
o Obtain a CT scan of the head with severe intoxication or
change in mental status that does not resolve rapidly.
o Assess cerebral edema and focal lesions.

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o Positive CT scan findings generally predict neurologic

complications.
o MRI is more accurate than CT scans for focal lesions and
white matter demyelination and is often used for follow-up
care.
o Serial CT scans may be necessary, especially with
mental status deterioration.

Unenhanced CT scan of the brain about 16 hours after injury shows

bilaterally symmetrical low attenuation lesions in the cerebellum (blue arrows),
globus pallidus (red arrows)
and caudate nuclei (white arrows).

The patient was in a house fire.

4. Other tests:
• Electrocardiogram:
o Sinus tachycardia is the most common abnormality.
o Arrhythmias may be secondary to hypoxia, ischemia, or
infarction.
• Neuropsychological testing:
o Formal neuropsychological testing of concentration, fine
motor function, and problem solving consistently reveal
subtle deficits in even mildly poisoned patients.
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These test , have been developed as possible means to assess

the risk of delayed neurologic squeal, to assess the need for hyperbaric
oxygen therapy, and to determine the success of hyperbaric therapy in
preventing delayed squeals.

Treatment
A) General measures :
1- Remove patient from the site of CO
exposure at once.
2- Maintain respiratory functions.

3- Consider endotracheal intubation to

facilitate ventilation in comatose
patients.
4- Stabilization of cardio-respiratory
status.
5- Early blood samples may provide much more accurate correlation
between HbCO and clinical status; however, do not delay oxygen
administration to acquire them.
6- Obtain an estimate of exposure time, if possible.

7- Avoid exertion to limit tissue oxygen demand.

B) Oxygen therapy :
* 100%oxygen inhalation is the only antidote for carbon monoxide
poisoning.

* It should be implied as fast as possible.

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* Blood oxygen tension is a

determinant of the rate of
carboxyhemoglobin elimination.

*This therapy should be used until:

a. COHb is below 10 % or
even normal in patients with
cardiovascular or
respiratory disease.
b. Symptoms disappeared.

Aim:
 Elimination of carbon monoxide from the body.

Mechanism:

• Oxygen competitively displaces Oxygen % Half-Life (min.)

CO from hemoglobin. While breathing
room air, this process is too slow it 21 (room air) 240 - 300
takes about 300 minutes. While on a
100% oxygen non-rebreather mask, 80 80 - 100
this time is reduced to about 90
minutes; with hyperbaric oxygen 100 50 - 70
therapy, the time is shortened to 32 100 (at 3
minutes. 20 - 25
atm.)

• CO removal can be speeded up by:

1-Raising the oxygen concentration, as with bottled gas
containing greater fractions of oxygen as Normobaric (100%) Oxygen
Therapy (NBO)
2-Placing the victim in a pressure chamber where he can be
treated with oxygen partial pressures of over 2000 mmHg for 30-120
minutes, as hyperbaric oxygen therapy (HBO).

• This increases the amount of oxygen dissolved in the blood

plasma and forces CO off the hemoglobin, allowing it to carry oxygen
once again.

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Types:

1) Normobaric (100%) Oxygen Therapy (NBO):

• Mask, tight-fitting, high-flow
oxygen (15 liters/min.), non-
rebreather are highly
recommended.
• Loose-fitting masks and Nasal
Prongs are not recommended.

2) Hyperbaric oxygen therapy (HBO):

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• It is breathing 100% oxygen while under increased atmospheric

pressure (3 atm).

• Advantage of HBO over NBO:

1. It reduces the half life of carbon
monoxide to 23 minutes
2. It restores cytochrome
oxidase aa3/C and helps to
prevent lipid peroxidation.
3. It helps in preventing the
delayed neurologic sequelae.
4. It enhances oxygen transport to
the tissues by plasma, partially
bypassing the normal transfer
through hemoglobin.

Indications of HBO:
Patients who are presented with morbidity and mortality risks that
include:

1-Pregnancy

Pregnant females often have a CO level that is 10-15% lower

than the fetus. Fetal Hb not only has a higher affinity for CO but
also has a left-shifted oxygen dissociation curve compared with
adult hemoglobin.
Exposure to CO causes an even farther leftward shift, in both
adult and fetal hemoglobin, and decreased oxygen release from
maternal blood to fetal blood and from fetal blood to fetal tissues.
Pregnant patients with CO-Hb levels greater than 10% should
be treated with HBO.

2- Cardiovascular dysfunction

3- Serious intoxication

4- Altered state of consciousness

5-Neurologic signs

6- Severe acidosis.

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Complications of HBO treatment:

1- Barotraumatic lesions (middle ear) and risk for rupture of the

tympanic membrane

2- Oxygen toxicity

The CNS manifest generalized seizures

3- Ocular effects (myopia, cataract growth).

4- Confinement anxiety

Note: Patients scheduled for HBO therapy need a careful pre-

examination and monitoring.

C) Symptomatic treatment:

1- Increased muscle activity and seizures should be treated with

dantrolene or diazepam

 Diazepam should only be given with appropriate

respiratory support.

2- Hypotension requires treatment with intravenous

fluids.
3- Vasopressors may be required to treat myocardial
depression.
4- Cardiac dysrhythmias are treated with standard
advanced cardiac life support protocols.
5- The delayed development of neuropsychiatric impairment is one of
the most serious complications of carbon monoxide poisoning. Brain
damage is confirmed following MRI or CAT scans.

 Extensive follow up and supportive treatment is often

required for delayed neurological damage.

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6- Unless severe, metabolic acidosis is treated with sodium bicarbonate.

 Treatment with sodium bicarbonate is controversial as
acidosis may increase tissue oxygen availability.
 Treatment of acidosis may only need to consist of oxygen
therapy.
7- Keep patient calm to reduce metabolic rate and oxygen
consumption and avoid physical exertion by the patient; insulate body
and warm, if hypothermic
8- Mangement of cerebral edema by mannitol or steroids.
9- Correct hypo or hyperglycemia.

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This is one suggested "Decision Tree" to diagnosing and managing

Acute CO Poisoning.
Optional: check orientation, phone #, address, date of birth, serial 7's,
digit span, forward & backward spelling of 3 & 4 letter words, and short-
term memory.
Abbreviations: ABG = arterial blood gases, F/U = follow-up, HBO =
hyperbaric oxygen (therapy), Hx = history, Si = signs, Sx = symptoms,
CXR = chest X-ray.

Prognosis
 Outcomes are often difficult to predict
following poisoning, especially patients who have symptoms of
cardiac arrest, coma, metabolic acidosis, or have high
carboxyhemoglobin levels.
o CO-hemoglobin (COHb) level usually does
not correlate well with symptoms or outcome; many patients
with CO-Hgb levels of 25-30% are treated.
o Death can result from severe cases.
o Even with proper treatment, some people develop long-term
brain damage, resulting in complications such as severe
memory loss, difficulty thinking, or other neurologic or
psychiatric problems.
o Others appear to have no long-term problems.

To Avoid Carbon Monoxide Hazards

• Use generators outdoors and away from windows, doors, and
vents.
• Follow manufacturer’s instructions.
• Install carbon monoxide (CO) alarms indoors.
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• Plug appliances directly into generator or use a heavy-duty

outdoor-rated extension cord.
• Connect generator to building wiring only by a qualified
electrician or utility company.

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 Toxic Gases

Chlorine Gas

#What is chlorine gas?

 Chlorine gas comes from chlorine, a common chemical used in
factories, labs, and in some household products. When liquid
chlorine mixes with air, it turns into
chlorine gas.

 Chlorine gas is a pulmonary irritant

with intermediate water solubility that
causes acute damage in the upper and
lower respiratory tract.

 Chlorine gas was first used as a

chemical weapon

#What does chlorine gas look like?

 It is yellow-green and has a strong smell, like bleach
 The density of the gas is greater than that of air, causing it to
remain near ground level and increasing exposure time.

#Methods of exposure
Inhalation is the main route of exposure to chlorine gas

♦ Chlorine gas is one of the most

common single, irritant, inhalation
exposures, occupationally and
environmentally.

• Possible sources of exposure

are :

 Industrial bleaching
operations
 Sewage treatment

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 Household accidents involving the inappropriate mixing

of hypochlorite cleaning solutions with acidic agents
 Transportation releases
 Swimming pool chlorination tablet accidents
 Storage tank failure
 Chemical warfare
• Large amounts of chlorine are produced in the industrial sector
• Toxic effects after inhalation exposure usually are mild to
moderate, and death is uncommon.

#Toxicokinetics
• Absorbed almost exclusively by inhalation
• Penetrates readily to alveolar
• Not systemically absorbed

Carbon monoxide Chlorine

Lighter than air Heavier than air

clear Yellow green & cloudy

Non irritant irritant

#Pathophysiology

• The intermediate water solubility of chlorine accounts for its effect

on the upper airway and the lower respiratory tract. Exposure to
chlorine gas may be prolonged because its moderate water
solubility may not cause upper airway symptoms for several
minutes.

• The odor threshold for chlorine is approximately 0.3-0.5 parts per

million (ppm); however, distinguishing toxic air levels from

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 Toxic Gases

permissible air levels may be difficult until irritative symptoms are

present.

#Mechanism of activity

• Chlorine is moderately soluble in water and reacts in combination to

form hypochlorous (HOCl) and hydrochloric (HCl) acids. Elemental
chlorine and its derivatives, hydrochloric and hypochlorous acids,
may cause biological injury. The chemical reactions of chlorine
combining with water and the subsequent derivative reactions with
HOCl and HCl are as follows:

• Cellular injury is believed to result from :

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 Toxic Gases

1. The oxidation of functional groups in cell components, from

reactions with tissue water to form hypochlorous and
hydrochloric acid,
2. The generation of free oxygen radicals.chlorine causes direct
tissue damage by generating free oxygen radicals

• Early response to chlorine gas depends on the

1) Concentration of chlorine gas.

2) Duration of exposure.
3) Water content of the tissues exposed.
4) Individual susceptibility.

#Pathologic findings
Pathologic findings are nonspecific.They include effect on

• Respiratory system:
• Acute inflammation of the nose, pharynx, larynx, trachea, and
bronchi.

• Severe pulmonary edema,

pneumonia, hyaline membrane
formation, multiple pulmonary
thromboses, and ulcerative
tracheobronchitis.

• Noncardiogenic pulmonary
edema is thought to occur when

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 Toxic Gases

there is a loss of pulmonary capillary integrity,Plasma exudation

results in filling the alveoli with edema fluid.

• Persistent hypoxemia is associated with a higher mortality rate.

• The hallmark of pulmonary injury associated with chlorine toxicity

is pulmonary edema, manifested as hypoxia

• Eye:
• The eye seldom is damaged severely by chlorine gas toxicity;

• Acute inflammation of the conjunctivae,burns and corneal

abrasions have occurred
•Acids formed by the chlorine gas
reaction with the conjunctival mucous
membranes are buffered, in part, by the
tear film and the proteins present in tears.
Acid burns to the eye typically cause
epithelial and basement membrane
damage but rarely damage deep
endothelial cells.

• Acid burns to the periphery of the

cornea and conjunctiva often heal
uneventfully,while burns to the center of the cornea may lead to
corneal ulcer formation and subsequent scarring

#To summarized::

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#Clinical picture:
• History:
• Cough (52-80%)
• Shortness of breath (20-51%)
• Chest pain (33%)
• Burning sensation in the throat and
substernal area (14%)
• Nausea or vomiting (8%)
• Ocular and nasal irritation (4-6%)
• Choking

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 Toxic Gases

• Muscle weakness
• Dizziness
• Abdominal discomfort
• Headache
• Physical:
•Decreased breath sounds
•Tachypnea
•Tachycardia
•Wheezing
•Nasal flaring
•Cyanosis
•Rhinorrhea
•Lacrimation
•Hoarseness of the voice or stridor
•acute respiratory distress syndrome
&noncardiogenic pulmonary edema

#Frequency:
• United States
Chlorine gas is one of the most common single, irritant, inhalation exposures,
occupationally and environmentally

• International
Internationally, chlorine gas accounts for the largest single cause of major toxic
release incidents. Use of chlorine internationally is parallel to use by the US in
chemical, paper, and textile industries and in sewage treatment.

Diagnosis
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• Laboratory Studies
• Arterial blood gas
o Abnormalities include hypoxia and metabolic acidosis.
o The metabolic acidosis may be hyperchloremic
(nonanion gap).
o A postulated mechanism for the production of this
acidosis is the absorption of hydrochloric acid following the
reaction of chlorine gas with water.
• Imaging Studies
• Chest x-ray (CXR) findings often are normal, but a CXR may
be indicated to rule out pulmonary edema, pneumonitis, and
ARDS.
• Ventilation perfusion scan
o Abnormal retention of radiolabeled xenon gas at 90
seconds suggests lower airway injury.
o Ventilation perfusion scans have been used to
determine lung damage in smoke inhalation.

• Other Tests
• PEFRs may reveal obstructive airway disease and response to
therapy.
• Monitor oxygen saturation.
• Obtain an electrocardiogram (ECG).
• Pulmonary function tests may indicate obstructive or
restrictive patterns.

Treatment
• Prehospital Care
Prehospital care with full face mask should protect against the effects
of chlorine gas. However, in the setting where providers should take
necessary precautions to prevent contamination. higher levels of
protection should be considered.

• Remove the individual from the toxic environment.

• Bring container, if applicable, so medical personnel can
identify toxic agent.
• Commence primary decontamination of the eye and skin, if
necessary.

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• Real-time measurement of chlorine gas, both quantitative

and qualitative, is possible through the use of mobile equipment.

Chlorine gas is denser than air and accumulates close to the

ground. Therefore, during chlorine-related accidents, people should
be instructed to seek higher altitudes to avoid excessive exposure.
Emergency Department Care
• Care of respiration
• Supplemental oxygen
o Maintain a PaO2 of 60 mm Hg or greater.
o Long-term (>24 h) elevated fraction of inspired oxygen
(FIO2) greater than 50% may result in oxygen toxicity.
• Decontamination
o Eye and skin exposures require copious irrigation with
saline.
o In cases of suspected ocular injury, determine initial pH
using a reagent strip. Continue irrigation with 0.9% saline
until the pH returns to 7.4.
o Topical anesthetics help limit pain and improve patient
cooperation.
o Following irrigation, perform slit lamp examination,
including fluorescein staining.
o Measure ocular pressures.
o Treat corneal abrasions with antibiotic ointment.
• Fluid restriction in patients with ARDS
• Treatment of bronchospasm
o Bronchodilators (inhaled albuterol or other beta-agonists
as terbutaline.)
o The role of inhaled ipratropium is not well defined.
o Lidocaine (1% solution) added to nebulized albuterol
results in both analgesic and cough-suppressant actions.
• Intubation for laryngospasm
o Fiberoptic aid may be required if significant edema is
present.
o Consider using the largest size endotracheal tube
possible to optimize pulmonary toilet.
• Hypoxemic respiratory failure
o Treat with positive-pressure ventilation.
o High positive end-expiratory pressure (PEEP) and
inverse ratio ventilation may be beneficial in ARDS.
o In an animal model, prone positioning immediately
following exposure to chlorine gas improved pulmonary
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 Toxic Gases

function, whereas treatment in the supine position was

associated with further compromise of pulmonary gas
exchange.
• Sodium bicarbonate
o The mechanism of action is thought to be through the neutralizing
of the hydrochloric acid formed when chlorine gas comes into
contact with water. Lack of clinical trials and the theoretical
possibility that an exothermic reaction may be produced when
bicarbonate mixes with hydrochloric acid have led some authors to
question its use. Nonetheless, several pediatric and adult case
reports did describe a clinical improvement in patients with
chlorine gas induced pulmonary injury who are treated with
inhaled sodium bicarbonate.
o
• Steroids
o Parenteral steroids, while advocated by some authors to
prevent short-term reactions and long-term sequelae, are not
recommended by others because of insufficient clinical trials.
• Animal studies suggest improvements in pulmonary function
and lung compliance with treatment of inhaled steroids,
• Prophylactic antibiotics are not recommended.
• Medications
Bronchodilators (albuterol(proventil-ventolin))

Beta-agonists, although not well studied in humans, have been widely

used for the management of respiratory symptoms in chlorine gas
exposure. They should be considered a first-line agent in the setting of
chlorine gas exposure and respiratory symptoms or signs.
Bronchodilatation through respiratory smooth muscle relaxation
improves the respiratory status of the person who is exposed to
chlorine gas.
Inhaled corticosteroids(budesonide(pulmicort-rhinocort)
Anti-inflammatory inhaled corticosteroids to improve respiratory
function following experimental chlorine gas exposure. Exact
mechanism of function in chlorine gas exposure unclear.
Aerosolized sodium bicarbonate
When inhaled, these agents may neutralize (if administered early) or
counteract the effects of inhaled chlorine.

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• Further Inpatient Care

• Consider hospitalization to observe and treat the patient with
chlorine gas exposure in a highly monitored setting in any of the
following cases:
o Symptoms persist after 6 hours.
o Patient was severely exposed.
o Child was exposed.
o Patient has a history of underlying respiratory or
cardiovascular disease.
• Some authors suggest observation for a minimum of 24 hours
because pulmonary edema may occur for 24 hours after exposure.
Pulmonary edema occasionally may induce severe hypoxemia in
minutes.
• Patients who are asymptomatic 24 hours after exposure may
be discharged from hospital.
• For a severe reaction, follow up with a pulmonologist.
• Further Outpatient Care
• No hospitalization is required for mild chlorine exposure or for
patients who remain asymptomatic.

Deterrence/Prevention
• Deterrence may decrease the number of accidental
exposures to chlorine gas.
• Proper descriptions on swimming pool chlorinator solutions
with detailed warnings to avoid mixing solutions would prevent a
great number of accidents.
• As accidental occupational exposures to chlorine gas
comprise a significant percentage of severe exposures, proper
methods of training and supervision are beneficial. Proper
enforcement of regulations covering these work situations should
be helpful.

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Complications
• Short-term effects of acute exposures of chlorine gas
o pneumonitis, often complicated by secondary bacterial
invasion.
o Smokers and those with asthma are most likely to
demonstrate persistence of obstructive pulmonary defects.
• Within 3-5 days, after the sloughing off of the mucosa, oozing
areas become covered with mucopurulent exudate. This can result
in chemical of chlorine gas
o Decreased lung function tests
o some patients displayed eventual repair of injured
pulmonary epithelium with fibrosis. Bronchiolitis obliterans
and emphysema have been described in patients following
acute exposures.
• Reactive airway dysfunction syndrome (RADS), or irritant-
induced asthma, is a variant of occupational asthma that occurs in
individuals who are acutely exposed to high concentrations of an
irritant product and develop respiratory symptoms in the minutes
or hours that follow. They develop persistent bronchial
hyperresponsiveness after the inhalational incident. A similar
pathology may occur with repeated exposures.

Prognosis
• Resolution of pulmonary abnormalities in most individuals
occurs over the course of one week to one month following
exposure.

Special Concerns
• The following populations are at higher risk of severe reaction
and progression to respiratory failure than other populations.
o Children and elderly individuals
o Those with underlying respiratory or cardiovascular
disease
o Smokers

Chronic Exposure
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• Chronic exposure to chlorine, usually in the workplace, may cause

corrosion of the teeth. Multiple exposures to chlorine have
produced flu-like symptoms and a high risk of developing reactive
airways dysfunction syndrome (RADS)

Carcinogenicity

• Chlorine has not been classified for carcinogenic effects. However,

the association of cigarette smoking and chlorine fumes may
increase the risk of cancer

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